Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
Anil K Tripathi
MD FICP FIACM FISHTM
Professor of Medicine and Head, Hemato-oncology Unit
Nodal Officer (AIDS Care)
Department of Medicine
CSM Medical University
(formerly King George’s Medical University)
Lucknow, Uttar Pradesh, India
(tripathiak2005@hotmail.com)
Kamal K Sawlani
MD
Professor and Head
Department of Medicine
UP Dental College and Research Centre
Lucknow, Uttar Pradesh, India
(kksawlani@rediffmail.com)
Offices in India
• Ahmedabad, Phone: Rel: +91-79-32988717, e-mail: ahmedabad@jaypeebrothers.com
• Bengaluru, Phone: Rel: +91-80-32714073, e-mail: bangalore@jaypeebrothers.com
• Chennai, Phone: Rel: +91-44-32972089, e-mail: chennai@jaypeebrothers.com
• Hyderabad, Phone: Rel:+91-40-32940929, e-mail: hyderabad@jaypeebrothers.com
• Kochi, Phone: +91-484-2395740, e-mail: kochi@jaypeebrothers.com
• Kolkata, Phone: +91-33-22276415, e-mail: kolkata@jaypeebrothers.com
• Lucknow, Phone: +91-522-3040554, e-mail: lucknow@jaypeebrothers.com
• Mumbai, Phone: Rel: +91-22-32926896, e-mail: mumbai@jaypeebrothers.com
• Nagpur, Phone: Rel: +91-712-3245220, e-mail: nagpur@jaypeebrothers.com
Overseas Offices
• North America Office, USA, Ph: 001-636-6279734, e-mail: jaypee@jaypeebrothers.com,
anjulav@jaypeebrothers.com
• Central America Office, Panama City, Panama, Ph: 001-507-317-0160, e-mail: cservice@jphmedical.com
Website: www.jphmedical.com
• Europe Office, UK, Ph: +44 (0) 2031708910, e-mail: info@jpmedpub.com
All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted in any form or by
any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the authors and
the publisher.
This book has been published in good faith that the material provided by authors is original. Every effort is made to ensure
accuracy of material, but the publisher, printer and authors will not be held responsible for any inadvertent error (s). In case of
any dispute, all legal matters are to be settled under Delhi jurisdiction only.
It is a matter of immense pleasure and gratification that we are bringing the second edition of the book Essentials of
Medicine for Dental Students. The book has received tremendous response all over the country. We have received
compliments as well as valuable suggestions. We are thankful to readers and all those who have sent their views.
We have tried to adhere to the latest curriculum prescribed by Dental Council of India. For ready reference, recent
curriculum of General Medicine as prescribed by Dental Council of India has been added in the book. Accordingly, we
have included some new topics or added more details such as halitosis, dysphagia, infectious mononucleosis, herpes,
acute respiratory distress syndrome, pneumothorax, lung cancer, interstitial lung disease, shock, cardiac arrest,
cardiorespiratory resuscitation, arrhythmias, Addison’s disease, etc. In particular, a chapter on “Medical Emergencies in
Dental Practice” has been specially added keeping in view of ever-growing need for dental surgeons to learn and practice
emergency medicine.
There was feedback from the students that the text in some of the chapters was too concised to comprehend and
remember. Hence, in this edition, we have reframed the language of the text, which has now become comfortable and
easy to retain. The running text has also been written in point-wise fashion. More figures and tables have been added for
better illustration of the subject.
The medical science is ever evolving. Newer understanding of the diseases, newer diagnostics and drugs need to be
included in the book to enable us to provide state-of-the art treatment. Hence, we have modified definitions, classifications
and treatment protocols in order to include recent advancements in the subject.
We sincerely hope that the present edition of the book will be even more useful for the students as well as practicing
dental surgeons. We look forward to receiving valuable views, comments and suggestions from our esteemed readers.
Anil K Tripathi
(tripathiak2005@hotmail.com)
Kamal K Sawlani
(kksawlani@rediffmail.com)
PREFACE TO THE FIRST EDITION
PREFA
Over the years, a customized and concise textbook of General Medicine for dental students and dental practitioners has
been much awaited. Students need a textbook that is easily readable, concise and in accordance with the prescribed
curriculum.
The primary objective of this book is to provide basic and practical information on the pertinent topics that will enable
the reader to understand and improve his/her diagnostic and therapeutic skills. Special attempt has been made to make the
book succinct without compromising on the required details.
The chapters are chosen according to the Dental Council of India guidelines. However, additional chapters on other
important subjects such as HIV/AIDS, malaria, stroke, pleural diseases have also been included. Emphasis has been
given on the clinical methods including history taking and physical examination which are described in the beginning of
each system. This will make a wholesome reading without much need to go for other books on clinical methods.
Each chapter contains relevant “Multiple choice questions” and “Fill in the blanks” to help the reader self-assess their
knowledge. In addition to them, a “Model test paper” is also provided at the end of the book which will enable the readers
to prepare for the competitive entrance tests.
The essence of learning General Medicine by dental students is in applying the concept and knowledge while they
deal with patients suffering from various medical disorders. In such endeavor, each chapter is followed by a section
“Implications on dental practice” which describes how the presence of medical disorders affects the management decisions.
While the book is intended primarily for dental undergraduate and postgraduate students, this should also be useful
for medical students and practitioners.
Although every attempt has been made to avoid any error or controversy, shortcomings are inevitable. Readers are
requested to offer their valuable comments and suggestions that will be of great help in improving the next edition.
AK Tripathi
KK Sawlani
ACKNOWLEDGMENTS
We are immensely thankful to Prof Saroj Chooramani Gopal, Vice Chancellor, CSM Medical University, Lucknow for
her constant guidance and blessings. We are indebted to Prof CG Agarwal, Ex-Head of the Department of Medicine,
KG’s Medical University who inspired us to write this book. We are highly grateful to Prof KCS Sanger for his scholarly
contribution and valuable suggestions. We are also thankful to Prof R Pradhan, Ex-Principal, UPDC & RC, Lucknow for
his valuable guidance. We extend our special thanks to Dr Sandeep Saxena and Dr PK Srivastava for their encouraging
support. We are indebted to Dr Satish Chandra, Dr Pawan Kumar, and Dr Sukanto K Das, residents in the Department of
Medicine, CSMMU, Lucknow for their help in reading the manuscript and providing photographs.
Our special thanks to Dr BD Agarwal, Professor of Medicine, Rama Dental College, Kanpur, Dr SP Verma, Lecturer
in Medicine, CSM Medical University, Lucknow, Dr Nitu Gupta, SMO, ART Center, CSM Medical University, Lucknow
and Dr Neeta Mishra, Associate Professor, Department of Oral Medicine and Radiology, UP Dental College and Research
Center, Lucknow for their support and contributions to the second edition of the book.
We owe to our family members for their constant support and encouragement without which the task could never have
been possible.
We are also indebted to our teachers and students who have been constant source of inspiration and learning. We
acknowledge the contributions of various experts and readers who provided us with their valuable comments and
suggestions.
Finally, we thank and highly appreciate the efforts of M/s Jaypee Brothers Medical Publishers (P) Ltd., New Delhi for
excellent and outstanding quality of the book.
CONTENTS
Clinical Methods 1 o
o
Hemolytic Anemia
Anemia of Acute Blood Loss
56
58
o History 1
CHAPTER 1
o Physical Examination 2
o Leukemia 58
o Definitions 13
o Multiple Myeloma 64
o Self Assessment 13
o Normal Hemostasis 64
o Platelet Disorders 67
Gastrointestinal and o
o
Von Willebrand’s Disease
Coagulation Disorders
69
69
Hepatobiliary System 15 o Splenomegaly 73
o Symptoms and Signs of Gastrointestinal o Lymphadenopathy 74
CHAPTER 2
Gastritis 22
Diseases 78
o Peptic Ulcer 23
o Diarrhea, Dysentery and Food Poisoning 25
o Cardiac Examination 81
o Malabsorption 28
o Investigations 82
o Liver: Structure and Function 30
o Acute Rheumatic Fever 83
o Jaundice 32
o Rheumatic Valvular Heart Disease 84
o Acute Hepatitis 35
o Aortic Stenosis (AS) 87
o Acute Viral Hepatitis 35
o Aortic Regurgitation (AR) 88
o Chronic Hepatitis 39
o Infective Endocarditis 89
o Cirrhosis of Liver 40
o Hypertension 92
o Portal Hypertension 42
o Ischemic Heart Disease/Coronary Artery
Disease 96
o Upper Gastrointestinal Bleeding 43
o Hepatic Encephalopathy 43
o Stable Angina 97
o Ascites 44
o Unstable Angina 99
o Hepatomegaly 46
o Acute Myocardial Infarction or STEMI 100
o Implications on Dental Practice 47
o Heart Failure 103
o Self Assessment 47
o Acute Pulmonary Edema (cardiogenic) 107
o Congenital Heart Disease 108
Hematological System 50 o Syncope 110
o Anemia 50 o Arrhythmia 112
CHAPTER 3
o Examination 122
o o Thyroid Disorders 188
CHAPTER 8
Investigations 125
o Pneumonia 126
o Calcium Metabolism 193
o Lung Abscess 128
o Parathyroid Disorders 195
o Bronchiectasis 129
o Pituitary Gland 196
o Bronchial Asthma 130
o Implications on Dental Practice 208
o Chronic Obstructive Pulmonary
o Self Assessment 209
o
Disease (COPD)
Pulmonary Eosinophilia
134
136
Infections 211
o Measles (Rubeola) 211
o
CHAPTER 9
Pulmonary Embolism 137
o Mumps 212
o Tuberculosis 139
o Rubella (German Measles) 213
o Respiratory Failure 144
o Chickenpox (Varicella) and Herpes
o Pleural Diseases 145
Zoster (Shingles) 214
o Pneumothorax 146
o Herpes Simplex 216
o Interstitial Lung Disease 147
o Infectious Mononucleosis 218
o Lung Cancers (Bronchogenic Carcinoma) 148
o Diphtheria 220
o Implications on Dental Practice 150
o Enteric Fever (Typhoid Fever) 221
o Self Assessment 151
o Gonorrhea 223
Renal Diseases 153 o
x
Syphilis 224
Malaria 228
o Investigations in Renal Disorders 154
o Nephrotic Syndrome 154
o Human Immunodeficiency Syndrome/
Acquired Immunodeficiency
o Nephritic Syndrome 156
Syndrome (HIV/AIDS) 231
o Acute Renal Failure (ARF) 158
o Chronic Renal Failure (CRF) 159
o Implications on Dental Practice 238
Contents
Anaphylaxis 245
o Hypoglycemia 245
o Diet and Nutrition 262
CHAPTER 13
o Adrenal Crisis 245 o Protein Energy Malnutrition (PEM) 263
o Excessive Bleeding 246
o Vitamins 264
o Dental Procedures in Pregnant Women 246
o Implications on Dental Practice 269
o Excessive Bleeding 245 o Self Assessment 270
o Dental Procedures in Pregnant Women 245
CHAPTER 14
o Acute Respiratory Distress Syndrome o Pulmonary Evaluation 271
(ARDS) 252 o Hematological Evaluation 271
o Cardiovascular Collapse 253 o Endocrinal Evaluation 271
o Cardiac Arrest 253 o Nutritional Evaluation 272
o Cardiopulmonary Resuscitation 253 o Evaluation of Other Organs 272
o Preoperative Laboratory Evaluation 272
Anaphylaxis and
Drug Allergy 256 Test Paper
Reference Laboratory Values
273
281
o Anaphylaxis 256
CHAPTER 12
Answers 285
o Drug Allergy 259 Index 289
o
xi
Implications on Dental Practice 260
o Self Assessment 260
THEOR
THEORYY SYLL ABUS
SYLLABUS
Clinical methods form the basis of the approach to a patient Presenting Complaints
by which a proper diagnosis is achieved. The skill of a This is also known as chief complaints. The patient is asked
clinician depends on his knowledge of theoretical as well about the main problems for which he has come to the doctor.
as practical aspects of the clinical methods. This skill is These main symptoms/problems are listed in a chronological
acquired and refined with experience. order (noted in the order of their appearance). Generally
the patient is allowed to tell by himself. Leading questions
HISTORY are avoided. The list should not be too long.
History is the physician’s abstraction of certain facts
developed in the course of the patient’s interview and History of Present Illness
arranged in a manner that facilitates diagnosis. The patient is then asked to narrate individual symptoms in
Proper history is important for making a correct details. Once this is over with, leading questions are asked
diagnosis. A careful evaluation by competent clinicians to clarify certain points or associations related to different
reveals that 82% of diagnoses are made by history, 9% by symptoms. For example, if the patient is complaining of
physical examination and 9% by the laboratory tests. A pain, details should be recorded about the site, severity,
history is not simply a collection of facts. It must also contain character, radiation, duration and timing, relieving and
information. Facts are the true statements made by the patient aggravating factors.
while information consists of facts arranged in useful a. Site: The exact site of pain is noted. Whether it is
manner. A general format is followed while taking a history localized or diffuse pain.
of the patient. The contents of history are recorded in the b. Severity: Does the pain interfere with routine daily
patient’s version and no part in the history should be distorted activities or keep the patient awake at night? Is the patient
or omitted. However, the focus and contents may vary from in severe agony or is he shouting?
patient to patient and also with the experience of the c. Character: Description of character of pain such as
clinician. burning, stabbing, pricking, colicky, and dull ache are
The standard format used for history taking is as follows; helpful. Colicky pain is the waxing and waning type of
1. Patient’s details (name, age, sex, marital status, occupation, pain and may cause the patient to roll about. Colicky
address) pain suggests obstruction of hollow structure like
2. Presenting complaints with duration intestine, ureter or common bile duct.
3. History of present illness d. Timing and duration: When does it start and when does
4. History of past illnesses it stop?
5. Treatment history e. Relieving factors and aggravating factors: Cardiac pain
6. Personal history occurs on exertion and is relieved by rest and nitrates.
7. Family history Pain of duodenal ulcer is relieved by eating.
8. Menstrual history (in females) Musculoskeletal pain may be relieved by change in the
posture and by simple analgesics. Anginal pain is Treatment History
relieved by sublingual nitrates. The details of medications taken are noted. History of any
The typical anginal (ischemic) pain is described in adverse effects of drugs is also asked. It is imperative to
Table 1.1. know what drugs the patient is taking currently so that drug
Symptoms pertaining to different systems are asked. interactions may be avoided. The history of intake of certain
Important symptoms regarding disorders of various systems drugs may help in knowing the cause of disease. For
are given in Table 1.2. example, steroids and NSAIDs can cause gastric erosion
and hematemesis.
History of Past Illness It is noted whether the patient has been compliant or
A detailed account is noted about any illness which occurred not. If not, the reason for the drug non-compliance is
in the past. A disease or symptom which has occurred in the discussed.
past could be a part of the present disease process or related
to the present problem. Personal History
For example, a patient with liver cirrhosis may give a The patient is asked about the consumption of alcohol,
history of jaundice or blood transfusion. tobacco, or smoking. His occupation should also be noted.
Certain occupations are associated with a higher incidence
TABLE 1.1: Characteristics of chest pain in stable angina
of a particular disease, e.g. persons working in a silica factory
Site of the pain Retrosternal or precordial are prone to develop silicosis. A history of stress at home
Character Squeezing, constricting, piercing, feeling of and office should also be recorded. Financial status of the
heaviness or pressure
Precipitating factors Physical exertion, cold exposure, heavy patient is also an important fact to be noted in the history.
meals, emotional stress, anemia, thyroid
2 Associated features
disease, vivid dreams (nocturnal angina)
Feeling of impending death, breathlessness,
apprehension, nausea, vomiting
Family History
Any history of genetic disorders in the family is enquired
Relieving factors Rest, sublingual nitroglycerin about. Any history of similar illness in other family members
Radiation Left shoulder, both arms, jaw, neck and cause of death of immediate relative should be recorded.
Duration Typically 2-10 minutes (>30 minutes History of hypertension, diabetes mellitus, tuberculosis,
suggests infarction)
cardiovascular diseases, and bleeding diastheses in other
family members should be noted.
Essentials of Medicine for Dental Students
3
History taking and simple observations can assess the intake suggests diabetes mellitus, thyrotoxicosis or
mental, emotional status and intelligence of the patient. State malabsorption.
of consciousness is noted. • Weight gain may occur due to hypothyroidism or fluid
• In a confusional state, the patient is subdued, drowsy retention.
and physically inactive. He is also disoriented about time, The most widely used method to measure obesity is body
place and person. mass index (BMI). BMI is calculated as weight in kg divided
• Delerium is a confusional state accompanied by by the square of height in meters (kg/m2). BMI upto 25 is
agitation, hallucination and illusion. These always normal, 25-29.9 is overweight and above 30 is obesity.
indicate disease of the nervous system. Abdominal obesity (increased waist-hip ratio: >0.9 in
TABLE 1.3: Points for general physical examination females, >1.0 in males) is an important risk factor for
• Mental and emotional state
coronary artery disease.
• Built of the body
• Temperature Temperature
• Pulse
Temperature is measured with a thermometer. Thermometer
• Blood pressure
• Respiration is placed in the mouth or in the axilla in adults while it is
• Anemia placed in the fold of the groin with thigh flexed or in the
• Jaundice rectum in case of small children.
• Cyanosis
• Oral cavity and throat
• Mouth temperature is 0.5C° higher than that of groin or
• Neck veins axilla. Rectal temperature is about 0.4°C (0.7°F) higher
• Thyroid than mouth temperature.
• Lymphadenopathy
• The evening (pm) temperature may be up to 0.5°C or
• Clubbing
• Peripheral edema 0.9°F higher than the morning (am) temperature in
• Skin and mucous membrane normal persons.
• The maximum normal is 37.2°C (98.9°F) at 6 am and
37.7°C (99.9°F) at 4 pm.
• A fever of more than 41.5°C (106.7°F) is known as
hyperpyrexia. A temperature less than 35°C (95°F) is
called hypothermia.
The fever may be continued, remittent or intermittent.
These classical patterns of fever are less commonly seen
due to early initiation of treatment with antipyretics and
antibiotics.
a. Fever which at no time touches the normal and does not
fluctuate more than 1°C during 24 hours is called
continued fever.
b. When the daily fluctuation in the temperature is more
than 2°C, the fever is of the remittent type. FIGURE 1.1: Palpation of the radial artery; the forearm of the
c. Fever which occurs only for several hours during 24 patient is in semiprone position with wrist semiflexed
hours is called intermittent fever. Intermittent fever can
be quotidian (occurs daily), tertian (occurs on alternate
days) or quartan (occurs every third day). Infection with
P. falciparum causes intermittent quotidian fever, P. vivax
and P. ovale cause tertian fever and P. malariae causes
quartan fever.
4 Pulse
Arterial pulse should be examined mainly for following
things:
a. Rate
b. Rhythm
c. Volume
Essentials of Medicine for Dental Students
d. Character
e. Radio-femoral delay
The rate and rhythm are assessed by palpating the radial FIGURE 1.2: Palpation of the left carotid artery with
artery (Fig. 1.1). The character of the pulse is better assessed the right thumb
by palpating the carotid artery (Fig. 1.2). Other peripheral
arteries like brachial, popliteal, posterior tibial and dorsalis roidism and drugs (beta blockers, verapamil, digoxin).
paedis can also be palpated. The pulse may be absent or Bradycardia may also be present in athletes.
weak in obstruction in the proximal part of the artery due to • Tachycardia (pulse rate >100/min) occurs due to fever,
thromboembolism and atherosclerosis. exercise, anxiety, thyrotoxicosis, anemia, tachyarrhythmias,
shock and drugs.
Rate: The pulse rate is determined by counting it for at least
• Pulse is slower than would be expected from the height
30 seconds. The normal pulse rate varies from 60-100 per
of fever in typhoid fever (relative bradycardia).
minute.
• Bradycardia is defined as pulse rate <60/min. Important Rhythm: Normally the rhythm of the pulse is regular. An
causes are raised intra-cranial pressure, heart blocks irregular rhythm is seen in atrial fibrillation (irregularly
and sinus node disease, cholestatic jaundice, hypothy- irregular) and frequent ectopic beats (regularly irregular).
Clinical Methods
Character: Initially the assessment of systolic BP is made by
• A low volume and slow rising pulse (parvus et tardus) palpatory method. The radial or brachial artery is palpated
is found in aortic stenosis (AS). while the cuff is inflated to raise pressure about 30 mm Hg
• A large bounding pulse (hyperkinetic pulse) is seen in above the level at which radial/brachial pulse disappears
hyperkinetic states (anemia, fever, anxiety, exercise), The stethoscope is placed over the brachial artery and cuff
patent ductus arteriosus, ventricular septal defect, and is deflated slowly (Figs 1.3A and B). The level at which
aortic regurgitation (AR). Korotkoff sounds appear (phase 1) is the systolic pressure
• Bisferiens pulse which has two systolic peaks is found and the level at which they disappear completely (phase 5)
in mixed lesion of AS and AR. is the diastolic pressure. When the pulse pressure (the
• Alternating strong and weak pulse (pulsus alternans) is difference between systolic and diastolic blood pressure)
present in severe left ventricular failure. is increased as in cases with hyperdynamic circulation
• Normally there is a fall in systolic arterial pressure of (aortic regurgitation, pregnancy, thyrotoxicosis, anemia,
<10 mmHg during inspiration. An accentuation in this arteriovenous fistula) the sounds may not disappear
phenomenon can lead to weakening or disappearance
of pulse during inspiration (paradoxical pulse). This is
found in cardiac tamponade and obstructive airway
disease.
Radio-femoral delay: The femoral pulse is weak and delayed
as compared with the radial pulse (radio-femoral delay) in
coarctation of aorta.
6
• Jugular veins are distended and pulsatile in congestive The “a” wave is absent in atrial fibrillation while it is
heart failure and pericardial effusion. Neck veins are prominent in tricuspid stenosis (TS). Prominent “Y” descent
also distended in cases of mediastinal tumors and is seen in tricuspid regurgitation.
retrosternal goiter but these are not pulsatile.
• Normally there is fall in the jugular venous pressure Respiration
(JVP) during inspiration. There may be a paradoxical Normal rate of respiration is 12-16 per minute in adults.
rise in the JVP during inspiration in constrictive The causes of fast breathing (tachypnea) are given in
Essentials of Medicine for Dental Students
pericarditis and cardiac tamponade (Kussmaul’s sign ). Table 1.5. Dyspnea is an abnormally uncomfortable
The venous pulse has three positive waves, a, c, and v, awareness of breathing. This could be due to respiratory
and two negative waves or descents, x and y. The a wave is diseases, cardiac diseases, anemia, acidosis, and
due to atrial contraction. This is followed by x descent (due psychogenic. Dyspnea, orthopnea and paroxysmal nocturnal
to descent of tricuspid valve ring) which is interrupted by a dyspnea are described in detail in Chapters 4 and 5.
small c wave. The v wave is due to passive filling of blood • Noisy breathing may occur due to obstruction of the
from veins into the right atrium during ventricular systole. respiratory passages at various levels. Obstruction at the
TABLE 1.4: Classification of blood pressure for adults level of larynx and trachea causes inspiratory stridor and
(>18 yrs) obstruction in bronchi and bronchioles produces
Category Systolic blood Diastolic blood wheezing.
pressure (mmHg) pressure (mmHg) • Rapid and deep respiration (Kussmaul’s breathing) is
Normal <120 <80 present in metabolic acidosis while rapid shallow
Prehypertension 120-139 80-89
Hypertension
breathing is a feature of restrictive lung disease.
Stage 1 140-159 90-99 • Cheyne-Stokes respiration is characterized by cyclical
Stage 2 >160 >100 waxing and waning of rate and depth of respiration
TABLE 1.5: Causes of tachypnea
Clinical Methods
• Recent exertion
• Anxiety
• Fever
• Metabolic acidosis
• Hysterical over-breathing
• Pulmonary and cardiac conditions causing hypoxia
• Cerebral disturbance
Pallor
• The presence of pallor depends on the thickness and
quality of the skin, amount of blood in the capillaries
and quality of the blood in the capillaries.
• The evidence of pallor is looked at palpebral conjunctiva
and mucous membrane of the mouth (Fig. 1.5). Other
sites are nailbed and palmar creases (Fig. 1.6).
• Generalized pallor is present in anemia. Pallor can also
be found in hypopituitarism, thick or opaque skin, and
diminished capillary blood flow as in shock, syncope,
left heart failure.
7
Jaundice
A
A yellowish discoloration of the skin and mucous membrane
due to deposition of bilirubin is known as jaundice (icterus).
The deposition of bilirubin in tissues occurs when the serum
bilirubin level is raised (hyperbilirubinemia). Sclerae have
a high affinity for bilirubin due to their rich elastin content.
• The normal total serum bilirubin level is 0.3-1.0 mg/dL.
Jaundice is clinically apparent in sclera when the
bilirubin level is raised above 3 mg/dL (Fig. 1.7).
• The clinical detection of jaundice is difficult in artificial
light. Hence, it should be examined preferably in day
light. Besides sclera, other sites to be looked for the
evidence of jaundice are mucosa of oral cavity
underneath the tongue and skin.
• Yellow discoloration of the skin can also occur in
carotenemia (carotenoderma) and exposure to B
quinacrine or phenols. Sclera is typically not involved FIGURE 1.6: A. Pallor of the palm; compare with palm of normal
in carotenemia. person (left) B. pale tongue
FIGURE 1.7: Jaundice visible over sclera
Clubbing
The enlargement of the distal portion of the fingers and toes,
due to proliferation of connective tissues, is known as
clubbing (Fig. 1.8A). The clubbing is graded as follows;
• Grade I: There is thickening of tissues at the nail base.
Clinical Methods
Respiratory diseases Central cyanosis
Chronic suppurative lung diseases • High altitude
• Lung abscess • Respiratory diseases (COPD, extensive pneumonia, pulmonary
• Bronchiectasis edema, massive pulmonary embolism)
• Empyema • Cardiac diseases (congenital cyanotic heart diseases,
Bronchogenic carcinoma Eisenmenger syndrome, heart failure)
Mesothelioma (pleural neoplasm) • Abnormal hemoglobin (methemoglobinemia, sulfhemo-
Pulmonary tuberculosis globinemia)
Fibrosing alveolitis Peripheral cyanosis
Cardiac diseases • Cold exposure
Congenital cyanotic heart diseases • Heart failure (reduced cardiac output)
• Fallot’s tetralogy • Arterial obstruction
• Eissenmenger syndrome • Venous obstruction
Subacute bacterial endocarditis
Gastrointestinal diseases Edema
Inflammatory bowel diseases
• Ulcerative colitis Edema is the presence of an excess of fluid in interstitial
• Crohn’s disease space causing swelling of the tissues.
Hepatic cirrhosis 1. Edema may be localized or generalized. Generalized
Idiopathic edema is known as anasarca, in which the fluid may
also accumulate in the pleural cavity (hydrothorax) and
peritoneal cavity (ascites). Edema over feet is known as
pedal edema. Causes of pedal edema are given in
9
Table 1.8.
2. Edema may be of the pitting or non-pitting type. Pitting
edema means formation of an indentation or pit
following the application of firm pressure for a sustained
period over the area of swelling (Figs 1.10A and B).
The mechanisms of edema can be described as follows:
a. The hydrostatic pressure in vascular system and
tissue colloid oncotic pressure tend to drive fluid
from the vascular to the extravascular space. On the
contrary, colloid oncotic pressure maintained by
plasma proteins in the vascular system and
hydrostatic pressure in the interstitial fluid promote
FIGURE 1.9: Central cyanosis the movement of fluid in the vascular compartment.
The development of edema is a result of the
slow. The extremities are cyanosed and cold while imbalance between these “Starling forces”. For
mucous membrane of the oral cavity and tongue are example, the edema in congestive heart failure is due
spared. Warming of the cyanotic extremity may increase to an increase in the vascular hydrostatic pressure. A
blood flow and abolish peripheral (but not central) decrease in the plasma colloid oncotic pressure is
cyanosis. the cause of edema in hypoalbuminic states like
c. Cyanosis due to heart failure is of mixed type, both nephrotic syndrome, malnutrition, and liver disease.
central and peripheral. The edema is of the pitting type.
TABLE 1.8: Causes of pedal edema b. Edema may result from damage to the capillary
Bilateral pedal edema endothelium which causes exudation of fluid and
Pitting type protein due to increased permeability. Injury to
• Congestive heart failure
• Nephrotic syndrome, acute nephritis
capillary endothelium may occur due to drugs,
• Liver cirrhosis infections, and trauma. Capillary permeability is also
• Malnutrition increased in hypersensitivity reactions. This type of
• Epidemic dropsy edema is usually localized, non-pitting and may be
• Drugs (calcium channel blockers, NSAIDs, steroids)
accompanied by other signs of inflammation.
Non-pitting type
• Myxedema c. In many forms of edema, the effective arterial blood
Unilateral edema volume is reduced. This in turn initiates physiological
• Filariasis mechanisms to restore the volume by renal salt and
• Thrombophlebitis water retention, which further adds up to the edema.
• Cellulitis
• Trauma Compensatory physiological responses are activation
• Regional lymph node resection of rennin-angiotensin-aldosterone system, and
increased secretion of vasopressin.
Edema generally appears first over the periorbital area
and is more marked in the mornings, in nephrotic syndrome
and acute nephritis (see Fig. 6.1). In heart failure, the edema
is more marked during the evenings and present over the
ankles and dorsum of the feet. In these conditions, edema
may become generalized later on. In bed-ridden patients,
10
the edema first appears in the presacral region.
Localized edema in a single limb is generally due to
either venous or lymphatic obstruction. For example, edema
of the leg may occur due to thrombosis of the popliteal or
femoral vein. Compression of axillary vein due to malignant
lymph nodes may cause edema of the arm.
Lymphatic obstruction due to resection of regional lymph
Essentials of Medicine for Dental Students
Lymph Nodes
Palpation of lymph nodes is an important part of general
examination (Fig. 1.11). Lymph nodes are examined for;
• size
• number
• texture
• tenderness
• mobility
• signs of inflammation over the nodes
Important groups of lymph nodes which must be
examined are submental, submandibular, preauricular,
postauricular, cervical (anterior and posterior chains),
FIGURES 1.10A and B: (A) Pressure applied over edematous supraclavicular, axillary and inguinals. For other details, see
limb (B) pitting edema Chapter 3.
TABLE 1.9: Causes of halitosis
Clinical Methods
Dental causes
• Dental decay-carries, exposed teeth
• Gum diseases
• Oral infections-abscess
• Oral cancer
• Xerostomia (dry mouth)
• Mouth breathing habit
• Tongue coating
Medical causes
• Sinus infections, cough and cold
• Allergies, post nasal drip
• Lung abscess
• Diabetic ketoacidosis (sweet and fruity)
• Renal failure (ammonical, urinary)
• Hepatic failure (fishy, mousy)
FIGURE 1.11: Palpation of the submandibular lymph nodes • Hiatus hernia
• Menstruation
Halitosis • Medications
Miscellaneous
Halitosis is an unpleasant odor or smell emerging from the • Certain foods- fish, dairy products, garlic, eggs
mouth or nostrils that is detected by the patient or others. It • Smoking
is also referred as bad breath, breath malodor, puppy breath, • Alcohol
• Stress
and dragon mouth. About 35% of world population is
• Certain professions
suffering from bad breath problem. Important causes of • High protein diets (Atkins diet)
halitosis are given in Table 1.9.
Foods Causing Bad Breath 11
Types of Halitosis 1. Sugars: bacteria cause breakdown of sugar and produce
1. Physiologic bad breath: This affects all normal healthy acidic environment.
persons and is caused by anaerobic bacterial overgrowth 2. Dense proteins/milk products: Cheese, yoghurt, ice
mainly on the tongue deep in the papillae. cream stay on the tongue and between teeth. Anaerobic
2. Pathologic bad breath: Occurs due to oral infections bacteria break down the proteins and produce VSC.
including carious teeth. 3. Acidic foods: Anaerobic bacteria multiply very fast in
3. Halitophobia: Some patients may complain of bad breath acidic medium and produce high levels of VSC. Acidic
in spite of treatment being given to them. It may be due foods include coffee, tomato juice, citrus fruit juices
to psychiatric illness. aerated drinks.
4. Transitory bad breath: This type occurs after 4. Onion, garlic, cabbage: When taken raw, smell comes
consumption of certain foods like garlic, onions, and from mouth because of sulphur compounds present in
certain medications. It usually lasts for hours/days. them.
Xylitol chewing gums: sugar free xylitol chewing gums are Lower limbs:
also useful. • Edema of feet, ankles
2. Following is not true in pulsus paradoxus:
Clinical Methods
DEFINITIONS
A. Found in cardiac tamponade
Certain terms are frequently used in clinical medicine. These
B. Disappears during expiration
have profound effects on presentations. Some important C. Inspiratory fall in blood pressure
terms are defined below. D. May be present in bronchial asthma
3. Following conditions are associated with bradycardia except:
Diagnosis A. Hypothyroidism B. Athletes
Diagnosis is an act or process of identifying or determining C. Hypotensive shock D. Raised intracranial tension
the nature of a disease by way of examination and assessment 4. Edema in both lower limbs can occur in:
of the symptoms and signs. A. Filariasis B. Cellulitis
C. Nephrotic syndrome D. Popliteal vein thrombosis
Diagnosis is an art wherein scientific methods are applied
5. Cyanosis in CHF is of following type:
to the elucidation of problems presented by a patient. A
A. Central
concept is formed about the etiology, pathology, and organ B. Peripheral
dysfunctions which constitutes the patient’s disease. C. Both, central and peripheral
Diagnosis provides a firm basis for the treatment and D. Not found
prognosis of the individual patients. 6. Which of the following is not matched correctly:
A. Pulsus Parvus et tardus — aortic stenosis
Clinical Diagnosis B. Pulsus besferiens—severe mitral stenosis
Diagnosis made by bedside methods without the help of C. Water hammer pulse—aortic regurgitation
D. Hyperkinetic pulse—thyrotoxicosis
laboratory tests.
7. Clubbing can be found in the following except:
Differential Diagnosis A. Bronchiectasis B. Lung abscess
C. Pneumonia D. Bronchogenic carcinoma
The recognition of a particular condition from amongst
others which closely resemble it in certain aspects.
8. Yellowish discoloration of sclera and skin occurs in the
following: 13
A. Carotinemia B. Hyperbilirubinemia
Prognosis C. Quinacrine ingestion D. Both A and B
Prognosis is a considered opinion of the probable E. All of the above
development and outcome of the disease based upon all the 9. Cyanosis is seen in:
relevant available facts of the case. A. Fallot’s tetralogy B. Methemoglobinemia
C. Sulfhemoglobinemia D. All of the above
Treatment 10. All of the following is true in peripheral cyanosis except:
A. It improves on warming
Treatment is the course of action adopted to deal with illness B. Best seen in oral mucous membrane
and control of the patient. C. Occurs in cases with low cardiac output
D. May occur following exposure to cold
Illness 11. Following is not matched properly:
Illness is defined by the totality of effects, predicaments, A. CHF _______ pedal edema
and repercussions of the disease, deformity, or circumstances B. Thyrotoxicosis _______ tachycardia
produced in the patient. C. High arterial CO2 _______ cyanosis
D. Orthopnea _______ mitral stenosis
SELF ASSESSMENT 12. Early morning periorbital edema suggests the disease of
following system:
Multiple Choice Questions A. Cardiac B. Renal
1. Rate and rhythm of the pulse is best appreciated by C. Hepatic D. All of the above
palpating: 13. “a” wave in JVP is absent in:
A. Brachial artery B. Radial artery A. Pericardial tamponade
C. Popliteal artery D. Femoral artery B. Complete heart block
C. Atrial fibrillation B. Fallot’s tetralogy
D. Hypotension C. Interstitial lung disease
14. Distended but nonpulsatile neck veins are found in: D. Conditions with peripheral cyanosis
A. Right heart failure B. Tricuspid stenosis 22. Clubbing may be present in the following except:
C. Mediastinal tumor D. Constricitive pericarditis A. Lung cancer
15. JVP is best examined in: B. Crohn’s disease
A. External jugular vein B. Internal jugular vein C. Infective endocarditis
C. Subclavian vein D. Any one of the above D. Left to right cardiac shunts
16. Sweet fruity odour is found in the oral cavity in case of: 23. Following is not properly matched:
A. Renal failure B. Hepatic failure A. Clubbing_______Fallot’s tetralogy
C. Diabetic ketoacidosis D. All of the above B. Cyanosis_______pulmonary edema
17. Blood pressure is generally measured by auscultating over C. Eisenmenger’s syndrome_______cardiac shunts with
following artery: left to right flow
A. Radial artery B. Brachial artery D. Pulmonary osteoarthropathy_______lung cancer.
C. Carotid artery D. Any of the above
18. The diastolic BP corresponds best with: Fill in the Blanks
A. First appearance of Korotkoff sound 1. Radio-femoral delay is found in _______.
B. Disappearance of Korotkoff sound 2. Pulsus alternans is present in _______.
C. Muffling of Korotkoff sound 3. Cyanosis appears when amount of reduced Hb exceeds
D. In between appearance and disappearance of korotkoff _______ g/dL.
sound 4. Rise in JVP during inspiration in constrictive pericarditis
19. The following can be measured by sphygmo-manometer and is called _______ sign.
palpating the artery: 5. Prominent Y descent in JVP is seen in _______.
A. Systolic blood pressure 6. Bradycardia is defined as pulse rate less than _______
14 B.
C.
Diastolic blood pressure
Both
per minute.
7. Tachycardia is defined as pulse rate more than _______
D. None per minute.
20. In coarctation of aorta, following is true: 8. Normal respiratory rate in adults is ______ per minute.
A. BP in lower limbs is higher than in upper limbs 9. Regularly irregular pulse is found in _______.
B. BP is equal in lower and upper limbs 10. Fishy mousy odour in the oral cavity suggests ______.
C. BP in upper limb is higher than in lower limbs 11. Cherry red discoloration of skin is found in _______ .
D. BP is generally not recordable in upper limbs 12. Waxing and waning respiration with intervening periods
Essentials of Medicine for Dental Students
21. Cyanosis is accompanied with clubbing in the following except: of apnea is called _______.
A. Eisenmenger’s syndrome
Chapter
Gastrointestinal and
2 Hepatobiliary System
any change in appearance of stools although it may systemic manner. This includes inspection, palpation,
present as iron deficiency anemia. percussion and auscultation.
Jaundice Inspection
Jaundice may result from prehepatic, intrahepatic and The patient should be supine and the abdomen should be
posthepatic causes (see chapter on Jaundice). adequately exposed. The inspection should be performed
under proper lighting conditions. Following points should
Other Symptoms particularly be noted;
• Difficulty in swallowing (dysphagia) and painful a. Shape of the abdomen: The abdomen may be distended
swallowing (odynophagia) are features of esophageal or sunken (scaphoid). The generalized distension of the
disease. abdomen may occur due to fat, fluid, flatus, feces or
• Hiccups can arise due to distension or irritation of the fetus. Localized distension could be due to organ
upper GI tract. However, they may also occur because enlargement or small bowel obstruction. Sunken
of non-GI causes. abdomen is seen in starvation and malignancy.
• Weight loss, anorexia and fatigue are non-specific b. Umbilicus: Umbilicus is everted and horizontal in
manifestations and can be seen in malignancy, ascites. Umbilical hernia may occur in massive ascites
malabsorption, inflammatory and psychiatric conditions. (Fig. 2.1).
Gastrointestinal and Hepatobiliary System
c. Movements of the abdominal wall: Movements of
abdominal wall are absent in peritonitis. Visible pulsations
can be seen normally in thin persons or can also be due to
aortic aneurysms. Visible peristalsis may be present in
gastric outlet obstruction and small bowel obstruction.
d. Prominent veins: Prominent superficial veins may be
present in inferior vena cava obstruction (Fig. 2.2) or
portal hypertension (caput medusae).
e. Skin: Skin over the abdomen is shiny and smooth in
marked distension. Purple striae are seen in Cushing’s
Syndrome. Striae atrophica or gravidorum are pink or
white linear marks produced by gross stretching of
abdomen as in ascites and pregnancy (Fig. 2.3).
FIGURE 2.1: Massive ascites with umbilical hernia f. Inspection of groin, genitalia and hernial sites should
also be done.
Palpation
• The patient is asked to bend the knees to relax abdominal
muscles and to breathe deeply.
• The palpation begins anti-clockwise from left iliac fossa.
• The palpation should be gently performed with warm
hands. Initially superficial palpation is done to find out
tender areas, which are to be examined in the end. 17
a. Organs such as liver, spleen, kidneys, ovaries, uterus
and urinary bladder are palpated to detect any
enlargement. Further details about the enlarged organs
like size, surface, borders, consistency, and tenderness
are noted.
FIGURE 2.2: Prominent veins over abdomen – Enlarged liver is palpable in the right hypochondrium.
It moves with respiration and the finger cannot be
insinuated between the costal margin and the lump
(Fig. 2.4). The upper border of the liver should also
be demarcated by percussion in order to assess the
size. (see hepatomegaly described elsewhere in this
chapter).
– Spleen is palpated in the left hypochondrium. It
moves with respiration and the finger cannot be
insinuated between the costal margin and the lump
(Fig. 2.5). A notch is felt at the medial border of the
spleen. This is not palpable bimanually.
– Kidneys are bimanually palpable and ballotable (it
can be pushed from the one hand to the other).
b. Any area showing tenderness or rigidity should be noted.
FIGURE 2.3: Abdominal stria in a patient with ascites Murphy’s sign may be present in acute cholecystitis.
c. Fluid thrill detects the presence of free fluid in the
abdomen (ascites). Place one hand flat in the lumbar
region of one side. Ask an assistant to put the side
of hand in the midline of the abdomen. Tap
the opposite lumbar region. A wave or thrill is felt by
the hand held flat in the other lumbar region (Fig. 2.6).
The assistant’s hand does not allow the transmission of
impulse through the abdominal wall. Fluid thrill is a sign
of tense and massive ascites.
Percussion
The normal note of the abdominal percussion is tympanitic
(resonant). Percussion is useful in confirming the
enlargement of liver and spleen and detecting fluid in the
FIGURE 2.4: Palpation of the liver peritoneal cavity(ascites).
Shifting dullness: Shifting dullness is a sign of moderate
ascites and may be absent when the ascites is tense.
Percussion is performed in supine patient from the midline
of the abdomen toward the flanks till dullness is detected
(Figs 2.7A and B). Keeping the hand on the abdomen in the
same position (at the point of dullness), patient is rolled
Auscultation
Essentials of Medicine for Dental Students
21
• Sturge-Weber angiomatosis Mechanical
Oropharyngeal tumours
Post surgical/ radiation changes
fear of swallowing or refusal to swallow (in hysteria, rabies, Zenker’s diverticulum
Retropharyngeal abscess/mass
tetanus, pharyngeal paralysis). Thyroid disorders
Plummer-Vinson syndrome
Classification Inflammatory lesions
Motor
Dysphagia is divided into following types;
Brain injury, cerebral palsy, parkinsonism, stroke
a. Oropharyngeal dysphagia: There is problem in Rabies, tetanus
transferring food from mouth to the esophagus. This Cranial nerve palsy, Guillain Barre syndrome
is associated with nasal regurgitation and pulmonary Myasthenia gravis, botulinum toxin
Myositis, myopathies
aspiration during swallowing. The causes of
oropharyngeal dysphagia can be subgrouped into (a)
mechanical and (b) motor dysphagia. Important causes TABLE 2.4: Causes of esophageal dysphagia
are given in Table 2.3.
Mechanical
b. Esophageal dysphagia: Difficulty in swallowing the
Esophageal cancer
food down the esophagus. Patients with mechanical Peptic stricture
obstruction complain of dysphagia mainly for solids Inflammatory esophagitis
whereas those with motility disorders have dysphagia for Schatzki’s ring (lower esophageal mucosal ring)
Posterior mediastinal mass
both solids and liquids. Causes are given in Table 2.4. Aortic aneurysm
Motor
Odynophagia Achalasia
Scleroderma
Odynophagia is a painful swallowing that may limit oral
Diffuse esophageal spasm
intake. Important causes are infectious esophagitis due to
c. Endoscopic removal of obstructing food bolus in acute Management
dysphagia 1. The treatment of acute gastritis consists of administration
d. Nutrition counselling of sucralfate suspension (1 g 4-6 hrly) and H2 receptor
antagonist (ranitidine 150 mg twice daily, famotidine
Medical
20 mg twice daily) or proton pump inhibitors
a. Proton pump inhibitors (for mucosal inflammation in
(omeprazole 20 mg once daily, rabeprazole 20 mg once
reflux disease)
daily, pantoprazole 40 mg once daily, lansoprazole 30
b. Antimicrobial agents (infectious esophagitis)
mg once daily).
c. Viscous lidocaine solution for symptomatic relief
2. The consumption of alcohol and drugs (NSAIDs) should
d. Anticholinergic medications in cases with drooling of
be avoided.
saliva and oropharyngeal dysphagia
3. Stress gastritis can be prevented by the administration
Endoscopic Therapy of sucralfate, H2 receptor antagonist or proton pump
a. Esophageal dilatation inhibitor in critically ill patients.
b. Esophageal stent placement
c. Pneumatic dilatation of lower esophageal sphincter Acute Gastritis Due to Infections
(LES) for achalasia. A variety of infections can lead to acute inflammatory
d. Botulinum toxin injection to LES in achalasia changes in the gastric mucosa. This presents as sudden onset
of epigastric pain, nausea and vomiting.
Surgical
H. pylori infection can lead to acute gastritis which
a. Laproscopic myotomy in achalasia generally progresses to chronic gastritis.
Acute bacterial infections (aerobic and anaerobic
22 GASTRITIS
Gastritis is a histological diagnosis characterized by
bacteria) can lead to progressive life-threatening necrotizing
gastritis (phlegmonus gastritis). The treatment includes
inflammation of the gastric mucosa. antibiotics and emergency gastrectomy.
Herpes simplex virus, CMV and Candida can cause
Acute Erosive and Hemorrhagic Gastritis
gastritis in immunocompromized patients such as AIDS.
Acute gastritis is usually erosive and hemorrhagic. Important
causes of erosive and hemorrhagic gastritis are: Chronic Gastritis
Essentials of Medicine for Dental Students
upon the biopsy sample. mechanism. However, these are not used as the first line
4. There may be anemia. Stool may be positive for occult therapy in active ulcers because other agents (PPI and H2
blood. Leukocytosis suggests complications such as receptor blockers) are more efficacious and better tolerated.
penetration or perforation. • Sucralfate (1 g 4 times daily) is used in addition to other
drugs in refractory ulcers.
Treatment • Bismuth containing compounds are given along with
General Measures antibiotics to eradicate H. pylori.
• Misoprostol is used to prevent ulcers due to NSAIDs.
1. Dietary restriction does not help; hence, it is not required.
2. Meals should be taken at regular intervals.
H. Pylori Eradication Therapy
3. Smoking should be stopped completely.
Triple drug therapy is employed to eradicate H. pylori
TABLE 2.5: Complications of peptic ulcer infection. The regimen includes two antibiotics and one PPI.
• GI hemorrhages Single antibiotic is not given to avoid the problem of
• Perforation resistance.
• Ulcer penetration (into pancreas, liver) • Commonly employed regimen includes Amoxycillin 1
• Gastric outlet obstruction
g twice daily plus Clarithromycin 500 mg twice daily
Gastrointestinal and Hepatobiliary System
plus twice a day PPI (omeprazole or rabeprazole 20 mg, Diarrhea is classified into:
lansoprazole 30 mg, pantoprazole 40 mg) for 14 days. – Acute (< 2 weeks)
Metronidazole can be used in place of Amoxicillin in – Persistent (2-4 weeks)
cases of penicillin allergy. – Chronic (> 4 weeks)
• Eradication of H. pylori is achieved in 85-90% cases.
Successful eradication reduces the recurrence of Acute Diarrhea
ulcer. Acute diarrhea is caused mainly by infections (90%). It may
• If infection persists after giving triple therapy, quadruple also be caused by drugs, ischemia, toxins and other
therapy (PPI, bismuth, tetracycline, metronidazole) is conditions. Causes of acute diarrhea are given in Table 2.6.
given.
Incubation Period
Therapy in Specific Cases The incubation period varies from few hours to days. It is
a. H. pylori associated ulcers if uncomplicated are treated few hours (1-6 hrs) in case of preformed toxin induced
with triple drug combination for 14 days. Thereafter PPI diarrhea while 12-24 hours in infective diarrhea.
or H2 receptor blocker must be continued for additional Pathogenic Mechanisms
2-6 weeks.
Pathogens can cause diarrhea via various mechanisms.
b. Treatment of active ulcer due to NSAIDs includes
These are described as below:
immediate withdrawal of the offending agent and
a. Toxin production: Bacterial toxins either preformed or
administration of PPI or H2 receptor antagonist. All such
produced in the gut can cause diarrhea. Such toxins are
patients should also be tested for H. pylori infection. If
exotoxins and include enterotoxins, cytotoxins, and
positive, eradication therapy should also be given.
neurotoxins. Enterotoxins disturb normal secretory
c. Preventive treatment with PPI or misoprostol is required
in high risk patients on NSAIDs such as age >60 years,
mechanisms and cause profuse watery diarrhea whereas
cytotoxins lead to inflammatory diarrhea by causing
25
history of ulcer disease, concurrent therapy with
destruction of mucosal cells. Some bacteria produce
corticosteroids or anticoagulants and serious underlying
exotoxins with both enterotoxin and cytotoxin activities.
medical illness. Use of COX-2 selective NSAIDs
Neurotoxins produced by S. aureus and B. cereus act on
reduces injury to the gastric mucosa.
the nervous system to produce vomiting.
Surgical Treatment b. Invasion: Inflammatory diarrhea or dysentery results
from the invasion and destruction of mucosal cells
a. Emergency surgery is performed in case of perforation
by Shigella or Enteroinvasive E. coli. Intraepithelial
and persistent hemorrhage.
multiplication and spread to adjacent cells also occurs.
b. Elective surgery is done in gastric outflow obstruction
c. Penetration: Salmonella typhi and Yersinia enterocolitica
and recurrent ulcer despite medical treatment.
penetrate intestinal mucosa and multiply in Peyer’s
DIARRHEA, DYSENTERY AND FOOD patches or intestinal lymph nodes. They disseminate from
POISONING these lymph nodes and cause fever.
26 – Cryptosporidium
Non-infectious Food Poisoning
• Diverticulitis • Food poisoning is gastroenteritis of infective or non-
• Inflammatory bowel disease (ulcerative colitis,Crohn’s disease)
• Metabolic (DKA, carcinoid)
infective origin.
• Sepsis • The important infective causes are S. aureus, salmonella,
• Drugs (NSAIDs, antibiotics) B. cereus and E. coli.
• Ischemic colitis • Non-infective causes are allergy to sea foods, fish or
Essentials of Medicine for Dental Students
absorbed and drags fluid along with it. This type of diarrhea diseases, biliary obstruction, cholestatic liver diseases and
ceases on fasting. Osmotic laxatives (antacids, lactulose, decreased enterohepatic circulation of bile salts.
sorbitol) and carbohydrate malabsorption, lactase deficiency)
are important causes of osmotic diarrhea. Mucosal Phase
The damage to the intestinal epithelium or resection of a
Essentials of Medicine for Dental Students
30
conditions such as celiac sprue and pernicious anemia. vitamins (A, D, B12, folate and K) and minerals (iron
and copper). Iron is stored in the form of ferritin and
Treatment hemosiderin.
1. Deficient nutrients are replaced.
2. Specific therapy depends on the cause: Liver Function Tests
a. Gluten diets (wheat, barley) should be avoided in The liver has numerous functions and no single test is
celiac sprue. enough to assess all its functions. However, certain tests
Essentials of Medicine for Dental Students
b. Tropical sprue is treated with tetracycline and folic are performed to assess some of the main functions of
acid for 6 months. the liver (serum albumin, serum bilirubin and prothrombin
c. Cotrimoxazole double strength tablet daily is given time) while other tests indicate the severity of damage
for 1 yr in Whipple’s disease. (aminotransferases) or obstruction to bile flow (alkaline
d. A one to two week course of antibiotics (fluoro- phosphatase).
quinolone, tetracycline, metronidaxole) is given in
malabsorbtion with bacterial overgrowth. Tests to Assess Excretory Functions
e. Milk products are avoided in lactase deficiency. a. Serum bilirubin: The normal level of serum total
bilirubin is 0.3-1.0 mg/dL. It is present in two forms,
LIVER: STRUCTURE AND FUNCTION unconjugated (0.2-0.7 mg/dL) and conjugated bilirubin
The liver is the largest organ of the body. It is situated in the (0.1-0.3 mg/dL). A rise in the level of conjugated
right hypochondrium under the diaphragm. Anatomically it bilirubin suggests liver or biliary tract disease. Isolated
is divided into right and left lobes. It has dual blood supply, elevation of unconjugated bilirubin is rare in liver disease
80% comes from the portal vein and the remainder from and it indicates hemolysis.
the hepatic artery. Two-third of the mass of the liver is b. Urine bilirubin: Conjugated bilirubin (not the
constituted by hepatocytes. Other important cell types are unconjugated bilirubin) is excreted in the urine when
Gastrointestinal and Hepatobiliary System
the plasma level of conjugated bilirubin is raised. Hence, b. Alkaline phosphatase: A significant rise in serum
the presence of bilirubin in the urine suggests liver alkaline phosphatase (ALP) suggests cholestasis
disease. (obstruction in the bile flow). It may be mildly raised in
c. Blood ammonia level: Blood ammonia level may be other liver diseases. The normal serum level is 30-120
raised in severe hepatic dysfunction and hepatic units/L. Alkaline phosphatase is also present in other
encephalopathy. It may also be high due to portal body tissues like bone, intestine, placenta and leukocytes.
shunting in portal hypertension. c. Serum 5’nucleotidase and gamma glutamyl transpeptidase
(GGT) are also raised in cholestasis. Hence, a
Tests to Assess Synthetic Functions concomitant rise in serum 5’nucleotidase or gamma
a. Serum albumin: Albumin is exclusively synthesized in glutamyl transpeptidase (GGT) along with ALP suggests
the liver. The normal value of serum albumin is 3.5-5.5 hepatic origin of alkaline phosphatase.
g/dL. It has a long half life of about 20 days, therefore a
low serum albumin suggests chronic liver disease. Imaging Techniques
b. Coagulation factors: The half life of most coagulation a. Ultrasonography: It is useful to screen for the evidence
factors is short; factor VII has the shortest half life of intrahepatic or extrahepatic cholestasis and gallstones
(six hours). Hence, measurement of prothrombin (Fig. 2.8). In addition, it can detect liver cysts, abscesses
time (PT) is helpful in the diagnosis and the prognosis
of acute parenchymal liver disease. Prothrombin
time may also be prolonged in obstructive jaundice
due to vitamin K malabsorption. Correction of PT after
administration of vitamin K suggests vitamin K
deficiency.
c. Miscellaneous: Other tests used to measure synthetic 31
functions of the liver include serum levels of α-1 anti-
trypsin, α-fetoprotein and ceruloplasmin.
Serum Enzymes
The liver contains thousands of enzymes. Many are present
in the serum in very low quantity. The elevation of these
enzymes in the serum indicates either damage to hepatocytes
or cholestasis.
a. Aminotransferases: Serum alanine aminotransferase or
serum glutamate pyruvate transaminase (ALT or SGPT)
and aspartate aminotransferase (AST or SGOT) are
raised in acute liver cell injury. The normal serum levels
of ALT and AST are 0-35 Unit/L. However, its elevation
does not correlate with the severity of the disease. A rise
in ALT is more specific to liver cell injury since AST
can also be raised in other conditions such as diseases
of myocardium, skeletal muscles, kidneys and brain. The
ratio of serum AST to ALT is less than one in viral
hepatitis whereas it is greater than two in alcoholic liver
FIGURES 2.8A and B: (A) Ultrasound showing stones in the
disease. They are usually not significantly elevated in
gall- bladder (B) Ultrasound showing impacted stone in the neck
obstructive jaundice. of gallbladder
and masses. Biopsy of a lesion can be done under • Other sites to be looked for the evidence of jaundice are
ultrasonographic monitoring. Ultrasonography may also mucosa of oral cavity underneath the tongue and skin.
detect portal hypertension (dilated portal vein, ascites, • Urine is dark yellow in color due to excretion of
splenomegaly and collateral vessels). conjugated bilirubin.
b. CT scan and MRI: These are useful in the evaluation of • Yellow discoloration of the skin can also occur in
parenchymal liver disease. Contrast enhancement can carotenemia (carotenoderma) and exposure to quinacrine
be used to differentiate the nature of space occupying or phenols. Sclera is typically not involved in
lesions. With MRI, vessels can be visualized without carotenemia.
use of IV contrast.
c. Endoscopic retrograde cholangiopancreatography Bilirubin Metabolism
(ERCP) and Percutaneous transhepatic cholangio- • Bilirubin is a product of heme metabolism. The breakdown
graphy (PTC): These help in the detection of the cause, of old red blood cells in the reticuloendothelial system
location and the extent of the biliary obstruction. ERCP (primarily spleen and liver) leads to the release of heme
can be used for therapeutic interventions such as stone (Fig. 2.9). Heme is further metabolized into biliverdin
extraction from common bile duct and for placing a stent. and subsequently to bilirubin. About 70-80% of bilirubin
Magnetic resonance cholangiopancreatography (MRCP) is derived from this mechanism. The rest comes from
is a sensitive and noninvasive technique of visualizing the breakdown of premature erythroid cells in bone
the biliary tree. marrow (ineffective erythropoiesis) and the catabolism
of myoglobin and cytochromes.
Liver Biopsy • This insoluble bilirubin binds reversibly and
Biopsy is a definitive method to diagnose the cause and noncovalently to albumin (unconjugated or indirect
The deposition of bilirubin in tissues occurs when the serum • The conjugated bilirubin is then transported to the
bilirubin level is raised (hyperbilirubinemia). duodenum via bile. Colonic bacteria metabolize the
• The normal total serum bilirubin level is 0.3-1.0 mg/dL. conjugated bilirubin into stercobilinogen which may be
With the use of Van den Bergh’s method, it has further oxidized to stercobilin. Stercobilinogen and
been shown that up to 30% of the total bilirubin (0.3 stercobilin are excreted in stool. A small amount of
mg/dL) may be the conjugated or direct reacting stercobilinogen is absorbed to reach the liver through
type. However, newer techniques have shown that in portal system and is re-excreted into the bile. A fraction
normal individuals, almost all bilirubin in the serum is escapes liver uptake and passes into urine as urobilinogen
unconjugated. and its oxidized form, urobilin.
• Sclerae have a high affinity for bilirubin due to their • The unconjugated bilirubin, because it is bound to
rich elastin content. Jaundice is clinically apparent in albumin, is not filtered through kidneys and therefore
sclera when bilirubin level is raised above 3 mg/dL. does not appear in urine. Hence, in unconjugated
• The clinical detection of jaundice is difficult in artificial hyperbilirubinemia (as in hemolysis), bilirubin is absent
light. Hence, it should be examined preferably in day in the urine (acholuric jaundice). However, urobilinogen
light. is increased in the urine. The presence of bilirubin in
Gastrointestinal and Hepatobiliary System
FIGURE 2.9: Bilirubin metabolism
TABLE 2.12: Urinary findings in different types of jaundice • The raised unconjugated bilirubin (>20 mg/dL) can lead
Urine Hemolytic Hepato- Obstructive
findings cellular
Normal to central nervous system manifestations in neonates
(kernicterus).
33
Urobilinogen +++ ++ – + • Liver transaminases and alkaline phosphatase are normal.
Bilirubin – ++ ++ – Unconjugated hyperbilirubinemia may result either from
overproduction of bilirubin or from impaired hepatic uptake
urine suggests predominant conjugated hyperbili- or conjugation of bilirubin. Table 2.13 shows the clinical
rubinemia (liver disease, obstructive jaundice). Urobi- and laboratory features in different types of jaundice.
linogen is absent in the urine in cases of obstructive a. Overproduction of bilirubin (prehepatic): This may
jaundice because bilirubin is not available in the occur in hemolytic disorders such as hereditary
intestine to be metabolized into stercobilinogen spherocytosis, sickle cell anemia, G6PD deficiency,
(Table 2.12). paroxysmal nocturnal hemoglobinuria and
autoimmune hemolytic anemia. Other causes include
Types of Jaundice
ineffective erythropoiesis, hemolytic reaction and
Jaundice is classically divided into two broad types, resolution of hematoma.
unconjugated hyperbilirubinemia and conjugated hyper- b. Impaired hepatic metabolism: The hepatic uptake
bilirubinemia. of bilirubin is impaired because of some drugs (like
Unconjugated hyperbilirubinemia: This is characterized rifampicin and probenecid) and in Gilbert’s syndrome.
by predominantly high levels of serum unconjugated The conjugation of bilirubin is impaired in Gilbert’s
bilirubin. syndrome and Criggler-Najjar syndromes because
• The color of urine is normal as there is no bilirubin. of decreased activity of the enzyme, glucuronyl
• The jaundice is generally mild (serum bilirubin <6 mg/ transferase.
dL). Most neonates develop mild rise in unconjugated
• Additionally patients may have anemia and splenomegaly. bilirubin because of incompletely developed hepatic
TABLE 2.13: Features of different types of jaundice
Prehepatic (hemolytic) Hepatic (Hepatocellular) Posthepatic (obstructive)
History Recurrent jaundice, positive Prodrome: fever, anorexia, Pain in abdomen, may
family history, anemia nausea be recurrent
Skin color Lemon yellow Yellow Dark yellow
Pruritus Absent Occasional (early phase) Present
Spleen Enlarged Occasional Not enlarged
Gallbladder Not palpable Not palpable May be palpable
Feces Normal Pale (if cholestasis) Pale
Urine color Colorless, yellow on standing Dark (bilirubin and Very dark
(urobilinogen) urobilinogen) (high bilirubin)
Tests for hemolysis Positive Negative Negative
Serum bilirubin Unconjugated (<6 mg/dL) Mixed Conjugated
ALT (SGPT) Normal Increased (+++) Minimally increased (+)
Alkaline phosphatase Normal Minimally high (+) High (+++)
Serum albumin Normal Low (in chronic disease) Normal
Prothrombin time Normal Prolonged Prolonged (correctible with vit K)
Important causes Hemolysis, Gilbert’s syndrome Viral hepatitis, drugs, alcohol Gallstones, carcinoma pancreas
functions (physiologic neonatal jaundice). Marked elevation transferases (ALT, AST) are raised out of proportion
of unconjugated bilirubin in premature infants can lead to to alkaline phosphatase. Clinical features of
kernicterus. hepatocellular jaundice are given in the Table 2.13.
Gilbert’s syndrome, an autosomal dominant disorder, is Causes of hepatocellular jaundice are given in
a common disorder with mild jaundice. Conjugation of Table 2.14.
34
bilirubin is also impaired due to decreased activity of c. Cholestatic jaundice (Obstructive jaundice): This
glucuronyl transferase enzyme. Serum bilirubin is generally type of jaundice results from the obstruction in the
less than 6 mg/dL. No treatment is required. bile flow which may be intrahepatic or extrahepatic.
Criggler-Najjar syndromes are characterized by Clinical features of cholestatic jaundice are given in
complete absence of activity of glucuronyl transferase (Type the Table 2.13. Causes of obstructive jaundice are
I) or reduced activity of the enzyme (Type II). The jaundice given in Table 2.15.
is severe and death occurs early in type I Criggler-Najjar
TABLE 2.14: Causes of hepatocellular jaundice
Essentials of Medicine for Dental Students
6 months. After disappearance of HBsAg, antibody of genus Hepacivirus of the flavivirus family. Six genotypes
against HBsAg (Anti-HBs) appears and persists for of HCV have been identified.
years and confers immunity. Presence of Anti-HBs • The route of transmission is parenteral (transfusion of
antibody means either previous infection or blood and blood products, IV drug abuse). Sexual and
vaccination. vertical spread is less common than in hepatitis B
b. The HBcAg is not found in the blood. However, infection. In the past it was responsible for 90% of post-
antibody to it (anti-HBc) appears early during the transfusion hepatitis.
illness. Presence of IgM anti-HBc indicates acute • Acute HCV infection is usually subclinical. Chronic
infection and IgG anti-HBc suggests chronic infection occurs in 70-80% cases. Cirrhosis and
infection (when HBsAg is positive) or recovery hepatocellular carcinoma can also occur.
(when anti-HBs is positive). • Extrahepatic manifestations like vasculitis, arthritis,
c. The presence of HBeAg indicates active viral glomerulonephritis and cryoglobulinemia may occur.
replication and high degree of infectivity. Anti-HBe Diagnosis: HCV contains several antigens leading to
appears as HBeAg disappears and its presence antibody formation which are used in its diagnosis. The
suggests low level of viral replication and decreased antibody is not protective and does not confer immunity.
infectivity. The most commonly used screening tests detect anti-HCV.
Gastrointestinal and Hepatobiliary System
These antibodies generally appear late and thus identify discoloration of eyes and skin. Clay-colored stool and
chronic infection. PCR test can detect HCV-RNA in the pruritus suggest cholestasis.
serum 1-2 weeks after infection and is used for the c. Recovery phase: The icteric phase is followed by an
confirmation of diagnosis and for the monitoring of therapy. improvement in general symptoms and a diminution of
jaundice. Complete clinical and biochemical recovery
Hepatitis D occurs within 1-2 months in hepatitis A and E and 3-4
Hepatitis D virus (HDV) is a RNA-defective virus . months in the majority of patients with hepatitis B. In
• It requires HBV for replication and causes hepatitis only about 5% cases recovery is delayed.
in the presence of hepatitis B infection. d. Signs: The sclera is yellow and the skin may show
• HDV infection can occur simultaneously with HBV (co- scratch marks due to pruritus. Tender hepatomegaly is
infection) or it can cause infection in patients suffering present in more than 50% cases. Splenomegaly and
from chronic hepatitis B (superinfection). lymphadenopathy may occur in 10-20% cases.
• Chronic HBV infection superimposed with HDV can
rapidly progress to cirrhosis. Complications
Diagnosis: The diagnosis is made by detecting antibody The most feared complication of acute hepatitis is fulminant
to hepatitis D antigen (anti-HDV) or by finding HDV-RNA hepatitis. It is primarily seen in hepatitis B and D, hepatitis
in serum. E during pregnancy and rarely in hepatitis A. Relapsing
jaundice and cholestasis may complicate hepatitis A. A
Hepatitis E serum sickness like syndrome (arthralgia, rash, angioedema)
Hepatitis E virus (HEV), a RNA virus, spreads by feco-oral may occur in hepatitis B. Extrahepatic complications are
route. It leads to water borne epidemics of hepatitis. seen in hepatitis B and C. Important complications are given
• The clinical features are similar to HAV infection.
• It does not cause chronic infection.
in Table 2.19.
37
• Acute fulminant hepatic failure occurs at high frequency Investigations
if the hepatitis occurs during pregnancy and is associated • During the early phase of hepatitis, there is significant
with high mortality. (>400 units/L) increase in the plasma ALT and AST.
Diagnosis: The diagnosis is made by detecting anti-HEV • This is followed by the rise in serum bilirubin level.
antibodies, IgM type during early phase and IgG type after However, in anicteric hepatitis, the rise in ALT and AST
recovery. is not associated with any rise in bilirubin.
38 disease.
• Serum ferritin is very high in hemochromatosis.
inactivated vaccine) is given intramuscularly followed by
a booster dose at 6-12 months. The dose is 1440 ELU
for adults and half the dose for the children. Travellers to
Treatment endemic area should receive it at least 4 weeks before the
a. Physical activity is restricted. However, bed rest is date of travel. This is also recommended for patients
recommended only in severe cases. with chronic hepatitis B or C to prevent hepatitis A
b. A high calorie diet is recommended. A good protein infection.
Essentials of Medicine for Dental Students
intake should be encouraged. The contents of the Passive immunization: Immune serum globulin is
diet should be palatable and according to the wish administered intramuscularly in the dosage of 0.02 ml/kg
and acceptability of the patient. Hospitalization and to the contacts soon after the exposure.
intravenous fluid (10% glucose) are indicated if oral
intake is not adequate or there is marked nausea and Hepatitis B
vomiting. Active immunization (pre-exposure prophylaxis):
c. Drugs which are hepatotoxic or those that are • Recombinant vaccines containing HBsAg are available.
metabolized in the liver should be avoided. • The standard regimen in adults is 20 µg IM in the deltoid
d. Alcohol intake should be avoided. region at 0, 1 and 6 months. For rapid immunity a
e. Bile salt sequestering agent (cholestyramine) reduces schedule of 0, 1, 2 and 12 months is followed. Children
pruritus in cases with cholestasis. need half the dose (10 µg) while immunocompromized
f. Patients with features of severe hepatic failure such as patients need 40 µg.
alteration in mental status (hepatic encephalopathy) and • The vaccine is particularly indicated in those at high
prolonged PT/bleeding should be hospitalized. risk of getting HBV infection (Table 2.20).
g. No specific therapy is recommended for acute viral • Many countries have included HBV vaccination in their
hepatitis except in acute HCV infection. Subcutaneous infant immunization program.
TABLE 2.20: High risk individuals who require hepatitis TABLE 2.21: Causes of chronic hepatitis
Passive immunization (post-exposure prophylaxis): to cirrhosis. The causes of chronic hepatitis are given in
• This is given to nonvaccinated persons who have Table 2.21.
exposure to HBV through mucous membrane and breaks Chronic hepatitis is classified on the basis of its cause,
in the skin such as accidental needle stick injury. its histological activity and its degree of progression.
• This is also indicated for newborn infants of HBsAg
positive mothers and in individuals who had sexual Chronic Viral Hepatitis
contact with persons with HBV infection. Hepatitis B and C can progress to chronic phase in 1-2%
• A dose of 0.06 ml/kg hepatitis B immunoglobulin and 80% cases respectively.
(HBIG) is given intramuscularly as soon as possible.
• Active immuni-zation with vaccine is also initiated Clinical Features
simultaneously if the person is unvaccinated. These are The clinical features of chronic viral hepatitis are fatigue
injected at different sites. and persistent or intermittent jaundice. Patients may present
Prognosis
with features of cirrhosis and its complications. Extrahepatic
presentations like arthralgia and arthritis, immune complex 39
• Clinical recovery is generally complete in 3-6 weeks. glomerulonephritis, polyartertris nodosa (hepatitis B) and
However, laboratory recovery may be delayed. Overall essential cryoglobulinemia (hepatitis C) may occur.
mortality is less than 1%.
• Hepatitis A patients recover completely without Laboratory Features
progressing to chronic liver disease. Some patients may High and fluctuating levels of serum aminotransferases are
have relapses up to one year. characteristic features. Serum bilirubin is only mildly raised
• The mortality rate in hepatitis B is low but rises higher whereas alkaline phophatase is usually normal. Serum
if superimposed with hepatitis D infection. albumin is low. Prothrombin time is increased in severe cases.
• Acute hepatitis is less severe and more likely to be Biopsy of the liver is required for assessment of
anicteric in hepatitis C. histological activity to grade the chronic hepatitis as mild,
• Hepatitis B and C can progress to chronic phase in moderate or severe.
1-2% and 80% cases respectively. However, 90% Serological tests are needed to identify the viral types
infants and neonates with hepatitis B infection develop and their replication patterns.
chronicity.
• Mortality in hepatitis E is particularly high (10-20%), if Treatment
it occurs during pregnancy. a. Chronic hepatitis B: The treatment of chronic hepatitis
B is needed if there are markers of viral replication and
CHRONIC HEPATITIS ALT is elevated to levels of twice above normal.
Chronic hepatitis is defined as persistent inflammation and Different drugs used are interferon alpha, lamivudine
necrosis of liver for at least 6 months. Progression is slow or adefovir dipivoxil. Interferon alpha is given sub-
in mild forms but severe forms progress rapidly and lead cutaneously in dosage of 5 million units daily or 10
TABLE 2.22: Treatment of chronic hepatitis Two of the commonest causes of cirrhosis are
Chronic hepatitis B viral hepatitis (B, D and C) and prolonged excessive use
Interferon alpha of alcohol. Important causes of cirrhosis are given in
5 million IU s/c daily × 16 weeks Table 2.23.
10 million IU s/c thrice a week × 16 weeks
Pegylated interferon alpha (weekly)
Oral drugs
Pathology
Lamivudine 100 mg OD a. The activation of stellate cells (fat storing cells, Ito cells)
Adefovir dipivoxil 10 mg OD is the central event in the development of cirrhosis
Entecavir 0.5-1 mg OD
Telbivudine irrespective of the cause. The activated stellate cells
Tenofovir transform into multifunctional cells upon interaction
Chronic hepatitis C with hepatocytes, Kupffer cells and cytokines. The
PEG interferon alpha 2a 180 mcg weekly
transformed cells form type I collagen leading to fibrosis.
or
PEG interferon alpha 2b 1.5mcg/kg weekly b. The cirrhosis can be micronodular typically in alcoholics
Plus where the regenerating nodules are small (<1 mm). The
Oral ribavirin 800-1200 mg/day macronodular form is characterized by larger nodules
Autoimmune hepatitis
Prednisolone
and is seen in posthepatitic or postnecrotic cirrhosis.
Azathioprim However, either form can occur at different stages of
Drug induced chronic hepatitis disease.
Withdrawal of causative drug c. Clinical features of the cirrhosis are derived from the
million units three times a week for 4 months. changes in the liver morphology as well as from liver
Lamivudine is used in daily oral dose of 100 mg. This is cell dysfunction (Table 2.24).
41
• Jaundice is generally absent or mild initially. It may of liver size and texture, ascites, portal hypertension and
become severe at later stages. splenomegaly.
c. Endoscopy: Upper gastrointestinal endoscopy is required
• Patient may present with features of portal hypertension
to detect esophageal varices and to exclude other causes
mainly abdominal distension due to ascites and
of upper gastrointestinal bleeding in the stomach and
splenomegaly, hematemesis and melena due to variceal
duodenum.
rupture or hepatic encephalopathy (Table 2.24).
d. Liver biopsy: Biopsy helps in the assessment of severity
• The signs of chronic hepatic dysfunction such as spider
of the cirrhotic changes. Typical histological features
nevi, palmar erythema, gynecomastia, testicular atrophy
may suggest the specific cause of the cirrhosis.
and loss of hair may occur due to disturbances in
hormonal metabolism. Females may have loss of libido, Management
menstrual abnormalities and breast atrophy. Palmar
Management includes general management, treatment of
erythema is redness of thenar and hypothenar eminences specific cause, management of the complications and liver
which may also be found in normal persons and in transplantation.
hyperdynamic circulation. Spider nevi are dilated a. General management:
central arterioles with radiating small vessels (like spider) • The diet should contain an adequate amount of
found mainly on the upper part of the body. They can protein and calories. However, protein intake should
also be seen in normal persons and also during be reduced in case of hepatic encephalopathy.
pregnancy. • Vitamin supplementation is helpful.
• Patients may have hemorrhagic manifestations such as • Salt restriction is required in case of ascites.
epistaxis and increased menstrual flow. • Medications which are hepatotoxic or metabolized
• Other features include parotid gland and lacrimal gland in liver should be given with caution.
enlargement, digital clubbing, Dupuytren’s contracture b. Treatment of specific cause: Alcohol abstinence is
and skin pigmentation. Complication of the cirrhosis is mandatory in alcoholic cirrhosis. Specific therapy is
given in Table 2.25. needed in hemochromatosis and Wilson’s disease.
c. Management of complications: (discussed later) The main clinical features are:
d. Liver transplantation: The most common indication for a. hemorrhage from rupture of varices (hematemesis)
liver transplantation is irreversible progressive chronic b. ascites
liver failure due to cirrhosis. c. splenomegaly
d. hypersplenism
Prognosis
e. hepatic encephalopathy
Overall the prognosis of cirrhosis is poor. Child Pugh’s Splenomegaly is the cardinal finding of portal hypertension.
classification is used for the grading and the prognosis. The Hypersplenism may give rise to thrombocytopenia and
prognosis is favorable if the cause can be corrected. Around leukopenia. Anemia is rare.
25% of the patients survive for more than 5 years. Collateral formation occurs around the esophagus and
PORTAL HYPERTENSION stomach (esophageal varices and gastric varices), the rectum
(hemorrhoids), retroperitoneal space and periumbilically in
Portal hypertension is elevation of portal venous pressure anterior abdominal wall. Collateral vessels in the anterior
above 10-12 mm Hg (normal 5-10 mm Hg). Portal abdominal wall may be visible as tortuous vessels radiating
hypertension results from (a) increased resistance to portal from the umbilicus (caput medusae).
blood flow and (b) high portal blood flow. More commonly, As a result of portal-systemic shunting, various toxic
portal hypertension occurs due to increased resistance. substances enter into systemic circulation without going to
The causes of portal hypertension are classified the liver. This is the basis for hepatic encephalopathy. Musty
according to the site of obstruction in relation to hepatic odor of the breath (fetor hepaticus) due to the presence of
sinusoids— (a) presinusoidal, (b) sinusoidal and (c) post- mercaptans can occur in hepatic encephalopathy.
sinusoidal. Causes of portal hypertension are given in
Table 2.26. Cirrhosis is the most common cause of portal Investigations
42 hypertension. Portal vein obstruction is the next most
common cause.
a. Endoscopy: Esophageal varices suggest the presence of
portal hypertension. However, it does not detect the
cause.
Clinical Features
b. Ultrasonography: It is useful in the evaluation of size
The clinical features result from portal-systemic collateral and texture of the liver, splenomegaly, diameter and flow
formation and portal venous congestion. As there are no pattern of the portal vein, ascites and collateral
valves in the portal vein, retrograde blood flow from portal
Essentials of Medicine for Dental Students
circulation.
venous system (high pressure) to systemic venous circulation c. CT scan and MRI: These are usually not needed.
(low pressure) occurs during portal hypertension. However, these are sensitive methods to detect
TABLE 2.26: Common causes of portal hypertension collaterals.
d. Portal venous pressure: Measurement of portal
Presinusoidal
Extrahepatic venous pressure is needed to confirm portal hypertension
• Portal vein obstruction (thrombosis, trauma, malignant and to determine the level of obstruction. Portal
diseases of pancreas) venography helps in knowing the site and cause of the
Intrahepatic
• Schistosomiasis
obstruction.
• Sarcoidosis, vinyl chloride
Sinusoidal Management
Cirrhosis
The management includes—(a) reduction of pressure in the
Metastatic liver disease
Postsinusoidal portal vein and (b) treatment of the complications.
Intrahepatic a. Reduction in the portal venous pressure: Propanolol and
• Veno-occlusive disease nidolol can be used to lower the portal venous pressure.
Extrahepatic
• Budd-Chiari syndrome (hepatic vein thrombosis)
Transjugular intrahepatic portosystemic shunt (TIPSS)
Gastrointestinal and Hepatobiliary System
and surgical decompression procedures are other options 5. Local measures:
to decrease portal venous pressure. a. Endoscopic intervention: It is most widely used as
b. Treatment of complications: Complications like upper the first line of treatment. Bleeding is stopped in the
GI bleed, ascites, spontaneous bacterial peritonitis majority of cases. Ligation of varices with bands and
(SBP), hepatic encephalopathy and hypersplenism are injection of sclerosing agent (sclerotherapy) are usual
managed as given below. procedures.
b. Balloon tamponade (with Sengstaken-Blakemore
UPPER GASTROINTESTINAL BLEEDING tube) is used when bleeding is massive and
Important causes of upper GI bleeding are given in Table endoscopy is not available.
2.27. Peptic ulcer is the most common cause of upper GI c. Esophageal transection may rarely be needed as a
bleeding. However, the most common cause of upper GI last resort.
bleeding in the cirrhotic patient is rupture of esophageal
varices. Bleeding in cirrhotic patients may also occur due Prevention of Variceal Bleeding
to congestive gastropathy or rupture of gastric varices. 1. Prevention of first hemorrhage (primary prevention)
The bleeding may be contributed by the presence of from varices is accomplished either (a) by the use of
coagulopathy, thrombocytopenia, gastric erosions and drugs. non-selective beta-blocker (propanolol) or (b) by
Variceal bleeding presents as painless hematemesis and prophylactic endoscopic banding.
melena. There may be circulatory shock if the bleeding is 2. Prevention of recurrent bleeding:
massive. GI bleeding can precipitate hepatic encephalopathy. a. Propanolol and band ligation are useful in reducing
Upper GI endoscopy is the best method to detect the recurrent variceal bleeding.
cause of bleeding. Endoscopy may also be used for b. TIPSS or portal-systemic shunt surgery may be
therapeutic interventions. required in patients not responding to the above
measures, however, the risk for hepatic encepha- 43
Treatment of Variceal Hemorrhage lopathy is increased.
1. Urgent hospitalization in ICU
2. Restore the intravascular volume by the blood HEPATIC ENCEPHALOPATHY
transfusion. Hepatic encephalopathy is a neuropsychiatric syndrome
3. Fresh frozen plasma is given to correct coagulopathy. secondary to acute or chronic hepatic failure or due to portal-
4. Reduction of portal venous pressure is achieved by: systemic shunt.
a. Vasopressin infusion (0.2-0.4 unit/min). The toxic substances absorbed from the intestine are
b. Somatostatin or its analogue octreotide (50-100 µg/ either not metabolized by the failing liver or bypass the liver
hr). through portal-systemic shunts. Thus, these harmful
c. TIPSS if bleeding does not respond to drugs and substances (mainly ammonia, mercaptans, short chain fatty
therapeutic endoscopic intervention. acids and false neurotransmitters) reach the central nervous
d. Emergency portosystemic shunt surgery is rarely system and result in alteration in consciousness and other
performed now. manifestations. The alteration in sensorium may range
TABLE 2.27: Causes of upper GI bleeding from mild confusion and disordered sleep patterns to deep
coma (hepatic coma). Flapping tremor (asterixis) and fetor
• Peptic ulcer disease hepaticus are usually present.
• Variceal rupture
• Erosive gastritis (drugs, alcohol, severe illness/stress)
• Gastric malignancy Precipitating Factors
• Mallory-Weiss tear (laceration at gastroesophageal Certain factors may precipitate the onset of encephalopathy
junction due to vomiting)
in otherwise stable cases of cirrhosis. These factors enhance
TABLE 2.28: Precipitating factors for hepatic encephalopathy Management of Hemorrhagic
• Gastrointestinal bleeding Tendency in Liver Disease
• Increased protein in the diet • The administration of vitamin K (10 mg for 3 days
• Constipation
subcutaneously) may be helpful in correction of
• Uremia
• Hypokalemia and alkalosis coagulopathy in cases with vitamin K malabsorption.
• Vigorous paracentesis • Fresh frozen plasma which contains all clotting factors,
• Infections is indicated in active severe bleeding or prior to surgery.
• Drugs (diuretics, sedatives, hypnotics)
• Portal-systemic shunt (TIPSS or surgery)
• Platelet transfusion may be needed in thrombocytopenia
with bleeding.
the production of ammonia or other toxic nitrogenous
substances or affect the CNS directly. The most common Hepatocellular Carcinoma
precipitating factor is upper GI bleeding. Other important Patients with cirrhosis are monitored periodically for the
factors are given in the Table 2.28. development of hepatocellular carcinoma. This is done by
the measurement of serum alpha fetoprotein level and
Treatment imaging techniques.
The treatment of hepatic encephalopathy includes following:
1. The precipitating factors should be identified and Hepatorenal Syndrome
removed. Renal failure occurring in the setting of cirrhosis and ascites
2. Protein should be withheld from the diet in severe cases without any evidence of specific cause of renal dysfunction
or restricted to less than 20 g/day. However, the amount is known as hepatorenal syndrome. Kidneys are intrinsically
of protein in the diet is increased gradually once the normal. The hepatorenal syndrome is believed to be due to
soft stools daily. fluid (<20 ml) in the peritoneal cavity. Ascites can be
4. Oral neomycin (0.5-1 g 6 hourly) can be used to reduce associated with normal or diseased peritoneum. The
gut bacteria and ammonia production. Metronidazole most common cause of ascites is cirrhosis with portal
(250 mg 8 hourly) can alternatively be used. Recently, hypertension. Tuberculosis and malignancies are the other
nonabsorbable agent rifaximin (400 mg orally three times important causes. Table 2.29 shows causes of ascites.
daily) has been found to be effective and safer than
neomycin and metronidazole. Pathogenesis
5. Sedatives and hypnotics should be avoided. However, Increased hydrostatic pressure in portal venous system,
short acting oxazepam may be given to agitated patients. dilatation of splanchnic arterial system, hypoalbuminemia
Flumazenil, a benzodiazepine antagonist may be helpful and reduced plasma oncotic pressure lead to loss of fluid
in some cases. from vascular compartment into peritoneal cavity. These
6. Zinc supplementation may sometimes help. changes cause reduction in the effective circulatory
7. Liver transplantation may be considered in nonresponding volume leading to increased activation of renin-angiotensin-
patients. aldosterone system, enhanced sympathetic activity, and
TABLE 2.29: Causes of ascites
46 refractory ascites.
Treatment of underlying cause: Specific treatment is
by the inflated lung. Hence, upper border of the liver should
also be ascertained by percussion in order to measure the
given in patients according to the cause. For example, span of liver, which is normally 12-15 cm in height.
antitubercular therapy is indicated in tuberculous ascites. Normally the upper liver dullness is at the level of fifth rib
in the right mid-clavicular line. Important causes of
Spontaneous Bacterial Peritonitis hepatomegaly are given in Table 2.30.
Spontaneous bacterial peritonitis (SBP) or primary bacterial TABLE 2.30: Causes of hepatomegaly
Essentials of Medicine for Dental Students
48 A. Hepatitis B
C. Hepatitis E
B. Hepatitis C
D. Wilson’s disease
C. Pernicious anemia
23. Stress ulcer may occur in:
D. Mallory-Weiss tears
13. Budd-Chiari syndrome results from the obstruction of: A. Head injury B. Trauma
A. Portal vein B. Biliary tract C. Burns D. All the above
C. Hepatic veins D. Hepatic artery 24. Hunger pain is found in:
14. All the following contribute to hepatic encephalopathy A. Duodenal ulcer B. Gastric ulcer
except: C. Gastric carcinoma D. Esophageal diseases
A. GI bleeding 25. Jaundice is clinically detectable when serum bilirubin
Essentials of Medicine for Dental Students
ANEMIA • The average life span of RBCs is 90-120 days and around
DEFINITION: Anemia is defined as a decrease in the 1% of RBCs are destroyed in the spleen and replaced
level of hemoglobin below normal for that age and sex. The by the marrow everyday.
normal hemoglobin level varies from 13-16 g/dL in the adult
Clinical Presentations
male and 12-15 g/dL in the female. The Table 3.1 shows the
values of RBC count, hematocrit and hemoglobin, below The symptoms and signs of anemia depend on a number of
which patient is diagnosed to have anemia. factors. Important factors are:
a. Severity of anemia
Normal Hematopoiesis b. Rapidity with which it develops
• Hematopoiesis in adult life takes place in the marrow of c. Cause of anemia
flat bones such as ribs, vertebrae, pelvic bones, sternum, d. Presence of comorbid diseases
scapula and the proximal ends of long bones. Patients, who develop anemia acutely, such as following
• All blood cells arise from a population of cells called massive bleeding, may be highly symptomatic whereas those
hematopoietic stem cells (Fig. 3.1). About 2.5 billion red with gradually developing anemia may have mild symptoms.
blood cells (RBCs), 1 billion granulocytes and 2.5 billion This is due to the development of various compensatory
platelets per Kg of body weight are produced each day. mechanisms in order to improve tissue oxygenation.
• The amount of hemoglobin is maintained by The symptoms and signs of anemia are due to the
erythropoietin, the hormone secreted by renal peritubular anemia per se or due to conditions which have resulted in
cells. anemia. Following are symptoms and signs due to anemia
itself.
TABLE 3.1: Values below which anemia is diagnosed General: Pallor, weakness, malaise, feverishness, tiredness,
Male Female vertigo, tinnitus
Central nervous system: Lack of concentration, decreased
RBC count (million/µL) <4.5 <4.0
Hemoglobin level (g/dL) <13 <12
memory, syncope, altered sensorium, seizures.
Hematocrit % <40 <37
Cardiorespiratory: Palpitation, dyspnea, angina, cardiomegaly,
congestive heart failure, flow murmur.
Hematological System
Gastrointestinal: Anorexia, nausea, distaste, stomatitis,
cheilosis, glossitis, dysphagia, malabsorption, hepatosple- • Hemoglobin , hematocrit
nomegaly. • RBC indices: MCV, MCH, MCHC, and Red cell distribution width
Others: Loss of libido, impotence, menstrual abnormalities. (RDW)
• Reticulocyte count and index
• Total and differential leukocyte count
Classification • Platelet count
Anemia has been classified in various ways. • Cell morphology: size, color, anisocytosis, and poikilocytosis
a. Traditionally it is classified into three groups: (a) dyshe- • Iron status: serum iron level, total iron binding capacity (TIBC), ferritin,
and marrow iron stain
matopoietic, (b) hemorrhagic and (c) hemolytic anemia. • Serum vitamin B12 and folic acid levels
b. Another classification is based on the morphology of • Bone marrow aspiration and biopsy
RBC (MCV, MCH, and MCHC) and is grouped into • Liver function and renal function tests
normocytic/microcytic/macrocytic and normochromic/
hypochromic types (Table 3.2). Investigations
c. However, the recent classification is based on reticulocyte Tests are needed to assess the type of anemia and also to
index, which is a measure of RBC production. The ascertain its cause. Table 3.4 shows the tests generally
reticulocyte index is increased (>2.5) due to increase in performed in anemic patients.
erythropoiesis as occurs in hemolytic and hemorrhagic • Mean corpuscular volume (MCV) of less than 80 fL is
anemias. A low reticulocyte index (<2) shows decreased called microcytosis and MCV of more than 100 fL is
marrow production or maturation defects during known as macrocytosis.
erythropoiesis (Table 3.3). • The variation in red blood cell size and shape is known
as anisocytosis and poikilocytosis respectively.
TABLE 3.2: Red blood cell indices (normal values)
1. Mean corpuscular volume (MCV) 90 + 8 fL
• Correction of reticulocyte count: The reticulocyte count
needs to be corrected according to the hematocrit. The 51
2. Mean corpuscular hemoglobin (MCH) 30 + 3 pg corrected reticulocyte count is further adjusted if
3. Mean corpuscular hemoglobin peripheral blood smear reveals prematurely released cells
concentration (MCHC) 33 + 2% (polychromasia). This is known as reticulocyte index.
Reticulocyte index is the main indicator of RBC
TABLE 3.3: Classification of anemia production.
a. Hypoproliferative (decreased production of red cells): normocytic
normochromic IRON DEFICIENCY ANEMIA (IDA)
1. Bone marrow failure: Aplastic anemia
2. Bone marrow invasion (myelophthisis): Infiltration, fibrosis IDA is the most common form of anemia prevalent
3. Mild to moderate iron deficiency worldwide.
4. Decreased stimulation by erythropoietin: Renal disease,
metabolic defects, inflammation Source and Daily Requirement
b. Maturation defect of RBC
Iron is mainly available from a diet rich in meat, liver, beans,
1. Nuclear defect (defect in DNA synthesis): B12 deficiency, folic
acid deficiency, drug toxicity, and refractory anemia jaggery and green vegetables. Milk is poor source of iron.
(Macrocytic) Daily iron requirement is 1 mg in males and 2 mg in females.
2. Cytoplasm defect (defect in hemoglobin synthesis): Severe iron
deficiency, thalassemias, sideroblastic anemia, and lead Metabolism
poisoning (Microcytic)
c. Hemolytic anemia • Iron is absorbed in the proximal small intestine in the
1. Intrinsic defects: Hereditary spherocytosis, G6PD deficiency, ferrous form. The absorption of iron is facilitated by the
and sickle cell anemia (HbS) presence of acid in the stomach and vitamin C, while
2. Extrinsic defects: Immune mediated, malaria, micro-angiopathic
antacids, calcium, phosphates, and phytates decrease it.
anemia, and toxins
d. Hemorrhagic anemia • Ferrous iron is transported by metal transporter to
enterocytes and stored in the form of ferritin. The iron
is transferred out of enterocytes by transporter ferroportin
into the circulation.
• Iron released into the circulation binds to transferrin and
is transported to sites of uses and storage. Hepatocytes,
enterocytes and macrophages serve as storage reservoir
of iron.
• Recently a liver hormone, hepcidin has been identified
as a principal hormone involved in iron regulation.
Hepcidin regulates the iron homeostasis by targeting
at villus enterocytes, macrophages and hepatocytes.
Thus, liver plays a central role in the regulation of iron
absorpion from the gut and in influencing the release of
FIGURE 3.2: Microcytic hypochromic anemia
iron from the storage sites.
52
and pregnancy. Decreased absorption due to gastrectomy,
Important investigations are peripheral blood examination,
achlorhydria or diseases of the small intestine can also lead
serum iron studies and bone marrow examination. (Fig. 3.2)
to IDA (Table 3.5).
a. The general blood picture is microcytic hypochromic.
Clinical Features b. Serum iron and ferritin are low while total iron-binding
capacity (TIBC) is increased. Transferrin saturation is
Besides having general symptoms of anemia, patients with
below 16%.
IDA may specifically have pagophagia, i.e. craving for ice,
c. Bone marrow stains for iron reveal decreased or absent
Essentials of Medicine for Dental Students
Intravenous iron therapy is indicated in following conditions: Treatment of underlying inflammatory disease usually
a. Patient is unable to tolerate oral iron corrects anemia. Iron therapy is not indicated.
b. Patient has malabsorption
c. The needs for iron are relatively acute as in pregnancy MEGALOBLASTIC ANEMIA
53
or following bleed Most important causes of megaloblastic anemia are
Previously used iron compound, iron dextran has been vitamin B12 deficiency (cobalamin) and folic acid deficiency.
associated with the risk of anaphylaxis which is almost never Vitamin B12 and folic acid are essential for DNA synthesis
seen with newer preparations like sodium ferric gluconate and their deficiency may lead to impaired cellular
and iron sucrose. proliferation and maturation. Rapidly dividing cells
particularly those of hematopoietic and gastrointestinal
Red Blood Cell Transfusion tissues are most affected. A large number of erythroblasts
Red cell transfusion is indicated in patients with severe in bone marrow fail to mature and are destroyed (ineffective
anemia where cardiorespiratory conditions warrant erythropoiesis). Leukopenia and thrombocytopenia occur
immediate intervention. In these situations, whole blood due to impaired proliferation and maturation of respective
must be avoided since it may cause volume overload. Whole progenitor cells.
blood is needed if there is continued and excessive blood
loss. Cobalamin
• The daily requirement of vitamin B12 (cobalamin) is
Anemia of Acute or Chronic about 2.5 µg.
Inflammation/Infection • Cobalamin is not synthesized in the human body and thus
Anemia of acute or chronic inflammation is one of the most must be supplemented in diet. The only dietary source of
common types of anemia which forms an important cobalamin are animal products like meat and dairy foods.
differential diagnosis of iron deficiency anemia because of • It is absorbed in the terminal ileum. The absorption is
similar general blood picture and low serum iron. This type facilitated by the intrinsic factor produced by the parietal
of anemia is characterized by mild to moderate anemia cells of the stomach.
• The cobalamin is largely stored in liver which may last
upto 3-6 years.
Folic acid
• Folic acid (pteroylmonoglutamic acid) is found in
foodstuff from both animal and plant sources. Dietary
folic acid may be destroyed by cooking.
• The body stores are relatively small and may last for
only a few months. The average daily requirement is
50-100 µg, although the demand may increase several
fold during pregnancy.
• It is mainly absorbed in the jejunum.
FIGURE 3.3: Pallor visible over face
Causes of Cobalamin and Folic Acid Deficiency
In tropical countries, megaloblastic anemia occurs mostly c. Neurological manifestations such as paresthesia,
due to folic acid deficiency because of malnutrition and ataxia, sensory-motor paraparesis (subacute combined
during pregnancy. Important causes of cobalamin and folic degeneration), forgetfulness, psychosis are found in
acid deficiency are given in Table 3.7. cobalamin deficiency and may occur even in the absence
of anemia.
Clinical Manifestations
The clinical manifestations are mainly due to the Investigations
red tongue are important and significant gastrointestinal characteristic of megaloblastic anemia (Fig. 3.4)
manifestations.
Hematological System
c. Lactate dehydrogenase (LDH 1) and unconjugated
bilirubin are raised due to ineffective erythropoiesis. a. Idiopathic
d. Bone marrow is hypercellular and reveals megaloblastic b. Secondary
changes. Megaloblasts are abnormally large RBC Drugs: chloramphenicol, sulphonamides, indomethacin, gold,
cytotoxic drugs, and anticonvulsants.
precursors with nuclei less mature than would be
Radiation
expected from the cytoplasmic development. Chemicals: DDT and benzene
e. Serum cobalamin and folate levels are determined to Viruses: hepatitis viruses, parvovirus, HIV-1, Epstein-Barr virus
detect the specific deficiency. Pregnancy
Paroxysmal nocturnal hemoglobinuria (PNH)
f. Serum levels of both methylmalonic acid and c. Inherited
homocysteine are increased in cobalamin deficiency Fanconi’s anemia
while only homocysteine level is increased in folate
deficiency. Clinical Features
g. Schilling test is performed to detect the malabsorption • The common presentations are bleeding and symptoms
of cobalamin. Auto-antibodies against intrinsic factor of anemia.
and parietal cells are found in pernicious anemia. • The excessive tendency to bleed is due to thrombocy-
topenia which may present as easy bruising, epistaxis,
Treatment gum bleeding, heavy menstrual flow and petechiae
Packed red cell transfusion is needed in case of severe (small pinpoint hemorrhage in skin and mucous
anemia with cardiac symptoms. In addition, treatment is membrane). Intracranial and retinal hemorrhages may
directed against the cause of the disease like antibiotics for also occur.
bacterial overgrowth in the intestine. • Neutropenia may predispose patients to develop
Cobalamin deficiency: Parenteral therapy with intramuscular
cyanocobalamin is preferred since deficiency is mostly due •
infections.
Lymphadenopathy and splenomegaly are absent. 55
to malabsorption. The treatment begins with a dose of 1000
µg (1 mg) per week for 8 weeks followed by 1000 µg each Investigations
month. The treatment is life long in case of pernicious a. Peripheral blood smear shows normocytic or macrocytic
anemia. anemia, decreased granulocyte and platelet count.
Folate deficiency: The usual dose of folic acid is 1 mg per Immature cells are absent. Reticulocytes are absent or
day orally. However, higher dosage upto 5 mg daily may be few.
needed in cases of malabsorption. Folinic acid is used in b. The diagnosis is confirmed by the bone marrow
methotrexate-induced anemia. aspiration and biopsy.
c. Other investigations include viral markers, chromosomal
APLASTIC ANEMIA studies, and tests for paroxysmal nocturnal hemoglo-
Aplastic anemia is characterized by pancytopenia (anemia, binuria (PNH). Chromosomal studies are done in
leukopenia and thrombocytopenia) and hypocellular bone children and younger adults to rule out inherited
marrow. In the majority of patients, the cause is not disorders like Fanconi’s anemia.
discernible (idiopathic) while the major known causes are
drugs, radiation and viral infections (Table 3.8). Treatment
a. Bone marrow transplantation: Allogeneic bone marrow
Pathogenesis transplantation (BMT) from HLA matched siblings is
The pathogenesis of bone marrow aplasia is generally curative and the preferred mode of therapy in young
believed to be immune mediated. However, some genetic patients (<40 years). However, this is limited by the
factors may predispose the individual to develop an high cost, nonavailability of matched donors and the
abnormal T cell immune response to exogenous stimuli significant morbidity and mortality. Moreover, this
(drugs, viruses) and subsequent marrow failure. facility is available only at a few centers.
b. Immunosuppressive therapy: Immunosuppressive TABLE 3.9: Classification of hemolytic anemias
agents such as anti-thymocyte globulin (ATG) or anti- Congenital (intrinsic)
lymphocyte globulin (ALG) along with cyclosporine is 1. Membrane defects: hereditary spherocytosis and hereditary
the treatment of choice for patients who cannot be given elliptocytosis
2. Hemoglobinopathies:
BMT.
a. Abnormal chain synthesis; thalassemia
c. Other drugs: The role of anabolic steroids is not clear, b. Amino acid substitution: sickle cell disease (Hb S), HbC,
though some patients may respond to them. HbD
d. Supportive therapy: 3. Enzyme defects: Glucose-6-phosphate dehydrogenase and pyruvate
kinase deficiency
• Severe anemia is managed with packed red cell
Acquired (extrinsic)
transfusion. 1. Immune: Autoimmune hemolytic anemia (AIHA)
• Platelet concentrates are used to maintain platelet 2. Non-immune:
count at or more than 10,000/ µL. Aspirin and a. Mechanical: Disseminated intravascular coagulation
NSAIDs which inhibit platelet function should be (DIC), toxemia of pregnancy, and artificial heart valve
b. Malarial and clostridium infections
avoided. c. PNH (intrinsic)*
• Infections should be aggressively dealt with broad- * PNH is characterized by acquired RBC membrane defect
spectrum antibiotics and antifungal agents. (intrinsic).
Granulocyte transfusion has also been used in
overwhelming infections. Aseptic precautions must Hemoglobinopathy
be observed to prevent infections. Normal hemoglobin (Hb) consists of heme and tetramer of
globin polypeptide chains. Major adult Hb (HbA,) has two
HEMOLYTIC ANEMIA
alpha chains and two beta chains (α2β2) and represents 98%
breakdown is immediately bound to a plasma protein, Reduction in alpha chain synthesis leads to alpha thalassemia
haptoglobin. The hemoglobin also binds with albumin to and that of beta chain leads to beta thalassemia. Hence in
form methemalbumin. In case of severe hemolysis the alpha thalassemia, excess beta chains form β4 tetramer called
haptoglobin binding capacity of plasma is reduced. Hence, HbH. In beta thalassemia, there is relative increase in the
free hemoglobin passes through renal glomeruli and amount of HbF and HbA2 as beta chains are missing and
is converted to ferritin and hemosiderin in proximal are substituted by gamma and delta chains respectively. Beta
tubules and passed in the urine (hemosiderinuria). Excess thalassemia major (Cooley’s anemia) is a severe disease and
hemoglobin that is not absorbed by proximal tubules is manifests in childhood. This condition is transfusion
passed as such in the urine (hemoglobinuria). Unconjugated dependent and generally fatal by 30 year of age. Beta
bilirubin is raised due to increased hemolysis (prehepatic thalassemia minor is mild disease, nontransfusion
or hemolytic jaundice). dependent, and patients can live full normal lives. In case
Hemolytic anemia can be acquired or hereditary. of severe thalassemia, the expansion of bone marrow (due
Hemolysis can occur due to defects in the RBC to extramedullary hematopoiesis) may cause bony
(intracorpuscular or intrinsic defects) or due to causes other deformities, pathological fractures and osteopenia.
than in RBC (extracorpuscular or extrinsic defects). The
Sickle cell anemia: Sickle cell anemia is caused by mutation
classification is given in Table 3.9.
in the beta globin gene that replaces the sixth amino acid
from glutamic acid to valine (Hb S, α2β26 Glu-val). Under TABLE 3.10: Red cell morphology in hemolytic anemias
Hematological System
hypoxic conditions, HbS polymerizes leading to sickling Spherocytes Hereditary spherocytosis and AIHA
of the RBCs which are more liable to hemolysis. Target cells Thalassemia
Microcytes Thalassemia
Clinical Features Schistocytes DIC, eclampsia, and artificial heart valve
Sickled cells Sickle cell syndrome
• The important clinical manifestations are anemia,
recurrent mild jaundice and splenomegaly.
TABLE 3.11: Findings suggestive of hemolysis
• Patients may have fever with chills during hemolysis.
• Other manifestations are gallstones (pigment stones) and Increased RBC destruction:
red brown urine (hemoglobinuria). a. High serum indirect bilirubin
b. Low serum haptoglobin
• The family history may be positive in hereditary disorders c. High serum LDH
like sickle cell disease, thalassemia and hereditary d. Hemoglobinuria and hemosiderinuria (in intravascular hemolysis)
spherocytosis. e. Decreased RBC life span
• A history of drugs and exposure to chemicals should Increased RBC production:
a. High reticulocyte count
also be obtained. This is important in patients with G6PD b. Nucleated RBCs in peripheral smear
deficiency. c. Erythroid hyperplasia in bone marrow
• Characteristic facial features due to marrow expansion
and growth retardation may be seen in inherited disorders e. Urine examination may reveal presence of hemosiderin
for example in thalassemia. or hemoglobin.
f. Serum iron and ferritin levels are normal.
Investigations g. Tests such as hemoglobin electrophoresis, osmotic fragility,
57
a. Peripheral blood smears reveal features of hemolysis Coombs’ test, Glucose-6-phosphate dehydrogenase
like anisocytosis, poikilocytosis, macrocytosis and target (G6PD) levels, sickling tests, and genetic studies are
cells. Characteristic RBC morphology is seen in specific helpful in the diagnosis of the specific causes.
causes (Table 3.10 and Fig. 3.5). h. Amniocentesis and chorionic villi biopsy are performed
b. Reticulocyte count is increased and is most useful in for prenatal diagnosis of inherited conditions like
the diagnosis of hemolytic anemia. thalassemia and sickle cell disease.
c. Bone marrow examination is generally not required.
d. Serum unconjugated bilirubin, methemalbumin, and Treatment
LDH are increased. Serum haptoglobin is decreased or Supportive treatment in form of packed cell transfusion may
absent (Table 3.11). be needed. However, repeated transfusion may lead to iron
overload which in turn may require treatment with chelating
agents, deferoxamine. Folic acid, 5 mg daily is given to
meet the increased demand. Following are other modes of
treatment in specific situations
a. Bone marrow transplantation is curative in thalassemia
and sickle cell disease.
b. Splenectomy may be needed in hereditary spherocytosis
and AIHA.
c. Steroids and other immune suppressive drugs are given
in immune-mediated anemias.
d. Factors including infections, dehydration, hypoxia
(in sickle cell disease) and drugs (primaquine,
sulphonamides) that may precipitate hemolysis in
FIGURE 3.5: Sickle cell anemia persons with G6PD deficiency should be avoided.
ANEMIA OF ACUTE BLOOD LOSS TABLE 3.12: Classification of acute leukemias
Acute blood loss due to trauma and surgery may lead to Acute myeloid leukemia
anemia. A loss of about 20% of blood volume (1 liter) can (French-American-British classification)
• M0 undifferentiated
be tolerated; however, a loss of more than 40% can lead to • M1 Myeloblastic
shock. • M2 Myeloblastic with differentiation
Anemia may be apparent only after volume replacement • M3 Promyelocytic
in patients with acute blood loss. • M4 Myelo-monocytic
• M5 Monoblastic
Other findings include raised total leukocyte count and • M6 Erythroleukemia
platelets, and presence of nucleated RBCs and immature • M7 Megakaryoblastic
leukocytes in the peripheral blood. Maximal rise in Acute lymphoblastic leukemia
• Pre B cell ALL
reticulocytes occur after 1 week. A rise in serum unconjugated
• T cell ALL
bilirubin and fall in serum haptoglobin may occur in case of • B cell ALL
bleeding in an internal cavity.
The management includes treatment of the underlying (Table 3.12). Newer World Health Organization (WHO)
conditions and the blood transfusion. Patient may need iron classification additionally includes cytogenetic and
replacement. molecular features.
depending on the type of cell of origin. • Wide spread bleeding may occur due to disseminated
In majority of cases the etiology of leukemia is not intravascular coagulation (DIC) which is mainly present
known. However, some are associated with ionizing in patients with acute promyelocytic leukemia (AML-
radiation, drugs (alkylating agents), toxins (benzene) and M3).
viral infections. There may be a genetic predisposition for • Malignant cells may also infiltrate various organs leading
the development of leukemia. to lymphadenopathy and hepato-splenomegaly.
• Gum hyperplasia may be seen in monocytic subtype
Acute Leukemias (M4, M5) of AML (Fig. 3.6).
Acute leukemias are broadly classified into acute • Other manifestations are stomatitis, sternal tenderness,
lymphoblastic leukemia (ALL) and acute myeloid leukemia testicular enlargement and infiltration of skin and
(AML). Acute lymphoblastic leukemia is more common in meninges.
children while acute myeloid leukemia is common in adults.
Diagnosis
Classification • Peripheral blood examination reveals the presence of
Acute leukemias are classified on the basis of cell of origin, blast cells with high, low or normal total leukocyte count
morphology and immunophenotypic characteristics (Fig. 3.7).
Treatment
Hematological System
The management of acute leukemia consists of supportive
and specific treatment.
a. Supportive treatment: Anemia is managed with infusion
of red cell concentrate. Platelet transfusion is needed to
treat bleeding manifestations and to maintain platelet
count above 10,000-20,000/µL. The chance of life-
threatening bleeding becomes more when platelet count
is <10,000/µl. Infections are treated with parenteral
broad spectrum antibiotics and antifungal drugs if
required.
b. Specific treatment: The objective of specific treatment
is to eliminate leukemic cells without affecting the
normal cells. However, the therapy may be associated
FIGURE 3.6: Gum hyperplasia in a AML-M5 patient with high morbidity and mortality. Hence, the decision
to administer a specific therapy to a particular patient is
based on the age, type of leukemia and the presence of
other associated illnesses.
• Chemotherapy: In chemotherapy, a combination of
various cytotoxic drugs is given under a standard
protocol. The first step is to achieve remission (normal
blood counts, normal bone marrow, and normal clinical
status). The initial induction phase is followed by the 59
consolidation phase and the maintenance phase. Table
3.13 shows drugs used in acute leukemias.
• Radiotherapy: Cranial irradiation along with intrathecal
methotrexate is given in ALL patients for CNS
prophylaxis.
Prognosis
The cure rate in AML is around 25-30% with chemotherapy
and 50-60% with BMT. The cure rate of >90% can be
achieved by chemotherapy in children with ALL (pre B type).
Typically the course of CML consists of three phases. severe infection and lymphadenopathy.
1. The initial phase is the chronic phase which, without
treatment, may last for 2-3 years. Investigations
2. This evolves into an accelerated phase which finally • The blood examination reveals high total leukocyte count
transforms into a terminal blast phase. (generally in lacs), normocytic normochromic anemia
3. The blast phase is like acute leukemia, which is and high platelet count.
mostly myeloblastic but in about 20% cases, it can • The presence of low platelet count denotes worsening
be lymphoblastic. of the disease.
• Large numbers of immature myeloid cells (metamye-
Clinical Manifestations locytes, myelocytes) are seen in the blood smear.
CML affects individuals in the third and fourth decade. The • Presence of 20% or more blast cells in bone marrow or
common presenting features are weakness, tiredness, weight peripheral blood is diagnostic of the blast phase of CML.
loss and abdominal fullness due to splenomegaly. However, • The diagnosis of CML is confirmed by the demonstration
some patients are asymptomatic at the time of diagnosis. of Philadelphia chromosome on cytogenetic analysis or
Seldom patients suffer from anemia and fever. Worsening the presence of bcr-abl fusion gene by molecular
anemia, splenomegaly, fever and bony pain may suggest techniques.
Treatment
Hematological System
• Bone marrow examination reveals infiltration with
• At present the only known curative method of treatment mature lymphocytes.
of CML is allogeneic bone marrow transplantation (Allo • Coombs test is positive in autoimmune hemolytic anemia.
BMT). However, most patients cannot avail this mode • Thrombocytopenia may occur due to immune destruction
of treatment due to the high cost, lack of proper donor or marrow failure.
or the high risk involved in the procedure particularly if • Serum immunoglobulin levels may be low which gives
the age is above 40 years. an idea about the degree of immunosuppression.
• Imatinib mesylate is the drug of choice for those who • Newer prognostic markers like CD38, ZAP 70 mutation
do not undergo Allo BMT. Imatinib mesylate is a new and VIg mutation are helpful in the management of CLL.
targeted drug which specifically inhibits the bcr-abl
tyrosine kinase. This can result in molecular remission Treatment
in around 60-70% patients. The usual dose is 400 mg Most patients do not require treatment in the early stage
oral daily. Newer tyrosine kinase inhibitor, Dasatinib is of the disease. Those with features of progressive disease
now available and is useful in patients who fail to such as symptomatic lymphadenopathy, anemia or
respond to imatinib. thrombocytopenia need chemotherapy. The therapy of
• The other useful agent is interferon alpha which is more choice is fludarabine based chemotherapy (fludarabine alone
toxic and less effective than imatinib. or in combination with cyclophosphamide and/or anti-CD
• Hydroxyurea is used to control the white blood cell count 20 monoclonal antibody) which provides better response
and has almost replaced the busulphan used previously. and survival.
• The blast phase is managed as acute leukemia. Alternatively oral chlorambucil may be given.
Alternatively imatinib in larger dosage (600 mg daily) Prednisolone is administered in cases of autoimmune
or dasatinib can be tried in blast phase.
Investigations
• The diagnosis of HD is made by lymph node biopsy.
Fine needle aspiration cytology (FNAC) may provide
doubtful results. Presence of Reed-Sternberg cells
(Owl’s eye appearance) is characteristic of the disease
FIGURE 3.9: Reed-Sternberg cell in Hodgkin’s lymphoma
(Fig. 3.9).
• Bone marrow examination, CT chest and abdomen are
done for the staging purposes.
• PET scan (Positron emission tomography) is useful to
document remission.
• Tests such as complete blood count, ESR, serum uric
acid, liver function and renal function tests are helpful
in planning and monitoring the treatment.
Staging
The disease stage is determined after clinical evaluation and
investigations. The Ann Arbor staging system is given in
Table 3.15.
Essentials of Medicine for Dental Students
Treatment
Localized disease: The patients with localized disease (IA,
IIA) are treated with 3 cycles of chemotherapy (ABVD-
FIGURE 3.10: Cervical lymphadenopathy
• A sizable number of patients have mediastinal TABLE 3.15: Ann Arbor staging system
lymphadenopathy.
• About one-third patients have B symptoms—fever, Stage I: Involvement of single lymph node region or lymphoid
structure*.
weight loss and night sweats. Stage II: Involvement of two or more lymph node regions on
• Unusual symptoms are generalized pruritus and pain in same side of the diaphragm.
involved lymph nodes following alcohol ingestion. Stage III: Involvement of lymph node regions or lymphoid
structures on both sides of the diaphragm.
Stage IV: Disseminated disease with liver or bone marrow
Classification involvement.
HD is classified into four types depending on histological A. No systemic symptoms
features (Table 3.14). B. weight loss >10 percent in 6 months, fever, and night sweats
*The lymphoid structures are defined as spleen, thymus, Waldeyer’s
The most common type of HD in USA is nodular ring, appendix and Peyer’s patches
sclerosis whereas mixed cellularity is the most common type
Clinical Features
Hematological System
doxorubicin, bleomycin, vinblastine and dacarbazine)
followed by radiotherapy of involved nodal areas. • The patients may present with localized or generalized
Extensive disease: Patients with B symptoms or extensive painless lymphadenopathy, hepatosplenomegaly and
disease receive complete course (6-8 cycles) of ABVD constitutional symptoms such as fever, weight loss and
chemotherapy. night sweats.
Long-term cure can be achieved in >90% patients with • Extranodal presentations are more common in NHL than
localized disease and in 50-75% patients with extensive in HD. These include involvement of bone marrow, gut,
disease. lungs, testis, thyroid, skin and brain.
• Patients may present with superior vena cava obstruction,
Nodular Lymphocyte Predominant Hodgkin’s intestinal obstruction and spinal cord compression.
Disease • Compared to HD, NHL is often disseminated at
Nodular lymphocyte predominant Hodgkin’s disease is a presentation.
distinct entity which is different from classical HD. In this Low-grade NHL is characterized by low proliferation rate,
type, the Reed-Sternberg cells are rare. The course of the insidious onset of symptoms and slow progression. High
disease is chronic and relapsing and sometimes it transforms grade NHLs have early onset of symptoms with aggressive
into diffuse large B cell NHL. course and are fatal if untreated.
Clot Lysis
The lysis of clot (fibrinolysis) and repair of vessel starts
after the clot formation. Physiological fibrinolysis activators,
tissue plasminogen activator (tPA) and urinary plasminogen
activator (uPA or urokinase) are released from the endothelial
FIGURE 3.12: Platelet plug formation cells and convert plasminogen into plasmin. Plasmin
66 FIGURE 3.13
degrades the fibrin polymer into small fragments, fibrin Disorders of Hemostasis
degradation products (FDPs) which are cleared by the Bleeding due to vessel or platelet disorders is generally
monocyte-macrophage scavenger systems. localized to superficial sites like the skin and mucous
membrane; it occurs immediately after trauma and
Coagulation Inhibitors is controlled by local measures. In contrast, bleeding
Essentials of Medicine for Dental Students
The formation of clot is limited to the site of injury only. due to coagulation disorders occurs in deeper tissues
This is tightly regulated by the coagulation inhibitors such (subcutaneous, muscle, joint, and body cavities), hours or
as antithrombin III, protein C and protein S. These even days after the injury and is not affected by local therapy.
collectively maintain the fluidity of blood. The disorders of hemostasis can be classified into three
TABLE 3.17: Coagulation test abnormalities in types:
various factor deficiencies a. Vessel wall abnormalities
a. Prolonged APTT: Factors XII*, XI, IX, VIII deficiency von Willebrand
b. Platelet disorders
disease 1. Decreased platelet count (thrombocytopenia)
b. Prolonged PT: Factor VII deficiency, early vitamin K deficiency 2. Platelet dysfunction
c. Prolonged APTT and PT: Factors II, V, X, late vitamin K deficiency, c. Coagulation disorders
warfarin, heparin
d. Prolonged Thrombin time (TT): Heparin, afibrinogenemia and 1. Congenital: Hemophilia A and Hemophilia B
dysfibrinogenemia 2. Acquired: Liver diseases, vitamin K deficiency, DIC
e. Clot solubility in 5M urea: Factor XIII deficiency (in this PT, APTT, and coagulation inhibitors (warfarin, heparin)
TT are normal)
Table 3.18 shows laboratory abnormalities in some
*no clinical bleeding occurs in Factor XII deficiency
common hemostatic disorders.
TABLE 3.18: Laboratory abnormalities in some common hemostatic disorders
Hematological System
Conditions Bleeding time Platelet count PT APTT Others
Hemophilia A Normal Normal Normal Raised Low factor VIII level
Hemophilia B Normal Normal Normal Raised Low factor IX level
Von Willebrand’s Disease Prolonged Normal Normal Raised Decreased vWF level, abnormal
platelet adhesion
Idiopathic thrombocytopenic Prolonged Low Normal Normal Increased megakaryocytes on bone
purpura (ITP) marrow examination
Disseminated intravascular Prolonged Low Raised Raised High FDP
coagulation (DIC) Low fibrinogen
Vessel Wall Abnormalities The causes of thrombocytopenia are given in Table 3.19.
The abnormalities of vessel wall, both congenital and
acquired, may result in purpura (bleeding in the skin and Idiopathic (Autoimmune) Thrombocytopenic
mucous membrane). Platelet count, platelet function Purpura (ITP)
and bleeding time are normal. Important causes are This is an autoimmune disorder in which antibodies (IgG)
senile purpura, Henoch-Schönlein purpura, vasculitis, are produced against platelet antigens (gp IIb/IIIa). The
paraproteinemia, scurvy and Ehlers Danlos syndrome. antibody-coated platelets are destroyed by phagocytic cells
in the spleen.
PLATELET DISORDERS
Clinical Features
The most common sites to observe bleeding in platelet
disorders are skin and mucous membrane. a. In children, the onset is generally sudden (acute ITP).
67
Collection of blood in skin is called purpura. Purpura appears 2-3 weeks after viral infection. In most
• Petechiae are small pinpoint hemorrhages into the dermis cases the condition is self-limiting.
due to the leakage of red blood cells through capillaries. b. The onset is insidious in adults and the disease may
• Ecchymoses are large subcutaneous collection of blood persist for years (chronic ITP). Chronic ITP is more
due to leakage from small arterioles or venules (common common in females.
bruises). The common presentations are skin and mucosal bleeding
• Deeper and palpable collection of blood is called in the form of petechiae, ecchymosis, gum bleeding,
hematoma. epistaxi, and menorrhagia (Figs 3.14 and 3.15). Bleeding
• The bleeding in mucous membrane may present as gum in gastrointestinal and genitourinary tract may also occur.
bleeding, epistaxis, and menorrhagia. Spleen is usually not palpable.
The normal platelet count is 1,50,000 to 4,00,000/µL.
Diagnosis
• The patient is usually asymptomatic if platelet count is
more than 1,00,000/µL. • The peripheral blood examination reveals low platelet
• Bleeding occurs only from severe trauma when the count.
platelet count is 50,000 to 1,00,000/µL.
• There is a tendency to easy bruising and purpura after TABLE 3.19: Causes of thrombocytopenia
minor trauma at counts between 20,000 to 50,000/µL. 1. Marrow disorder (decreased production)
• Patients with counts lower than 20,000/µL bleed a. Marrow failure – aplasia, hypoplasia
b. Infiltration – tumor, fibrosis
spontaneously and may have intracranial or internal
c. Vit B12/Folate deficiency
bleeding. 2. Splenic sequestration: splenic tumor and portal hypertension
• It is to be noted that bleeding does not always correlate 3. Increased destruction of circulating platelets
with the platelet count; patient may bleed at a higher a. Immune: ITP, SLE, drug induced, lymphoma, CLL, and HIV
b. Non-immune: DIC, sepsis, prosthetic valve, and TTP
platelet count and vice versa.
a. The initial treatment is with oral prednisolone 1-2 mg/
kg/day. In most patients, platelet count improves within
few days. The dose of prednisolone is tapered when the
platelet count becomes normal.
b. In case of severe and life-threatening bleeding,
intravenous immunoglobulin (IV Ig) is given in the
dosage of 1g/kg for 1-2 days.
c. Splenectomy is indicated when there is no response to
medical therapy or an unacceptably large dose of steroid
is needed to maintain adequate platelet count. Most
patients will respond to splenectomy which is curative
in around 70-80% cases.
d. Patients who fail to respond to steroid and splenectomy
may be given danazol, vincristine, azathioprim, cyclo-
phosphamide or cyclosporine. Monoclonal antibody
(anti-CD20) has also been used in some cases with
success.
FIGURE 3.14: Purpuric rashes on the face e. Platelet transfusion provides only a transient effect and
is reserved only for cases with life-threatening bleeding.
68
Prolonged bleeding time despite normal platelet count
indicates functional disorder of platelets. There may be
defect in the platelet adhesion, aggregation or granule
release. Important causes are given in Table 3.20. Commonly
used drugs, aspirin and clopidrogel cause inhibition of
platelet function. Aspirin irreversibly inhibits platelet
cyclooxygenase I (COX –I) thus blocking synthesis of
Essentials of Medicine for Dental Students
69
although its plasma level is normal. by the deficiency of factor VIII (Hemophilia A) or factor
3. Type III vWD is the most severe form where vWF is IX (Hemophilia B). The disease manifests in males while
nearly absent. females are carriers (Fig. 3.16). Rarely it may also manifest
in females in case the father is a hemophilic and mother is
Clinical Features carrier or if the patient has Turner’s syndrome (45 XO).
In most cases, mild symptoms in form of epistaxis, gum Clinical Manifestations
bleeding, menorrhagia and superficial bruises may be The clinical manifestation of hemophilia depends on the
present. Gastrointestinal bleeding may also occur. Excessive severity of deficiency of the factor VIII or IX.
hemorrhage may be observed after trauma, dental extraction The bleeding is spontaneous in severe cases (Factor activity
or surgery. Unlike hemophilia, hemarthrosis (bleeding in <1%) while it may occur after minor trauma or surgery in
joints) do not occur. moderate cases (level 1-5%).
• People with mild disease (factor activity 5-40%) rarely
Investigations
bleed spontaneously but can bleed following severe
• Platelet count is normal. trauma or surgery.
• Bleeding time and APTT are prolonged. • Severe cases generally manifest in early childhood when
• The factor VIII activity is low. the child starts crawling or walking whereas mild and
• The plasma vWF level is reduced. moderate cases may clinically manifest later in life.
• The platelet adhesion activity of vWF as measured by • The bleeding occurs mainly in joints (hemarthrosis),
ristocetin cofactor assay is reduced. muscles (hematoma), viscera or in retroperitoneum but
it can involve any organ system.
Treatment • The most common joint involved is the knee joint
a. Mild bleeding episodes can be managed by giving (Fig. 3.17). Ankle, elbow and hip joints are also involved.
desmopressin (DDAVP) which increases the vWF level. Warmth, pain and swelling are initial presentations of
joint involvement. Recurrent bleeding in the joint can
lead to synovial thickening, destruction of cartilage,
fibrosis and deformity of joints.
• Calf and psoas muscles are most commonly affected with
hematoma. Bleeding into iliacus muscle often causes
femoral nerve palsy. Patients can also develop large
calcified mass of blood with inflammation that may be
mistaken as tumor (pseudotumor syndrome).
• Hematuria is also common in hemophilia.
• Intracranial and oropharyngeal bleeding may be fatal.
Investigations
• Activated partial thromboplastin time (APTT) is
prolonged.
• Prothrombin time (PT), bleeding time and platelet count
are within normal limits.
• Diagnosis is confirmed by the assay of factor VIII or
IX.
• Prenatal diagnosis can be made by chorionic villi biopsy
or amniocentesis.
bleeding.
• Physiotherapy is indicated once active bleeding stops
to prevent joint deformity.
• Non-steroidal anti-inflammatory drugs and intramuscular
injections should be avoided.
Specific Therapy
• Specific therapy of hemophilia A includes intravenous
administration of factor VIII. The dose, frequency and
duration of factor administration depend on the severity
of the bleeding. A dose of 1 unit/kg factor VIII raises
the activity of the factor by 2%. An increase to around
20-50% activity is generally needed to control bleeding.
The chances of transmission of infections such
as hepatitis, Parvovirus and HIV with uses of plasma
derived factor can be eliminated by the use of
FIGURE 3.17: Hemarthrosis of the knee recombinant factor.
Hematological System
• In case the factor is not available, cryoprecipitate which Most patients have prolonged PT and APTT. Prolon-
is rich in factor VIII, fibrinogen and vWF may be used. gation in PT correlates with bleeding risk. Treatment
• Mild hemophilics may benefit from desmopressin includes parenteral vitamin K and infusion of fresh frozen
(DDAVP) which increases factor level to 2-3 folds. plasma as it contains all coagulation factors.
• Antifibrinolytic agents like ε-amino caproic acid Protein C, protein S and antithrombin III are also
(EACA) and tranaxemic acid can be used in minor dental synthesized in the liver. Deficiency of these coagulation
and oral mucosal bleed. These agents inhibit inhibitors favours coagulation and can predispose the
plasminogen activator in oral tissue and stabilize the clot patients to develop DIC.
formation. EACA is given orally or IV in dosage of 100
Disseminated Intravascular Coagulation (DIC)
mg/kg upto 10g initially followed by 50 mg/kg upto 5 g
6 hourly for 2-7 days. EACA can also be used as a Disseminated intravascular coagulation is characterized by
mouthwash. Tranexamic acid can be given in dosage of widespread coagulation in the microcirculation leading to
0.5-1 gm 8 hourly orally. The filling of carious tooth consumption of coagulation factors and platelets.
requires single infusion of factor VIII combined with Mechanism: Endothelial damage in septicemia and other
antifibrinolytic agents for 3-4 days after the procedure. situations cause release of the endothelial tissue factors
In case of major oral and periodontal surgery and which activate the coagulation process. Thromboplastin
extraction of permanent teeth, the patient needs released from placenta, damaged tissue and injured brain
hospitalization and regular infusion of factor VIII along also activates the coagulation cascade. The formation of
with EACA. fibrin stimulates the fibrinolytic system generating fibrin
degradation products (FDP). The deficiency of coagulation
Therapy of Hemophilia B factors and platelets leads to hemorrhagic manifestation
which is further exacerbated by the activation of the
The specific treatment of hemophilia B is the intravenous
administration of factor IX. Desmopressin and
fibrinolytic system. The important causes of DIC are
mentioned in Table 3.21.
71
cryoprecipitate are not effective.
Clinical Features
Acquired Coagulation Disorders
• Since DIC leads to both thrombosis and bleeding, the
Acquired coagulation disorders are common and generally manifestations are either in the form of tissue infarction,
complex. There is deficiency of multiple coagulation factors. digital ischemia and gangrene or bleeding at various
Most common acquired coagulation disorders are DIC, sites. Spontaneous oozing from venipuncture sites or
hemorrhagic diathesis due to liver disease, vitamin K wounds is an important clue to the diagnosis of DIC.
deficiency and complications of anticoagulant therapy.
TABLE 3.21: Causes of DIC
Liver Diseases Infections
• Gram-negative bacterial infections
• Most of the coagulation factors are synthesized in liver. • Gram-positive bacterial infections
Hence, there may be deficiency of these factors in liver • Fungal infections
diseases. • Malaria
• Vitamin K absorption is reduced in cholestatic liver Obstetric
• Retained dead fetus
diseases leading to decreased synthesis of vitamin K • Amniotic fluid embolism
dependant factors (II,VII, IX, X). • Abruptio placentae
• The bleeding in liver diseases is compounded by the Malignancies
• Lung, pancreas, prostate cancer
presence of anatomical lesions like esophageal varices,
• Acute promyelocytic leukemia
gastritis and peptic ulcer disease. Tissue injury
• Thrombocytopenia can occur in patients having chronic • Burns
liver disease with splenomegaly (hypersplenism). • Head injury
• DIC can present as recurrent deep or superficial vein TABLE 3.22: Important causes of neutropenia
thrombosis, particularly in cancer patients. Drug induced
• Microangiopathic hemolysis can lead to anemia. • Anti-cancer drugs, antibiotics (sulphonamides, chloramphenicol),
anticonvulsants (carbamazapine), and antithyroid drugs
Investigation Hematological diseases
• Aplastic anemia, acute leukemia, myelofibrosis, tumor invasion and
The DIC is suspected when there is a suggestive clinical megaloblastic anemia
situation (as mentioned in Table 3.21) along with following Infections
laboratory findings: • Tuberculosis, typhoid, kala azar, malaria, infectious mononucleosis,
and HIV
a. Low platelet count
Autoimmune
b. Increased PT and APTT • Systemic lupus erythematosus, and Felty’s syndrome Congenital
c. Low plasma fibrinogen level • Cyclic neutropenia
d. Elevated plasma FDP (d-Dimer assay)
e. Schistocytes (fragmented RBC) on peripheral blood
smear. Manifestations
The manifestations depend on the severity and duration
Management of neutropenia and the type of underlying illness.
This includes the following steps: Oral ulcers are usual in agranulocytosis. The patient
1. Prompt management of underlying disorders such as: develops fever and infections mainly of oropharynx,
a. antibiotics in septicemia perirectal area, sinuses, lungs and skin. Common organisms
b. delivery of fetus in obstetric complications responsible for infections are gramnegative enteric bacilli,
2. Patients with bleeding manifestations should receive Pseudomonas spp., Staphylococcus spp., Candida and
Aspergillus.
72
fresh frozen plasma (FFP) to replace coagulation factors
and platelet transfusion to correct thrombocytopenia. A careful history of exposure to drugs, toxins and
3. Heparin is indicated in patients where the predominant duration of illness should be asked. A careful examination
manifestation includes thrombosis and gangrene. Role of oropharynx and perirectal area should be done. The
of heparin in patients with bleeding manifestations presence of lymphadenopathy and hepatosplenomegaly
is controversial. However, it may be given in such should also be noted.
situations where the bleeding is not controlled despite
Investigations
Essentials of Medicine for Dental Students
Hematological System
Growth factors (G-CSF or GM-CSF) are used to reduce the
chance and severity of neutropenia after chemotherapy and • Chronic myeloid leukemia
radiation therapy. • Portal hypertension
• Myelofibrosis
SPLENOMEGALY • Malaria
• Kala azar
Spleen is a reticuloendothelial organ which lies in the left
upper quadrant of abdomen. The important functions of Clinical Manifestations
spleen are: The symptoms due to splenomegaly are abdominal
a. Removal of old and defunct red blood cells from discomfort and pain. Massive splenomegaly may cause early
circulation satiety and abdominal bloating due to abdominal
b. Synthesis of antibodies in the white pulp compression. Splenic infarction may result in severe pain
c. Removal of antibody-coated bacteria and blood cells radiating to the left shoulder. Repeated splenic infarction in
d. Spleen can form blood cells when the bone marrow sickle cell disease may lead to splenic destruction
is unable to meet the demand (extramedullary (autosplenectomy). Rupture of enlarged spleen can occur
hematopoiesis). spontaneously or due to trauma and this may be fatal.
e. It also serves as a reservoir (store) for platelets and Pancytopenia may occur in patients with splenomegaly
neutrophils. (hypersplenism).
Increase in the normal function can lead to splenomegaly.
Causes of splenomegaly are given in Table 3.23. Diagnosis
The spleen is normally not palpable. If palpable, it is A detailed history and clinical examination are helpful in
enlarged (Fig. 3.18). The direction of enlargement is towards knowing the underlying cause of splenomegaly. One should
right iliac fossa. The maximum diameter of spleen on
ultrasonographic assessment is around 13 cm. Massive
particularly look for the presence of fever, bleeding,
lymphadenopathy and hepatomegaly. The following 73
splenomegaly is defined as the spleen palpable more than 8 investigations can be helpful in making a diagnosis:
cm below costal margin. The common causes of massive 1. Complete blood count
splenomegaly are mentioned in Table 3.24. 2. Bone marrow examination
3. Imaging (ultrasonography, CT scan)
TABLE 3.23: Causes of splenomegaly 4. Screening for infections and autoimmune diseases
5. Endoscopy of the upper gastrointestinal tract.
Hyperplasia in response to infection
• Malaria and kala azar
• Infectious mononucleosis, cytomegalovirus infection, HIV infection,
and viral hepatitis
• Endocarditis, tuberculosis, typhoid fever, and septicemia
• Histoplasmosis
Hyperplasia due to excessive function of red cell removal
• Spherocylosis, thalassemia, and early sickle cell disease
Hyperplasia in response to immune disorder
• Felty’s syndrome, SLE, and sarcoidosis
Extramedullary hematopoiesis
• Myelofibrosis and marrow infiltration
Congestive splenomegaly
• Portal hypertension (cirrhosis, hepatic vein obstruction, portal vein
thrombosis)
Infiltration of spleen
• Leukemias, lymphomas, Myeloproliferative disorders, amyloidosis,
and storage diseases (Gaucher’s disease, Niemann-Pick disease).
FIGURE 3.18: Splenomegaly
LYMPHADENOPATHY
Enlarged lymph nodes may be localized or generalized. The
Table 3.25 shows important causes of lymphadenopathy.
Generalized lymphadenopathy is defined as the enlargement
of three or more noncontiguous lymph node areas. Inguinal
lymph nodes of upto 2 cm size and submandibular lymph
nodes of upto 1 cm are generally considered normal.
• Lymphadenopathy may be the presenting symptom or it
may be noticed incidentally when examined for other
reasons.
• In more than two-third of the cases, the cause of
lymphadenopathy is nonspecific or reactive.
• The enlargement of supraclavicular and scalene lymph
nodes is always abnormal. The left supraclavicular node
can be enlarged in metastasis from GI malignancy
(Virchow’s node, Fig 3.19).
TABLE 3.25: Causes of lymphadenopathy
Infections
• Viral: EBV, CMV, and HIV FIGURE 3.20: Cervical lymphadenopathy
• Bacterial: Streptococci, Staphylococci, and tuberculosis
• Spirochaetal: syphilis • The most common site of localized lymphadenopathy
74 • Fungal: histoplasmosis, and coccidioidomycosis
• Parasitic: filariasis, kala azar, and toxoplasmosis
Malignancies
is the neck (Fig. 3.20) which is generally due to upper
respiratory infections, oral and dental lesions and viral
• Primary: lymphomas, ALL, and CLL illnesses (infectious mononucleosis and others). In India,
• Metastasis: from various primary sites tuberculosis is an important cause of lymphadenopathy.
Immunological diseases
• Metastasis from cancer of head and neck, lung and
• Rheumatoid arthritis, SLE, and drugs (phenytoin)
Miscellaneous thyroid may also lead to cervical lymphadenopathy.
• Sarcoidosis and amyloidosis • Generalized lymphadenopathy may be found in
Essentials of Medicine for Dental Students
Diagnosis
History: A detailed history of the presence of fever, weight
loss, cough, sore throat, pain in lymph nodes, occupation,
sexual behavior and drug intake is taken.
Examination:
a. The lymph nodes are examined for the size, texture,
tenderness, mobility and for the signs of inflammation
over the node (Fig. 3.21).
• Hard, fixed and nontender lymph nodes are
FIGURE 3.19: Left supraclavicular lymphadenopathy metastatic.
(Virchow’s node) • Rubbery lymph nodes are found in lymphoma.
Hematological System
5. Painful infarcts in the jaws in sickle cell disease may be
mistaken for toothache or osteomyelitis.
6. Patients with splenectomy are more prone to infections.
Hence, dental procedures in such patients should be done
under prophylactic antibiotics.
7. Infection and bleeding pose major problem in the dental
management in patients with aplastic anemia. Gingival
bleeding may be controlled by the use of local hemostatic
measures and use of systemic antifibrinolytic agents
(tranexamic acid, aminocaproic acid). Oral infection can
be reduced by use of chlorhexidine oral rinses.
8. Cyclosporin (used in patients with aplastic anemia) can
result in gingival swelling.
9. Intramuscular injections and nerve block anesthesia are
FIGURE 3.21: Examination of cervical lymph node
avoided in patients with thrombocytopenia. However,
• Matted lymph nodes are characteristic of tuber- intraligamentary anesthesia can be used safely.
culosis. 10. Oral ulcers, advanced periodontal disease, pericoronitis
b. The presence of skin lesions, hepatomegaly and and pulpal infections can lead to life-threatening
splenomegaly should be noted. septicemia in patients with severe neutropenia. The
c. Careful oral, dental and throat examination is performed patients should be given appropriate antibiotics and
in cases with cervical lymphadenopathy. mouth rinses.
d. Abdominal and mediastinal lymphadenopathy may only
be detected by imaging.
11. Oral bleeding, oral ulcers, gingival infiltrates, oral
infections and cervical lymphadenopathy may be the 75
Investigations: The following investigations are helpful in presenting features of leukemias. Hence, the dentist may
making a diagnosis: be the first clinician to suspect the disease.
1. Complete blood count 12. Spontaneous gingival bleeding is common when platelet
2. Lymph node biopsy/FNAC count is below 20,000/mm3.
3. X-ray chest, ultrasonography, CT scan 13. A history of any bleeding manifestations (including
4. Bone marrow examination family history) must be asked in patients undergoing
5. Screening for infections and autoimmune illnesses dental procedures. In case of such history, investigations
should be performed to diagnose or exclude hemostatic
IMPLICATIONS ON DENTAL PRACTICE disorders.
1. Elective oral surgical and periodontal procedures should 14. A history of anticoagulant therapy must be noted.
be avoided in patients with severe anemia. Increased Non-surgical treatment can be carried out provided the
bleeding and impaired wound healing may occur in PT/ INR is not grossly above the therapeutic range
presence of anemia. and trauma is minimal. Surgical treatment is not
2. Glossitis, burning mouth, angular stomatitis and recommended for those who have INR >3.5. At an INR
aphthous stomatitis can be early manifestations of iron, <3.5 where bleeding is expected (in procedures like
vitamin B12 or folate deficiency. These may occur before multiple extractions, removal of wisdom teeth, full
the appearance of anemia. mouth or arch extraction) local measures should be used
3. Iron syrups may lead to staining of teeth. This can be along with the reduction of INR to 2-3. Extensive flap
prevented by using sodium ironedetate. surgery or multiple bony extraction may require an INR
4. General anesthesia is not administered if Hb level is <10 of <1.5.
g/dL. Hemolytic anemias, particularly sickle cell disease 15. The transfusion of blood and blood components should
may pose difficult problem during general anesthesia. be done if absolutely necessary to avoid the risk of
transfusion-associated infections such as HIV, hepatitis 13. Most of the coagulation factors are synthesized by:
B, hepatitis C, syphilis, malaria, cytomegalovirus and A. Kidneys B. Bone marrow
parvovirus. C. Liver D. Capillary endothelial cells
14. Most of the bilirubin is formed in:
SELF ASSESSMENT A. Liver B. Spleen
C. Gallbladder D. Red blood cells
Multiple Choice Questions 15. Platelet dysfunction can be found in following except:
1. Raised PT and PTT are seen in: A. vWD B. Uremia
A. Thrombocytopenia B. vWD C. Aplastic anemia D. Aspirin therapy
C. DIC D. Hemophilia. 16. The following can be found in aplastic anemia except:
2. Which of the following manifestations is characteristic of A. Thrombocytopenia B. Splenomegaly
hemophilia: C. Low reticulocyte count D. Infections
A. Gum bleeding B. Petechiae 17. Which one of the following is seen in ITP:
C. Hemarthrosis D. Epistaxis A. Raised bleeding time B. Raised PT
3. Gum hypertrophy can be seen in: C. Raised PTT D. High plasma FDP
A. AML B. CLL 18. A 20-year girl develops excessive and prolonged bleeding
C. CML D. ALL following tooth extraction. Tests reveal raised PTT, normal
4. Gum bleeding can occur in: PT, normal platelet count. The most probable diagnosis is:
A. ITP B. Acute leukemia A. vWD B. ITP
C. vWD D. All of the above C. Hemophilia D. DIC
5. Microcytic hypochromic anemia is seen in all except: 19. Following are vit K dependent coagulation factors:
A. Thalassemia B. Iron deficiency A. VIII, IX, and IX B. II, VII, IX, X
C. Folate deficiency D. Pyridoxine deficiency C. II, V, VII, IX D. V, VII, X, XII
6. In hemolytic anemia the following can occur:
76 A. Indirect hyperbilirubinemia
B. Splenomegaly C. Gallstones
20. The mechanism of action of tranexamic acid is:
A. Anticoagulation
B. Antifibrinolysis
D. All of the above C. Enhancing platelet aggregation
7. Which is true in vWD: D. All of the above
A. Normal PT 21. The following are found in DIC:
B. Normal APTT A. Thrombocytopenia B. Excessive bleeding
C. Decreased platelet count
C. Thrombosis D. All the above
Essentials of Medicine for Dental Students
Hematological System
A. Microcytosis B. Koilonychia 10. Coombs’ test is positive in ________anemia.
C. Raised reticulocyte count 11. Most common inherited bleeding disorder is ________.
D. Low plasma ferritin 12. Hard, fixed and non-tender lymphadenopathy
28. The therapy of choice in bleeding secondary to liver suggests a diagnosis of ________.
dysfunction is: 13. Virchow’s node is ________.
A. Cryoprecipitate B. Fresh frozen plasma 14. Fish tapeworm can cause________deficiency anemia.
C. Factor VIII D. Platelet transfusion 15. Vegetarians are prone to develop________deficiency.
16. Massive splenomegaly is defined as ________.
Fill in the Blanks 17. Localized lymphadenopathy most commonly occurs
1. The most common type of leukemia in children is in ________region.
________. 18. Matted lymph nodes are seen in________.
2. Philadelphia chromosome is present in patients 19. The daily dose of oral iron for treatment of iron
of________. deficiency anemia is________.
3. Oral anticoagulant therapy is monitored by ________ 20. The MCV is________in pernicious anemia.
test. 21. The most common cause of microcytic hypochromic
4. PTT is used to monitor________therapy. anemia is________.
5. Koilonychia is seen in ________. 22. Normal absolute eosinophil count is________.
6. The plasma level of haptoglobin is________in 23. The life span of RBC is________.
hemolytic anemia. 24. Hypersegmented neutrophils are characteristically
7. Imitanib mesylate is used in the therapy of ________. found in________anemia.
8. Spontaneous bleeding can occur in thrombocytopenia 25. Schilling test is useful in the diagnosis of________
if platelet count falls below________. anemia.
77
Chapter
4 Cardiovascular System
SYMPTOMS AND SIGNS OF CARDIOVASCULAR TABLE 4.1: The New York Heart Association (NYHA)
DISEASES grading of dyspnea
Grade 1 No breathlessness
Symptoms Grade 2 Breathlessness on severe exertion
Following are important symptoms in patients with cardiac Grade 3 Breathlessness on mild exertion
Grade 4 Breathlessness at rest
diseases:
• Dyspnea
Paroxysmal nocturnal dyspnea (PND): PND is a condition
• Chest pain
when patients may wake up in the night with complaints of
• Palpitation
severe breathlessness and wheezing. Patient is relieved by
• Oedema
sitting upright or standing. Patient usually opens window
• Syncope
or door for fresh air. PND is a variant of orthopnea and is
• Fatigue
due to same mechanisms. In advanced failure, patient may
not be able to lie supine at all.
Dyspnea
Dyspnea is an abnormally uncomfortable awareness Palpitation
of breathing. Main causes of dyspnea are diseases of
Palpitation is an unpleasant awareness of the beating of the
cardiovascular system and pulmonary system (see also chapter
heart. It may occur due to abnormalities in the rate, rhythm
5). In cardiovascular system this is mostly due to heart failure.
or force of contraction of the heart.
In heart failure elevated pulmonary venous and capillary
• Important causes of palpitation are atrial, junctional and
pressure leads to pulmonary congestion. Pulmonary
ventricular tachyarrhythmias.
congestion leads to decreased lung compliance and
• Rapid irregular palpitation is due to atrial fibrillation.
increased airway resistance. Hence, an extra effort is needed
• Other causes are extrasystole, high cardiac output states
to ventilate lungs. Other mechanisms of dyspnea are
(anemia, thyrotoxicosis) and valvular regurgitation
respiratory muscle fatigue and acidosis. Rapid, shallow
(mitral regurgitation, aortic regurgitation).
breathing is characteristic of cardiac dyspnea.
Dyspnea is classified in four grades depending on Chest Pain
severity, that is, level of exertion required to provoke its
Chest pain is the common presentation in the cardiac disease,
onset (Table 4.1). The breathlessness in cardiac patients may
although it can also occur in diseases of the lungs, chest
be on exertion, at rest or in the supine position (orthopnea).
wall or in anxiety states (Table 4.2).
Orthopnea: Orthopnea, breathlessness on lying flat, is due
• The chest pain due to ischemic heart disease typically is
to redistribution of fluid from abdomen and lower
constricting, heavy or choking in character, occurs in
extremities to chest in recumbent position (increased venous
retrosternal area, may radiate to left arm or shoulder
return) and elevation of diaphragm.
and is provoked during exertion. The pain may be
Cardiovascular System
accompanied by sweating, nervousness, breathlessness
or marked anxiety (see Chapter 1: Table 1.1).
• The chest pain may also occur due to aortic dissection,
pericarditis, pneumothorax or esophagitis.
• The pain in pericarditis is sharp central or to the left
side of the chest which increases on deep inspiration
and during coughing or postural changes.
Fatigue
Fatigue is an important symptom of cardiac failure. It is
due to decreased oxygen delivery to muscles.
Edema in heart failure is a manifestation of systemic venous infarction. A syncopal attack due to heart blocks is known
congestion and increased salt and fluid retention which as Stokes-Adams attacks. (see page 114)
occurs as compensatory mechanism. Edema generally
presents first in the dependent parts of the body. This is Hemoptysis
usually bilateral and presents initially in feet, and is more Patients with mitral stenosis may have hemoptysis. Pink
marked at the end of the day (Fig. 4.1). However, edema frothy sputum associated with sudden severe breathlessness
may be localized in the sacral area in bed-ridden patients and cough signifies pulmonary edema.
(see also Chapter 1).
Syncope
General Examination
The clinical examination in a cardiac patient should include
79
Syncope is defined as transient loss of sensorium due a complete general examination together with a systemic
to decreased cerebral blood flow. There is generally a cardiac examination. Other relevant systems are also
spontaneous recovery. Important cardiac causes of syncope examined for making a complete diagnosis.
are arrhythmias, aortic stenosis and massive myocardial A thorough examination is mandatory. One should
specifically look for chest deformities, anemia, cyanosis,
TABLE 4.2: Causes of chest pain clubbing of fingers and toes, edema, hepatomegaly,
a. Cardiac causes cutaneuos signs of infective endocarditis, arterial pulses,
• Myocardial infarction jugular venous pulsations and blood pressure.
• Pericarditis
• Dissection of aorta
Anemia
b. Non-cardiac causes
• Functional Anemia may be a precipitating factor in ischemic heart
• Disease of thorax disease and heart failure. It can be present in infective
Herpes zoster
Costochondritis
endocarditis.
Myalgia
Pleurisy Cyanosis
Pneumothorax
Cyanosis is a bluish discoloration of the skin and mucous
Pulmonary embolism
c. Extrathoracic causes membrane caused by increased concentration of reduced
• Esophagitis hemoglobin (>4 g %) in superficial blood vessels. Cyanosis
• Peptic ulcer is looked for at lips, nailbeds, malar area, ear lobes and the
• Cholecystitis
• Pancreatitis
mucous membrane of the oral cavity. Cardiac causes of
cyanosis are cyanotic congenital heart disease (Fallot’s
tetralogy, Eisenmenger’s syndrome) and pulmonary edema.
Cyanosis in congestive heart failure can be both central and
peripheral types (see also Chapter 1).
Edema
Edema which pits on digital pressure is a feature of cardiac
failure (Fig. 4.1). Later the edema may progress to anasarca.
Clubbing
Clubbing of fingers and toes is found in cyanotic heart disease
and infective endocarditis (Fig. 4.2).
Arterial Pulse
Arterial pulse should be examined for the rate, rhythm,
FIGURE 4.4: Palpation of the right carotid artery with the left
thumb
Blood Pressure
Blood pressure is measured in both arms and also in the
lower limb. In coarctation of aorta, the arterial pressure in
the upper limb is much higher than in lower limbs. The
pulse pressure is wide in AR, anemia and pregnancy whereas
it is narrow in AS. Hypotension may occur in cardiac failure
FIGURE 4.2: Clubbing in cyanotic heart disease (see Chapter 1).
Cardiovascular System
Jugular Venous Pulse • Pulsations in left parasternal area and epigastrium may
A raised jugular venous pressure (JVP) is a sign of be seen in cases of right ventricular enlargement.
right heart failure. The JVP may rise during inspiration • Pulmonary component of second heart sound (P2) is
in constrictive pericarditis and cardiac tamponade palpable in second left parasternal area in case of
(Kussmaul’s sign). “a” wave is absent in atrial fibrillation pulmonary hypertension.
whereas it is prominent in tricuspid stenosis (TS). • A thrill (palpable murmur) may be palpable in systolic
Prominent “Y” descent is seen in tricuspid regurgitation (see phase (MR, AS, ventricular septal defect) or diastolic
Chapter 1). phase (MS, AR) in corresponding areas.
Auscultation
Others
• The first heart sound (S1) corresponds to the closure of
• Inspiratory crepitations over the lung bases are present
mitral and tricuspid valves. It is loud in MS and muffled
in patients with heart failure. In patients with pulmonary
in MR.
edema, coarse crepitations are heard widely along with
• The second heart sound corresponds to the closure of
wheezing.
aortic (A2) and pulmonary valve (P2). The pulmonary
• Tender hepatomegaly may be present in cases with heart
component of the second heart sound (P2) is loud in
failure.
pulmonary hypertension and soft in pulmonary stenosis.
• Splenomegaly can be found in subacute infective
Aortic second sound (A2) is soft in AS. There is a wide
endocarditis.
and fixed split of second heart sound in atrial septal
• Ascites may occur in severe heart failure.
defect (ASD).
• Abdominal bruit over renal area may be found in
• The presence of third heart sound (S3) in children may
hypertension due to renal artery stenosis.
CARDIAC EXAMINATION
be physiological. However, after the age of 40 yrs it may
signify ventricular failure. 81
• The fourth heart sound (S 4) occurs due to vigorous
atrial contraction with a noncompliant ventricle (as in
Inspection and Palpation
hypertension, AS).
• The lowermost and outermost distinct cardiac pulsation • Opening snap (OS) is audible due to forceful opening
is known as cardiac impulse or apex beat. It is normally of the mitral valve in diastolic phase preceding the murmur
situated in the fifth intercostal space just medial to and is heard in cases of noncalcific mitral stenosis.
mid clavicular line. The apex beat may be shifted inferiorly • Ejection click may be heard due to opening of the
or laterally in cardiac enlargement. The stenosed aortic or pulmonary valve.
apex beat is insignificant in cases of pericardial The murmurs are found because of turbulent flow
effusion and mitral stenosis (MS) whereas prominent within the heart and great vessels. An increased flow
in mitral regurgitation (MR), aortic regurgitation across the normal valve may also generate murmur (innocent
(AR) and aortic stenosis (AS). The apex beat is or functional murmur). The murmurs are generally
palpated to determine its location and character. It is defined by characters such as site, loudness, quality, timing
“tapping” in character in MS while thrusting in AS and and radiation. Different murmurs found in heart diseases
AR. are mentioned in Tables 4.3 and 4.4.
TABLE 4.3: Auscultatory findings in rheumatic valvular heart disease
Mitral stenosis Loud S1, Loud P2 Opening snap Mid-diastolic murmur
Mitral regurgitation Soft S1, Loud P2 Pansystolic murmur
Aortic stenosis Soft A2 Ejection click Ejection systolic murmur
Aortic regurgitation Soft A2 Early diastolic murmur
TABLE 4.4: Types of murmur and their causes
Pansystolic MR, TR, VSD
Ejection systolic AS, PS
Early diastolic AR, PR
Mid-diastolic MS, TS, Austin Flint in AR
Continuous PDA
INVESTIGATIONS
Chest X-ray
Chest X-ray is useful in detecting cardiomegaly (Fig. 4.5).
Dilatation of individual chambers can also be recognized on
X-ray of the chest. It may also reveal signs of increased
pulmonary blood flow (pulmonary plethora) and pulmonary
hypertension.
Echocardiography Others
This very useful noninvasive procedure is employed to Myocardial perfusion imaging with radioactive thallium,
diagnose structural and functional abnormalities of the heart magnetic resonance imaging (MRI) and positron emission
and the presence of cardiac vegetations. Doppler tomography (PET) are other techniques employed in patients
echocardiography can detect the abnormal direction of flow with cardiac diseases.
Treatment Pathophysiology
1. Eradication of streptococci: A 10 day course of The size of the orifice of normal mitral valve is 4-6 cm2.
erythromycin (250 mg 6 hourly oral) or oral penicillin The orifice is progressively narrowed by fibrosis and
V (500 mg twice daily) is administered to all patients to calcification of valve leaflets, fusion of commissures and
eradicate streptococcal infection. Alternatively, a single shortening of chordae tendineae. Mitral valve orifice less
intramuscular injection of benzathine penicillin G (1.2 than 2 cm2 is hemodynamically significant and becomes
million units) may be given. “critical” at <1 cm2. The obstruction to the flow of blood
2. Bedrest: This is required in patients with severe carditis. through the stenosed mitral valve during diastole causes a
This is also helpful in reducing joint pain. The duration rise in left atrial pressure. This leads to the hypertrophy and
Investigations
1. ECG may reveal the evidence of left atrial (LA)
enlargement, right ventricular (RV) hypertrophy and atrial
fibrillation (Fig. 4.7).
2. Chest X-ray shows findings suggestive of LA
FIGURE 4.7: Atrial fibrillation
enlargement and pulmonary congestion.
3. Echocardiography is the most sensitive and specific of
non-invasive methods to diagnose the valvular disease. 3. Digoxin is given to control ventricular rate in patients
It may reveal structural abnormalities of the valves, size with AF. Beta blocker and calcium antagonists (verapamil,
of cardiac chambers, pulmonary artery pressure, diltiazem) can also be used.
ventricular dysfunction and presence of thrombi. 4. Oral anticoagulant (warfarin) is given to patients with a
Transesophageal echocardiography provides better history of thromboembolic events or to those with AF
information than transthoracic echocardiography. (INR of 2.0-3.0).
4. Cardiac catheterization is used to assess associated 5. Prophylaxis should be given to all patients to prevent
valvular lesions and to detect coronary artery disease. rheumatic fever (see prophylaxis for rheumatic fever).
6. Prophylaxis for infective endocarditis should be given
Treatment
prior to procedures (see prophylaxis for endocarditis).
Medical Recent guidelines recommend prophylaxis only if there
Medical treatment of mitral stenosis consists of:
1. Restriction of physical activity.
is a prior history of endocarditis.
85
Surgical
2. Sodium restriction and diuretics are used in heart failure. Surgical intervention is needed when patient remains
symptomatic despite medical treatment or when mitral
TABLE 4.7: Clinical signs of mitral stenosis stenosis is severe.
Malar flush (mitral facies) 1. Mitral valvotomy
Atrial fibrillation (irregularly irregular pulse) a. Percutaneous balloon valvotomy is indicated when
Cardiac examination mitral valve is noncalcified and without regurgitation.
Tapping apex beat
Diastolic thrill in mitral area The procedure involves the passing of catheter across
Auscultation the valve and inflation of the balloon to dilate the
• Loud first heart sound orifice.
• Opening snap
• Mid-diastolic murmur in mitral area (low pitched,
b. Open valvotomy is carried out in patients where
rumbling) balloon valvotomy is not possible or in cases with
Signs of pulmonary hypertension restenosis. In this procedure the fusion of the valve
Loud P 2
is loosened and calcium deposit and thrombi are
Right ventricular heave
Signs of raised pulmonary capillary pressure removed.
Pulmonary crepts 2. Mitral valve replacement: The mitral valve is replaced
Signs of right heart failure
when there is critical MS (<1 cm2 orifice size) and/or
Raised JVP
Tender hepatomegaly there is associated significant mitral regurgitation.
Bilateral pitting pedal edema Replacement is also done when the mitral valve is severely
Ascites and pleural effusion in severe cases
distorted and calcified.
Mitral Regurgitation (MR) TABLE 4.9: Clinical signs of mitral regurgitation
Mitral regurgitation (MR) is the backflow of blood from Atrial fibrillation (irregularly irregular pulse)
the left ventricle to the left atrium during systole. Rheumatic Cardiac examination
Hyperdynamic and shifted apex beat
heart disease is the principal cause of MR. Other important
Systolic thrill in mitral area
causes are mitral valve prolapse, ischemic heart disease, Auscultation
dilated cardiomyopathy and connective tissue diseases like • Soft first heart sound
Marfan syndrome. Myocardial infarction, infective • Apical S 3 (third heart sound)
• Pan systolic murmur in mitral area
endocarditis and trauma can lead to acute MR (Table 4.8). Signs of pulmonary hypertension
Loud P 2
Pathophysiology Right ventricular heave
Signs of raised pulmonary capillary pressure
Mitral regurgitation leads to gradual dilatation of LA with
Pulmonary crepts
little increase in pressure. However, chronic volume Signs of right heart failure
overload leads to left ventricular (LV) dilatation. Eventually Raised JVP
the pressure in the LV and LA rises leading to breathlessness Tender hepatomegaly
Bilateral pitting pedal edema
and pulmonary congestion. On the contrary, there is sudden Ascites and pleural effusion in severe cases
elevation of LA pressure in acute MR causing severe
pulmonary edema. of cardiac chambers, pulmonary artery pressure,
ventricular dysfunction and presence of thrombi.
Clinical Manifestations
Doppler echocardiography is needed to detect and
The symptoms of chronic MR are similar to that of MS and estimate the MR. Transesophageal echocardiography
the main symptoms are fatigue, exertional dyspnea and provides better information than transthoracic
86 orthopnea. Thromboembolic events are less common.
Patients with acute severe MR commonly present with acute
echocardiography.
4. Cardiac catheterization is used to assess the severity of
pulmonary edema. Clinical signs are listed in Table 4.9. MR, to detect associated valvular lesions and coronary
artery disease.
Investigations
1. ECG may reveal the evidence of LA and LV enlargement, Treatment
RV hypertrophy and atrial fibrillation.
2. Chest X-ray shows findings suggestive of LA and LV Medical
Essentials of Medicine for Dental Students
enlargement and pulmonary congestion. Medical treatment of mitral regurgitation consists of:
3. Echocardiography is the most sensitive and specific of 1. Restriction of physical activities that cause fatigue and
non-invasive methods to diagnose valvular disease. It breathlessness.
may reveal structural abnormalities of the valves, size 2. Sodium restriction and diuretics are used to reduce
pulmonary congestion.
TABLE 4.8: Causes of mitral regurgitation (MR) 3. Digoxin is given to control ventricular rate in patients
with AF and to improve the ventricular systolic function.
Chronic MR 4. Vasodilators like ACE inhibitors are given in chronic
Rheumatic fever
Mitral valve prolapse
MR to reduce regurgitation and improve forward output.
Infective endocarditis (damage to valve) Intravenous nitroprusside or nitroglycerine is useful in
Ischemic acute MR.
Dilated cardiomyopathy (dilatation of ventricle/mitral valve ring)
5. Oral anticoagulant (warfarin) is given to patients with
Acute MR
Infective endocarditis history of thromboembolic events or to those with AF.
Myocardial infarction (papillary muscle rupture) 6. Prophylaxis should be given to all patients to prevent
Trauma rheumatic fever.
Cardiovascular System
7. Prophylaxis for infective endocarditis should be given with decreased coronary supply. Angina may occur even in
prior to procedures. Recent guidelines recommend the absence of coronary artery disease.
prophylaxis only if there is a prior history of
endocarditis. Clinical Manifestations
87
and calcification of a normal valve, (b) calcification of a dysfunction and presence of thrombi. Doppler
bicuspid valve and (c) rheumatic aortic valve stenosis. echocardiography is needed to detect associated AR.
Rheumatic AS is always accompanied with mitral valve 4. Cardiac catheterization is mainly required to accurately
involvement and presence of AR. Aortic stenosis in children assess the severity of AR, LV dysfunction and to detect
is commonly congenital in origin (Table 4.10). the presence of coronary artery disease.
Pathophysiology
TABLE 4.11: Clinical signs of aortic stenosis
The obstruction to the left ventricular outflow causes
pressure overload on the LV which subsequently leads to General examination
Slow rising pulse with delayed peak (pulsus parvus et tardus)
concentric LV hypertrophy. The increase in cardiac output Carotid thrill
during effort is limited by the valve stenosis. This can cause Narrow pulse pressure
syncope and hypotension. Left ventricular failure occurs Cardiac findings
Inspection and palpation
when it is unable to overcome the obstruction.
• Forceful and sustained apex beat
Ischemic symptoms (angina) may result due to increased • Systolic thrill at base of the heart radiating to carotid artery
oxygen demand by hypertrophied myocardial mass together Auscultation
• Soft or absent A2
TABLE 10: Causes of aortic stenosis (AS) • S4 at apex (S3 if LVF)
• Harsh ejection systolic murmur best at aortic area and radiating
Degeneration/calcification of normal valve toward carotid artery
Calcification of bicuspid aortic valve Others
Rheumatic fever • Basal crackles (crepts) in lungs due to pulmonary congestion
Congenital AS • Signs of RV failure may be present in severe cases
Treatment TABLE 4.12: Causes of aortic regurgitation
Medical Valvular
• Rheumatic fever
Medical treatment of aortic stenosis consists of: • Endocarditis
1. Strenuous physical activities should be avoided. • Trauma
2. Sodium restriction is advised in presence of CHF. • Congenital bicuspid aortic valve
• Syphilis
Diuretics are used with caution to avoid hypotension. • Ankylosing spondylitis
3. Digoxin is given to improve the ventricular systolic Aortic root disease
function in patients with LVF. • Aortic dissection
4. Oral anticoagulant (warfarin) is given if there is AF. • Marfan syndrome
• Hypertension
5. Prophylaxis for infective endocarditis should be given • Syphilis
prior to procedures. Recent guidelines recommend • Ankylosing spondyltis
prophylaxis only if there is a prior history of endocarditis.
6. Statins have been shown to reduce the progression of
degenerative calcific AS. Clinical Manifestations
• The patients remain asymptomatic for years. Palpitations,
Surgical
particularly on lying down are generally an early
1. Aortic valve replacement: All symptomatic adult patients
symptom. Later on, patients present with dyspnea on
with severe AS should be considered for aortic valve
exertion followed by orthopnea and PND. Angina may
replacement.
also occur frequently in severe AR.
2. Percutaneous balloon aortic valvuloplasty: it is useful in
• The presentations in acute severe AR are pulmonary
88
children with congenital non-calcific AS.
edema and/or cardiogenic shock (tachycardia, cold
extremities, hypotension, cyanosis). The clinical signs
AORTIC REGURGITATION (AR)
are listed in Table 4.13.
• Aortic regurgitation (AR) is the backflow of blood from
the aorta through an incompetent aortic valve into the Investigations
left ventricle during diastole. 1. ECG shows the evidence of LV hypertrophy and ST-T
• Aortic regurgitation (AR) may be either due to valvular changes.
involvement or dilatation of aortic root or both. 2. Chest a X-ray reveals cardiomegaly and aortic root
Essentials of Medicine for Dental Students
• The important causes of valvular involvement are dilatation. Features of pulmonary congestion may be
rheumatic disease, endocarditis, trauma and congenital present.
bicuspid aortic valve. Marfan syndrome and severe 3. Echocardiography may reveal structural abnormalities
hypertension can lead to aortic root dilatation and AR. of the valves, size of cardiac chambers, pulmonary artery
Syphilis and ankylosing spondylitis can cause AR because pressure, ventricular dysfunction and presence of
of valvular involvement and aortic dilatation (Table 4.12). thrombi. Doppler echocardiography is needed to assess
the severity of AR.
Pathophysiology
4. Cardiac catheterization is mainly required to detect the
Regurgitation causes volume overload leading to dilatation presence of coronary artery disease.
and hypertrophy of the LV. The stroke volume is increased
to maintain the effective cardiac output. This is the basis Treatment
for peripheral arterial signs in AR. As the LV function
deteriorates, the effective forward output declines even Medical
during rest. Myocardial ischemia may occur even in the Medical treatment of aortic regurgitation consists of:
absence of concomitant coronary artery disease (CAD). 1. Strenuous physical activities should be avoided.
TABLE 4.13: Clinical signs of aortic regurgitation Surgical
Cardiovascular System
Aortic valve replacement and/or aortic root repair: All
General examination
symptomatic patients with chronic AR should be considered
Peripheral signs of AR
• Collapsing or water hammer pulse for aortic valve replacement. However, surgery may also be
• Dancing carotids (pulsatile and prominent carotid arteries) advisable in asymptomatic patients who show evidence of
• Quincke’s sign (alternate flushing and paling of progressive cardiomegaly or deteriorating LV function.
skin at root of nail on pressure)
Acute AR: Repair of aortic root abnormalities and aortic
• Pistol shot sound over femoral arteries (Traube’s sign)
• Duroziez sign (to and fro murmur over femoral artery when
valve replacement should urgently be performed in patient
it is compressed) with acute AR. Patients may be stabilized by vasodilators or
• de Musset’s sign (head nodding with the pulse) ionotropes before surgery.
Blood pressure
• Increased pulse pressure (low diastolic pressure) INFECTIVE ENDOCARDITIS
• Hill’s sign: systolic BP in lower limbs is higher (>20 mm Hg)
than in upper limbs.
Infective endocarditis is microbial infection of endothelium
Cardiac findings of the heart. The infection most commonly occurs at the
Inspection and palpation site of pre-existing endocardial damage in heart valves (native
• Heaving and laterally displaced apex beat or prosthesis) and endocardium of the chambers. Similar
• Diastolic thrill at left sternal border process involving arterial endothelium in arteriovenous
Auscultation
shunts, patent ductus arteriosus and coarctation of aorta is
• Soft or absent A2
• S3 , (S4 occasionally)
known as infective endarteritis.
• High pitched blowing early diastolic murmur best at left
sternal border Pathology
• Other murmurs include ejection systolic murmur at aortic
area radiating to carotid artery and low pitch mid-diastolic
The endothelium may get damaged due to high pressure jet
injury as occurs in valvular or congenital heart disease. The
89
murmur over mitral area (Austin flint murmur).
damaged surface of endothelium invites platelet adhesion
Others
• Basal crackles (crepts) in lungs due to pulmonary congestion. and aggregation and fibrin deposition (nonbacterial
• Signs of RV failure (edema and hepatomegaly) may be thrombotic endocarditis). Organisms which enter into the
present in severe cases. blood stream through mucosa, skin or sites of focal infection
may colonize the platelets-fibrin deposit and form
vegetation. These vegetations can grow in size and cause
2. Sodium restriction and diuretics are advised in presence obstruction or can be dislodged as emboli. Locally, it can
of CHF. lead to abscess formation and damage to the tissues like
3. Digoxin and vasodilators (ACE inhibitors) are given to valves, chordae tendinae and myocardium. Virulent organisms
improve the ventricular systolic function in patients with such as S. aureus may even colonize normal endothelium.
LVF. Long-acting nifedipine has been found to delay the • Ventricular septal defect (VSD), mitral regurgitation,
need for operation. aortic stenosis, aortic regurgitation are particularly
4. Oral anticoagulant (warfarin) is given if there is AF. susceptible to endocarditis.
5. Prophylaxis for infective endocarditis should be given • Whereas conditions with low pressure shunt (atrial septal
prior to procedures. Recent guidelines recommend defect) are at low risk of developing endocarditis.
prophylaxis only if there is a prior history of endocarditis. • Intravenous drug abusers are prone to develop right sided
6. Nitroprusside or ionotrope is given in acute AR to stabilize (tricuspid valve) endocarditis.
the patient before surgery. Endocarditis is classified into acute and subacute types
7. Treatment of precipitating or underlying causes (syphilis, depending on manifestations and their clinical course
endocarditis) should be commenced. (Table 4.14).
TABLE 4.14: Acute and subacute infective endocarditis
Acute Subacute
1. Rapid course 1. Indolent course
2. Rapid valve destruction and abscess formation 2. Slow structural damage
3. Metastatic spread common 3. Less common
4. Clubbing, splenomegaly and petechial hemorrhages 4. Clubbing, splenomegaly and petechial
not found hemorrhages are seen
5. Fatal if not promptly treated 5. Prolonged course unless complicated by ruptured mycotic
aneurysm or embolism
6. Causative organism: Staph. aureus, pneumococci, 6. Strep. viridans, enterococci, HACEK group
Beta hemolytic streptococci
• The most common organism causing subacute b. Meningitis, embolic infarcts and intracranial bleeding
endocarditis is Viridans group of streptococci. These due to rupture of mycotic aneurysms are neurological
are commensals in the upper respiratory tract and may presentations.
enter the blood following brushing, chewing or dental c. Septic emboli may disseminate infection to distant
procedures. Other organisms like Enterococcus faecalis, organs such as skin, spleen, kidneys, bone and
S. bovis may arise from urinary tract or bowel. meninges. Embolic events may also be associated
• Staphylococcus aureus is the most common cause of acute with infarction at various sites.
endocarditis. Prosthetic valve endocarditis is generally d. Immune complex deposition can lead to glomerulo-
due to coagulase negative Staphy. epidermidis, a normal nephritis and hematuria.
skin commensal.
• HACEK group of gram-negative bacteria (Hemophilus, Investigations
90 Actinobacillus, Cardiobacterium, Eikenella and
Kingella) can also cause native valve endocarditis.
1. Blood culture: The most important test is blood culture
which tells about the organism and guides in antibiotic
• Other uncommon organisms which cause endocarditis
therapy. Venous blood samples are taken 30 minutes
are fungi (Candida), rickettsia, chlamydia and anaerobes.
apart from three different sites. Aseptic technique is
essential and the sample should be taken prior to
Clinical Manifestations
antibiotic therapy except in severe cases. Serological
Endocarditis is suspected in any patient with cardiac disease tests may be useful if blood culture is negative.
Essentials of Medicine for Dental Students
Cardiovascular System
Treatment
endocarditis
The treatment of infective endocarditis should be prompt
and adequate. The principles of treatment are: 1. Penicillin G 2-4 million units IV 4 hrly
2. Gentamicin 1 mg/kg IV or IM 8 hrly
1. The antibiotics should be administered parenterally to
3. Ceftriaxone 2 g IV OD
achieve high serum concentration since the vegetation 4. Ampicillin/amoxycillin 2 g IV 4 hrly
is avascular. 5. Naficillin or Oxacillin 2 g IV 4 hrly
2. The therapy is generally of prolonged duration. The dose 6. Cefazolin 2 g IV 8 hrly
7. Vancomycin 15 mg/kg IV 12 hrly
and duration should be meticulously adhered to ensure 8. Rifampicin 300 mg orally 8 hrly
the proper response.
3. The antibiotics should preferably be bactericidal. Surgery
4. The selection of antibiotics should be based on culture Surgery is often needed in patients with prosthetic valve
reports and minimum inhibitory concentration (MIC) endocarditis and fungal endocarditis who have (a) heart
values. Empirical therapy may be initiated in acute severe failure due to valve damage, (b) no response to antibiotics,
cases after drawing blood samples for culture. The (c) large vegetations and (d) abscess formation.
antibiotics are later changed, if necessary, based on
sensitivity reports. Prophylaxis
The list of antibiotics commonly used, their dosage and • Antibiotic prophylaxis prevents only a small number of
indications are given in Tables 4.15 and 4.16. cases of infective endocarditis. Bacteremia associated
with routine daily activities like chewing brushing, and
Empirical Therapy flossing is similar as with dental procedures like tooth
Empirical therapy is given when the culture is negative or extraction. It has been seen that cardiac tissue is exposed
before culture and sensitivity reports are available.
Ceftriaxone plus gentamicin is given in subacute native valve
to bacteremia causing oral cavity organisms many times
greater with routine daily activities than from dental 91
endocarditis. Vancomycin is added to the above regime in procedures. As per American Heart Association recent
case of prosthetic valve endocarditis. guidelines antibiotic prophylaxis is now recommended
only for patients at highest risk (Table 4.17).
TABLE 4.16: Common regimens used in IE
Organism Sensitivity Regimens
Streptococci Penicillin susceptible (MIC <0.1 µg/ml) Penicillin G (4 weeks)
Penicillin G plus Gentamicin (2 weeks)
Ceftriaxone (4 weeks)
Vancomycin (4 weeks)
Relatively penicillin resistant (MIC 0.1-0.5 µg/ml) Penicillin G (4-6 weeks) plus gentamicin (2 weeks)
Moderately penicillin resistant (MIC 0.5-0.8 µg/ml). Penicillin G plus Gentamicin (4-6 weeks)
Enterococci Penicillin G or Ampicillin or Vancomycin plus
Gentamicin (4-6 weeks)
Staphylococci
Native valve Methicillin susceptible Naficillin or Oxacillin or Cefazolin (4-6 weeks)
plus Gentamicin (3-5 days)
Vancomycin (4-6 weeks)
Methicillin resistant Vancomycin ( 4-6 weeks)
Prosthetic valve Methicillin susceptible Naficillin or Oxacillin (6-8 weeks)
plus Gentamicin (2 weeks) plus Rifampicin (6-8 weeks)
Methicillin resistant Vancomycin (6-8 weeks) plus Gentamicin (2 weeks)
plus Rifampicin (6-8 weeks)
HACEK group Ceftriaxone (4 weeks)
Ampicillin plus Gentamicin (4 weeks)
Fungal Amphotericin B plus flucytosine
• Patients with valvular and congenital heart disease who TABLE 4.19: Dental procedures for which endocarditis
prophylaxis is advised in patients at high or
are at high risk of endocarditis should receive
moderate risk for endocarditis
prophylactic antibiotics (Table 4.18) before undergoing
any procedure which may cause bacteremia. Antibiotic 1. Extractions
2. Periodontal procedures, cleaning causing gingival bleeding
prophylaxis is not advised for other cardiac lesions.
3. Implant placement, reimplantation of avulsed teeth
• The patients must be advised to maintain good dental 4. Endodontic instrumentation (root canal) or surgery beyond
and oral health. In patients with poor oral hygiene, routine the apex
chewing and brushing of teeth may cause bacteremia. 5. Subgingival placement of antibiotic fibers or strips
6. Placement of orthodontic bands but not brackets
Hence, daily personal care and annual professional dental 7. Intraligamentary injections (anesthetic)
care is advised.
• Tooth extraction, periodontal surgery, root canal therapy, TABLE 4.20: Oral procedures not requiring prophylaxis for
scaling, removal of tartar and tooth implantation are infective endocarditis
procedures that require antimicrobial prophylaxis (Tables • Local anesthetic agent (non-intraligamentary)
4.19 and 4.20). In addition, respiratory, gastrointestinal • Intracanal endodontic procedure
and genitourinary procedures also require prophylaxis. • Operative and prosthodontic procedures with or
without retraction cord
• Patients with atrial septal defect, surgically repaired VSD • Adjustment of orthodontic appliance
and PDA, prior coronary artery bypass surgery and • Placement of removable prosthodontic or orthodontic
implanted pacemakers and defibrillators do not require appliances
prophylaxis (Table 4.21). • Impression taking
• Exfoliation of primary teeth
• Oral radiography
• Placement of rubber dams
TABLE 4.17: Cardiac lesions (high risk) for which antibiotic
• Suture removal
92 prophylaxis is recommended before dental procedures
• Fluoride treatment
Cardiovascular System
Essential Hypertension
prophylaxis is not recommended
Patients with elevated arterial blood pressure without any
• Atrial septal defect (ostium secondum) identifiable cause are said to have essential or primary or
• Mitral valve prolapse without regurgitation and/or thickening
idiopathic hypertension. More than 90% patients with
• After surgical repair of ASD,VSD, or PDA
• Coronary artery bypass surgery (CABG) performed more than 6 hypertension belong to this category. Pathogenesis of
weeks prior to treatment essential hypertension is not clearly understood. However,
• Physiological, functional heart murmurs this is thought to be multifactorial. Important environmental
• Cardiac pacemakers
• Implanted defibrillators, previous rheumatic fever or Kawasaki
factors include high salt intake, heavy alcohol use, obesity
disease without valvular dysfunction and sedentary lifestyle. Genetic factors may also be
responsible in some ethnic groups.
There is no definite dividing line between normal and
elevated arterial blood pressure. However, hypertension is Secondary Hypertension
defined as a level of blood pressure at which there is In secondary hypertension, a specific cause is identified.
increased risk for target organ damage and the benefits of Important causes are given in Table 4.23. The most common
treatment outweighs the cost and hazards. cause of secondary hypertension is renal disease. Secondary
The seventh US Joint National Committee on hypertension should be suspected if onset of hypertension
Prevention, detection, evaluation, and treatment of high is at <35 years or >55 years of age or there is abrupt onset
blood pressure (JNC VII) defined normal blood pressure as of severe hypertension at any age.
<120 mmHg systolic and <80 mmHg diastolic. The
classification of blood pressure is given in Table 4.22. Effects of Hypertension on Target Organs
• Isolated systolic hypertension is defined as systolic blood There is an increased chance of damage to the vascular bed
pressure of 140 mmHg or more together with diastolic
pressure <90 mmHg.
of several organs mainly retina, heart, brain, kidneys and
large arteries.
93
• Labile hypertensives are those patients who some times 1. Retinal: Retinal changes depend on the severity of
have blood pressure in the hypertensive range. hypertension. These are classified into four grades (grade
• Accelerated hypertension is defined as significant recent I-IV) based on the presence of arteriolar thickening,
increase in blood pressure over previous hypertensive nicking, hemorrhages, exudates and papilledema.
level associated with rapidly progressive end organ
TABLE 4.23: Important causes of secondary hypertension
damage.
• Presence of papilledema (swelling of optic disk) along Renal disorders
with other features of accelerated hypertension signifies • Renovascular stenosis
• Parenchymal renal disease, particularly glomerulonephritis
malignant hypertension. • Polycystic kidney disease
Endocrinal disorders
TABLE 4.22: Classification of blood pressure
• Pheochromocytoma
for adults (>18 years)
• Cushing’s syndrome
Category Systolic blood pressure Diastolic blood • Primary hyperaldosteronism
(mm Hg) pressure (mm Hg) • Acromegaly
Normal <120 <80 • Hypo- and hyperthyroidism
Prehypertension 120-139 80-89 Drugs
Hypertension • Oral contraceptives
Stage 1 140-159 90-99 • Corticosteroids
Stage 2 >160 >100 • Sympathomimetic drugs
• Cyclosporine
Note: Blood pressure values are based on the average of two or more readings Miscellaneous
taken at each of two or more visits after an initial screening. When systolic and • Toxemia of pregnancy
diastolic values fall into different categories, the higher category should be • Coarctation of aorta
selected for classification. • Raised intracranial pressure
2. Cardiac: These include left ventricular hypertrophy, TABLE 4.24: Investigations in patients with hypertension
pulmonary edema and high incidence of coronary artery Basic investigations in all patients
disease. • Urine analysis for protein, blood and glucose
3. Central nervous system (CNS): Stroke (infarction and • Fasting blood sugar
• Serum creatinine and blood urea nitrogen
hemorrhage), transient ischemic attacks (TIA), hyper- • Serum sodium and potassium
tensive encephalopathy (coma, seizures) are important • Serum lipid profile
effects on CNS. • Electrocardiography
Investigations in special group of patients
4. Renal: Effect on kidneys consists of proteinuria and
• Chest X-ray and echocardiography
renal failure. • Renal ultrasonography and angiography
5. Large vessels: Hypertension leads to accelerated athero- • Serum calcium and phosphate
sclerosis and aneurysmal dilatation. • Thyroid stimulating hormone (TSH)
• Urinary cortisol and catecholamine
• Plasma renin activity and aldosterone
Clinical Features
• The majority of patients asymptomatic and is diagnosed Management
on routine clinical examination. However, symptoms due The management of hypertension includes general measures
to raised blood pressure are occipital headache, dizziness, and drug therapy.
palpitation and fatigue. General measures (lifestyle modification):
• Patient may also present with symptoms related to target 1. Relief of stress: Patients are advised to avoid unnecessary
organ damage like epistaxis, hematuria, blurred vision, tension. Relaxation techniques may also be practised.
TIA, angina and breathlessness. 2. Salt restriction: Dietary restriction of sodium chloride
• Symptoms pertaining to underlying cause may be present; upto only 5 g per day helps reduce blood pressure in
Cardiovascular System
1. Diuretics: Thiazides are the most frequently used
Dose range (daily) diuretics to treat hypertension. The side effects of
Diuretics thiazides such as hyperuricemia, hypertriglyceridemia
Hydrochlorthiazide Oral 12.5-25 mg and hypokalemia can be minimized by restricting the
Frusemide Oral/IV 20-320 mg dose of hydrochlorothiazide to 25 mg per day. A
Torsemide Oral 5-10 mg
Spironolactone Oral 25-100 mg
combination of thiazide and potassium sparing agents
Beta blockers (spironolactone, amiloride) may also be used. Loop
Atenolol Oral 25-100 mg diuretics are used hypertensive crisis and renal failure.
Metoprolol Oral 50-300 mg 2. ACE inhibitors and angiotensin receptor blockers (ARB):
Carvedilol Oral 12.5-50 mg
Bisoprolol Oral 2.5-20 mg Angiotensin converting enzyme inhibitors (enalapril,
Nevivilol Oral 2.5-10 mg lisinopril, ramipril) and ARB (losartan, valsartan) have
Calcium channel antagonist good antihypertensive effect and cause significant
Amlodipine Oral 2.5-10 mg
reduction in death, acute MI and stroke. These agents
Diltiazem Oral 90-360 mg
Verapamil Oral 80-480 mg also reduce the progression of nephropathy in type II
ACE inhibitors diabetes. ARBs have lesser side effects like cough and
Enalapril Oral 2.5-40 mg angioedema than ACE inhibitors. These drugs are
Ramipril Oral 1.25-20 mg
Lisinopril Oral 5-40 mg
contraindicated in bilateral renal artery stenosis.
ARBs 3. Long acting calcium channel antagonist (amlodipine)
Losartan Oral 25-100 mg is particularly useful in elderly patients with isolated
Valsartan Oral 80-320 mg systolic hypertension. Other agents are less commonly
Irbisartan Oral 150-300 mg
Telmisartan Oral 20-80 mg used. These groups of drugs can cause pedal edema.
Olmisartan Oral 20-40 mg
95
4. Beta adrenergic antagonists: These agents lower heart
Alpha blockers rate and cardiac output. The cardioselective agents which
Prazosin Oral 1-20 mg
are preferred include atenolol and metaprolol. They are
Terazosin Oral 1-20 mg
Centrally acting agents used with caution in patients with congestive heart
Clonidine Oral 0.1-1.2 mg failure, heart blocks and asthma.
Methyldopa Oral 250-2000 mg 5. Other groups of drug occasionally used in hypertension
Vasodilators
Hydralazine Oral 40-300 mg
are:
a. alpha adrenergic receptor blockers: prazosin,
doxazosin
TABLE 4.26: Mechanism of action and side effects of antihypertensive drugs
Drugs Mechanism of action Side effects
• Beta adrenergic Blockage of sympathetic effects on heart, Heart failure, heart blocks, bradycardia, Raynaud’s
antagonists decreased heart rate and cardiac output phenomenon, impotence, may precipitate broncho-
spasm
• Calcium channel Arterial vasodilatation Pedal edema, flushing, headache, rash,
blockers tachycardia (nifedipine), gum hyperplasia
• ACE inhibitors Inhibits ACE and blocks the production of Dry cough, angioneurotic edema, hypotension,
angiotensin II leading to arterial and venous dilatation taste disturbance, hyperkalemia
• ARBs Block angiotensin receptors and cause Angioedema, rash, hyperkalemia
vasodilatation
• Diuretics Cause natriuresis and decrease intravascular Thiazide; hyperglycemia, hypercalcemia,
volume, may result in mild vasodilatation hyperlipidemia, hypokalemia and hyponatremia
Loop diuretics; hypocalcemia,hypokalemia and
deafness
K sparing; gynaecomastia, hyperkalemia
b. centrally acting agents: clonidine, methyldopa Hypertensive urgencies is defined as substantial increases
c. vasodilators: hydralazine, minoxidil and in blood pressure usually with systolic >220 mmHg or
d. agents with mixed alpha and beta adrenergic diastolic >120-130 mmHg. It also includes hypertension
antagonist action: labetalol, carvedilol. with disk edema, progressive end organ complications rather
than damage and severe perioperative hypertension. In this
Treatment Guidelines situation, BP must be reduced in several hours. Parenteral
The treatment of hypertension depends on: therapy is usually not needed.
a. The level of blood pressure Hypertensive emergencies include hypertensive
b. The presence of target organ damage encephalopathy, hypertensive nephropathy, intracranial
c. The presence of cardiovascular risk factors (see Table hemorrhage, unstable angina, myocardial infarction, acute
4.30) left ventricular failure with pulmonary edema, aortic
d. Presence of other disease dissection and eclampsia. Malignant hypertension is
1. Prehypertension: Lifestyle modification should be characterized by nephropathy or encephalopathy with
advised. Drug therapy may be needed in case of presence accompanying papilledema.
of other cardiac risk factors or end organ damage. Control of blood pressure is vital for preventing ongoing
2. Hypertension (Stage 1 and 2): In addition to lifestyle end organ damage. Rapidly acting parenteral agents are used.
modification, drug therapy is indicated. The goal of Excessive and rapid decline in the BP should be avoided as
therapy should be to achieve a blood pressure level of it may lead to cerebral hypoperfusion and coronary
less than 140/90 mmHg (130/80 mmHg in diabetics). insufficiency. The goal is to attain a decline of 20-25% in
Thiazides are preferred initially as monotherapy. Other the mean arterial pressure or a diastolic pressure of 110
drugs (ACE inhibitors, ARBs, beta blockers or calcium mmHg. Thereafter, the reduction in blood pressure is
96
channel blockers) may also be considered as attained gradually over several days. The parenteral drugs
monotherapy. However, combination therapy (preferably used are nitroprusside, nitroglycerine, dizoxide, esmolol,
diuretic plus another agent) may be used where the blood labetalol, enalaprilat and hydralazine. Intravenous frusemide
pressure is not controlled by monotherapy. The choice is given as an adjunct. Sublingual nifedipine should be
of drug also depends on the presence of co-existing avoided in the acute management because it is associated
conditions (see Table 4.27). with adverse cardiac events.
Cardiovascular System
The ischemic heart disease can clinically manifest as:
disease/IHD
• angina pectoris (stable or unstable)
1. Stable angina • myocardial infarction
2. Acute coronary syndromes (ACS) • arrhythmias
a. Unstable angina
• heart failure
b. Non ST segment elevation myocardial infarction (NSTEMI)
c. ST segment elevation myocardial infarction (STEMI) • sudden death
3. Heart failure
4. Arrhythmias STABLE ANGINA
5. sudden cardiac death
6. Asymptomatic Stable angina results from transient myocardial ischemia
arising because of imbalance between myocardial oxygen
TABLE: 4.29: Causes of ischemic heart disease supply and demand. The reduced perfusion results from
Atherosclerosis of coronary arteries fixed ‘stable’ obstruction due to atheroma of the coronary
Spasm of coronary artery arteries (Fig. 4.8).
Vasculitis involving coronary artery
Emboli
Clinical features:
Congenital anomalies of coronary arteries
• The term angina, derived from Greek language means
choking or strangulation.
Pathogenesis of Coronary Atherosclerosis • Stable angina is characterized by central chest pain or
discomfort classically precipitated by exertion or stress
Atherosclerosis starts in second or third decade of life. The
and relieved by rest. The detailed characteristics of pain
collection of lipoproteins within intimal layer of the coronary
are given in Table 4.31.
97
artery is the initial event. These lipoproteins undergo
• Diabetics and elderly may present with breathlessness,
modification into oxidized LDL and subsequently are taken
fatigue and faintness rather than chest pain. Symptoms
up by migrated monocytes in the intima (foam cells). Most
other than chest pain are known as anginal equivalents.
foam cells die and result in formation of a lipid rich center.
• The physical signs are generally normal. The patient
This necrotic area is surrounded by smooth muscle cells
may have signs of cardiomegaly, mitral regurgitation,
which lay down extracellular matrix that forms the bulk of
pulmonary edema and third or fourth heart sound (gallop
the advance atheromatous lesion (atheromatous plaque or
rhythm).
atheroma). Monocyte-mediated cytokines also play an
important role in the evolution of the atheromatous plaque.
The risk factors for atherosclerosis/cardiovascular disease
are given in Table 4.30.
98
or without T wave inversion during chest pain is specific reduce the myocardial oxygen demand by decreasing
finding in stable angina. the preload and afterload on the heart. Nitroglycerine
a. Stress Testing 0.4 to 0.6 mg is given sublingually for acute relief of the
anginal pain. For long-term therapy, isosorbide dinitrate
1. Exercise ECG: This is used to diagnose IHD and to
(10-20 mg 8 hrly) or isosorbide mononitrate (20-60 mg
estimate the prognosis. The ECG is done on a treadmill
once or twice daily) is given orally. Nitroglycerine
protocol wherein the recording is made during and after
ointment or transdermal patches are also available.
exercise. The symptoms like chest pain, fatigue,
c. Beta blockers: These reduce myocardial oxygen demand
Essentials of Medicine for Dental Students
• Captopril
• Enalapril
stratified into low and high risk groups. High risk
6. Plaque stabilization therapy patients are subjected to coronary arteriography and
HMG –coA reductase inhibitors subsequent PTCA or CABG. Low risk patients should
• Atorvastatin undergo early stress test to ascertain the need for
• Simvastatin
• Rosuvastatin angiography.
101
FIGURE 4.9: ECG of lateral wall myocardial infarction (early or hyperacute) showing ST segment elevation in leads I, aVL, V4 and V6
FIGURE 4.10: ECG of lateral wall myocardial infarction (recent) showing Q waves and prominent T wave inversion in leads I, aVL, V4 and V6
FIGURE 4.11: ECG of lateral wall myocardial infarction (old) showing Q waves in leads I, aVL, V4 and V6
and other complications such as pericardial effusion, evidence of active internal bleeding. Bleeding is the
mitral regurgitation, ventricular septal defect and left most frequent side effect of fibrinolytic therapy.
ventricular thrombus. Streptokinase can result in hypersensitivity reaction.
d. Other tests: Chest X-ray may reveal pulmonary edema. b. Primary percutaneous intervention (PCI): Primary
Leukocytosis, raised ESR and CRP can also be present. percutaneous intervention (angioplasty, stenting) is
Lipid profile, serum electrolytes, urea and creatinine are expensive and available at select centers. When
also measured. performed by experienced operators it appears to be
more effective than fibrinolysis. This can also be
Management performed in case of contraindication or failure of
1. Hospitalization: Patient should be hospitalized in fibrinolytic therapy (rescue PCI).
coronary care unit (CCU) with facilities of continuous 6. Anticoagulant therapy: Unfractionated heparin is given
ECG monitoring and defibrillator as promptly as possible as intravenous infusion to maintain the patency of infarct
since many patients die within the first 24 hours of onset related artery. Later, oral anticoagulant is given for
of symptoms of MI and over half occur within first hour prolonged use where indicated.
due to ventricular fibrillation. Patient should be confined 7. ACE inhibitors are given to prevent ventricular
to bedrest. The goal is a door-to-needle time of <30 min remodeling. This is continued indefinitely in patients with
and door-to-balloon time of <90 min. hypertension or heart failure.
2. Oxygen therapy: Oxygen is administered for initial few 8. Other measures: Patients are on bed rest for at least 12
hours and continued if hypoxemia is present. hours. Gradually, the activity is increased depending on
3. Antiplatelet agents: Aspirin (nonenteric coated) in the the tolerance. Liquid diet is started when chest pain
dosage of 160-325 mg should be given to the patient to subsides. Later on, low fat, high fiber diet is prescribed.
102
chew. Later aspirin is continued in the dosage of 75-162 Laxatives are given to relieve constipation. Sedative
mg orally daily. Clopidogrel (300 mg loading dose (diazepam, lorazepam) is generally given for proper
followed by 75 mg/day) can be used if there is allergy sleep.
or intolerance to aspirin. 9. Risk stratification: Patients are stratified into low and
4. Relief of pain: high risk groups depending on presence of persistent
• Sublingual nitroglycerine (0.4 mg) is given for pain ischemia, heart failure and symptomatic ventricular
relief. This may be given at interval of 5 minutes. arrhythmias. High risk patients are subjected to coronary
Intravenous nitroglycerine is started if pain reoccurs angiography and subsequent PTCA or CABG. Low risk
Essentials of Medicine for Dental Students
or there is associated hypertension. patients should undergo early stress test to ascertain the
• Morphine also can be used for pain relief (2-4 mg need for angiography.
IV).
Secondary prevention: The secondary prevention of MI
• Intravenous beta blockers such as metoprolol are also
includes long-term administration of aspirin or clopidrogrel,
helpful for pain relief followed by daily oral therapy.
beta blockers, ACE inhibitors, control of risk factors like
5. Reperfusion therapy: This is given to restore the flow in
cessation of smoking, statin therapy for hyperlipidemia,
the infarct related artery and to limit the infarct size.
control of blood pressure and blood sugar, weight reduction
a. Fibrinolytic agent like streptokinase or tPA (tissue
in obese and regular exercise. Oral anticoagulants may be
plasminogen activator) is given through intravenous
required in some cases.
infusion. Alternatively, reteplase or tenecteplase can
be administered as bolus (Bolus fibrinolytics). It Complications of MI
should be administered as soon as possible. However, The complications include
it can be useful if given within 6 hours of 1. Arrhythmia: Ventricular fibrillation is the major cause of
presentation. The contraindications are history of early death in MI. Other co mmon arrhythmias are
cerebrovascular accident, severe hypertension and atrial fibrillation and heart blocks.
Cardiovascular System
2. Pump failure or cardiogenic shock where more than Pathophysiology
40% myocardium is damaged. This is an important cause The pump failure leads to low cardiac output, which
of inhospital mortality. activates counter-regulatory neurohormonal mechanisms
3. Recurrent ischemia or chest pain such as
4. Pericarditis, Dressler’s syndrome • activation of renin angiotensin aldosterone system
5. Thromboembolism (RAAS)
6. Ventricular remodeling • stimulation of sympathetic system
7. Left ventricular aneurysm • increased vasopressin secretion
8. Mechanical complications like ventricular rupture and The net effects of these mechanisms are sodium and fluid
cardiac tamponade, mitral regurgitation and rupture of retention and vasoconstriction. These tend to improve
interventricular septum. cardiac output; however, these are also responsible for
various manifestations of heart failure due to systemic and
HEART FAILURE pulmonary congestion. Natriuretic peptides are released from
Heart failure (HF) is a clinical syndrome in which the heart the stretched myocytes and mediate vasodilatation, diuresis
and sodium loss.
is unable to pump adequate amount of blood to meet the
metabolic demands of the body. Abnormality in cardiac
Symptoms and Signs
structure or function may be responsible for the inability of
Symptoms and signs in CHF are due to
heart to pump blood adequately.
• heart failure per se
Causes • underlying causes of heart failure
• precipitating factor
Heard failure generally occurs due to defect in the myocardial
103
Clinical features of heart failure are given in Table 4.34 and
contractility. Ischemic heart disease and cardiomyopathy
4.35. Mechanisms underlying clinical features are given in
are the most common causes of HF. Causes of HF are listed
Table 4.36.
in detail in Table 4.33.
Symptoms of HF mainly arise due to increased
pulmonary and systemic venous and capillary pressure and
Precipitating Factors
reduced cardiac output. The important symptoms are
In certain situations, the load over an already burdened dyspnea, orthopnea, paroxysmal nocturnal dyspnea,
myocardium is suddenly increased leading to HF. Important weakness and fatigue, edema and abdominal pain.
precipitating causes are infection, arrhythmias, anemia, Dyspnea is the most important symptom and is
excessive physical exertion, emotional stress and fluid mutifactorial in origin. The most important mechanism of
over load. Pregnancy, thyrotoxicosis and accelerated dyspnea is accumulation of interstitial and alveolar fluid due
hypertension may also precipitate HF. to increased pulmonary capillary pressure. Initially, the
TABLE 4.33: Important causes of heart failure TABLE: 4.34: Symptoms and signs of heart failure
104
increased jugular venous pressure, pitting edema and tender
• Ascites, pleural effusion*
Increased pulmonary venous pressure (left heart failure) hepatomegaly. Pulsus alternans is regular pulse with regular
• Dyspnea, orthopnea, PND alteration in pulse amplitude (alternate low and large volume
• Hemoptysis (pink frothy sputum) pulse), and is a sign of severe heart failure.
• Central cyanosis
• Crackles on auscultation Lung examination reveals inspiratory rales (crepitations)
• Pleural effusion* over the bases. In severe cases with pulmonary edema,
Due to decreased cardiac output and increased afterload coarse rales and wheezes all over lung fields are found
• Cold clammy skin (cardiac asthma). Third and fourth heart sounds are often
• Peripheral cyanosis
Essentials of Medicine for Dental Students
105
d. Systolic or diastolic heart failure: Heart failure due to of brain natriuretic peptide (BNP) has been shown to
impaired myocardial contraction is called systolic HF be a highly sensitive and specific test for the diagnosis,
while failure of ventricle to relax and fill normally is prognosis and monitoring of the HF. High BNP level can
called diastolic HF. The causes of diastolic HF are differentiate cardiac asthma from the dyspnea of
constrictive pericarditis, restrictive cardiomyopathy and pulmonary origin.
ischemic heart disease.
Treatment
TABLE 4.37: Clinical features of left heart failure
The treatment of HF includes:
Symptoms • correction of the underlying cause
Dyspnea • removal of the precipitating factors
Orthopnea
Paroxysmal nocturnal dyspnea (PND) • control of congestive heart failure.
Acute pulmonary edema
Signs Correction of Precipitating Factors
Pulmonary rales (crackles, crepitations)
Third heart sound
Precipitating factors in patients with underlying heart disease
Pulsus alternans should be searched and corrected. Some important factors
Pleural effusion are:
• Excessive salt and fluid intake
TABLE 4.38: Clinical features of right heart failure • Excessive activity
Raised jugular venous pressure (JVP)
• Arrhythmias
Tender hepatomegaly • Infections
Bilateral pitting pedal edema • Anemia
Ascites • Pulmonary embolism
Pleural effusion
• Noncompliance in therapy
Control of Heart Failure • Potassium sparing agents are often used in
combination with other diuretics to minimize
Control of HF can be achieved by general measures and
hypokalemia. Spironolactone in low dosage (25
drug therapy.
mg daily) has been shown to improve morbidity
1. General measures:
and mortality in advanced HF.
• Reduced physical exertion lowers myocardial
b. Vasodilators: Activation of renin-angiotensin-
oxygen demand and thus controls failure. Absolute
aldosterone system (RAAS), adrenergic nervous
bed rest may be needed in severe heart failure. In
system and increased secretion of vasopressin cause
stable patients, regular isotonic exercises are advised.
vasoconstriction and salt and fluid retention.
• The salt intake is reduced to half of the normal or
Vasodilators help in HF as they reduce preload and
even less than 2 g per day in some cases.
afterload through venodilatation and arterial dilatation
• Weight loss in obese patients is also helpful in
respectively.
controlling heart failure.
• ACE inhibitors improve exercise tolerance and
2. Drug therapy: Drugs may help in HF by reducing preload
reduce morbidity and mortality in patients with
and afterload and improving myocardial contractility.
HF. They also prevent the onset of failure in
This can be achieved generally with the help of more
patients with left ventricular dysfunction.
than one class of drugs (Table 4.39).
• Angiotensin II receptor blockers (ARB) are
a Diuretics: Diuretics lead to increased urinary sodium
equally effective as ACE inhibitors and have less
excretion and reduction in plasma volume. This
incidence of cough.
lowers the preload to the heart.
• Nitrates and hydralazine are also useful for
• Thiazide diuretics can be used alone in mild HF
chronic oral administration.
and in combination with other class of diuretics
106
• Intravenous nitroglycerine, sodium nitroprusside
in severe HF.
or nesiritide (recombinant BNP) is indicated in
• Loop diuretics are given in severe HF and in cases
acute severe HF.
with renal impairment. Intravenous frusemide
c. Ionotropic agents: They improve myocardial
causes venodilatation and is useful in acute
contractility. Various types of ionotropic agents
pulmonary edema.
include:
TABLE 4.39: Drugs used in heart failure • Digitalis: Digitalis relieves symptoms of HF and
1. Diuretics is particularly indicated in patients of HF with
Essentials of Medicine for Dental Students
Cardiovascular System
These agents act by counteracting the adverse effects
of enhanced adrenergic stimulation. Beta blockers 1. Acute respiratory distress syndrome (ARDS)
are started in low dosage initially and the dose is a. Infections
increased gradually with care. b. Inhaled toxins
c. Aspiration of gastric contents
3. Other measures:
d. Disseminated intravascular coagulation
• Anticoagulant therapy: Anticoagulant therapy is e. Acute pancreatitis
given to patients with heart failure and atrial f. Multiple trauma
fibrillation or to patients with severe heart failure g. Anaphylaxis
2. High altitude
to prevent thromboembolism. 3. Narcotic overdose
• Antiarryhthmic therapy: Amiadarone is given to
control ventricular arrhythmias upright may provide some relief. Additionally, patients may
• Pacing: Biventricular pacing resynchronizes have excessive sweating and cyanosis. The sputum may be
the cardiac contraction and improves the profuse, pink frothy or blood stained. The examination may
performance in severe heart failure with reveal cold extremities, tachycardia and tachypnea with
conduction abnormalities prominent use of accessory muscles of respiration,
• Circulatory support: Mechanical circulatory hypotension. There are extensive rales (crackles, crepitations)
support like intra-aortic balloon pump is helpful and wheezes on lung auscultation. Cardiac examination will
in intractable cases reveal findings of underlying heart disease.
• Cardiac transplantation: Cardiac transplantation
is considered in patients with refractory severe Investigations
end stage heart failure. • The chest X-ray may reveal cardiomegaly and signs of
107
pulmonary edema (prominent interstitial and hilar
ACUTE PULMONARY EDEMA (CARDIOGENIC) shadows, Kerley B lines, pleural effusion).
Acute pulmonary edema is characterized by the accumulation • Echocardiography may help in differentiating cardiac
of fluid in the pulmonary interstitium and alveoli due to from noncardiac causes.
increase in the pulmonary venous and capillary hydrostatic • A rise in serum brain natriuretic peptide (BNP) level
pressure. The lungs become less compliant, airways favors acute left ventricular failure as a cause of
resistance increases and the capillary-alveolar gas exchange pulmonary edema.
is compromised.
Non-cardiac pulmonary edema is characterized by high Management of Cardiogenic Pulmonary Edema
venous and capillary permeability with low hydrostatic Acute pulmonary edema is a life-threatening condition and
pressure. needs prompt management.
108
should be adequately managed.
VSD is the most common type of CHD. There is incomplete
septation of the ventricles. The defect is most commonly
CONGENITAL HEART DISEASE
present at the junction of membranous and muscular portion
Congenital heart disease (CHD) may present in early of the interventricular septum. VSD can occur alone or can
childhood or may remain asymptomatic till adult life. Its be accompanied by other defects like aortic regurgitation.
incidence is around 1% of live birth. Congenital abnormalities The septal defect allows blood to shunt from left ventricle
are due to multifactorial environmental and genetic causes. (high pressure) to right ventricle (low pressure). The right
Rubella infection in mother is associated with patent ductus
Essentials of Medicine for Dental Students
Cardiovascular System
large VSD. There is an increased incidence of respiratory
infection. In advanced cases, cyanosis and digital clubbing • Large ASD is closed surgically. Eisenmenger syndrome
appear due to reversal of shunt. There is a pansystolic is a contraindication for surgery.
murmur best heard at left sternal border in smaller VSD
• Isolated secondum lesion has a low risk of developing
(Maladie de Roger’s murmur). However, the murmur is
infective endocarditis, hence prophylaxis is generally not
softer in large VSD as the RV pressure is elevated.
needed.
Investigations
Patent Ductus Arteriosus (PDA)
Echocardiography is used to detect the location and size of
the VSD. The ECG may show biventricular hypertrophy In fetal life, the blood from the pulmonary artery does
and chest X-ray reveals pulmonary plethora (prominent not go to lungs but flows into the aorta through a
pulmonary vascular markings). communication, ductus arteriosus. However, the ductus
closes soon after the birth as the blood from pulmonary
Treatment artery goes to lungs. In some, the ductus fails to close, a
• Small defects should be watched as they may close condition known as PDA. This is more common in females
spontaneously. Surgery is indicated in larger defects. and is sometimes associated with other congenital
• Eisenmenger syndrome is a contraindication for surgery abnormalities.
where the only option is heart-lung transplantation. In PDA, the blood flows from high pressure (aorta) to
• In VSD, there is a moderate risk of developing infective low pressure (pulmonary artery) side, resulting in left to
endocarditis. Hence, endocarditis prophylaxis is right shunt. Pulmonary artery pressure rises with the rise in
mandatory before any procedure. pulmonary vascular resistance. As the pressure in pulmonary
artery exceeds that of aorta, right to left shunting occurs,
Atrial Septal Defect (ASD) the blood flow reverses (Eisenmenger syndrome). This leads
ASD occurs more commonly in females. The commonest
type of ASD is osteum secundum. Other types are osteum
to cyanosis, more in the feet than in upper part of the body,
also called differential cyanosis. 109
primum and sinus venosus. Atrial septal defect may be
accompanied by mitral stenosis (Lutembacher’s syndrome). Clinical Manifestations
A large amount of blood shunts from LA to RA. The right
Patients with small shunt are generally asymptomatic for
ventricular volume and pulmonary flow are increased which
years. However, there may be retarded growth and
may lead to pulmonary hypertension. The pulmonary
development in children with large shunt. With the onset of
hypertension can in turn lead to elevated RV pressure and
reversal of shunt (right to left) as pressure in RV exceeds cardiac failure, the patients develop dyspnea. The arterial
that of LV. This condition is known as Eisenmenger syndrome. pulse is generally high volume. Cardiac finding includes
a continuous ‘machinery’ murmur in the left second
Clinical Manifestations intercostal space often with a thrill. In advanced cases, P2
ASD is generally asymptomatic in early life. However, there becomes loud and the murmur is shortened. Patients develop
is an increased tendency for recurrent respiratory infection. cyanosis and features of right heart failure (Eisenmenger
Later during the fourth or fifth decade, it may present as syndrome).
atrial fibrillation, heart failure and Eisenmenger syndrome.
Important clinical signs include wide and fixed splitting of Investigations
second heart sound and a systolic flow murmur over the The echocardiography is used to detect the location and
pulmonary area. size of the PDA. The ECG may show evidence of RV
hypertrophy. Chest X-ray reveals pulmonary plethora and
Investigations enlargement of heart.
Echocardiography is used to detect the location and size of
the ASD. The ECG may show incomplete right bundle Management
branch block. Chest X-ray reveals pulmonary plethora and The large PDA is occluded with an implantable device in
enlargement of the heart. infancy before pulmonary hypertension develops. However,
surgery in small PDA is indicated to reduce the chance of Management
endocarditis but may be delayed until later childhood. Surgical correction of the coarctation is indicated in all except
A prostaglandin synthetase inhibitor (ibuprofen or very mild cases. Balloon dilatation is used to correct
indomethacin) may induce closure in the first week of life postsurgical restenosis.
if there is no intrinsic abnormality of ductus.
Tetralogy of Fallot
Coarctation of Aorta
The tetralogy consists of following 4 components;
Congenital narrowing of aorta (coarctation) occurs most 1. Ventricular septal defect
commonly just below the origin of left subclavian artery. 2. Pulmonary stenosis
“Acquired” coarctation of aorta may result due to trauma 3. Overriding of VSD by aorta
or arteritis (Takayasu’s disease). This is more common in 4. Right ventricular hypertrophy
males and may be associated with other congenital This is the most common cause of cyanotic CHD. The
anomalies like bicuspid aortic valve and “berry aneurysms” pulmonary flow is reduced due to RV outflow obstruction.
of cerebral arteries. This results in shunting of desaturated blood from RV to
LV across the VSD leading to cyanosis, clubbing and
Clinical Features polycythemia. The cyanosis increases during feeding or
• If severe, it may cause heart failure in the newborn. crying while it may reduce in squatting posture. There is
• In adults, headache may occur because of hypertension. ejection systolic murmur in the pulmonary area. The
Blood pressure is raised in upper extremities (in vessels complications include infective endocarditis, cerebral
above narrowing) but is normal or low in lower infarction or abscess and polycythemia.
limbs.
• Collateral vessels are well developed on chest and back stenosis and closure of VSD. In case of hypoplastic
(involving periscapular, intercostals and internal pulmonary artery, an initial palliative shunt between
mammary arteries). Bruit may be heard over collaterals. pulmonary artery and subclavian artery is created to
• Rupture of “berry aneurysm” may cause cerebral facilitate definitive correction.
hemorrhage. • Prophylaxis for infective endocarditis is indicated even
• Dissection of aorta and infective endocarditis are other after surgical correction.
complications.
SYNCOPE
Investigations
Syncope is defined as a transient loss of consciousness due
ECG may show LVH. Chest X-ray reveals dilated ascending to diminished cerebral perfusion. Syncope is characterized
aorta and indentation at the site of coarctation (the “3” sign). by loss of postural control and spontaneous recovery.
Notching of ribs due to collaterals may be seen. It may be preceded by symptoms of ‘presyncope’ such as
Echocardiography, CT and MRI are helpful in the diagnosis lightheadedness, visual blurring, dizziness, sweating and
and evaluation of the severity of coarctation. nausea.
Cardiovascular System
Causes of Syncope is immediately made to lie down (recumbent position)
The causes of syncope can be classified into: at the earliest.
1. Cardiovascular disorders • Venous pooling which may occur during prolonged
2. Vascular disorders standing or sitting posture reduces the filling of the
ventricle. The underfilled ventricle vigorously contracts
3. Cerebrovascular diseases
due to increased sympathetic activation which in turn
There are some situations which may resemble syncope
stimulate myocardial mechanoreceptors and vagal
(Table 4.42).
afferent fibers. This causes vasodilation (due to
sympathetic inhibition) and bradycardia (increased
Cardiac Syncope
parasympathetic activity). Vasodilatation and bradycardia
Arrhythmia is the most common cause of syncope due to produce hypotension and syncope.
cardiac cause. The syncope can occur in profound
bradycardia or tachyarrhythmia. Under these conditions, the Postural Hypotension (Postural Syncope)
decreased stroke volume can lead to cerebral hypoperfusion. • Postural hypotension (orthostatic hypotension, OH) is a
The syncope due to atrioventricular block is known as fall in systemic arterial pressure on assumption of upright
Stokes-Adams attack. posture. It is defined as a sustained drop in systolic
(>20 mm Hg) or diastolic (> 10 mm Hg) blood pressure
Vasovagal Syncope within 3 minutes of standing (see also Chapter 10).
• This is the most common cause of “common faint” in • The common causes of postural (orthostatic)
normal persons. hypotension are defective postural reflexes and drugs.
• The precipitating factors are hot or crowded environment, There is fall in the systemic arterial pressure on
severe pain, extreme fatigue, prolonged standing, hunger assumption of an upright posture.
•
and emotional situations.
The vasovagal syncope occurs generally in the sitting
• These defective postural reflexes are generally due to
autonomic peripheral neuropathy such as in diabetes, 111
and standing posture. Hence, it is essential that the patient parkinsonism and aging.
• Hypovolemia because of diuretic therapy, excessive
TABLE 4.42: Causes of syncope sweating, diarrhea, or hemorrhage may also lead to
postural syncope.
1. Cardiovascular disorders
Arrhythmias • Drugs that cause postural syncope mainly include
Sinus bradycardia vasodilators, diuretics and antidepressants.
Heart blocks
Ventricular and supraventricular tachycardia Seizures and Syncope
Aortic stenosis
Hypertrophic obstructive cardiomyopathy The seizures may easily be confused with syncope. However,
Left ventricular dysfunction careful history and examination may reliably differentiate
2. Disorders of vascular tone and blood volume these situations. The important differences are listed in Table
Vasovagal syncope 4.43.
Postural hypotension
Carotid sinus sensitivity
Cough or micturition syncope Investigations
3. Cerebrovascular disease • Tests like ECG, echocardiography, Holter ECG and
Vertebrobasilar insufficiency
electrophysiological studies may be needed to diagnose
Basilar artery migraine
Conditions which resemble syncope the cause of syncope.
Hysterical fainting • Upright tilt test is used to confirm the diagnosis of
Anxiety vasovagal syncope.
Hypoglycemia • Other tests like EEG, CT, MRI scan may be needed to
Seizures
diagnose any neurological cause.
TABLE 4.43: Differences between syncope and seizures
Seizure Syncope
Premonitory symptoms None or aura Lightheadedness, nausea, blurring of vision
Sweating, palpitation
Precipitating factors Usually none Emotional stress, postural hypotension, prolonged standing
Posture Any posture Usually erect
Rapidity of onset Immediate Gradual
Period of unconsciousness Prolonged (minutes) Transient (seconds)
Facial appearance Cyanosis and frothing Pallor
Associated findings Motor seizures, tongue biting, Motor movement uncommon and transient
urinary incontinence
Recovery Prolonged headache, confusion, Rapid and uneventful
focal neurological signs
• Atrial tachycardia.
the syncope. 2. Ventricular tachyarrhythmias
• Patients should try to assume a recumbent position as a. Ventricular ectopic beats (extrasystoles, premature
beats)
soon as they feel premonitory symptoms. b. Ventricular tachycardia (VT)
• Patients who have recurrent syncope should avoid c. Ventricular fibrillation (VF)
climbing ladders, swimming alone, driving or operating d. Tosades de pointes
C. Bradyarrhythmias
machines.
1. Sick sinus syndrome (SSS)
2. Atrioventricular (AV) block
ARRHYTHMIA a. First-degree block
Abnormalities in the rhythm of heart rate are known as b. Second-degree block
Mobitz type I (Wenckebach) block
arrhythmias. Cardiac arrhythmias result from abnormalities Mobitz type II block
of impulse generation, conduction or both. c. Third-degree (complete) heart block
Arrhythmias may present with palpitations, dyspnea, 3. Bundle branch block
a. Right bundle branch block (RBBB)
syncope, fatigue, light headedness, angina, exercise
b. Left bundle branch block (LBBB)
intolerance and skipped beat. Palpitations are suggestive of
TABLE 4.46: Intravenous dosage of some commonly
Cardiovascular System
Diagnostic tools for detecting arrhythmia are following:
a. 12 lead ECG: An ECG during baseline and at the time of used anti-arrhythmic drugs
arrhythmia is initial investigation. • Adenosine: 6 mg IV as a rapid bolus followed by 12 mg after 1-2
b. Continuous ambulatory ECG monitoring: Continuous min if needed
ambulatory monitoring of ECG for 24-48 hours is useful • Digoxin: 0.5 mg IV over 20 min followed by 0.25 or 0.125 mg
for diagnosis of transient arrhythmias that occur with increments to 1.5 mg in 24 hours
sufficient frequency. Correlation between symptoms and • Diltiazem: IV bolus of 0.25/kg mg over 2 min, repeat bolus of
0.35 mg/kg if required
heart rate recordings aids in diagnosis of arrhythmia.
• Verapamil: 5-10 mg over 2-3 min, can be repeated after 15-30
c. Exercise ECG: is helpful in diagnosis of exercise induced min
arrhythmia or to assess response to exercise. • Amiodarone:150 mg IV over 10 min, maintain at 1 mg/min
d. Event recorder: They record ECG on activation by the infusion for 6 hours
patients when they feel symptoms. This can be kept by • Lidocaine: 1-2 mg/kg at 50 mg/min, maintain at 1-4 mg/min
the patients for a month or more. These can also be • Ibutilide: 1 mg over 10 min, followed by second infusion of 1 mg
implanted subcutaneously for up to 1-2 years and are • Flecainide: 50 mg every 12h
useful for patients with infrequent arrhythmia or • Propafenone: 150 mg over every 12h
symptoms. • Metoprolol: 2.5-5 mg IV bolus over 2 min
e. Electrophysiological studies (EPS): EPS is an invasive • Esmolol: 0.5 mg/kg over 1 min
procedure to induce arrhythmia to know their origin. It
is particularly useful in supraventricular arrhythmias
(SVT) and ventricular arrhythmias (VT).
BRADYARRHYTHMIAS
Anti-arrhythmic drugs
Bradyarrhythmia is a rhythm when heart rate is less than 60
Anti-arrhythmic drugs are classified into four classes based
upon their actions (Table 4.45 and 4.46).
beats per minute.
113
TABLE 4.45: Classification of anti-arrhythmic drugs Sinus Bradycardia
Sinus bradycardia is defined as sinus rate of 60 beats/min
Class I Drugs that block sodium channels (membrane
stabilizing effects) with a normal P wave in ECG). In healthy individuals
Ia Prolong action potential: Quinidine particularly in athletes, heart rate may normally be less than
Procainamide 60/min.
Disopyramide
Ib shorten action potential: Lidocaine Symptoms: It may cause fatigue, confusion and syncope
Mexiletine due to reduced cerebral perfusion. It may also cause
Phenytoin breathlessness and angina on exertion.
Ic no effect on action potential: Flecainide
Propafenone Causes: Causes of sinus bradycardia are hypothyroidism,
Class II Beta-blockers, slow AV conduction: Atenolol hypothermia, myocardial ischemia, primary sinus node
Metoprolol
Esmolol
disease, drugs (digoxin, beta blockers, calcium channel
l-sotalol blockers like diltiazem and verapamil, amiodarone.
Class III drugs which prolong action potential: Amiodarone
Diagnosis: ECG reveals rate of <60/min with normal P wave.
d-Sotalol
Ibutilide PR interval, QRS complexes, ST-T wave pattern are
Dofetilide normal.
Bretylium
Class IV slow calcium channel blockers: Verapamil Treatment: In symptomatic patients, the treatment is directed
Diltiazem towards. the underlying cause. Atropine (0.5 to 2.0)
Miscellaneous: Adenosine intravenously can be given in acute symptomatic patients.
Digoxin
Cardiac pacing (transcutaneous or transvenous) may be
Atropine sulphate
required.
Sick Sinus Syndrome conduction delay. ECG reveals no change in PR
Sick sinus syndrome (SSS) is a group of rhythm interval prior to block or non-conducted P wave.
disturbances that result due to sinus node dysfunction. It Type II block may progress into complete heart
includes patients with sinus pause or sinus arrest, tachybrady block. Permanent pacemaker is indicated.
syndrome and sinoatrial exit block. c. Complete (third-degree) heart block:Complete (third-
Symptoms: Patients with SSS may present with palpitation, degree) heart block is a more advanced form in
dizziness, confusion, syncope because of pauses with which transmission of atrial impulses to ventricles
sinoatrial or ventricular activity, intermittent tachycardia and through AV node is completely blocked. Ventricle
bradycardia. escape rhythm maintains a regular, slow ventricular rate
of <45 beats/min. No increase in heart rate occurs with
Causes: Sick sinus syndrome occurs most commonly in
exercise.
elderly patients and arises from intrinsic disease (fibrosis,
Symptoms: Patient may be asymptomatic or may present
degenerative) of sinus node or cardiac conduction system.
with dyspnea and fatigue. Syncope may occur during
Sinus arrest is a condition when sinus node fails to generate
transition partial heart block to complete heart block
an impulse intermittently.
due to ventricular asystole, which may last for few
Treatment: Sinus pauses that result in ventricular asystole
seconds to minutes.
for 3 sec are indications for permanent pacing.
Causes: Causes may be congenital or acquired. Acquired
causes of complete block are myocardial ischemia/
Atrio-ventricular Block
infarction, drugs (digoxin, beta blockers), degeneration
AV bock is condition when atrial impulse is not conducted
of conduction tissue, infiltrative diseases ( amyloidosis,
or conduction is delayed to ventricles.
sarcoidosis), infectious diseases (Chaga’s disease, Lyme
114 a. First-degree heart block is due to delay of impulse
conduction in AV node. ECG reveals prolonged PR
disease) and rheumatological diseases.
Diagnosis: Examination of patient reveals “cannon” a
interval (greater than 0.2 seconds). Important causes are
waves in jugular veins, varying intensity of first heart
increased vagal tone, antiarrhythmic drugs, ischemia,
sound, changing systolic blood pressure level, slow and
electrolytes disturbances and conduction system disease.
regular pulse rate of <45/min.
It is usually asymptomatic and no treatment is required.
Treatment: Permanent pacing is indicated if cause is not
However it may worsen heart failure in patients with
pre-existing heart disease. In symptomatic patients, dual reversible.
Essentials of Medicine for Dental Students
115
Paroxysmal atrial tachycardia with atrio-ventricular precipitate or worsen heart failure in patients with
block (PAT with block) is associated with digitalis ventricular dysfunction or structural heart disease.
intoxication. Multifocal atrial tachycardia (MAT) is It may be asymptomatic and discovered on routine
seen in chronic obstructive pulmonary disease and examination or ECG. Causes of atrial fibrillation are
heart failure. Treatment with beta blockers, calcium given in table 4.47.
channel antagonists or digitalis is given to slow Management of AF: Paroxysmal AF attacks are
the ventricular rate. In digitalis intoxication, the well tolerated and do not require treatment. In
digitalis is stopped and normal potassium levels are symptomatic patients beta blockers are used
maintained. Digoxin antibodies with phenytoin and especially if it is associated with coronary artery
propanolol are used in refractory condition. disease, hypertension or heart failure. Class Ic drugs
Recurrent tachycardia or tachycardia not responding like flecainide or propafenone are also useful.
to drugs is treated by radiofrequency catheter ablation
TABLE 4.47: Common causes of atrial fibrillation
or surgical ablation.
3. Atrial flutter is characterized by single large re-entry Valvular heart disease (especially mitral valve disease)
circuit within the atrium. ECG reveals flutter waves Ischemic heart disease
(saw-toothed appearance) with atrial rate of around Hypertension
300 beats/min. It is commonly associated with 2:1, Hyperthyroidism
3:1, 4:1 block so heart rate is usually less than the Congenital heart disease
Acute alcohol ingestion
atrial rate (75-150/min). Block is increased by carotid
Pericardial disease
sinus massage or intravenous adenosine and is
Pulmonary diseases
helpful in diagnosis. Therapy includes (a) Restoration
Drugs (theophylline etc.)
of sinus rhythm by direct current (DC) cardioversion, Idiopathic (Lone AF)
(b) digoxin, beta blockers or diltiazem may be
Radiofrequency ablation and overdrive atrial pacing or exertion may precipitate or induce arrhythmia. It is due
are other modes of treatment in refractory cases. to re-entry in the right atrium and AV node.
Management of persistent, AF includes: ECG reveals normal regular QRS complexes at a rate of
a. Rate control 140-240/min.
b. Prevention of thromboembolism Symptoms are awareness of fast heart beat (palpitations),
c. Rhythm control. breathlessness or syncope. It may present with angina or
heart failure if there is structural heart diseases. Polyuria
Rate Control
may also occur because of release of atrial natriuretic peptide
Rate control of AF is done by agents which prolong (ANP) due to increased atrial pressures.
conduction through AV node like beta blockers, calcium
channel blockers (diltiazem, verapamil) and digoxin. Management
• Carotid sinus massage and other methods which increase
Prevention of Thromboembolism
vagal tone (Valsalva maneuver, facial immersion in cold
Loss of atrial contraction and atrial dilatation produces stasis water) may terminate the attack. If physical methods
of blood and may precipitate thrombus formation in left
are not effective, intravenous adenosine, verapamil,
atrium. Chronic warfarin ingestion in patients at risk for
diltaizem, flecainide or betablockers may terminate the
embolic stroke (cerebrovascular accident) is the most
attack.
effective therapy for preventing stroke associated with AF.
• SVTs presenting with hemodynamic instability
The INR is maintained between ‘2.0-3.0’.
(hypotension, pulmonary edema) require emergency DC
In patients who have AF for >48 hours, anticoagulation
cardioversion.
with warfarin is recommended for at least 3 weeks before
cardioversion. • For recurrent attacks, prophylactic oral therapy with
116
a verapamil, diltiazem, beta blockers or digoxin may
Rhythm Control be given. It can also be cured by catheter ablation
Restoration of sinus rhythm can be achieved with electrical techniques.
direct current (DC) cardioversion or chemical cardioversion
Atrioventricular re-entrant tachycardia (AVRT)
(using antiarrhythmic drugs). If AF is present for <48 hours
and Wolf-Parkinson-White (WPW) Syndrome
immediate DC cardioversion or chemical cardioversion (with
intravenous ibutilide or flecainide or propafenone) can be This is due to long circuit involving atria, His bundle and
done. ventricles. There is an abnormal connection which connects
Essentials of Medicine for Dental Students
Cardiovascular System
due to tachycardia, this condition is known as Wolff-
Parkinson-White (WPW) syndrome. It is defined as three or more consecutive VPCs. It has to
The ECG appearance may be indistinguishable from be differentiated from SVT with aberrant conduction.
AVNRT. • The usual mechanism is re-entry or abnormal
automaticity or triggered activity in ischemic tissue.
Management • It may be sustained (>30 sec) or non sustained (<30
• Carotid sinus massage or intravenous adenosine may sec). Patient may be asymptomatic or presents with
terminate the attack. syncope or symptoms due to reduced cerebral perfusion
• If atrial fibrillation occurs, it is treated by DC cardio- (dizziness) or dyspnea.
version. • VT is a frequent complication of acute myocardial
• In symptomatic patients, prophylactic therapy is infarction or cardiomyopathy. It may also occur in
indicated. Flecainide, propafenone or amiodarone is used coronary artery disease, mitral valve prolapse, and
for prophylaxis. myocardits.
• Digoxin and verapamil are never used in atrial fibrillation • VT is unfavorable sign in patients with heart disease
associated with WPW syndrome because they shorten and may cause hemodynamic compromise or degenerate
the refractory period of the accessory pathway and may into ventricular fibrillation.
allow a higher rate of conduction and may precipitate • ECG shows tachycardia with a rate of >120/min with
ventricular fibrillation. broad, bizarre QRS complexes.
• In symptomatic patients, catheter ablation of accessory
pathway is curative. Ventricular Fibrillation (VF)
It is characterized by rapid and irregular ventricular activation
Ventricular Tachyarrhythmias resulting into disorganized contraction of ventricle leading
to hemodynamic collapse, cardiac arrest and sudden death. 117
Ventricular Premature Beats (VPBs) • The patient is pulseless and becomes unconscious and
Ventricular premature beats (VPBs) or ventricular extrasystole respiration ceases.
or ventricular ectopic beats (VEBs) is characterized by wide, • The ECG reveals irregular, rapid oscillations (250-400/
bizarre QRS complexes that differ from normal beats in min). The QRS complexes and T waves are not
morphology and there is no preceding P wave. identifiable.
• Every second or third beat if immature, the condition is Treatment of VT and VF:
known as ventricular bigeminy or trigeminy. • Immediate DC cardioversion is the primary therapy for
• VPC may disappear with exercise and rhythm may pulseless VT or VF.
become normal if there is no cardiac disease. • Intravenous antiarrhythmic agents may also be required
• Patient may complain of skipped beat or may be if patient is resistant to defibrillation. In well tolerated
asymptomatic. VT, intravenous amiodarone or lidocaine is indicated.
• VPC occurring in patients with heart disease are Electrolyte imbalance, hypoxemia, acidosis should be
associated with increased chances of sudden cardiac corrected because these can worsen the situation.
death due to ventricular fibrillation. • Treatment of recurrent symptomatic ventricular arrhy-
Treatment: In asymptomatic patients with no cardiac disease, thmia includes administration of chronic antiarrhythmic
no treatment is required. If frequent, the underlying agents (beta blockers, amiodarone)
cause (hypokalemia,hyperkalemia,hypomagnesemia, • Nonpharmacologic treatment of VT/VF includes
hyperth- yroidism and heart diseases) should be treated. implantable cardiac defibrillator (ICDs) and radio-
Beta blockers are agents of first choice in symptomatic frequency catheter ablation to interrupt the arrhythmia
patients with VPC. focus or circuit.
• Torsades de pointes is a form of VT in which QRS 14. Sudden change in the posture from supine to standing
morphology twists around the baseline. It may occur in following dental procedures may cause postural
hypokalemia, hypomagnesemia or after any drug that hypotension and syncope, particularly in patients using
prolongs QT interval. It has poor prognosis. diuretics and calcium channel blockers.
15. Oral abnormalities such as enamel hypoplasia, delayed
IMPLICATIONS ON DENTAL PRACTICE eruption of both dentitions, positional anomalies, bluish
1. Patients with cardiac disease should receive dental white “skimmed milk” appearance of teeth and
treatment in minimal stressful environment. Anxiety, vasodilatation in the pulps may be associated with
exertion and pain should be minimized. cyanotic congenital heart disease.
2. The blood pressure may preferably be measured before 16. Patient with left ventricular failure should be managed
any dental procedure to ensure that this is normal or in partially reclining or erect position. Supine position
controlled. A high blood pressure may result into may worsen dyspnea.
precipitation of other related problems such as angina
or heart failure. SELF ASSESSMENT
3. Besides general examination, precordium should be
auscultated to rule out any lesion in the heart. Multiple Choice Questions
4. Irregular pulse, engorged jugular veins and tachypnea 1. Differential cyanosis can be seen in:
A. Bronchiectasis B. PDA
may indicate the presence of cardiac disease.
C. ASD D. Methemoglobinemia
5. Angina may present as pain in the mandible, teeth and
2. “a” wave in JVP is absent in:
other oral tissues. A. Complete heart block B. Severe HF
6. A history of hypertension, ischemic heart disease or any C. AF D. All the above
9. General anesthesia should be avoided for at least three C. Fallot’s tetralogy D. Pulmonary stenosis
months in patients with recent onset angina. 6. Most common congenital cyanotic heart disease is:
10. Elective dental surgery should be deferred for A. Fallot’s tetralogy B. Eisenmenger syndrome
6 months following acute MI. C. Tricuspid atresia D. Pulmonary atresia
7. Clubbing may be found in all except:
11. Prophylaxis for infective endocarditis is mandatory in
A. Acute infective endocarditis
cases where there is a risk.
B. Fallot’s tetralogy
12. Cardiac patients on anticoagulant drugs or aspirin are at C. Bronchiectasis
increased risk of bleeding following dental procedures. D. Brochogenic carcinoma
Hence, these drugs should preferably be stopped a week 8. Following features can be present in SABE except:
before the procedure. A. Splinter hemorrhages B. Anemia
13. Calcium channel blockers may cause gingival swelling C. Erythema nodosum D. Splenomegaly
and lichenoid lesions in the oral cavity. ACE inhibitors 9. Most common organism causing SABE is:
A. S. aureus B. HACEK group
can cause loss of taste, burning sensation in oral cavity,
C. Strep. viridans D. Enterococci
and angioedema. Dry mouth can result due to 10. Following may be found in rheumatic AS except:
antihypertensive drugs such as diuretics, beta blockers A. Water hammer pulse B. Forceful apex beat
and clonidine. C. Syncope D. Angina
11. Prophylaxis for infective endocarditis is not indicated in: C. Renal
Cardiovascular System
A. Implanted pacemaker B. Secondum ASD D. Primary hyperaldosteronism
C. CABG D. All the above 21. The diuretic preferred in acute pulmonary edema is:
12. Following is the feature of ASD: A. Loop diuretics B. Potassium sparing
A. Continuous murmur C. Thiazides D. All
B. High chance of SABE
C. Wide and fixed second heart sound Fill in the Blanks
D. Commonest type of congenital heart disease 1. Differential cyanosis is seen in _________.
13. Following can be found in mitral stenosis except: 2. Austin flint murmur is found in_________.
A. Loud S1
3. Carey-Coombs murmur in present in_________.
B. Mid-diastolic murmur at apex
4. Reversal of shunt in VSD is known as_________.
C. Opening snap
D. Aortic ejection click 5. Graham-Steel murmur is found in_________.
14. “T” wave in ECG is due to: 6. Maladie de Roger’s murmur is found in_________.
A. Atrial depolarization 7. Continuous machinery murmur is a feature of
B. Atrial repolarization _________.
C. Ventricular depolarization 8. Most common type of ASD is_________.
D. Ventricular repolarization 9. Antihypertensive drug that can cause gum swelling
15. All are features of LVF except: is_________.
A. Orthopnea B. Hepatomegaly 10. Brain natriuretic peptide (BNP) measurement is
C. Pulmonary edema D. S 3 helpful in the diagnosis of_________.
16. Which antihypertensive drug is contraindicated in 11. Prehypertension is defined as Systolic BP___and
bradycardia: diastolic_________.
A. Amlodipine B. Atenolol 12. Patients with coronary artery bypass surgery require
C. Thiazide D. None
17. The most common form of hypertension is:
13.
prophylaxis for infective endocarditis (Yes/No)
Janeway’s lesions are seen in_________.
119
A. Renovascular B. Essential hypertension
14. Berry’s aneurysm is a feature of_________.
C. Endocrinal D. Drug induced
18. Stokes-Adams attack is due to: 15. Mycotic aneurysm is found in_________.
A. AF B. Complete heart block 16. Hill sign is present in_________.
C. Atrial extrasystole D. Severe hypertension 17. Wide fixed splitting of second heart sound is found
19. The preferred antihypertensive agent in diabetics is: in_________.
A. Beta blocker B. ACE inhibitor 18. First heart sound is_________in mitral stenosis.
C. Diuretics D. Centrally acting drugs 19. Crackles are feature of_________ ventricular failure
20. Most common cause of secondary hypertension is: (right or left).
A. Pheochromocytoma 20. Drugs used for the prophylaxis of rheumatic fever
B. Eclampsia are 1_______, 2______ and 3_______.
Chapter
5 Respiratory Diseases
Cough
Cough is one of the most important symptoms in respiratory
diseases. It may be acute (less than 3 weeks) or chronic
FIGURE 5.1: Anterior and posterior aspects of the lung (Table 5.2)
Contd...
Respiratory Diseases
The cough may be dry or associated with sputum
May have hemoptysis Bronchogenic
(productive cough). carcinoma
• Dry cough can occur in bronchial asthma, early phase Lung paren- dry initially followed by Pnemonia
of pneumonia and interstitial lung diseases. Episodic chyma productive cough,
dry cough particularly in the night may be an early rusty sputum
Dry, distressing Interstitial fibrosis
symptom of asthma.
Often nocturnal, pink Pulmonary edema
TABLE 5.1: Important causes of dyspnea frothy sputum
Acute dyspnea Chronic dyspnea
a. Respiratory causes a. Respiratory causes The cough may have different characteristics based on
• Asthma • COPD the sites involved. These are given in table 5.3.
• Acute exacerbation of • Interstitial lung
COPD disease Sputum
• Pneumonia • Pleural effusion
• Pneumothorax
Sputum production is a common symptom in respiratory
• Pulmonary embolism diseases. Its characteristics such as amount, colour and
• ARDS consistency are helpful in making the diagnosis.
• Foreign body inhalation • Large amount of sputum is produced in bronchiectasis
• Laryngeal edema
and lung abscess while scanty thick sputum is found in
b. Cardiac causes b. Cardiac causes
• Acute pulmonary edema • Chronic heart asthma.
failure • Sputum is mucoid, scanty and thick in chronic
c. Other causes c. Other causes bronchitis.
• Metabolic acidosis • Anemia
• Purulent yellow or green sputum signifies infection.
(uremia, diabetic ketoacidosis) • Obesity
• Foul smelling sputum is present in anaerobic infection.
121
• Psychogenic
• Pink frothy sputum suggests pulmonary edema.
TABLE 5.2: Causes of cough • Patients with bronchiectasis or lung abscess may
Acute cough Chronic cough bring out large amount of sputum in a particular posture
Upper respiratory tract Chronic bronchitis
which forms the basis of ‘postural drainage’ in the
infection management.
Pneumonia Post-nasal drip
Aspiration Gastroesophageal reflux Hemoptysis
Pulmonary edema Asthma
Pulmonary embolism Drugs (ACE inhibitors) The coughing of blood in the sputum is called hemoptysis.
The blood may be coughed up alone (frank hemoptysis) or
• Common causes of productive cough are there may be streaking of sputum with blood. Expectoration
bronchiectasis, chronic bronchitis, pneumonia, lung of 200 to 600 ml blood in 24 hours is defined as massive
abscess and tuberculosis. hemoptysis. Hemoptysis should be differentiated from
TABLE 5.3: Characteristics of cough bleeding from other sites such as gums, nose and stomach.
Site of origin Character of cough Common causes The differentiating features between hemoptysis and
Pharynx Persistent, throat pain Pharyngitis, post nasal
drip TABLE 5.4: Differences between hemoptysis and hematemesis
Larynx Harsh, painful, persis- Laryngitis, tumour, Hemoptysis Hematemesis
tent. whooping cough, vocal 1. Bright red appearance 1. Coffee ground or dark red
May have stridor cord palsy (bovine 2. Presence of cough or 2. Presence of vomiting or
cough) other respiratory other abdominal symptoms
Trachea Persistent, painful, stridor Tracheitis, tumour symptoms
Bronchi Dry or productive, Bronchitis, Bronchial 3. Alkaline pH 3. Acidic pH
4. Melena generally not 4. Associated with black tarry
wheeze asthma
found stool (melena)
Contd...
TABLE 5.5: Causes of hemoptysis pleural inflammation and malignancies involving pleura. The
pain due to pleural inflammation may occur in pneumonia
Respiratory
• Chronic bronchitis and pulmonary infarction if parietal pleura is involved. Chest
• Tuberculosis pain due to cardiac diseases should be differentiated from
• Bronchogenic carcinoma that of pleural origin. Important differentiating points are
• Bronchiectasis given in Table 5.6.
• Pulmonary infarction
• Pneumonia
Cardiac EXAMINATION
• Mitral stenosis
• Left ventricular failure
General
Others The general examination in the patients with respiratory
• Goodpasture’s syndrome disease is of great importance. Particularly one should look
• Wegener’s granulomatosis
• Hemorrhagic disorders
for the physique, cyanosis, digital clubbing, elevation of
• Anticoagulant therapy JVP, edema and lymph node enlargement.
Physique: Weight loss may be apparent in cases of
hematemesis (bleeding from gastrointestinal tract) are given tuberculosis, chronic suppurative lung diseases and
in Table 5.4. malignancies of the lung or pleura.
Common causes of hemoptysis are chronic bronchitis, Cyanosis: Patients with respiratory failure may have
pulmonary tuberculosis, and bronchogenic carcinoma. Other central cyanosis. This may occur acutely in extensive
causes are given in Table 5.5. pneumonia, pulmonary edema and massive pulmonary
embolism. Chronically cyanosis is present in COPD. The
Wheezing presence of polycythemia in COPD may lead to cyanosis
even in mild hypoxemia.
122
Wheeze is a high pitched continuous musical sound heard
due to narrowing of airways. This may be noticed by the Clubbing: Digital clubbing may be found in patients with
patient or relatives or others as in case of asthma. chronic suppurative lung diseases (bronchiectasis, lung
A low pitched inspiratory sound heard in the obstruction abscess, empyema), primary and metastatic lung cancers,
of larynx or trachea is known as ‘stridor’. mesothelioma, chronic interstitial lung disease and advanced
pulmonary tuberculosis. The presence of digital clubbing
Chest Pain along with swelling above the wrist and ankle due to
Chest pain in respiratory diseases is mainly due to the periostitis of long bones (hypertrophic pulmonary
Essentials of Medicine for Dental Students
involvement of parietal pleura. The pain is sharp “stabbing” osteoarthropathy) is particularly associated with
which increases on deep inspiration and coughing (pleuritic bronchogenic carcinoma. Clubbing develops rapidly in
chest pain). The causes of pleuritic pain are conditions with patients with lung abscess and bronchogenic carcinoma.
(see Table 1.6)
TABLE 5.6: Differences between pain of
pleural and cardiac origin Edema: Pedal edema can be found in patients with
respiratory disease and it indicates the presence of cor
Pleural origin Cardiac origin
pulmonale (right ventricular enlargement secondary to
Site is usually lateral, axilla or back Central, retrosternal
pulmonary disease) and right ventricular failure.
Character of pain is stabbing, cutting Heaviness or constriction
or tearing type Swelling over the face and neck may also occur in
Referred to abdomen or back Referred to neck or left superior vena cava obstruction due to enlarged lymph nodes
upper limb or malignant mass.
Aggravated by respiratory movement Aggravated by exertion, Lymph node enlargement: The enlargement of lymph
or cough emotions
Relieved by rest or decreased Relieved by rest or nodes, mainly axillary and cervical may indicate tuberculosis
movement of chest nitroglycerine or carcinoma lung. Other groups of lymph nodes like
Examination reveals pleural rub Pericardial rub may be mediastinal, hilar and paratracheal can only be detected by
localized to the site of pain present imaging.
Respiratory Diseases
Respiratory System Examination
The respiratory system, like other systems, should be
examined under four headings: inspection, palpation,
percussion and auscultation.
124
• Crackles are bubbling or clicking brief interrupted Vocal resonance: In consolidation, spoken or whispered
sounds produced by the explosive opening of small sounds are auscultated louder and more clearly over the
airways due to sudden changes in gas pressure. Fine chest wall. These are called bronchophony and whispering
crackles are heard in interstitial fibrosis and early pectoriloquy respectively. The voice may sound nasal or
pulmonary edema while coarse crackles are heard bleating over the level of pleural effusion (aegophony).
TABLE 5.8: Chest examination findings in common conditions
Condition Inspection/palpation Percussion Auscultation
Essentials of Medicine for Dental Students
Consolidation • Reduced chest wall movement • Dull note • Bronchial breath sounds
(Pneumonia) over the affected area • Crackles
• No mediastinal shift • Increased vocal resonance
• Increased vocal fremitus • Whispering pectoriloquy present
Pleural effusion • Reduced movements over • Stony dull note • Diminished or absent breath sounds
affected side
• Mediastinal shift to opposite side • Pleural rub rarely (above effusion)
• Decreased vocal fremitus • Aegophony
Pneumothorax • Reduced movements over • Hyper-resonant • Diminished or absent breath sounds
affected side
• Mediastinal shift to opposite side
• Decreased vocal fremitus
Emphysema • Reduced movements bilaterally • Normal or hyper- • Diminished vesicular breath sounds
• Barrel shaped chest resonant liver dullness with prolonged expiration
• No mediastinal shift masked
• Decreased vocal fremitus • Wheezes
Chronic bronchitis • Movement normal or • Normal note • Vesicular breath sounds with
symmetrically reduced prolonged expiration
• No mediastinal shift • Wheezes
• Normal vocal fremitus • Coarse crackles
Respiratory Diseases
The chest examination findings in common respiratory • Forced expiratory volume (FEV1) is the amount of
disease are given in Table 5.8. gas exhaled in the first second of this maneuver which
is around 80 % of the FVC in normal subjects (Figs
INVESTIGATIONS 5.5A and B).
Chest X-ray: Chest radiograph is an important initial • Forced vital capacity (FVC) is the total amount of
investigation in patients with respiratory diseases. gas which can be forcefully exhaled following a
Consolidation, pleural effusion, pneumothorax, cavity and maximal inhalation.
infiltrates can be reliably diagnosed. • In obstructive lung diseases such as COPD, asthma,
Posteroanterior (PA) view is the standard view. Lateral and bronchiectasis, the FEV1/ FVC ratio is reduced.
view provides additional information in certain conditions
like minimal pleural effusion (lateral decubitus view) and
mediastinal lesions. Comparison with old films is sometimes
helpful to detect new lesions or any change in size.
Sputum examination: Examination of the sputum
provides useful information. Gram staining, AFB (Acid Fast
Bacilli) smear and culture/sensitivity of the sputum are needed
to diagnose pulmonary infections. Malignant cells can be
seen in sputum in cases of bronchogenic carcinoma.
Nebulization with hypertonic saline can be used to
obtain sputum samples. Sample can also be obtained by
bronchoscopy or trans-tracheal aspiration.
Computed tomography: This is useful in the diagnosis
and staging of lung and pleural malignancies. High resolution FIGURE 5.4: Lung volumes 125
CT is particularly helpful in the diagnosis of bronchiectasis,
interstitial fibrosis and pulmonary embolism.
Radioisotope imaging: Combined ventilation-perfusion
scanning is useful in the diagnosis of pulmonary
thromboembolism.
Pulmonary angiography is the definitive method of
diagnosing pulmonary emboli.
Arterial blood gas (ABG) analysis: Partial pressures of
oxygen (PaCO2), carbon dioxide (PaO2) and pH can be
measured in arterial blood sample. This is helpful in the
assessment of the degree and type of respiratory failure.
Bronchoscopy: Trachea or bronchi are directly visualized
by flexible or rigid bronchoscope. Samples from airways
can also be obtained by bronchial washings, aspiration or
biopsy. Foreign body can be removed by bronchoscopy
(Therapeutic bronchoscopy).
Pleural biopsy and aspiration: These are helpful in the
detection of the cause of pleural effusion.
Spirometry: Lung volumes are measured by spirometry
(Fig. 5.4). This is most useful in differentiating obstructive FIGURES 5.5A and B: Spirometry in (A) normal person (B)
from restrictive lung diseases. patient with obstructive lung disease
• The ratio is normal or raised in restrictive lung TABLE 5.9: Common pathogens causing CAP
diseases such as pulmonary fibrosis. Bacteria
• Peak expiratory flow rate (PEFR) can be measured Streptococcus pneumoniae
by a portable meter and is helpful in the diagnosis Mycoplasma pneumoniae
Hemophilus influenzae
and management of patients with asthma.
Clamydia pneumoniae
Staphylococcus aureus
PNEUMONIA Legionella sps.
Pneumonia is defined as the infection of the lung
Viruses
parenchyma (alveoli and distal airways) and interstitium of Influenza
the lung. Adeno viruses
Respiratory syncytial viruses
Etiology
Pneumonia is more common at extremes of age and in TABLE 5.10: Common pathogens causing HCAP
winter months.
Non-MDR pathogens MDR pathogens
• The risk factors for developing pneumonia are smoking,
Streptococcus pneumoniae Pseudomonas aeruginosa
alcohol use, immunocompromised states (HIV disease, Hemophilus influenzae Methicillin resistant S. aureus
end stage renal disease), diabetes mellitus, congestive Methicillin sensitive S. aureus Acinetobacter spp.
heart failure, COPD and malignancies. Enterobacteriacae Enterobacteriacae
(E. coli, klebsiella) (antibiotic resistant)
• Pneumonia is broadly divided into two types: Community
acquired pneumonia (CAP) and Health care associated
pneumonia (HCAP). and dental caries. Pseudomonas infection is common in
oropharyngeal secretions colonized with pathogenic within 24 hours. The lung parenchyma is highly
microorganisms. Other routes are gross aspiration, vascular and edematous with plenty of bacteria and
aerosolization, hematogenous spread from a distant site and scanty neutrophils.
spread from adjacent tissues. • Second stage (red hepatization) is characterized by
the presence of numerous erythrocytes, neutrophils,
Organisms desquamated epithelial cells and fibrin in alveoli
More than 100 organisms including viruses, bacteria, fungi resulting in a red and airless lung, and a consistency
and parasites are reported to cause pneumonia. Common similar to that of liver.
organisms responsible for CAP and HCAP are listed in Table • In the third stage (grey hepatization), lung parenchyma
5.9 and 5.10, respectively. becomes grey, dry and friable.
By far the most common organism causing CAP is S. • Finally, in the stage of resolution, the exudates are
pneumoniae (>50%). The etiological organism may vary digested and removed by scavenger cells or coughed
according to the age of the patient and the specific clinical out.
situations. P. carinii occurs in HIV infection while anaerobic b. Bronchopneumonia: This type is most commonly seen
and gram-negative bacilli (mixed etiology) can cause in HCAP. There is neutrophilic exudate in bronchi and
pneumonia due to aspiration in patients with stroke, epilepsy, bronchioles with peripheral spread of infection to alveoli.
TABLE 5.12: CURB-65 criteria
Respiratory Diseases
One or several lobes of the lung may be involved.
Generally lower and posterior segments of lobes are C confusion
affected. U blood urea nitrogen >20 mg/dL
c. Interstitial pneumonia: This is seen in viral and R respiratory rate >30 min
B blood pressure systolic <90 mm Hg or diastolic <60 mm Hg
pneumocystis jiroveci pneumonia. There is predominant
65 age >65 years
involvement of the interstitium, alveolar wall and
connective tissue around the bronchovascular tree. The
Complications
pattern may be patchy or diffuse.
d. Miliary pneumonia: Hematogenous spread of pathogens The complications of pneumonia are given in Table 5.13.
to the lung may result into diffuse and discrete 2-3 mm
Investigations
lesions resembling millet seeds.
1. Radiological: Chest X-ray shows homogeneous opacity
Clinical Manifestations localized to the lobe or segment (lobar consolidation)
The onset may be sudden or insidious, and the disease may or diffuse infiltrates in bronchopneumonia (Fig. 5.6).
be mild or severe. Fever with chills or rigors, cough (dry Other findings may include pleural effusion, lung abscess
or productive), pleuritic chest pain, breathlessness are and hilar lymphadenopathy. Pneumatoceles may be seen
typical manifestations of pneumonia. Other symptoms are in S. aureus pneumonia.
headache, nausea, vomiting, diarrhea, altered sensorium, TABLE 5.13: Complications of pneumonia
myalgia and arthralgia. The signs of lobar pneumonia are
1. Pulmonary
depicted in Table 5.11. • Parapneumonic pleural effusion
The severity of pneumonia is indicated by respiratory • Empyema
127
rate >30 per minute, pulse rate >125 per minute and blood • Suppurative pneumonia/lung abscess
• ARDS
pressure less than 90 mmHg. Other markers of severity are
• Pneumothorax (in S. aureus pneumonia)
altered mentation, hypoxia (PaO2<60 mmHg), hyponatremia, 2. Extrapulmonary
acidosis and azotemia. Pneumonia due to certain organisms • Hepatitis, pericarditis, meningoencephalitis
like P. aeruginosa, Klebsiella spp, E. coli, S. aureus are • Multiorgan failure
• Ectopic abscess formation
associated with high mortality rate. The CURB-65 criteria
(Table 5.12) are helpful in deciding whether patient should
be treated on out-patient basis or hospitalized. Patients with
two or more criteria need hospitalization.
TABLE 5.11: Respiratory signs in lobar pneumonia
128
2. Supportive therapy: Oxygen therapy is given to all
hypoxemic patients. Those who do not respond may need LUNG ABSCESS
mechanical ventilation. Intravenous fluids may also be Suppurative pneumonia is characterized by destruction of
required in hospitalized patients. lung parenchyma by the inflammatory process generally
3. Antibiotic therapy: The antibiotics should be started as leading to micro-abscess formation. When a large collection
early as possible. If possible, the specimen should be of pus occurs within the lung parenchyma lined by chronic
sent for culture and sensitivity before starting antibiotics. inflammatory tissue, the condition is known as lung abscess.
The etiology is commonly unknown; hence, the initial The most commonly involved areas are dependent
Essentials of Medicine for Dental Students
choice of antibiotics is empirical. However, this may be segments of the lungs: posterior segments of the upper lobes
modified once culture reports are available. and superior segments of the lower lobes in supine position.
a. In out-patients with CAP, the preferred empirical
antibiotic options are macrolide or doxycycline or Risk Factors
fluoroquinolones (with activity against S. pneumoniae) Aspiration of oropharyngeal secretion is the most important
(Table 5.14). A 10-14 days therapy is generally cause of lung abscess. Predisposing factors for aspiration
required. include:
b. Emperical antibiotic options for hospitalized patients • Altered consciousness due to any cause (alcohol, drugs,
with CAP are following. These are given intravenously. seizures, stroke and general anesthesia)
The duration of treatment is 10-14 days. • Impaired swallowing due to esophageal disorders
1. Beta lactum (cefatrixone 1-2 gm/day or Cefotaxime (achalasia, gastroesophageal reflux)
2 gm 6 hrly) plus a macrolide or fluoroquinolones • Vocal cord palsy.
2. Beta lactam/beta lactamase inhibitor (ampicillin/ • Poor oral hygiene and gross oral sepsis is also
sulbactam or piperacillin/tazobactam) plus associated with greater risk of pulmonary infection due
macrolide or fluoroquinolones to aspiration.
TABLE 5.15: Causes of cavitatory lung disease
Respiratory Diseases
Causative Organisms
Mostly the lung abscess is caused by mixed bacterial flora, 1. Lung abscess
both aerobic and anaerobic. 2. Tuberculosis
3. Fungal infections
• Common aerobic pathogens responsible for lung abscess
4. Cavitating carcinoma
are S. pneumoniae, S. aureus, S. pyogenes, H. influenzae, 5. Pulmonary infarction
E. coli and Pseudomonas. 6. Wegener’s granulomatosis
• Anaerobic bacteria such as bacteroides, Prevotella,
• Sputum or pulmonary secretion obtained by broncho-
Fusobacterium and Peptostreptococcus species are
scopy is cultured for both aerobic and anaerobic
generally responsible in cases with poor dental hygiene
organisms.
or oral sepsis.
• CT thorax can be helpful to exclude the presence of
tumor or other underlying causes in patients not
Clinical Features
responding to treatment.
The presentation is generally insidious in anaerobic infection
while more acute presentation is typical of aerobic infection. Treatment
Important symptoms are high remittent fever, weight loss,
Medical
malaise, night sweats, cough with large amount of purulent
sputum. The foul smelling sputum suggests anaerobic • The antibiotic therapy should be chosen according to
infection. Chest pain may occur due to pleural involvement. the organism isolated.
General examination may reveal clubbing. Respiratory • The therapy is generally given for prolonged period
examination shows signs of consolidation or cavity such as (6-8 weeks) until the radiographic resolution of the
cavity.
bronchial breath sound and coarse crackles.
129
• Commonly, a combination of penicillin (amoxicillin) and
Diagnosis metronidazole is effective. However, with the emergence
of beta lactamase producing organisms, clindamycin
• The chest X-ray may show, in early stages, a homogenous
(150-300 mg 6 hrly) is now considered standard therapy.
opacity due to consolidation. This may cavitate and Beta lactam/beta lactmase inhibitors may also be used.
present as large cavity with air fluid level (Fig. 5.7). • Postural drainage is also helpful in the management of
Other causes of cavitatory lung disease should be lung abscess.
excluded (Table 5.15).
Surgical
Surgical intervention like percutaneous drainage or lobectomy
is needed in case there is no response to medical treatment
or there is a large abscess.
BRONCHIECTASIS
Abnormal and permanent dilatation of bronchi is called
bronchiectasis. There is inflammation of the medium sized
airways leading to the destruction of the wall. The
inflammatory cells, chiefly neutrophils are primary mediators
and they release proteolytic enzymes leading to destruction
and fibrosis of bronchial structures. Repeated obstruction
and infections are important factors. Common causes of
bronchiectasis are suppurative pneumonia and tuberculosis.
FIGURE 5.7: X-ray chest showing lung abscesses with
Other important causes of bronchiectasis are given in Table
horizontal air fluid level 5.16.
TABLE 5.16: Important causes of bronchiectasis • Sputum examination and culture guide in choosing the
Congenital antibiotics.
• Kartagener’s syndrome*
• Cystic fibrosis Treatment
Acquired
• Suppurative pneumonia
• The main steps in the management of bronchiectasis
• Tuberculosis are antibiotics, postural drainage and inhaled
• Post-viral infection (in children, adenovirus, influenza virus) bronchodilators.
• Foreign body • Surgery is indicated in cases of massive hemoptysis
• Bronchial tumor
• Allergic bronchopulmonary aspergillosis (ABPA) and localized bronchiectasis which fail to respond to
adequate medical therapy.
* Kartagener’s syndrome includes bronchiectasis, sinusitis and situs
inversus.
Complications
Clinical Manifestations The complications of bronchiectasis are amyloidosis, cor
Chronic persistent or intermittent cough with large amount pulmonale and abscess at distant site.
of purulent sputum is the main symptom. Patient may also
have fever, weight loss and hemoptysis. Recurrent lung BRONCHIAL ASTHMA
infection may lead to pneumonia and pleurisy. Asthma is a disease of the airways in which there is a chronic
Clinical examination reveals digital clubbing and anemia. inflammation and increased responsiveness to a wide variety
Lung signs are non-specific and include basal coarse of stimuli, leading to reversible airway obstruction. Patients
crackles and wheezes. There may be signs of right heart generally have paroxysms of cough, wheeze and dyspnea,
failure (cor pulmonale). interspersed with symptom-free periods.
Clinical Features
The symptoms of bronchial asthma may be episodic or
persistent.
• Episodic asthma is characterized by paroxysm of
dyspnea, cough and wheezing which occurs more
commonly in children and young adults. The attacks
may be mild or severe and may last for hours, days or
rarely weeks. Between episodes, the patients are usually
asymptomatic.
• In older non-atopic patients, the asthma is chronic and
persistent. Symptoms are worse in the early morning.
This can be confused with the COPD.
Examination
• The examination may reveal tachypnea, tachycardia and
involvement of accessory respiratory muscles. FIGURE 5.9: Peak expiratory flowmeter
Chest X-ray: This is usually normal. However, it may c. To prevent exacerbation
appear hyperinflated. This is also helpful in ruling out other d. To normalize exercise capacity
conditions. Avoidance of factors: The identification of allergens is
Arterial blood gas analysis: Initially PaCO2 is low. A possible only in a few cases. Wherever possible, the exposure
normal or high PaCO2 is a sign of impending respiratory to such agents must be avoided.
failure. PaO2 <60 mmHg signifies severe bronchoconstriction
Desensitization: Desensitization by repeated administration
and respiratory failure.
Others: Peripheral blood may show eosinophilia. Sputum of allergen has not been proven effective in most studies.
may also contain an increased number of eosinophils. Drug therapy: The drugs used in asthma can be grouped
as:
Management a. Quick relievers: which inhibit smooth muscle
The overall aim of management should be contraction and cause bronchodilatation (Table 5.18)
a. To abolish or minimize symptoms b. Long-term control medications: which prevent or
b. To attain the best possible PEF reverse inflammation (Table 5.19).
132 Anticholinergics
Ipratropium bromide
Tiotropium inhaled no major side effects
Note: Long acting inhaled adrenergic agents (salmeterol, formoterol) and theophylline also have anti-inflammatory properties.
Chronic Persistent Asthma
Respiratory Diseases
2. Repeated dosage of short-acting adrenergic drugs
A stepwise approach is chosen according the severity of (salbutamol 2.5-5 mg or terbulaline 5-10 mg) is given
disease. Once the disease is controlled, a step down therapy through a nebulizer at an interval of 20-30 minutes. The
is attempted. PEFR should be recorded frequently to assess the
Step 1: Inhaled short acting adrenergic agents (salbutamol, response. Metered dose inhaler with a spacer device can
terbutaline) are used as needed for minor alternatively be used. Ipratropium bromide can be added
symptoms. to get additional bronchodilator effect.
Step 2: If the symptoms are not controlled with occasional 3. Systemic steroids: This is essentially needed in all cases
inhaled adrenergic drugs as mentioned above, of severe asthma. Prednisolone (30-60 mg daily) or
low dose of inhaled steroid is added. Mast cell methylprednisolone is given orally or intravenously.
stabilizers can be used prophylactically before 4. Others:
exposure to allergens, exercise or cold air. a. Mechanical ventilation is needed in patients with
Step 3: The dose of inhaled steroid is escalated. An inhaled coma, respiratory arrest, exhaustion and deteriorating
long acting adrenergic agent such as salmeterol or blood gases despite adequate treatment.
formoterol can be added. Sustained release b. IV fluid is administered to prevent dehydration.
theophylline may also be used orally. c. Antibiotics are not used routinely. These are only
Step 4: In addition to drugs used in step 3, leukotriene given if infection is present.
modifiers and inhaled ipratropium bromide are d. Opiates, sedatives or tranquillizers are contraindicated.
tried.
Step 5: Regular oral steroid in the lowest effective dosage Patient Education and Monitoring of Therapy
is added to step 4 regimen to control symptoms. • The patients are educated about the nature of disease
134 cough and sputum. advances, dyspnea becomes more severe and occurs even
2. Emphysema is defined as irreversible destruction and during rest.
enlargement of airspaces distal to terminal bronchioles. In mild cases, the physical examination may be normal.
Pure forms of these two conditions are rare and in the • Chest examination reveals vesicular breath sound
majority of cases they coexist. with prolonged expiratory phase and generalized
wheeze. The crackles (crepitations) may be heard
Etiological Factors mainly in the lower zones.
• Cigarette smoking is the most important etiological factor • The patient with predominant emphysema shows
Essentials of Medicine for Dental Students
for COPD. There is a positive correlation between the barrel shaped chest (increased AP diameter), loss of
intensity of smoking (number of cigarettes and duration cardiac and liver dullness and diminished vesicular
of smoking) and the development of COPD. However, breath sound.
individual susceptibility varies since only 15 % smokers • The use of accessory respiratory muscles, breathing
develop clinically significant COPD. with pursed lips and lack of cyanosis characterize
• Air pollution in the environment may also be associated emphysema (pink puffers).
with the development of COPD. • Cyanosis and right heart failure are more common
• Other factors are occupational exposure to dusts, and seen earlier in the course of disease in patients
bronchial hyper-responsiveness and low birth weight. with predominant chronic bronchitis (blue bloaters).
• Severe alpha-1 antitrypsin deficiency is a proven genetic The signs are also depicted in Table 5.20.
risk factor for the development of emphysema.
Investigations
Pathophysiology 1. Pulmonary function tests: (see also page 131) Spirometric
The important pathological changes in the airways are demonstration of airway obstruction without significant
inflammation, hypertrophy of the mucous secreting glands reversal is the hallmark of the diagnosis of COPD.
TABLE 5.20: Clinical signs in COPD
Respiratory Diseases
Treatment
General Treatment of COPD can be described as of (a) chronic stable
• Cyanosis phase, and (b) acute exacerbation
• Signs of right heart failure
Pedal edema, raised JVP, hepatomegaly, ascites
Chronic Phase
• Signs of CO2 retention
Flapping tremor (asterixis), bounding pulse Most forms of therapy are directed to relieve the symptoms
obtundation and to decrease the frequency and severity of acute
• Pursed lip breathing exacerbations. These measures do not alter the natural course
• Wasting and weight loss
Respiratory of the disease. However, cessation of smoking, oxygen
• Use of accessory muscles of respiration (scalenae, therapy in chronically hypoxic patients and lung volume
sternocleidomastoid) reduction surgery (LVRS) in selected patients are known to
• Indrawing of intercostal muscles during inspiration (Hoover’s influence the natural history of COPD.
sign)
• Increased AP diameter of the chest
a. Smoking cessation: All patients with COPD should be
• Loss of cardiac dullness and liver dullness encouraged to stop smoking since it improves the rate
• Diminished vasicular breath sounds of decline in the pulmonary function. The patients should
• Prolonged expiratory phase be educated and adequately counseled. Bupropion or
• Generalized wheeze
nicotine replacement therapy may be employed to enhance
• Crackles mostly at bases
the chance of smoking cessation.
b. Oxygen therapy: Long-term oxygen therapy at home is
Significant reversibility of the obstruction (as seen in required in patients with PaO2 <55 mmHg or in patients
asthma) is defined as 15% or more increase in FEV1 with PaO 2 55-60 mmHg who have pulmonary
hypertension, heart failure or polycythemia. Oxygen is
135
after two puffs of beta adrenergic agonist. An abnormal
FEV1 (< 80% predicted) with an FEV1/VC ratio of < given in low concentration (2 liters/min) for at least 15
70% strongly suggests COPD. A normal FEV1 excludes hours a day.
the diagnosis of COPD. Lung volumes (total lung c. Bronchodilators: Bronchodilators are given for
capacity and residual volume) are increased due to air symptomatic relief. Anticholinergic agents (ipratropium
bromide, tiotropium) are used in inhaler form. Beta
trapping.
agonists like salbutamol (short acting) or salmeterol and
2. Chest X-ray may demonstrate bullae, hypertranslucent
formeterol (long acting) are also useful. The addition of
lung fields, flattened diaphragms and prominent
beta agonists with anticholinergic agents provides
pulmonary arterial shadows. The X-ray is also helpful
incremental response. Oral theophylline may result in
in excluding other conditions presenting with chronic
improved exercise tolerance and quality of life in
cough and dyspnea. CT is used to diagnose emphysema
moderate to severe COPD.
and to detect its severity.
d. Corticosteroids: Inhaled corticosteroids have been shown
3. Arterial blood gas analysis reveals hypoxemia (low
to decrease the frequency of acute exacerbations of
PaO 2 ) and hypercarbia (high PaCO 2 ). Diffusing COPD. Low dose inhaled steroids are thus indicated in
capacity of the lung for carbon monoxide (DLco) is severe COPD. However, chronic use of oral
markedly low in emphysema. corticosteroid is not recommended in view of side effects.
4. Serum alpha-1 antitrypsin level should be measured in e. Antibiotics: Respiratory infections must be treated
young patients with family history of COPD. promptly as they may precipitate acute exacerbation. The
most common bacteria responsible for infection are S.
Complications pneumoniae and H. influenzae. The antibiotics of choice
The complications of COPD include, (a) pneumothorax are amoxicillin, amoxicillin-clavulanate combination or
due to rupture of bullae, (b) respiratory failure (type II) clarithromycin given for at least 5-10 days. Influenza
and (c) cor pulmonale. vaccine is recommended annually.
f. Pulmonary rehabilitation: Exercise and pulmonary 5. Diuretics are given in case of raised jugular venous
rehabilitation programs improve dyspnea and quality of pressure (JVP) and edema.
life. 6. Mechanical ventilatory support (invasive and non-
g. Surgery: invasive) may be required in patients with severe
• Lung volume reduction surgery (LVRS) may be respiratory distress, severe hypoxia and hypercapnia.
indicated in patients with emphysema. It improves
pulmonary functions and symptoms and also PULMONARY EOSINOPHILIA
provides mortality benefit. Pulmonary eosinophilia or pulmonary infiltrates with
• Surgical resection is also required in patients with eosinophilia (PIE) are distinct syndromes characterized by
large bullae. the presence of pulmonary infiltrate and eosinophilia
• Severe COPD is an important indication for lung (peripheral eosinophil count >500/µL). The most common
transplantation. cause of PIE in tropical countries is parasitic infestation
and ABPA (allergic bronchopulmonary aspergillosis)
Acute Exacerbation in developed countries. Other causes of PIE are listed in
The acute exacerbation of COPD presents as fever, Table 5.22.
increased breathlessness and cough, production of increased
volume of purulent sputum and some times as right heart Tropical Eosinophilia
failure. The patients may have cyanosis and impaired • Tropical eosinophilia is caused by filarial infection.
sensorium. • The manifestations are due to allergic and inflammatory
Acute exacerbation of COPD should be differentiated reactions elicited due to clearance of microfilaria by the
from other conditions presenting as acute onset dyspnea lungs.
136
(Table 5.21). • The main presenting features are paroxysmal dyspnea,
Chest X-ray, arterial blood gas analysis, ECG, blood wheeze, cough and low grade fever.
counts, urea and electrolytes and sputum culture are • Peripheral blood examination shows eosinophilia (>3000/
generally performed to assess severity of the exacerbation µL) and X-ray chest generally reveals diffuse miliary
and to exclude other causes. opacities. Total serum IgE level and anti-filarial antibody
Most patients require hospitalization. The main steps in titer are specifically elevated.
the treatment include: • The treatment includes diethylcarbamazine (DEC) in
1. Oxygen therapy dosage of 4-6 mg/kg body weight daily for 14 days.
Essentials of Medicine for Dental Students
2. Antibiotics are given to treat respiratory infections. Acute eosinophilic pulmonary infiltrate may also occur
3. Bronchodilators: The dose and frequency of broncho- due to passage of helminthes larvae through lungs (Loeffler’s
dilators are escalated. These are administered initially Syndrome).
by nebulization. Intravenous infusion of aminophylline
is needed if there is no response. TABLE 5.22: Causes of pulmonary infiltrates
4. Short course of oral corticosteroid hastens recovery with eosinophilia (PIE)
and reduces chances of subsequent relapses.
1. Parasitic infestation
TABLE 5.21: Differential diagnosis of • Ascaris, microfilaria, ankylostoma, toxocara, strongyloides
acute exacerbation of COPD 2. ABPA
3. Drug induced
Pneumonia • Nitrofurantoin, penicillin, sulphonamide, PAS, phenyl
Pneumothorax butazone
Left ventricular failure 4. Conditions with unknown etiology
Pulmonary embolism • Hypereosinophilic syndromes
Acute severe asthma • Churg-Strauss syndrome (multisystem vasculitis)
Airways obstruction • Eosinophilic pneumonias
TABLE 5.24: Causes of pulmonary embolism
Respiratory Diseases
Allergic Bronchopulmonary Aspergillosis (ABPA)
• Aspergillus fumigatus is the most common cause of 1. Deep vein thrombosis (in lower limb)
ABPA. 2. Non-thrombotic causes
a. Amniotic fluid embolism (tear of placental margin, fetal
• The features include asthma, raised serum IgE, skin
membrane leak)
reaction to A. fumigatus, evidence of peripheral b. Air embolism
eosinophilia (>1000/µL ) and pulmonary infiltrates. c. Fat embolism (long bone fractures, blunt trauma)
• The sputum culture may be positive for the A. fumigatus. d. Tumor embolism (choriocarcinoma)
e. Septic emboli (Infective endocarditis affecting tricuspid and
• The treatment requires long-term use of glucocorticoids. pulmonary valves)
Investigations
1. Demonstration of AFB: The diagnosis of tuberculosis
is based on the demonstration of AFB in the smear of
the sputum or in other specimens such as tissue biopsy
materials or body fluids. Ziehl-Neelsen or Auramine
fluorescence staining is usually done for this purpose. If
the patient is not passing sputum, nebulization with
hypertonic saline can be used to induce sputum
expectoration. Samples can also be obtained by gastric
lavage (in children), bronchoalveolar lavage or
transbronchial biopsy.
2. Culture methods: The culture provides confirmation of FIGURE 5.14: X-ray chest showing right sided massive pleural
the diagnosis by the isolation and identification of M. effusion with mediatinal shift
(Fig. 5.13). However, any type of radiographic pattern Treatment
such as consolidation, collapse, pleural effusion or The main aims of treatment of tuberculosis are:
miliary can be seen in tuberculosis (Fig. 5.14). 1. To cure the patients of tuberculosis
5. Skin test: Purified protein derivative (PPD) skin test 2. To decrease transmission of tuberculosis to others
(using Montoux method or Heaf method) is positive (a) 3. To prevent relapse
in persons infected with M. tuberculosis, (b) in persons 4. To prevent morbidity and mortality from active
sensitized by non-tuberculous mycobacteria and (c) in tuberculosis
those who have received BCG vaccination. A positive 5. To prevent late effects of tuberculosis.
skin test does not tell about the active disease. A positive
test in those who have not received BCG may suggest Anti-tubercular Drugs
the diagnosis of tuberculosis. The test may be negative The anti-tubercular drugs are bactericidal or bacteriostatic
in miliary tuberculosis and in immunocompromised in nature. The bactericidal drugs are used to rapidly reduce
patients with tuberculosis. the number of viable organisms and render patients non-
6. Histopathological tests: The FNAC (fine needle infectious. These also have sterilizing activity (kill all bacilli),
aspiration cytology) or biopsy specimens from the hence, they prevent relapse. Bacteriostatic drugs are used along
involved tissue may typically reveal caseous granuloma. with the bactericidal drugs to prevent emergence of resistance.
AFB can be demonstrated in tissue specimens. The tissue First line drugs: The first line drugs are rifampicin (R),
can be cultured to demonstrate mycobacteria. isoniazid (H), pyrazinamide (Z) and ethambutal (E). Isoniazid
7. Other tests: and rifampicin are active against all population of TB bacilli
• The hematological findings include anemia, raised while pyrizinamide and streptomycin are active against certain
ESR and C reactive protein. population of TB bacilli. In addition, pyrazinamide is active
142 • The fluid (pleural, pericardial, peritoneal) is exudative against bacilli in acid environment inside macrophages and has
in nature. good CSF penetration. Streptomycin is particularly active
• Liver biopsy and bone marrow biopsy specimens against extracellular bacilli. The dosage and side effects of
may also be examined for the evidence of granuloma anti-tubercular drugs are given in Table 5.27.
and AFB.
TABLE 5.27: Anti-tubercular drugs and their dosage
Drugs Mode of action Daily dose Intermittent Common side effects
mg/kg (thrice weekly)
Essentials of Medicine for Dental Students
mg/kg
Isoniazid (H) Bactericidal 5 10 Hypersensitivit y, neuropathy, hepatitis
Rifampicin (R) Bactericidal 10 10 Hepatitis, thrombocytopenia, flu like symptoms,
hypersensitivity, drug interactions
Pyrazinamide (Z) Bactericidal 25 35 Gout, hepatitis, hypersensitivity
Ethambutol (E) Bacteriostatic 15 30 Optic neuritis, hypersensitivity, colour blindness for
green
Streptomycin (S) Bactericidal 15 15 Vestibular toxicity, deafness, hypersensitivity, renal
toxicity
Second line drugs: The Second line drugs (Table 5.28) (twice or thrice weekly). The response to therapy is
are less efficacious and more toxic. These are used when monitored through clinical improvement, X-ray chest and
first line drugs fail. culture or smear examination.
Initial phase: The aim is to rapidly kill the bacilli, resolve
Treatment Regimen symptoms and bring out sputum conversion (AFB negative)
The treatment consists of the initial phase and the so that the patient becomes non-infectious. Generally, a
continuation phase. The schedule is daily or intermittent combination of 3-4 drugs is used for 2-3 months.
TABLE 5.28: Second line anti-tubercular drugs
Respiratory Diseases
alcoholics, elderly, malnourished, diabetics, pregnant
Oral agents ladies and HIV patients.
• Ethionamide • Corticosteroids are useful if given with antitubercular
• Cycloserine drugs in seriously ill patients (miliary TB), and meningeal,
• PAS pericardial, pleural or ureteric diseases to prevent
• Fluoroquinolones: Gatifloxacin, Levofloxacin,
Moxifloxacin, Ofloxacin adhesions.
Injectible agents • Surgery may be needed in patients with massive and
• Streptomycin (S) recurrent hemoptysis, constrictive pericarditis, lymph
• Kanamycin node suppuration, empyema and spinal cord compression.
• Amikacin
• Capreomycin
Other drugs National Guidelines
• Clofazimine Patients with tuberculosis are grouped into four categories
• Thioacetazone and the treatment regimens are chosen accordingly
• Amoxicillin-clavulinic acid
• Linezolid
(Table 5.29).
Note: Less severe form of extrapulmonary TB includes lymph nodes, unilateral pleural effusion, bone excluding spine, peripheral joint or skin
involvement. Severe form of extrapulmonary TB includes meningitis, military TB, pericarditis, peritonitis, bilateral or extensive pleural effusion, spinal,
genitourinary, intestinal TB.
more of the injectable drugs: amikacin, kanamycin or Chemoprophylaxis
capreomycin. • Chemoprophylaxis has been applied in (a) tuberculin
negative individuals to prevent occurrence of infection
Directly Observed Treatment, Short Course (DOTS)
in high risk situations (b) treating tuberculin positive
Patients swallow the drugs before a health personnel or cases to prevent disease.
some other responsible person. This ensures that the TB • In India where a large majority of the population is
patient takes the right drugs, in the right dosage at the right tuberculin positive, it may be an expensive preposition.
intervals. DOTS helps to improve cure rate and to reduce Hence, chemoprophylaxis has been recommended in all
the chance of drug resistance. known recent tuberculin converters or in household
contacts of newly diagnosed active cases regardless of
Complications of Pulmonary Tuberculosis tuberculin positivity.
The complications of TB are given in Table 5.30. • Isoniazid is given for 6 months or isoniazid plus
rifampicin for 3 months or rifampicin alone for 4 months.
Vaccination
Most countries recommend the use of Bacillus Calmette RESPIRATORY FAILURE
Guérin (BCG) vaccination. This contains attenuated strain Respiratory failure is defined as a condition in which lung
of M. bovis. function is inadequate to meet the metabolic requirement of
• Intradermal route is recommended for the administration the individual. The dysfunction can be in one or more
of the vaccine at the lower deltoid area. components of the respiratory system such as airways,
• In India, it is recommended to be administered to infants respiratory muscles, alveolar units and pulmonary vessels.
after birth or at the first contact of the infant with the Respiratory failure manifests as hypoxemia (PaO2 <60
145
ventilation are not available. • The clinical examination reveals pleural rub and other
b. Chronic: This is characterized by the presence of features of primary underlying disease. The disappearance
hypoxemia, hypercapnea with near normal pH due to of rub and chest pain suggests recovery or the
compensatory rise in bicarbonate (HCO3). The most development of pleural effusion.
important cause is COPD. The treatment is directed • The management of pleurisy includes treatment of the
toward the cause. A controlled long-term oxygen therapy primary cause and the symptomatic control of pain.
may be helpful. Analgesics and anti-inflammatory drugs are used for
c. Acute on chronic: Any precipitating event such as acute pain relief. Codeine is helpful in suppressing the cough
infection, airways obstruction and cardiac failure can
and chest pain.
lead to acute deterioration in patients with chronic
respiratory disease. The treatment consists of control Pleural Effusion
of precipitating events and controlled low concentration
Pleural effusion is defined as excessive accumulation of
oxygen therapy.
fluid in the pleural space. The collection of grossly purulent
Type III Respiratory Failure TABLE 5.32: Common causes of pleural effusion
Type III Respiratory Failure type of respiratory failure can
Transudative
occur as a result of lung collapse, generally during Congestive heart failure
perioperative period. That is why this is also called as peri- Cirrhosis with ascites
operative respiratory failure. It can be avoided by frequent Nephrotic syndrome
change in position and chest physiotherapy. Exudative
Tuberculosis
Pneumonia
Type IV Respiratory Failure Malignancy
Type IV Respiratory Failure occurs due to hypoperfusion Pulmonary embolism
of respiratory muscles in patients with shock. Respiratory Connective tissue diseases
Pancreatitis
failure occurs due to increased demand by respiratory
fluid is known as empyema. Presence of blood and lymphatic PNEUMOTHORAX
fluid in pleural space is called hemothorax and chylothorax Presence of air in the pleural space is known as
respectively. Important causes of pleural effusion are pneumothorax. Incidence of pneumothorax is highest in
pneumonia, tuberculosis, cardiac failure, cirrhosis and tall young males, smokers and those with apical subpleural
malignancy. Other causes are mentioned in Table 5.32. blebs.
Pathogenesis
There are inflammatory changes in the air spaces and
alveolar walls initially which gradually involve interstitium
and vessels. Eventually, chronic inflammation leads to
fibrosis. In granulomatous type, lymphocytes, macrophages
and epithelial cells organize into discrete granuloma in the
lung parenchyma.
Clinical features
Progressive dyspnea is the most common presenting
symptom whereas tachypnea and basal end inspiratory
FIGURE 5.15: Right sided pneumothorax crackles is the important sign. Other symptoms and signs
are given in the Table 5.34.
Management
Common causes of ILD
a. Primary spontaneous pneumothorax: It can be initially
managed by simple aspiration. Thoracoscopy with
stapling of blebs is indicated if lung expansion does not
Important causes of ILD are
a. Idiopathic interstitial pneumonia 147
occur or patient develops recurrent pneumothorax. b. Occupational: fumes, gases, asbestos, organic and
b. Secondary spontaneous pneumothorax: It is treated with inorganic dust
tube thoracostomy with underwater seal drainage. c. Sarcoidosis
Alternatively, thoracoscopy with stapling of blebs can d. Connective tissue diseases: SLE, rheumatoid arthritis
be performed. e. Drugs and others
c. Traumatic pneumothorax: It should be treated with tube
thoracostomy. Two tubes are needed in case of hemo- Investigations
pneumothorax, one to be placed in upper part to drain a. Chest X-ray: The findings are nonspecific. Most
air and another in lower part to drain blood. common findings are bibasilar reticular pattern, nodular,
d. Tension pneumothorax: This is a medical emergency. A and mixed pattern (Fig. 5.16).
large bore needle should be inserted into pleural space TABLE 5.34: Clinical features of ILD
through second anterior intercostals space. Later
thoracostomy should be done and the needle removed. Symptoms:
Progressive dyspnea
e. Supportive treatment: This includes oxygen inhalation Dry cough (or minimal sputum)
and management of shock. Fatigue, weight loss
Chest pain, hemoptysis (uncommon)
INTERSTITIAL LUNG DISEASE Signs:
Tachypnea
Interstitial lung disease (ILD) is a group of diseases Cyanosis, clubbing (rare)
involving parenchyma of the lung: the alveoli, alveolar Bilateral basal end inspiratory crackles
epithelium, capillary endothelium and spaces between these Wheezes (occasional)
Signs of cor pulmonale
structures.
Etiology of Lung Cancers
The most common cause of lung cancer is cigarette smoking.
Various carcinogens and tumor promoters are inhaled during
smoking.
a. In active smokers, the relative risk of developing lung
cancer is 13 fold while it is 1.5 fold in passive smokers.
b. The chance of developing cancer is even more in case a
smoker has COPD.
c. The chance of developing lung cancer depends on the
amount and duration of cigarette smoking (cigarette pack
years).
d. The risk of ling cancers reduces following smoking
cessation.
Apart from smoking, thoracic radiation therapy increases
the incidence of lung cancer.
instruments can cause lung abscess. INR are estimated before the procedure. A level of INR
9. Numerous dental products and materials such as <2.5 is safe for dental care including simple extraction.
toothpaste, tooth enamel dust, methyl methacrylate may 20. Tuberculosis is unlikely to be transmitted to the dental
exacerbate the asthma. staff unless the patient is having active pulmonary
10. Elective dental procedure should only be done when tuberculosis or the dental staff is immunocompromised.
asthma is well controlled. Patients are asked to bring Hence, dental treatment is best deferred until the active
the asthma medication with them. tuberculosis has been treated.
21. Patient with tuberculosis and HIV infection can have
11. The history of allergy to aspirin or NSAIDs should
oral lesions in the form of chronic oral ulcerations and
always be asked in asthmatic patients as these agents
candidiasis.
may precipitate asthmatic attacks.
22. Mycobacteria are resistant to many disinfectants.
12. Use of beta blockers may preferably be avoided in
Hence, heat sterilization should be used.
asthmatic patient.
23. The drug interaction with anti-tubercular agents must
13. If the patient develops acute asthmatic attack during
be considered while prescribing the dental treatment.
dental procedure, the procedure is stopped and all
24. Rifampicin can cause red saliva.
C. Ethambutol
Respiratory Diseases
SELF ASSESSMENT
D. Streptomycin
Multiple Choice Questions 10. Hepatitis can be caused by:
1. Following part of lung is mostly involved in lung abscess: A. Rifampicin
A. Middle lobe of the lung B. Isoniazid
B. Posterior segment of lower lobe C. Pyrazinamide
C. Superior segment of lower lobe and posterior of D. All of the above
upper lobe 11. Significant improvement in FEV 1 after bronchodilator
D. Posterior segment of upper lobe and superior of inhalation is seen in:
lower lobe A. COPD
2. Following are causes of cavity in lung except: B. Bronchiectasis
A. Lung abscess C. Bronchial asthma
B. Tuberculosis D. None of the above
C. COPD 12. Following indicates severe asthma except:
D. Wegener’s granulomatosis A. Pulsus paradoxus
3. Which is not a clinical manifestation of lung abscess: B. Cyanosis
A. Clubbing C. PaO2 >80 mm Hg
B. Chest pain D. Silent chest
C. Copious amount of sputum 13. Clubbing can be found in all except:
D. Episodic dyspnea with wheeze A. Lung abscess
4. Kussmaul’s breathing is seen in: B. Lung cancer
A. Metabolic alkalosis C. Pneumonia
B. Respiratory alkalosis D. Bronchiectasis
C. Metabolic acidosis 14. Hemoptysis can be present in:
D. Respiratory acidosis
5. Polycythemia is seen in:
A.
B.
Pulmonary tuberculosis
Chronic bronchitis 151
A. Emphysema C. Mitral stenosis
B. Pleural effusion D. All the above
C. Bronchial asthma 15. Tropical pulmonary eosinophilia is associated with:
D. Lung abscess A. Aspergillus infection
6. Stony dull note on percussion is present in: B. Nitrofurantoin
A. Pleural effusion C. Filaria
B. Pneumothorax D. Malaria
C. Pulmonary fibrosis 16. Fibro-cavitatory lesion is feature of:
D. Bronchial asthma A. Primary tuberculosis
7. Following is the sign of consolidation: B. Post-primary tuberculosis
A. Bronchial breath sound C. Miliary tuberculosis
B. Increased vocal fremitus D. All of above
C. Whispering pectoriloquy 17. Following can be used in the treatment of pulmonary edema
D. All of above except:
8. Most common source of pulmonary embolism: A. Morphine
A. Splenic vein B. Frusemide
B. Arteriovenous fistula C. Beta blockers
C. Leg and pelvic veins D. Nitrates
D. Subclavian vein 18. The most common symptom in pulmonary embolism is:
9. Peripheral neuropathy can be caused by: A. Chest pain
A. Isoniazid B. Fever with chills
B. Rifampicin C. Dyspnea
D. Hemoptysis
19. Following is preferred for the definitive diagnosis of acute Fill in the Blanks
pulmonary embolism: 1. Enlargement of_________secondary to lung disease
A. D-dimer test is called cor pulmonale.
B. Arterial blood gas analysis 2. Foul smelling sputum suggests infection due to
C. Ventilation perfusion scan _________organisms.
D. Spiral CT 3. Pink frothy sputum can be present in _________.
20. Following can be found in pulmonary infarction: 4. Most common cause of community acquired
A. Dyspnea pneumonia is _________.
B. Pleuritic chest pain 5. Most common cause of hospital acquired pneumonia
C. Hemoptysis is _________.
D. All the above 6. Barrel shaped chest is seen in _________.
21. Following are the causes of type I respiratory failure except: 7. FEV1/FVC ratio is_________in COPD.
A. Pneumonia 8. Interrupted brief explosive sounds on lung
B. Pulmonary embolism auscultation is known as_________.
C. Respiratory muscle paralysis 9. Continuous musical adventitious lung sound is called
D. Pulmonary edema _________.
22. Domiciliary oxygen therapy is indicated in: 10. Inspiratory sound heard in case of tracheal obstruction
A. Pneumonia is called_________.
B. COPD 11. Healed calcified parenchymal lesion in primary tuber-
C. Pulmonary eosinophilia culosis is called as_________lesion.
D. None of the above 12. Cyclical waxing and waning of respiration intervened
23. Following drugs are used in patients with eosinophilia with a short period of apnea is known as _________
except: breathing.
A. Prednisolone 13. The most common cause of chronic type II
152 B.
C.
Hydroxyurea
Diethyl carbamazine
respiratory failure is_________.
14. The drug of choice in tropical pulmonary eosinophilia
D. Nitrofurantoin is_________.
24. Hyper-resonant note and absent breath sounds are features 15. Pink puffers are associated with the disease
of: _________.
A. Pleural effusion 16. Pleural rub is a sign of_________.
B. Pneumothorax 17. Nasal or bleating sounds on lung auscultation are
C. Pneumonia called_________.
D. Pulmonary fibrosis
Essentials of Medicine for Dental Students
Creatinine clearance (140-age) weight in kg • The edema is due to low plasma oncotic pressure
resulting in leakage of fluid into the interstitium
=
(ml/min ) 72 serum creatitine ( mg/dL )
154 (in females, the value is multipled by 0.85)
(underfilling hypothesis) and/or primary salt and water
retention by kidneys.
However, GFR can be measured more accurately • Escape of fluid into the interstitium causes low
by radionuclide studies using 125I-iothalamate, diethylene intravascular volume which results into activation of
triamine-penta-acetic acid labeled with technetium renin-angiotensin- aldosterone axis and the sympathetic
(99mTc-DTPA), or dimercaptosuccinic acid labeled with system, increased secretion of vasopressin (ADH), and
technetium (99mTc-DMSA). decreased secretion of atrial natriuretic peptide. The net
d. Imaging studies include plain X-rays, ultrasound, result is renal salt and water retention and increased
Essentials of Medicine for Dental Students
intravenous urography (IVU), CT scan, MRI, renal intravascular volume and further leakage of fluid into
arteriography and renal venography. interstitial space.
e. Renal biopsy: Light microscopy, electron microscopy
and immunofluorescence of the biopsy specimen are
TABLE 6.3: Causes of nephrotic syndrome
helpful in the diagnosis, prognosis and treatment of
various renal disorders. Primary renal disorders (idiopathic)
f. Other investigations may be required in specific situations Minimal change disease
Membranous glomerulopathy
to know the etiology of renal diseases such as antinuclear Focal and segmental glomerulosclerosis
antibody (ANA) in SLE, serum protein electrophoresis Membranoproliferative glomerulonephritis
in myeloma and serum IgA level in IgA nephropathy. Systemic diseases and others
Diabetes mellitus
Amyloidosis
NEPHROTIC SYNDROME Infections (HIV, hepatitis B, hepatitis C, plasmodium malariae)
Nephrotic syndrome is characterized by massive proteinuria Drugs (gold, penicillamine, NSAIDs, captopril)
Autoimmune (systemic lupus erythematosis, rheumatoid arthritis)
(>3.5 g per 1.73 m2 body surface area per 24 hr), hypoal-
Malignancies (Hodgkin’s disease, carcinoma breast, colon, and lung)
buminemia, edema, hyperlipidemia and hypercoagulability.
Renal Diseases
• The fall in oncotic pressure due to hypoalbuminemia
leads to compensatory increase in synthesis of lipids by
liver. There is also an altered metabolism of lipids. Both
these mechanisms result in hyperlipidemia.
• Hypercoagulability is due to increased urinary loss of
antithrombin III and altered levels of protein C and S.
• Infections may occur more commonly due to increased
urinary loss of immunoglobulins.
• Vitamin D deficiency that occurs due to enhanced
excretion of cholecalciferol binding protein may cause
hypocalcemia and secondary hyperparathyroidism.
• Loss of transferrin in the urine may lead to iron-
unresponsive microcytic hypochromic anemia.
Clinical Features
Edema is the main presenting feature of nephrotic syndrome.
FIGURE 6.2A: Anasarca in nephrotic syndrome - facial and
In children, edema is often seen only in the face (Fig. 6.1).
upper limb edema
However in adults, initially it may be present in the dependant
parts (lower extremities) but later on it may become
generalized edema known as anasarca (Figs 6.2A and B).
In the morning, the face and upper limb may be more
affected. Fluid collection can present as pleural fluid, ascites,
or pulmonary edema. Fever may occur due to infection. 155
Other uncommon features are arterial and venous
thrombosis, pulmonary embolism, and renal vein thrombosis.
Urine out put is generally normal. Hypertension and
hematuria are rare.
Investigations
156
• Minimal change disease is the most common histological
type found in children whereas membranous Prognosis
glomerulopathy is most common in adults with nephrotic Remission occurs in 90% children and 50% adults in minimal
syndrome. change disease. About 20-30% patients with membranous
nephropathy develop chronic renal failure.
Treatment
General Measures NEPHRITIC SYNDROME
1. Control of edema: The salt in diet is restricted to 1-2 Nephritic syndrome arises due to acute glomerular
Essentials of Medicine for Dental Students
gm per day. Diuretics (thiazide or loop diuretics or both) inflammation (glomerulonephritis, GN) and is characterized
are used judiciously because these can lead to electrolyte by sudden onset (days to weeks) of:
imbalance and hypotension. • Oliguria
2. Reduction of proteinuria: ACE inhibitors and ARBs are • Edema
useful in reducing proteinuria in patients. The daily protein • Hypertension
loss is compensated by adequate dietary protein intake. • Hematuria
3. Management of hyperlipidemia: This is managed with • Subnephrotic proteinuria (<3 g/day)
the lipid lowering drugs such as statins (simvastatin, • Worsening renal function
atorvastatin, and rosuvastatin). Dietary modification and
exercise are also helpful. Pathophysiology
4. Management of hypercoagulable states: Anticoagulation The renal blood flow and glomerular filtration rate (GFR)
is needed in patients with the evidence of thrombosis. are reduced because of obstruction of glomerular capillaries
5. Others: Vitamin D (1,25-dihydroxycholecalciferol) by inflammatory cells and glomerular cell proliferation.
supple-mentation is required in patients with evidence Impaired GFR and increased reabsorption of salt and water
TABLE 6.4: Causes of nephritic syndrome
Renal Diseases
Investigations
1. Idiopathic
(a) Urine examination
Proliferative glomerulonephritis (focal or diffuse)
Rapidly progressive glomerulonephritis(RPGN) The urine examination reveals dysmorphic red blood cells,
2. Post-infectious red blood cell cast, and proteinuria. 24 hours urine output is
Streptococci
Bacterial endocarditis
measured which is low.
Hepatitis B (b) Blood Examination
Malaria
3. Multisystem disorders • Blood urea and creatinine are raised.
SLE(lupus nephritis) • Other tests which help in diagnosing different types of
Henoch-Schönlein purpura
GN are serum complement levels (C3), anti-GBM
Goodpasture’s syndrome
Wegener’s granulomatosis antibody, ANCA (anti-neutrophil cytoplasmic antibody),
antinuclear antibody (ANA), and ASO titers.
• Tests like serum electrolytes, arterial blood gases, and
by tubules result in edema and hypertension. Injury to the complete blood count may be needed.
glomerular capillary wall leads to the appearance of
dysmorphic RBC, red blood cell cast and protein in the (c) Renal biopsy
urine. Hematuria is often macroscopic. The biopsy of kidney is the gold standard for the diagnosis,
treatment plan and the prognosis of the disease. Light
Clinical Features microscopy, immunofluorescence, and electron microscopy
The onset is often sudden. The presenting features are of biopsy specimen are helpful in distinguishing the major
decreased urine output and edema. A urine output less than types of acute nephritis.
400 ml per day is defined as oliguria while less than
50-100 ml per day is called anuria. Hypertension and Treatment 157
hematuria are often present. Patients also have generalized General Measures
symptoms such as anorexia, nausea, vomiting, headache 1. Control of edema and volume overload: The salt in diet
and malaise. is restricted to 1-2 g per day. Water intake is restricted
to the urine output plus 500 ml/day. Diuretics (thiazide
Causes
or loop diuretics or both) are used carefully.
The important causes of nephritic syndrome are given in 2. Control of hypertension: The blood pressure is controlled
Table 6.4. with antihypertensive agents. This helps in decreasing
The nephritic syndrome is classified on the basis of proteinuria and slowing the progression of the disease.
pathological features into three broad categories. The types The target BP should be 130/80 mm Hg.
of nephritic syndrome along with the serological markers 3. To minimize protein loss: ACE inhibitors and ARBs are
are described in Table 6.5. The most common type is useful in reducing proteinuria. However, these agents
immunecomplex glomerulonephritis. can cause hyperkalemia and a rise in creatinine; hence
TABLE 6.5: Types of nephritic syndrome
Pathogenic type Serological features Immunofluorescence Important causes
1. Immune complex GN Low C3 Granular deposition of Ig and C3 – Idiopathic
– Post-infectious
– SLE
2. Anti-GBM disease Anti-GBM antibody + Linear deposition of Ig and C3 – Anti-GBM disease
– Goodpasture’s syndrome
3. Pauci-immune GN ANCA+ Absent Ig and C3 – Wegener’s
granulomatosis
serum potassium and serum creatinine should be Important causes of ARF are classified in the Table 6.6.
monitored. The most common type of ARF is prerenal failure. This is a
4. Dialysis: Dialysis may be needed to control hyper- response to renal hypoperfusion in situations like hypotension
volemia and uremia. and volume depletion. However, prolonged and severe
hypoperfusion may lead to renal parenchymal injury, a type
Specific Measures
of intrinsic renal failure (acute tubular necrosis).
• Corticosteroids (prednisolone, methylprednisolone) and
other immunosuppressive drugs (cyclophosphamide, Clinical Manifestations
azathioprine, cyclosporine and mycophenolate mofetil) The clinical manifestations of ARF are often due to azotemia
are occasionally used for the control of glomerular (retention of nitrogenous waste products such as urea and
inflammation, however their role is debatable. creatinine) and are nonspecific. The clinical features also
• Antibiotic is given in post-streptococcal glomeru- depend on the underlying cause of renal failure.
lonephritis. • Usual symptoms are nausea, vomiting, malaise, and
• Patients who do not respond to immunosuppressive anorexia.
therapy and progress to end stage renal disease (ESRD) • Cardiac manifestations include pulmonary edema due
require dialysis or renal transplantation. to fluid retention, pericardial effusion and arrhythmias.
• Encephalopathic features such as drowsiness, confusion,
Prognosis
asterixis, seizures and coma may occur.
The course of the disease varies according to the cause and • There may be a bleeding tendency due to platelet
histopathological types. Majority of patients with post- dysfunction and altered coagulation.
streptococcal nephritic syndrome remit spontaneously • Features of hyperkalemia and metabolic acidosis are
158
and few patients (<5%) may develop rapidly progessive common.
glomerulonephrits (RPGN) or ESRD. • Anemia occurs due to blood loss or decreased RBC
production.
ACUTE RENAL FAILURE (ARF) • Infection is a serious complication and the most common
Acute renal failure is defined as sudden decline in renal ability cause of death in ARF patients.
to maintain fluid and electrolyte homeostasis and to excrete
nitrogenous wastes. Clinically ARF manifests as rising blood Management
urea and serum creatinine levels or decreased urine output The management of ARF is generally aimed at maintaining
Essentials of Medicine for Dental Students
over hours or days. Acute renal failure may be oliguric or fluid, electrolyte and acid-base balance. This requires a
nonoliguric. regular fluid intake and output recording and frequent
estimation of urea, creatinine and electrolytes. The recovery
TABLE 6.6: Causes of acute renal failure
of renal function occurs in most patients with ARF.
1. Prerenal failure 1. Fluid management: Intravenous fluid replacement is
Hypotension or volume contraction (blood or fluid loss)
done in patients with hypovolemia in prerenal ARF. In
Heart failure
2. Intrinsic renal failure other types of ARF, fluid intake is restricted according
Acute tubular necrosis to the urine output (500 ml plus urine output in last 24
Glomerulonephritis hours). Diuretics are used in cases with volume
Interstitial nephritis
Reno-vascular diseases
overload.
3. Postrenal failure (Obstructive) 2. Diet management: Adequate caloric intake should be
Ureteric obstruction (stone, clot, tumor, external compression) maintained to avoid excessive catabolism. Protein intake
Bladder outlet obstruction (prostate hypertrophy/carcinoma,
is restricted upto 0.6 gm/kg/day. Salt, potassium and
stone, clot)
phosphorus intake should also be restricted.
Renal Diseases
3. Management of metabolic complications: Hyperkalemia 9. Removal of obstruction: Measures to remove obstruction
is managed with the use of calcium, insulin, bicarbonate in the urinary tract should be undertaken.
and glucose. Sodium bicarbonate is given to control
acidosis. Hypocalcemia and hyperphosphatemia require CHRONIC RENAL FAILURE (CRF)
prompt management. Chronic renal failure is defined as irreversible loss of renal
4. Adjustment of drug dosage: The dosage of the drugs is function which develops over a period of months to years.
adjusted according to the severity of renal failure. Eventually clinical symptoms and signs ensue due to severe
Nephrotoxic drugs should be avoided. loss of metabolic, excretory and endocrinal functions of
5. Management of anemia: Severe anemia is managed by the kidneys (uremia). Blood urea and serum creatinine are
blood transfusion. Erythropoietin, though useful in CRF raised. Important features of CRF are given in Table 6.7.
is not helpful in ARF. Now the term “chronic renal disease (CRD)” or “chronic
6. Bleeding complications: Bleeding can be controlled by kidney disease (CKD)” are preferred over CRF.
the use of desmopressin or estrogen. Regular use of End stage renal disease (ESRD) is a severe stage
antacids reduces the incidence of gastrointestinal of CRF (GFR 10-15 ml/min), in which the patient is
hemorrhage. permanently dependant on renal replacement therapy to avoid
7. Control of infections: Aseptic precautions should be life-threatening uremia.
practised to avoid infections. Prompt use of antimicrobial Newer classification of CRF (CKD): According to the
agent is necessary to manage infection. estimated GFR, chronic kidney disease is classified as per
8. Dialysis: Majority of patients improve on conservative guidelines issued by the National Kidney Foundation, USA.
management. However, the dialysis is indicated in (Table 6.8)
following situations:
Causes of CRF
159
• refractory hyperkalemia
• acidosis Diabetes mellitus and hypertension are most common causes
• volume overload of CRF. Other important causes are glomerulonephritis,
• uremic complications (encephalopathy, pericarditis polycystic renal disease, tubulointerstitial diseases, and
and seizures). obstructive nephropathies.
Peritoneal dialysis and hemodialysis are equally effective.
Management
TABLE 6.7: Important features of CRF 1. Diet management: Adequate caloric intake should be
maintained to avoid excessive catabolism. Protein intake
Chronic features (>3 months) of uremia
Hypertension is restricted up to 0.6 g/kg/day to reduce accumulation
Anemia of nitrogenous waste products and to slow down the
Renal osteodystrophy progression of renal failure. Fluid, salt, potassium and
Isosthenuria (fix low specific gravity of urine) phosphorus intake should also be restricted.
Broad cast in the urine
Small contracted kidneys (on ultrasonography) 2. Management of metabolic complications: Hyperkalemia
is managed with the use of calcium, insulin, bicarbonate
and glucose. Sodium bicarbonate is given to control
TABLE 6.8: Newer classification of CRF (CKD) acidosis.
Stage Description GFR (ml/min/ 3. Management of renal osteodystrophy: Hyperpho-
1.73m2) sphatemia is management by restriction of phosphate
1 kidney damage with normal/increased GFR >90 (milk, cheese, eggs) in the diet and use of phosphate
2 kidney damage with mildly decreased GFR 60-89 binding drugs such as calcium carbonate and aluminium
3 Moderately decreased GFR 30-59 hydroxide gel. Supplementation of vitamin D (1-alpha
4 Severely decreased GFR 15-29
5 kidney failure <15
hydroxyl vitamin D3 or 1,25-dihydroxy vitamin D3) and
calcium is needed to correct hypocalcemia.
IMPLICATIONS ON DENTAL PRACTICE
1. Poor oral health is common in patients with chronic
renal failure.
2. Elective dental care is avoided in patients with acute
renal failure.
3. Elective dental procedures are better tolerated on non-
dialysis days.
4. Blood pressure measurement is advised at every visit.
5. Complete blood count, platelet count and bleeding time
should preferably be done in uremic patients before dental
procedures.
6. Peritoneal dialysis is generally not a contra-indication
for dental procedures.
FIGURE 6.3: Patient on hemodialysis 7. Hemorrhagic complications are more common during
dental treatment in patients with uremia. This can present
4. Management of proteinuria: ACE inhibitors and ARBs as gingival bleed or hematoma formation following
are helpful in reducing proteinuria and slowing the periodontal procedures. Hence, appropriate care must
progression of renal damage. be taken and hemostatic agents (tranexamic acid,
5. Control of blood pressure: Hypertension must be DDAVP) may be used.
controlled rigorously with a target of blood pressure 8. Uremic patients are immunocompromised. Hence, these
less than 130/80 mmHg. In CKD patients with diabetes patients need meticulous oral hygiene and frequent check
160
mellitus or proteinuria greater than 1 gm/24 hrs, BP should up to maintain oral health to reduce the incidence of
preferably be reduced to 125/75 mm Hg. infection from dental origin.
6. Adjustment of drug dosage: The dosage of the drugs is
9. The incidence of hepatitis B, hepatitis C and HIV is more
adjusted according the severity of renal failure.
in patients on hemodialysis. Screening and appropriate
Nephrotoxic drugs should be avoided.
precautions should be exercised.
7. Management of anemia: Erythropoietin (subcutaneous
10. Nephrotoxic drugs must be avoided. The dosage and
or intravenous) is useful in the management of anemia.
frequency of administration of medications should be
Iron stores must be adequate to ensure response to
adjusted according to renal function.
Essentials of Medicine for Dental Students
Renal Diseases
D. Wegner’s granulomatosis C. Oliguria
3. Dysmorphic red blood cells in urine are found in: D. Small contracted kidneys
A. Bladder cancer B. Renal stone 13. Following are the features of CRF:
C. Glomerulonephritis D. Prostatism A. Hypercalcemia and hyperphosphatemia
4. Prerenal ARF can occur in: B. Hypocalcemia and hypophosphatemia
A. Massive blood loss C. Hypocalcemia and hyperphosphatemia
B. Severe diarrhea D. Hypercalcemia and hypophosphatemia
C. Heart failure 14. The key component of nephrotic syndrome is:
D. All of the above A. Anasarca B. Hypoalbuminemia
5. Which of the following is usually not a feature of minimal C. Massive proteinuria D. Hyperlipidemia
change disease: 15. The following is not seen in nephritic syndrome:
A. Massive proteinuria B. Hypoproteinemia A. Hematuria B. Oliguria
C. Oliguria D. Hyperlipidemia C. Proteinuria D. None of the above
6. The most important abnormality in ARF is: 16. Insulin is used in the treatment of:
A. Ketosis A. Hyperkalemia B. Hypercalcemia
B. Metabolic acidosis C. Hypernatremia D. Hypermagnesemia
C. Metabolic alkalosis 17. Following are present in case of nephrotic syndrome:
D. All of the above A. Massive proteinuria B. Hyperlipidemia
7. The most important electrolyte disturbance in renal failure C. Renal vein thrombosis D. All of the above
is: 18. Most common cause of nephrotic syndrome in children is:
A. Hyponatremia B. Hypernatremia A. Minimal change disease
C. Hypokalemia D. Hyperkalemia B. Membranous glomerulopathy
8. Amount of protein normally excreted in urine per day is: C. Diabetes mellitus
A. 1 gm
C. 150 mg
B. 500 mg
D. No protein is present
D. Amyloidosis 161
9. Microalbuminuria is defined as excretion of following amount Fill in the Blanks
of albumin daily:
A. Less than 30 mg B. 30-300 mg 1. The amount of proteinuria in nephrotic syndrome is
C. 300-650 mg D. More than 650 mg more than ________ per day.
10. Following is the commonest systemic cause of nephrotic 2. The oliguria is defined as urine out put less than
syndrome: ________ per day.
A. SLE B. Diabetes mellitus 3. The retention of nitrogenous waste products due to
C. Leukemia D. Gold therapy renal insufficiency is called ________.
11. The commonest cause of death in ARF is: 4. Normal level of blood urea is ________.
A. Infections B. Pulmonary edema 5. Normal serum creatinine level is________.
C. Hypertension D. Hypocalcemia 6. Normal level of serum total protein and albumin is
12. Following feature is specific for chronic renal failure: ________.
A. Hyperkalemia 7. In end stage renal disease, the GFR is _______/min
Chapter
7 Nervous System
A basic knowledge of cranial nerves is desirable for dental Sinusitis and other local nasal disorders
practitioners since patients may present with a number of Head injury
Subfrontal meningioma
symptoms pertaining to the oromaxillary area. There are Bacterial meningitis
twelve cranial nerves. These are named as follows:
I Olfactory Common substances such as clove oil, peppermint oil,
II Optic soap or fruits are used to test the sense of smell. Each
III Oculomotor nostril is tested separately. However, local causes like
IV Trochlear sinusitis etc. should be ruled out before contributing the
V Trigeminal dysfunction due to the neurological cause.
VI Abducent
VII Facial Optic Nerve
VIII Vestibulocochlear The optic nerve is the nerve of sight. It is composed of the
IX Glassopharyngeal axons of the cells in the ganglionic layer of the retina. The
X Vagus optic nerve emerges from the back of eyeball and passes
XI Acessory through optic canal to enter in the cranial cavity where it
XII Hypoglossal unites with the opposite optic nerve to form the optic
chiasma. From the optic chiasma fibers run in optic tract.
Olfactory Nerve The fibers from the medial half of retina cross the midline
Olfactory nerve, which carries the sensation of smell, arises in optic chiasma and enter the optic tract of opposite side,
in the olfactory mucous membrane from receptor nerve cells, while the fibers from the lateral half of each retina pass in
situated in upper part of the nasal cavity. The nerve fibres the optic tract of the same side. Most of the fibers in the
pass through the cribriform plate of the ethmoid bone and optic tract end by synapsing with nerve cells in lateral
enter the olfactory bulb in the cranial cavity. Olfactory tract geniculate body. The axons of nerve cells in lateral
connects the olfactory bulb to the olfactory area of the geniculate body pass as the optic radiation to the visual
cerebral cortex. cortex of the cerebral hemisphere.
The presentation of olfactory nerve damage may be lack Few fibres from the optic tract pass to prerectal nucleus
of smell sense (anosmia) or altered sense of smell and superior colliculus and are concerned with light reflexes.
(parosmia). Hallucination of smell may occur as aura of Following are different components of optic nerve testing:
temporal lobe seizure. Important causes of anosmia are given • Visual acuity
in Table 7.1. • Visual fields
Nervous System
• Color vision eye due to pituitary tumors, inflammatory and traumatic
• Pupillary examination lesions extending out of sella turcica. Binasal hemianopia is
due to bilateral lesion of outer aspect of optic chiasma.
Visual Acuity
Visual acuity is measured by Snellen’s chart. Patient is placed Color Vision
at a distance of 6 meters and asked to read letters on the Colour vision is tested using Ishihara’s pseudoisochromatic
chart. This tests the distant vision. Normal eye can read plates consisting of multicolor dots outlining certain digits.
down the letters upto seventh line from top (visual acuity 6/ Most common color vision anamoly is red green deficiency,
6). In case of very poor visual acuity (1/60) when patient is which is inherited as sex-linked recessive condition.
not able to read the top letters from a distance of 1 meter, Acquired causes of defective color vision are macular and
other tests are performed. These are counting fingers (CF), optic nerve disease.
hand movements (HM), perception of light (PL) or no
perception of light (no PL). Pupillary Examination
Near vision is tested with the help of test types of varying
The pupillary light reflex consists of optic nerve fibres
sizes from the ordinary reading distance. The near vision is
as afferent component and parasympathetic fibres in
recorded as the smallest type patient can read comfortably.
occulomotor nerve as efferent. The light shown in one eye
Smallest print is N5.
results in constriction of pupil in the same eye (direct
Visual Field pupillary reaction) as well as in other eye (consensual
Different methods to test visual field are (a) confrontation pupillary reaction). The absence of direct papillary light
test using a finger (b) red pin confrontation test (c) perimetry. reaction but the presence of consensual reaction indicates
When the size of test object is 5 mm, the field of vision is the lesion of the optic nerve in that eye. This is performed
100 degrees laterally, 60 degrees medially, 60 degrees
superiorly and 75 degrees inferiorly.
using swinging light test (swinging torch test).
163
Scotoma is known as a zone of loss of vision in the Accommodation Reflex
visual field. The scotoma can be central or paracentral. Pupillary accommodation reflex includes meiosis (pupils
Important cause of unilateral central scotoma is optic neuritis. become smaller) and convergence of the eyes on
Unilateral paracentral scotomas are due to vascular disease accommodating for the near objects. This is impaired in the
(retinal embolism or retinal artery branch occlusion). Bilateral lesions of third nerve and in autonomic neuropathies.
paracentral scotomas are due to vitamin B12 deficiency or Argyll Robertson pupil: The pupil is small and irregular.
alcoholism. Glaucoma can cause comma shaped defect in Accomodation reflex is present while there is no light reflex.
visual field (paracentral ‘arcuate’ scotoma) due to damage This is seen in neurosyphilis.
of nerve fibres in retina or optic nerve.
Adie pupil (tonic pupil): There is absence or delayed
Loss of vision in one half of visual field is known as
papillary constriction to light or to accommodation. It is of
Hemianopia. When vision is lost in same half of visual
little clinical significance.
fields in both eyes it is known as homonymous. Right
homonymous hemianopia means right half of the field in Horner’s syndrome: This is due to paralysis of cervical
both eyes is affected. Quadrantanopia is a term used to sympathetic nerve. Sympathetic nerve fibres originating in
describe blindness in one quadrant of visual field. Loss of the lower cervical and upper thoracic region of the spinal
vision in outer half of field (temporal halves) in both eyes is cord pass through the ophthalmic division of the Fifth cranial
known as bitemporal hemianopia. Binasal hemianopia is loss nerve to the eye. Sympathetic activity mediates papillary
of visual field in inner or nasal halves of visual fields. dilatation and elevation of the upper lid through the
Hemianopia may occur due to lesions in optic nerve or contraction of smooth muscles of levator palpebrae
chiasma (incongruous) or post-geniculate lesions superioris. Features of Horner’s syndrome are:
(congruous). Bitemporal hemianopia is due to damage of • Pupillary constriction
fibres in optic chiasma derived from the nasal part of each • Slight drooping of the upper lid (ptosis)
• Absence of papillary dilatation in the dark Trochlear Nerve
• Loss of cilio-spinal reflex The trochlear nerve leaves the midbrain and passes forward
• Impaired sweating of the face on the side of lesion in middle cranial fossa in the lateral wall of the cavernous
sinus. It then passes through superior orbital fissure to enter
Oculomotor Nerve the orbital cavity. It supplies the superior oblique muscle of
The occulomotor nerve after emerging from the anterior the eyeball and helps in turning the eyeball downward and
surface of mid-brain passes forward between the posterior laterally.
cerebral and superior cerebellar arteries and continues in Infranuclear lesions of the trochlear nerve may result in
the middle cranial fossa in the lateral wall of cavernous sinus. impaired downward movement when eyeball is in medial
It then passes through superior orbital fissure to enter the position.
orbital cavity. The occulomotor nerve supplies the following
muscles of the eye: Trigeminal Nerve
• Levator palpebrae superioris Trigeminal nerve is the largest cranial nerve. It has a sensory
• Superior rectus root and a small motor root. It leaves the anterior side of
• Inferior rectus pons and passes through the posterior cranial fossa to reach
• Inferior oblique the apex of petrous temporal bone in the middle cranial
It also supplies the ciliary muscles and constrictor fossa. Here the sensory root forms the trigeminal ganglion.
pupillae muscles of the iris. The three divisions namely ophthalmic (V1), maxillary (V2)
The functions of the oculomotor nerve are and mandibular(V3) arise from the ganglion.
• Lifting the upper eyelid a. The opthalamic division is sensory and supplies skin of
• Turning the eye upward, downward and medially forehead and scalp as far as the vertex, the conjunctiva
164
• Constriction of pupil of the eye, cornea, the upper eyelid, lacrimal gland, the
• Accommodation of the eye mucous membranes of the paranasal sinuses, the nasal
The test is done by asking patient to look in different cavity and the skin of nose as far as the tip.
directions. Horizontal and outward movement of eye ball is b. The maxillary division is also sensory and it passés
called abduction whereas horizontal inward movement is through foramen rotundum to supply the skin overlying
termed adduction. Vertical upward movement is termed the maxilla, upper lip, the lower eye lid and its conjuctival
elevation and downward is termed depression. Superior and surface, the teeth of upper jaw, the maxillary sinus, the
inferior recti act as elevator and depressor alone when the palate, and the mucous membrane of the nose.
Essentials of Medicine for Dental Students
eye is in abduction. Inferior and superior oblique act as c. The mandibular division is both motor and sensory. These
elevator and depressor respectively when eye is in adduction. roots pass through the foramen ovale. The sensory fibers
Lower motor neuron lesion (infranuclar lesion) of III, supply the skin of the lower part of cheek, the skin over
IV and VI cranial nerves leads to weakness of individual or the mandible, the lower lip and the side of the head. It
group of muscles. While upper motor neuron lesions also supplies the teeth of lower jaw, temporomandibular
(supranuclear lesion) lead to paralysis of conjugate joint, mucous membrane of the check, the floor of the
movement of the eye. mouth and the anterior part of the tongue.
The infranuclear lesion of the occulomotor nerve may The motor fibers supply:
lead to following abnormalities: • Muscles of masticulation
• No movement of eyeball in medial and upward • Mylohoid muscle
direction, movement is possible in lateral direction • Anterior belly of the digastric muscle
and slightly downwards • Tensor veli palatine of the soft palate
• Lateral and downward displacement of the eye • Tensor tympani of the middle ear
• Dilatation of the pupil The sensory component of the trigeminal nerve is
• Loss of accommodation reflex of the pupil. examined by testing the touch, pain and cold sensations in
Nervous System
the areas supplied. The lesion of the whole trigeminal nerve
leads to loss of sensations in the skin and mucous membrane
of the face and nasopharynx. Lacrimal and salivary
secretions may be diminished. Trophic ulcers may develop
in the mouth, nose and cornea. Lack of salivary secretion
may also alter taste perception.
The motor component of trigeminal nerve is tested by
asking the patient to clench the teeth. Normally temporal
and masseter muscles become prominent which can be
easily palpable. Muscles do not become prominent on the
paralyzed side. While opening the mouth, jaw deviates to
the paralyzed side. This is because of uninhibited action of
lateral pterygoid muscles which push the jaw to the paralyzed
side.
FIGURE 7.1: Right VI nerve palsy
Corneal reflex: The corneal reflex may be absent either
due to lesion of Vth nerve (afferent component of the reflex) The facial nerve controls facial expression, salivation
or due to facial nerve (efferent component of the reflex) and lacrimation. It also carries the taste sensation from the
This is tested by touching the lateral edge of cornea with a anterior two-third of the tongue, floor of the mouth and the
fine cotton wisp. Normally this leads to the blinking of the palate. The taste fibers pass from the lingual nerve (a branch
eyes. Alternatively it can be tested by lightly blowing puff of fifth cranial nerve) into the chorda tympani, to join the
of air into each cornea. facial nerve above stylomastoid foramina. The sensory
component of facial nerve carries sensations from the part
Abducens Nerve
The Abducens nerve emerges between the pons and the
of the skin of external ear. Examination of the facial nerve
is described under ‘facial nerve palsy’. Innervation of tongue
165
medulla oblongata and passes forward in the middle cranial is given in Table 7.2.
fossa along with internal carotid artery through the cavernous
TABLE 7.2: Innervation of the tongue
sinus. It then passes through superior orbital fissure to enter
Sensory Taste
the orbital cavity.
It supplies the lateral rectus muscle and its function is Anterior two third – V nerve Anterior two third – VII nerve
Posterior one third – IX nerve Posterior one third – IX nerve
to turn the eyeball laterally.
Infranuclear lesions of the vith nerve may result in
Taste sensation examination: Patient is asked about the
inability to move eye outward (Figure 7.1) with diplopia
loss or change in the taste. The examination is done by
(double vision) and convergent squint because of unopposed
applying solutions one by one on the surface of protruded
action of medial rectus.
tongue. The solutions generally used for different taste
Facial Nerve modalities are sugar (sweet), common salt (salt), citric acid
(sour) and quinine (bitter). The patient is asked to indicate
Facial Nerve emerges as two roots between the pons and
the medulla oblongata and passes laterally in the posterior the nature of taste before withdrawing tongue inside the
cranial fossa with the VIII nerve and enters the internal mouth. This is to differentiate the impairment of taste
acoustic meatus in the petrous part of temporal bone. The sensation in anterior or posterior parts of the tongue.
nerve then enters the facial canal and laterally through the Ageusia is defined as loss of taste sensation.
inner ear. It emerges from the canal through the stylomastoid
foramen. The nerve then passes through the parotid gland Vestibulocochlear Nerve
and divides into branches which innervate the muscles of Vestibulocochlear nerve consists of vestibular and cochlear
the face and scalp except the levator palpebrae superiorosis. fibers. These fibers leave the brain between the pons and
It also supplies the platysma, stylohoid, posterior belly of the medulla oblongata. After crossing the posterior cranial
the diagastric and the stapedius muscle of the middle ear. fossa it enters the internal acoustic meatus with the facial
nerve. The vestibular fibers originate from the vestibule and Vagus Nerve
semicircular canals and are concerned with the sense of The Vagus Nerve has both motor and sensory components.
position and movements of head. The cochlear fibers It emerges from the anterior surface of the medulla oblongata
originate from the cochlea to the internal ear and are and passes laterally in the posterior cranial fossa. It then
concerned with hearing. passes through the jugular foramen and descends through
Important symptoms of vestibular dysfunction are the neck along with carotid arteries and internal jugular vein
vertigo, giddiness and unsteadiness. In vertigo, external within the carotid sheath. After passing through the
objects seem to move around the patient. Auditory mediastinum, it pierces the diaphragm and terminates in the
manifestations include tinnitus, hyperacusis, and auditory abdomen.
hallucination and delusion. Tinnitus means persistent ringing Vagus nerve innervates the heart and great vessels, the
in the ears. In hyperacusis, there is excessive sensitivity to larynx, trachea, bronchi, lungs and alimentary canal (from
sound and it occurs due to paralysis of stapedius muscle. pharynx to splenic flexure of colon). It also supplies liver
and pancreas and other glands associated with alimentary
Tests of Hearing canal.
a. Hearing is tested by producing whispered and Accessory Nerve
conventional voice at varying distances. The Accessory nerve is a motor nerve and has cranial root
b. Hearing may also be tested using vibrating tuning fork and a spinal root. The cranial root emerges from the anterior
(512 Hz). Rinne test and Weber test are used to diagnose surface of the medulla oblongata and runs laterally in the
sensoryneural and conductive hearing loss. posterior cranial fossa. The spinal root arises from nerve
c. Audiometry is used to measure the extent of hearing cells in the anterior column of the upper five segments of
loss and to locate the site of lesion. the cervical part of the spinal cord. The nerve ascends
Glassopharyngeal nerve has both motor and sensory Examination of IX, X, and XI cranial nerves
components. It emerges from the anterior surface of the
Due to common innervations of various structures by IX,
medulla oblongata and passes laterally in the posterior cranial
X and XI cranial nerves, symptoms are generally common
fossa. It then passes through the jugular foramen and
and overlapping.
descends through the upper part of neck to the tongue.
The motor fibers supply the stylopharyngeus muscle, PALATAL PARALYSIS
parasympathetic fibers supply the parotid gland, and sensory
Unilateral paralysis of palate may not lead to symptoms or
fibers carry general sensations and taste sensation from the
symptoms are very minimal. However, bilateral paralysis of
posterior part of the tongue and pharynx. It also innervates
palate may produce following:
carotid body and carotid sinus.
• There is regurgitation of fluid during swallowing through
The function of this nerve is to assist swallowing and the nose. This is due to paralysis of soft palate.
promoting salivation. • Patient is not able to pronounce the words which require
The loss of taste sensation in the posterior part of the closure of nasopharynx. For example, ‘egg’ and ‘rub’
tongue occurs if the glassopharyngeal nerve is damaged. are pronounced as ‘eng’ and ‘rum’ respectively.
Nervous System
• Dysphagia (difficulty in swallowing) for solid foods may The hypoglossal nerve is examined by asking the patient
occur in lower motor neuron lesion and markedly for to protrude the tongue, move the tongue from side to side
liquids in upper motor neuron lesion. and to lick each cheek with the tongue. In unilateral lesion,
Examination of palatal movement is performed by asking the tongue deviates to the paralyzed side on protrusion.
the patient to say ‘ah’. In case of bilateral paralysis there is Presence of wasting or fasciculations on the tongue indicates
no movement of the palate. Palate will remain flat and lower motor neuron lesion of the hypoglossal nerve.
immobile on the side of paralysis and median raphe is pulled
toward the other side in case of unilateral lesion. EXAMINATION OF A COMATOSE PATIENT
Palatal reflex: It may be impaired in the lesion of IX or Consciousness: It is a state when patient is aware of self
X cranial nerves. Normally there is reflex contraction of the and the environment. The person is able to respond to
palate when the back of the pharynx is tickled. internal as well external changes/needs.
Laryngeal paralysis: The innervation of larynx is given in Sleep: This is a normal variation in consciousness. Patient
Table 7.3. can be aroused to a normal state of consciousness either
• Bilateral damage of superior laryngeal branch of vagus spontaneously or by external stimuli from the state of sleep.
nerve leads to hoarse voice. Confusional state: It is an altered state of consciousness
• Unilateral paralysis of recurrent laryngeal nerve (branch characterized by clouded alertness and disorientation.
of vagus nerve) leads to blurred speech and bovine cough Delerium is a confusional state with marked agitation.
(patient cannot cough clearly and effectively). Bilateral Drowsiness: It is like light sleep, which cannot be easily
paralysis may cause stridor or respiratory obstruction. aroused and the alertness can only be maintained for brief
Laryngoscopic examination reveals characteristic period. Once awakened, patient is usually disoriented and
features of vocal cord paralysis. tends to fall asleep despite verbal stimulation.
Examination of spinal part of accessory nerve: Trapezius
and sternomastoid muscles are tested for the evidence of
Stupor: It is a condition where arousal can occur only by
vigorous stimuli and arousal is brief and incomplete. 167
lesion in the spinal part of the XI nerve. Patient is asked to Coma: It is a state of persistent loss of consciousness, where
shrug the shoulder against resistance for testing trapezius patient is unarousable and unable to respond to external
muscle. There is weakness in the rotation of chin toward events or inner needs like hunger. The coma indicates
the opposite side in sternomastoid paralysis. disorders of arousal mechanisms in the brain.
168
f. Unilaterally dilated pupil signifies third cranial nerve
are given in Table 7.4.
damage whereas bilaterally dilated or unresponsive
Diagnosis pupils suggests severe midbrain lesion, atropine or
methyl alcohol intoxication, and severe anoxic
Early diagnosis of underlying cause is of vital importance.
encephalopathy. Bilaterally small or pin point
The diagnosis is based on history, general physical and
pupils are seen in narcotic overdose, metabolic
neurological examination and the laboratory investigations.
encephalopathy and thalamic or pontine lesions.
History TABLE 7.5: The Glasgow Coma Scale
Essentials of Medicine for Dental Students
Nervous System
impaired respiration, pooling of secretions in the oral cavity
occurs because of tonic contractions of muscles of a. EEG: This may help in the diagnosis and classification
respiration. Increased tone in laryngeal muscles may cause of seizure disorders. Characteristic EEG changes in petit
‘ictal cry’. Tongue bite may occur due to contraction of mal seizures (3 Hertz spike and wave activity)
jaw muscles. Increased sympathetic manifestations such differentiate it from complex partial seizures.
as tachycardia, hypertension and dilatation of the pupils may b. Brain imaging: CT or MRI is indicated in patients with
also occur. focal seizures, focal neurological signs or if age of onset
Clonic phase: Tonic phase lasts for a minute and is is more than 20 years (Fig. 7.2).
followed by ‘clonic phase’ characterized by jerky movements c. Metabolic: Serum electrolytes, urea, calcium, blood
for a few minutes. Subsequently, the patient goes in a state glucose and liver function tests are done to rule out any
of muscular flaccidity and unresponsiveness (post-ictal metabolic cause.
phase). There may be bladder or bowel incontinence. TABLE 7.7: Causes of seizures
Patient gradually regains consciousness over minutes
to hours and may have postictal headache, confusion, Idiopathic
Genetic
muscle ache and fatigue for hours. Neurofibroma
The presence of aura suggests partial seizure with Inborn errors of metabolism
secondary generalization. Trauma
Birth trauma
Head injury
Absence Seizures (Petit mal)
Metabolic
• This occurs in childhood and ceases after 20 years of Alcohol withdrawal
age. Hypoglycemia
Hypocalcemia
171
• This is characterized by brief lapses of sensorium with
Hyponatremia
loss of postural control. Hypoxia
• These are too subtle to be noticed or referred to as day Renal failure
dreaming. Liver failure
Intracranial space occupying lesions
• The attacks are much briefer (seconds) and more
Tuberculoma
frequent than complex partial seizures. Neurocysticercosis
• There is no post-ictal confusion. Brain abscess
• There may be mild motor movements like blinking of Brain tumor
Cerebrovascular diseases
eyes, chewing and hand clonus.
Hemorrhage
• This is associated with characteristic EEG pattern. Emboli
Infections
Causes of Seizures Encephalitis
Meningitis
The etiology depends on the age of the patient. A list of HIV
causes of seizures is given in Table 7.7. Toxoplasmosis
• Hypoxia, metabolic derangements, congenital defects Inflammatory
and birth trauma are important causes of seizures in SLE
Sarcoidois
neonates. Degenerative
• Febrile seizures are more common in early childhood. Alzheimer’s disease
• Head trauma is common cause of seizures in young Drugs
adults. Lignocaine
Quinolones
• In older people, cerebrovascular disease, tumors and Penicillins
degenerative disorders are important cause of seizures. Theophylline
• Metabolic and electrolyte imbalance, drugs, and systemic Chloroquine, Mefloquine
Psychotropic agents
illnesses can cause seizures at any age.
5. Other tests: Blood count, ESR, X-ray chest, CSF • These precautions should be taken until a good control
examination, ANA and other specific tests may be of seizures is obtained.
needed to diagnose infective or inflammatory causes.
Immediate Care of Seizures
Differential Diagnosis • The patient is shifted to a safer place, away from danger
The seizures should be differentiated from transient ischemic (water, fire and machine).
attacks (TIA), syncope (see page 100) and pseudoseizures. • The patient is turned to the semi-prone position to
Pseudoseizures do not occur during sleep and are not prevent aspiration.
associated with unconsciousness, cyanosis, incontinence • The patient should not be left alone until full recovery
and tongue bite. There are no post-ictal headache, confusion from seizures as there may be drowsiness and confusion
and focal neurological deficit. EEG changes and high serum in the post-ictal stage or the seizures may reoccur.
prolactin level are features of “true” seizures and not found • Nothing should be given by mouth until the patient has
in pseudoseizures. Pseudoseizures may occur in hysterical fully recovered.
reactions and malingering and may be precipitated by • If convulsions continue for a prolonged duration (>5
emotional stress. minutes) or reoccur without the patient regaining
consciousness, hospitalization is a must.
Management
Treatment of the Underlying Condition
General Precautions
If the cause of seizures is a metabolic abnormality (electrolyte
• The patient should refrain from working with dangerous
abnormality or glucose abnormality) it should be corrected
equipments and should avoid swimming, fishing, or
effectively. In case of drug induced seizures, the offending
cycling.
172 • He should also avoid any activity such as driving where
loss of consciousness is dangerous. The patient should
drug should be withdrawn. Structural CNS lesions like
brain tumor, abscess and vascular malformation must be
treated appropriately. The antiepileptic treatment may not
avoid working near fire or at a height.
be required once the underlying condition has been well
treated.
Nervous System
most patients, seizures can be controlled by a single
drug. In some, a combination of two or more drugs is Type of epilepsy Drug(s) of choice
required to control the seizures. Partial or secondary generalized seizures Carbamazepine
• If seizures are refractory to medical treatment, the patient Phenytoin
may benefit from surgical interventions. Valproic acid
Primary generalized seizures Valproic acid
Lamotrigine
Monitoring Absence seizures Valproic acid
Patient should be monitored for the side effects of the Ethosuximide
Myoclonic Valproic acid
medication. Blood counts, liver function tests, renal function Clonazepam
tests are done at regular intervals. Serum level of drug can
be measured to guide appropriate dosage and to check the Management
compliance. The status epilepticus should be treated as emergency. The
patient should be hospitalized.
Duration of Therapy
1. Airway is maintained and oxygen is administered.
Treatment should be continued until there have been no 2. Intravenous line is started, a blood sample is withdrawn
seizures for at least 2-3 years. The dosage of the drugs should for laboratory analysis and intravenous dextrose (50%
be tapered and withdrawn gradually over 2-3 months. dextrose 25-50 ml) is promptly given. The initial laboratory
tests include glucose, electrolytes, calcium, urea, creatinine,
Status Epilepticus
liver transaminases and complete blood count.
Status epilepticus refers to continuous seizure activity or 3. Intravenous diazepam (10 mg) or lorazepam (4 mg) is
intermittent seizures with impaired consciousness in given slowly in 2 minutes. This can be repeated once
interictal period. This can be convulsive (tonic clonic) or
nonconvulsive type. Practically seizure activity lasting for
after 15 minutes if seizures are not controlled.
4. If seizures continue beyond 30 minutes, intravenous
173
more than 5 minutes should be managed as status epilepticus. phenytoin (20 mg/kg) at a rate not more than 50 mg/
min is given. Alternatively, fosphenytoin can be given.
Causes This may be repeated in a dosage of 5-10 mg/kg. One
Abrupt drug (antiepileptic drugs) withdrawal or should monitor for cardiac arrhythmia and hypotension.
noncompliance is the most common cause of the status 5. Phenobarbitone (IV 20 mg/kg) at a rate not more than
epilepticus. Other causes are metabolic disorders, intracranial 50 mg/min is given if seizures are still uncontrolled. An
infections and structural lesions of the brain. additional dose of 5-10 mg/kg may be repeated if needed.
TABLE 7.8: The anti-epileptic drugs
Drug Daily dose (adult) Important side effects
Phenytoin 300-400 mg Ataxia, diplopia, drowsiness, gingival hyperplasia, folate deficiency, osteomalacia
Carbamazepine 200-2000 mg Ataxia, diplopia, drowsiness, blood dyscrasia, hepatotoxicity, hyponatremia
Valproic acid 400-2000 mg Rashes, liver damage, drowsiness, blood dyscrasia
Phenobarbital 60-180 mg Ataxia, confusion, drowsiness, rash,
Clonazepam 1-12 mg Ataxia, drowsiness
Gabapentin 300-2400 mg Ataxia, drowsiness
Lamotrigine 25-500 mg Ataxia, drowsiness, diplopia, rash
Ethosuximide 500-1500 mg Ataxia, rash, blood dyscrasia
Primidone 250-1000 mg Ataxia, confusion, drowsiness, rash, megaloblastic anemia
Topiramate 200-600 mg Ataxia, confusion, drowsiness, renal stones
Tiagabine 32-56 mg Ataxia, confusion, drowsiness, paraesthesia, depression
Oxycarbazepine 900-2400 mg As for carbamazepine
Levetiracetam 1000-3000 mg Sedation, fatigue, psychosis
Zonisamide 200-400 mg Sedation, headache, psychosis, renal stone
Respiratory depression and hypotension are important • The pus may form in the subarachnoid space which
adverse events. may lead to adhesions.
6. Uncontrolled seizures are finally managed by general • Adhesions may result in obstruction to CSF flow
anesthesia and neuromuscular blockade along (hydrocephalus) and cranial nerve damage.
with ventilatory support. Anesthetic agents used are • Cerebral infarction may occur due to obliterative
midazolam, propofol and pentobarbitone. endarteritis.
7. Once the status is controlled, long-term anti-epileptic
• Cerebral edema can lead to raised intracranial pressure
medications are started.
(ICP) and coma.
8. The underlying cause is identified if any and treated
accordingly.
Clinical Manifestations
Complications The classical triad is fever, headache and neck rigidity. The
Important complications of status epilepticus are cardio- majority of patients develop impairment in sensorium.
respiratory dysfunction, hyperthermia, rhabdomylosis and Nausea, vomiting and photophobia are also common.
irreversible neurological damage. Patients with meningococcal meningitis may develop rash
and adrenocortical failure with shock (Waterhouse
MENINGITIS Friderichsen syndrome). Other features are seizures and
Meningitis means inflammatory changes in the meninges signs of raised ICP (Table 7.11).
and the subarachnoid space. Involvement of brain
parenchyma along with meninges is known as meningoen- Signs of Meningeal Irritation
cephalitis. • Neck rigidity is the pathognomonic sign of meningeal
Causes: Meningitis is generally due to infective causes. irritation (Figs 7.3A and B). This is demonstrated as an
174
These could be viruses, bacteria or fungi. The noninfective increased resistance to passive flexion of the neck. Other
causes of meningitis are SLE, sarcoidosis, or neoplastic causes of neck rigidity are diseases of the cervical spine,
invasion. posterior fossa tumor and subarachnoid hemorrhage.
Meningitis can be classified into three main categories: • Kernig’s sign is elicited when the patient is lying supine.
• acute purulent (pyogenic, septic, bacterial) The thigh is flexed on the abdomen with the knee flexed
• viral (aseptic)
• chronic meningitis (tuberculous, fungal). TABLE 7.10: Causes of bacterial meningitis
Neonates
Acute Bacterial Meningitis
Essentials of Medicine for Dental Students
Gram-negative bacilli
The organisms responsible for acute bacterial meningitis Group B streptococci
are variable and may differ with the age of the patients. The Listeria monocytogenes
Children
most common organisms in adults are S. pneumoniae and
H. influenzae
N. meningitides. A list of various organisms responsible for S. pneumoniae
acute meningitis is given in Table 7.10. N. meningitides
Bacterial meningitis is either secondary to bacteremic Adults
illness or due to spread of infection from adjacent structures S. pneumoniae
N. meningitidis
like ear, sinus, nose or fractured skull. Old age, alcoholism,
H. influenzae
diabetes, splenectomy are additional risk factors. Listeria monocytogenes
Meningococcal meningitis results from air borne infection Elderly
that initially leads to nasopharyngeal colonization. S. pneumoniae
N. meningitidis
Listeria monocytogenes
Pathology
Gram-negative bacilli
• Pia-arachnoid is congested and infiltrated with Posttraumatic/post-surgical
inflammatory cells. S. aureus
Nervous System
(Fig. 7.4). Passive extension of the knee causes pain
and spasm of the hamstrings. This is due to irritation of
meninges in the lower spine.
• Brudzinski’s sign is elicited when the patient is in a
supine position. Passive flexion of the neck results in a
spontaneous flexion of hips and knees.
Investigations
CSF examination: Diagnosis is made by lumbar puncture
and CSF examination. CT scan is performed to rule out the
presence of intracranial space-occupying lesion prior to
lumbar puncture particularly in cases with signs of increased
ICP, focal neurological signs and seizures. Lumbar puncture
in such cases may lead to fatal brain stem herniation.
The CSF is examined for pressure, cell count, protein,
glucose, smear stain for bacteria and culture. PCR may
rarely be needed. The findings of CSF examination of normal
and patients with meningitis are given in Table 7.12.
Blood examination: There is generally leukocytosis.
Blood culture may be helpful in the detection of organism.
Treatment
after obtaining a blood sample for culture. However, CSF • Ceftazidime is active against P. aeuroginosa and is
should be obtained as soon as possible. preferred over ceftriaxone or cefotaxime in hospital-
Empirical treatment is started before the CSF culture acquired meningitis, posttraumatic and postsurgical
and gram stain report is available. It is directed against the meningitis.
most common microorganisms present in a particular age Duration of Therapy
group (Table 7.14). Antimicrobials used against specific
The duration of antibiotic therapy depends on the type of
organisms in meningitis are given in Table 7.15. organism. A one-week therapy is given in case of H.
• Ceftriaxone or cefotaxime provides adequate influenzae and N. meningitides infection. S. pneumoniae
coverage against S. pneumoniae, H. infuenzae, Group needs antibiotic therapy for two weeks whereas
B streptococci and N. meningitides. L. monocytogenes and gram-negative bacilli infections
• Vancomycin is added to cover cephalosporin resistant require a 3 weeks therapy.
S.pneumoniae.
Adjunctive Therapy
176 • Ampicillin is added to cover L. monocytogenes in
patients less than 3 months of age or more than 55 The use of dexamethasone has decreased morbidity and
mortality in pneumococcal meningitis in adults. This is also
years and also in immunocompromised patients.
beneficial in pneumococcal and H. influenzae meningitis in
TABLE 7.13: Drugs and their dosage used in
bacterial meningitis
infants and children. Ten milligrams of dexamethasone is
given 15-20 minutes before or concurrent with the first
Agent Daily adult dose, frequency of administration
dose of antibiotic. Therapy is continued at the same dosage
Ceftriaxone 4 g/d, 12 h every 6 hours for 4 days.
Cefotaxime 12 g/d, 4 h
Essentials of Medicine for Dental Students
to headache. Migraine
Tension headache
Cluster headache
Classification Benign paroxysmal headache
The headache is classified as primary and secondary Secondary headache
Intracranial causes
(Table 7.16). Secondary headache has underlying cause and Subdural and intracerebral hematoma
the clinical features vary accordingly. The mechanism of Subarachnoid hemorrhage
Essentials of Medicine for Dental Students
primary headache is poorly known and it is probably due to Brain abscess, meningitis, encephalitis
disturbances in serotonergic neurotransmission. Obstructive hydrocephalus
Vasculitis
Benign intracranial hypertension (pseudotumor cerebri)
Approach to a Case of Headache Cerebral ischemia or infarction
A detailed history is important in the case of headache. The Extracranial causes
Giant cell arteritis (temporal arteritis)
onset, severity and the site of headache are important. Sinusitis
• Acute severe headache may suggest subarachnoid Glaucoma
hemorrhage or meningitis. Optic neuritis
• Hemicranial headache is a feature of migraine. Dental diseases
Temporomandibular joint disease
• Inquiry should be made about precipitating factors like Disease of cervical spine
alcohol, emotional stress, foods or medications. Systemic causes
• Chewing movements may exacerbate the pain due to Fever, hypoxia, hypercapnia, hypertension, anemia, allergy
Drugs (nitrates)
temporomandibular joint disease, trigeminal neuralgia and
Depression
glossopharyngeal neuralgia.
Treatment
Nervous System
The headache typically starts with nonspecific prodromal
symptoms like malaise and irritation followed by an aura of
Avoidance of Trigger Factors
a focal neurological event. There is severe throbbing
hemicranial headache with nausea, vomiting, photophobia The trigger factors are identified and best avoided. Alcohol,
and phonophobia. The patient prefers to be in quiet and red wine, chocolate are avoided. Adequate sleep should be
darkened room and to go to sleep. The aggravating factors ensured. Meals should not be missed.
for the headache are menses, red wine, hunger, lack or excess Treatment of Acute Attack
of sleep, alcohol, emotional or physical stress, perfumes and • Rest in a quite darkened room is helpful.
oral contraceptive pills. The deactivators or relieving factors • Analgesics (aspirin, paracetamol and other NSAIDs) are
are sleep, pregnancy and triptans. Family history of migraine usually effective if taken early at the onset of headache.
is often present. This is often combined with dopamine antagonists
The most common aura is visual, which is in the form (metoclopramide, domperidone, prochlorperazine).
of scotomas, hallucinations and fortification spectra. The • Severe attacks may be treated with triptans (sumatriptan,
latter is pathognomonic for migraine and is characterized zolmitriptan) and ergotamine. These are 5-HT (serotonin)
by silvery zig zag lines marching across the visual fields for agonists and are potent constrictors of extracranial
20 to 25 minutes. vessels. Triptans can be given orally, subcutaneously or
intranasally. The usual dose of sumatriptan is 6 mg
Variants of Migraine subcutaneously repeated at one hour (not more than
Basilar migraine: The neurological symptoms are in two doses per day) or 25-100 mg orally which may be
the form of vertigo, diplopia, and dysarthria. These repeated at 2 hours (maximum 200 mg/day). These are
symptoms are followed by headache and impaired contraindicated in patients with coronary artery disease,
uncontrolled hypertension and migraine with neurological
179
sensorium. Transient blindness may also occur, particularly
in young females. deficits.
Ophthalmoplegic migraine: This is characterized by pain • Ergotamine is best effective when taken early during
around the eye, nausea, vomiting and diplopia. Diplopia is prodromal phase. The initial dose is 1-2 mg orally which
due to transient external ophthalmoplegia mainly involving may be repeated at every 30 minutes to a maximum of
third cranial nerve and rarely sixth nerve. 10 mg per day or 16 mg per week. It is contraindicated
Facial migraine (carotidynia, lower-half headache): The in coronary artery disease and pregnancy. This is given
pain occurs repeatedly in jaw, neck and periorbital area. orally often in combination with 100 mg caffeine.
There may be an associated throbbing headache. The pain Dihydroergotamine (DHE) can be given parenterally
is accompanied with tenderness and prominent pulsations (1-2 mg IM, SC) at the onset of the headache.
Intravenous DHE (1 mg) along with prochlorperazine
of cervical carotid artery. There may be soft tissue swelling
(5-10 mg) is effective during severe attacks.
over the artery. The condition is more common in older
• Narcotic analgesics (meperidine) can be used in severe
patients and it is generally precipitated by dental trauma.
acute attacks. However, this should not be used for
Pathophysiology of Migraine chronic headaches to prevent addiction and tolerance.
The mechanism of migraine is multifactorial and complex. Prophylactic Therapy
It has definite genetic predisposition and is influenced by This is necessary if migrainous headache occurs more than
strong environmental components. Headache and related 3 times a month. The drugs are taken daily. It may take
symptoms are caused by dilatation of the extracranial vessels 2-6 weeks before the drugs are effective. A prolonged
whereas focal neurological dysfunctions are due to treatment is required. Once the response is obtained,
intracranial vasoconstriction. Neurotransmitters such as the dose can be tapered and withdrawn. The common
serotonin and dopamine are implicated in the genesis of the drugs used for prophylaxis are given in Table 7.17. Most
migraine. Other possible mechanisms are activation of dorsal patients respond to low dose amitriptyline, propranolol or
raphe neurons in upper brainstem. valproate.
TABLE 7.17: Drugs used for prophylactic Preventive therapy is generally effective. The drugs
therapy of migraine
used are propranolol, amitriptyline,valproate, verapamil,
Drug Dosage (daily) cyproheptadine. Lithium carbonate and prednisolone are also
Propranolol 80-320 mg effective.
Amitriptyline 10-50 mg (at night)
Sodium valproate 300-1000 mg Headache Due to Raised Intracranial Pressure
Cyproheptadine 4-16 mg
Methysergide 4-8 mg Headache due to raised intracranial pressure is worse in the
Verapamil 80-240 mg morning upon waking and improves as the patient becomes
upright. It may be associated with vomiting. It may worsen
Tension Headache on bending forward, coughing or straining. The headache
This is a very common type of headache which is is relieved by simple analgesics.
experienced by the majority of the population at some time Intracranial mass lesions and hydrocephalus are main
or other. causes of raised intracranial pressure. It is rare for mass
• The headache is constant, generalized and may continue lesion to present with severe headache alone; seizure or
for weeks or months. focal neurological deficits are usual presenting features.
• It is commonly described as a dull, tight, pressure or
FACIAL PAIN
band like sensation.
• Pain is less noticeable when the patient is busy and The pain in the facial area may be due to various causes.
becomes worse at the end of the day. Most cases are due to dental problems, trigeminal neuralgia,
• Emotional stress, noise and fatigue may precipitate the post-herpetic neuralgia and atypical facial pain. Provocation
headache. of pain due to hot, cold or sweet foods is typical of dental
• It is common in middle-aged males and there is no family in the facial region supplied by second and third divisions
history. of the trigeminal nerve.
• The pain occurs periodically at a specific time of the
day, generally in the early morning. The pain is severe TABLE 7.18: Causes of facial pain
and lasts for 30-90 minutes. There is unilateral periorbital
pain associated with nasal congestion, lacrimation, 1. Trigeminal neuralgia
2. Atypical facial pain
rhinorrhea or redness of the eye. 3. Postherpetic neuralgia
• Horner’s syndrome may occur during the attack. 4. Glossopharyngeal neuralgia
• Patients may remain asymptomatic for weeks or months 5. Other causes:
before another bout of headache (cluster) occurs. Glaucoma
Sinusitis
• Alcohol triggers the attack. Mastoiditis
Treatment of acute attack with oral drugs is unsatisfactory. Dental problems
Inhalation of 100% oxygen (7 L/min for 15 minutes) is the Temporomandibular joint disease
Jaw pain due to angina pectoris
most effective modality of treatment for acute attack.
Giant cell arteritis
Subcutaneous sumatriptan (6 mg) may be effective.
Pathogenesis Atypical Facial Pain
Nervous System
There is demyelination of the trigeminal nerve root at the point Atypical facial pain occurs usually in middle-aged depressed
of their entry into the pons. The demyelination is commonly females. It is a constant pain often burning type which is
due to the compression mainly by aberrant blood vessels centered on the maxilla, but may spread to the rest of the
(superior cerebellar artery, tortuous vein). In a few patients face on the affected side. Sometimes it may involve
it may occur due to multiple sclerosis or brainstem tumor. other side of the face, neck or back of the head. Tricyclic
antidepressant, analgesics, carbamazepine or phenytoin may
Clinical Features be tried. The response to therapy is poor.
Trigeminal neuralgia is characterized by episodes of sudden,
severe, sharp lancinating pain in the area of lips, gums, Glossopharyngeal Neuralgia
cheek and chin. The pain lasts for a few seconds or Glossopharyngeal nerve (IX cranial nerve) supplies taste
sometimes persists for a minute or two. The pain is sensation to the posterior one-third of the tongue and
so severe that patients may flinch as if a motor tic sensation to the posterior pharynx (along with X nerve).
(hence called tic douloureux). The pain is triggered by Glossopharyngeal neuralgia is similar in quality to trigeminal
chewing, speaking, smiling and touching trigger zones in neuralgia but is less common. Pain occurs on one side of
the trigeminal territory. There is a tendency for remissions the throat in the area of tonsillar fossa which may radiate to
and relapses. the ear. In some the pain may remain localized in the ear.
Examination does not reveal any neurological sign. The pain may be initiated by swallowing, coughing, chewing
Presence of neurological signs and sensory loss suggest or yawning. Pain may be accompanied by syncope in some
multiple sclerosis or posterior fossa tumor. cases. Sensory and motor examination is normal. No cause
is demonstrable in most cases; however, multiple sclerosis
Investigations
CT and MRI may be needed to detect the underlying cause
may be responsible for the pain in some.
Medical treatment is the same as for trigeminal neuralgia. 181
such as multiple sclerosis and tumors. High resolution MR Carbamazepine is the drug of choice. Microvascular
angiography is helpful in visualizing aberrant vessels. decompression and partial rhizotomy can be done in
refractory cases.
Treatment
Medical: The drug of choice is carbamazepine (upto Post-herpetic Neuralgia
1200 mg/day). If not controlled, other drugs such as Post-herpetic neuralgia is the complication of herpes zoster
phenytoin (300-400 mg daily) or gabapentin (upto 2400 mg/ (shingles) infection. It occurs more commonly in elderly
day) are tried. Baclofen (10-20 mg thrice a day) may be patients when first division of trigeminal nerve is involved.
used alone or in combination with carbamazepine or Pain is continuous and burning in character throughout the
phenytoin. affected territory of trigeminal nerve. Even a light touch
Surgical: This is tried when medical treatment fails. may precipitate the pain. Pain may last for years. Simple
• The most common therapy is heat lesion of the trigeminal analgesics may be helpful. Phenytoin (300 mg/day),
ganglion or nerve (radiofrequency thermal rhizo-tomy). carbamazepine (upto 1200 mg/day), gabapentin (upto 3200
• Injection of alcohol in Meckel’s cave has been practiced mg/day) may be tried if analgesics fail to control the pain.
in the past. Excessive damage of the nerve may lead to Tricyclic agents (amitryptiline) alone or along with
loss of sensation in the face (anesthesia dolorosa). phenothiazine are often effective in severe cases.
• Posterior craniotomy and microvascular decompression
is quite effective and generally done in younger patients. FACIAL NERVE PALSY
• Gamma radiosurgery to the trigeminal root is a The facial nerve (VII cranial nerve) arises from the pons,
recent noninvasive effective tool to treat trigeminal passes through the facial canal and exits from the skull
neuralgia. though stylomastoid foramina. It then passes through the
FIGURE 7.6: Facial nerve palsy (There is loss of nasolabial
fold and drooping of angle of mouth on right side)
FIGURE 7.5: Pathway of VII cranial nerve
• The patient is unable to whistle or blow.
parotid gland and subsequently divides into branches • If the nerve to stapedius is damaged, there is hyperacusis
(Fig. 7.5). It provides motor innervation to all muscles of (sensitivity to loud sounds).
the facial expression and the stapedius. Through its branch, There is loss of taste in the anterior two-third of the
the chorda tympani, it carries taste sensation from the tongue on the same side. There is no sensory loss over the
(see also ‘examination of the cranial nerve’) Causes of Facial Nerve Palsy
The involvement of facial nerve at its origin in the pons or
Features of Facial Nerve Palsy at any site throughout its course may lead to infranuclear
The findings of motor lesion of unilateral facial nerve are as facial palsy (lower motor neuron type). The causes of the
follows: lesion at different sites are given in Table 7.19. Important
• There is loss of facial expression at the side of the palsy. causes of supranuclear palsy are cerebral thrombosis,
Essentials of Medicine for Dental Students
• Furrows of the forehead are absent. cerebral embolism, cerebral hemorrhage and brain tumor.
• The eye is more widely open and the eyelids do not Melkersson-Rosenthal syndrome is triad of recurrent
close completely on the side of lesion. facial nerve palsy, recurrent facial edema and plication of
• There is drooping of the corner of the mouth. When the tongue.
patient is asked to smile or show his teeth, the angle of
the mouth at the side of the lesion does not move TABLE 7.19: Causes of infranuclear facial nerve palsy
(Fig. 7.6).
Pons: Infarction, tumor, multiple sclerosis
• There is loss of nasolabial fold on the affected side Cerebellopontine Acousticneuroma
(Fig. 7.6). angle:
• On attempted closure of the eye lids, the eye ball on the Temporal bone: Chronic suppuratve otitis media (CSOM),
cholesteatoma, Bell’s palsy, Ramsay Hunt
paralyzed side rolls up (Bell’s phenomenon). It is a normal
syndrome, dermoid, carotid body tumor
phenomenon which is preserved and can be visualized Outside skull: Parotid lesions, trauma, lymph node swelling
in facial nerve paralysis. Others: Guillain-Barré syndrome, sarcoidosis
• Food collects between teeth and the lips. (uveo-parotid fever, Heerfordt syndrome),
diabetes mellitus, leprosy, lyme disease,
• Saliva dribbles from the angle of the mouth on the
Melkersson-Rosenthal syndrome
paralyzed side.
TABLE 7.20: Features of supranuclear and infranuclear
Nervous System
Ramsay Hunt syndrome is a complication of herpes zoster
facial palsy
infection of geniculate ganglion associated with facial palsy
and vesicular eruption in external auditory canal and pharynx. Supranuclear facial palsy Infranuclear facial palsy
Facial diplegia is bilateral facial infranuclear palsy seen 1. Upper motor neuron 1. Lower motor neuron lesion
in Guillain-Barré syndrome and sarcoidosis. lesion
2. Upper part of face 2. Whole face involved
relatively spared
Localization of the Site of Lesion in 3. May be associated 3. Aphasia not present
Infranuclear Facial Palsy with aphasia
4. Usually accompanied 4. May be accompanied with
1. Lesion outside the stylomastoid foramina: with hemiplegia on hemiplegia on opposite
a. If the lesion of the facial nerve is outside the same side (un-crossed side (crossed hemiplegia)
stylomastoid foramen, only motor manifestations are hemiplegia)
5. Taste sensation not 5. Taste sensation may be
present. involved
involved
b. Taste is not involved as chorda tympani joins the 6. Emotional facial 6. Emotional facial movement
facial nerve in the facial canal before the facial nerve movement preserved not preserved
emerges from the stylomastoid foramen.
c. There is no hyperacusis. equally involved in infranuclear facial palsy. This is because
2. Lesion in the temporal bone: upper part of the face is innervated by both motor cortices
a. The lesion of the facial nerve in facial canal near the whereas the lower part of the face is innervated by the
middle ear may cause hyperacusis in addition to loss opposite hemisphere only.
of taste. • Supranuclear facial palsy is often associated with
b. Other cranial nerves (auditory and vestibular) are paralysis of the arm and leg of the same side or aphasia.
also involved if the lesion is near the internal auditory
183
• The taste sensation in the anterior two-third of the tongue
meatus. is not involved in supranuclear type.
3. Lesion in the pons: In the pontine lesion, sixth cranial • Emotional facial movements are also preserved in
nerve may also be involved and there may be hemiplagia supranuclear type.
of the opposite side (crossed hemiplagia). • In supranuclear type, the lesion is on the opposite side
If the recovery of motor function is incomplete, aberrant of the palsy whereas it is on the same side of the palsy
regeneration can cause synkinesis, i.e., movement of one
in infranuclear type.
muscle can cause movement of another or all muscles; for
• Important causes of supranuclear palsy are cerebral
example, closure of eye can cause deviation of the angle of
thrombosis, cerebral embolism, cerebral hemorrhage and
the mouth. Lacrimal gland fibers may join with fibers of
brain tumor.
other muscles so that while eating, tears may also flow
(crocodile tears). Orbicularis oculi fibers may join with
Bell’s Palsy
orbicularis oris resulting in the closure of eyelids when the
mouth is opened (jaw winking). This is the most common type of facial palsy. It is a type of
idiopathic infranuclear (lower motor neuron type) facial palsy,
Supranuclear Facial Palsy the cause of which is not known. The site of involvement
The damage of corticonuclear fibers from motor cortex to is facial canal. Bell’s palsy has been associated with
facial nucleus may cause supranuclear facial palsy (upper reactivation of herpes simplex type I infection, but its causal
motor neuron type). The infranuclear facial paralysis must role is not established.
be differentiated from supranuclear type of facial palsy.
(Table 7.20) Clinical Features
In supranuclear facial palsy, the upper part of the face Onset is abrupt or subacute and the maximum weakness
(frontalis, orbicularis oculi) is involved to a lesser extent occurs in 48 hours. Pain around the ear may occur prior to
than the lower part of the face whereas whole of the face is or along with the weakness. Motor manifestations are the
same as described earlier. Bell’s phenomenon is present. Causes
There is loss of taste in the anterior two-thirds of the tongue Stroke may be ischemic (thrombotic and embolic) or
on the same side. Hyperacusis occurs on the side of lesion hemorrhagic. Important causes of stroke are given in
if nerve to stapedius is also involved. There may be Table 7.21. Risk factors for stroke are given in Table 7.22.
diminished salivation and tear secretion.
Clinical Manifestations
Investigations
There is an acute onset of neurological dysfunction. The
MRI may show swelling and enhancement of geniculate presentation is variable and depends upon the vessel
ganglion and facial nerve. EMG has prognostic value. involved. Patients generally present with headache, sudden
loss of consciousness and seizures.
Treatment
Symptomatic: This includes massage of the facial muscles
TABLE 7.21: Causes of stroke
and protection of the eye during sleep to prevent corneal
damage. A lubricating eye drop is used to avoid dryness. Ischemic stroke
Specific: Administration of glucocorticoids with or without Thrombosis
Lacunar infarction
acyclovir improves the outcome. The dose of prednisolone Large vessel thrombosis
is 60-80 mg daily for 5 days and then tapered over the next Embolic
5 days. Acyclovir is given in a dosage of 400 mg 5 times From artery
daily for 10 days. Combination of prednisolone with Carotid bifurcation
Cardioembolic
acyclovir is more effective than prednisolone alone. Atrial fibrillation
Myocardial infarction
Prognosis
184
Infective endocarditis
Valvular lesions
Over 80% of the patients recover completely in a few weeks Others
time. Patients with complete paralysis have a less favorable Hypercoagulable states
prognosis than those with incomplete paralysis. Vasculitis
Meningitis
Hemorrhagic
CEREBROVASCULAR DISEASES
Hypertension
Cerebrovascular diseases mainly include ischemic stroke, Trauma
hemorrhagic stroke and vascular anomalies such as Anticoagulant therapy
Essentials of Medicine for Dental Students
Aneurysm
intracranial aneurysms and arteriovenous malformation. The AV malformation
incidence of cerebrovascular diseases increases with age. Blood dyscrasias
• Stroke or cerebrovascular accident are characterized Brain tumor
by abrupt onset of symptoms and neurologic deficits
attributable to focal vascular cause. TABLE 7.22: Risk factors for stroke
• Ischemia may be transient and there may be recovery
Hypertension
from the neurological deficit within few hours but always Heart diseases (AF, CHF, IE)
within 24 hours. This is known as Transient ischemic Diabetes mellitus
attack (TIA). TIAs are usually embolic. TIA is a risk Smoking
Hyperlipidemia
factor for future stroke.
Age (old age)
• A reversible ischemic neurological deficit (RIND) is Gender (male)
similar to TIA persisting for >24 hours but resolves Previous vascular event
within a week. (MI, stroke, peripheral embolism)
• In some patients, the deficit continues to worsen after AF = Atrial fibrillation, CHF = Congestive heart failure,
IE = Infective endocarditis, MI = Myocardial infarction
about 6 hours of the onset (stroke-in-evolution).
Treatment
Nervous System
• Involvement in the carotid artery area (anterior
circulation) leads to hemiplegia (weakness of upper and Following are the main components of management of
lower limbs of one side) and cortical sensory loss on stroke:
the opposite side of the involved hemisphere. 1. Medical support: The patient should be urgently
• Aphasia (loss of speech) may occur in left hemispheric hospitalized. The medical management includes control
involvement. of blood pressure, maintenance of fluid and electrolytes
• Vertebrobasilar strokes (posterior circulation ) produce and control of intracranial pressure (with IV mannitol).
unilateral or bilateral motor sensory deficits of cranial 2. Thrombolysis: This is indicated in early ischemic stroke
nerves and brain stem signs. Symptoms like vertigo, within 3 hours of onset of symptoms. Recombinant tissue
nausea, vomiting, dizziness, dysarthria, ataxia are more plasminogen activator (rTPA) is used for thrombolysis.
common in posterior circulation strokes. 3. Aspirin in doses of 160-325 mg daily is indicated for
• Sudden onset of severe headache and neck rigidity acute and long-term management of ischemic stroke.
suggests subarachnoid hemorrhage. 4. Anticoagulation is required to prevent recurrent embolic
strokes. Warfarin is used for chronic anticoagulation
Investigations and the target INR should be 2-3 (in case of prosthetic
• CT or MRI head is performed to diagnose the type valve 2.5-3.5).
(ischemic or hemorrhagic) and site of lesion (Fig. 7.7). 5. Carotid endarterectomy is indicated in patients with
• Other tests done are carotid Doppler (to diagnose carotid >70% carotid stenosis. It decreases the risk of stroke
stenosis), echocardiography (to rule out cardiac lesions) and death.
and CSF analysis. 6. Modification of risk factors includes the control of blood
• Complete blood count, platelet count, PT, APTT and pressure, blood sugar, serum lipids and cessation of
•
electrolytes are also performed.
Tests such as blood sugar, lipid profile and ECG are
smoking.
7. Physiotherapy and rehabilitation. 185
done to find out the presence of risk factors.
• Specific tests may be needed to diagnose an uncommon IMPLICATIONS ON DENTAL PRACTICE
underlying cause. 1. In patients of epilepsy, fixed prosthesis is placed rather
than removable appliances because latter may dislodge
during the seizure.
2. Gingival growth occurs in patients taking phenytoin.
3. There is no need to increase the dose of anticonvulsant
therapy in well-controlled epilepsy prior to dental
treatment. Routine use of sedation is not indicated.
4. Seizure may occur during the dental procedures. Hence,
one should be aware of the management of patients
during seizures.
5. Drugs may precipitate seizures or may interfere with
the anticonvulsant drugs. Avoidance or the dose
adjustment of the drugs may be required.
6. Accumulation of food debris in the vestibule and the
plaque on the teeth may occur on the affected side in
cases of facial palsy. Saliva may trickle from the angle
of mouth and lead to angular stomatitis.
7. There is loss of taste in the anterior two-third of the
tongue on the same side and there may be diminished
FIGURE 7.7: MRI brain showing intracerebral hemorrhage salivation and tear secretion in Bell’s palsy.
8. CSF leak (CSF rhinorrhea) and recurrent bacterial C. Chronic suppurative otitis media(CSOM)
meningitis may occur as a result of maxillofacial fracture D. Sroke (Cerebrovascular accident)
involving the cribriform plate of the ethmoid. 8. In status epilepticus, the initial drug to be given is:
9. Patients with maxillofacial injuries should be given A. Phenytoin B. Diazepam
C. Phenobarbitone D. Carbamazepine
prophylactic antibiotics because of risk of bacterial
9. Drug of choice for partial seizures is:
meningitis.
A. Phenytoin B. Clonazepam
10. Patients with trigeminal neuralgia may develop oral C. Carbamazepine D. Gabapentin
complications as they may be reluctant to brush their teeth. 10. Which one is not true about trigeminal neuralgia:
11. Migrainous neuralgia must be differentiated from pain A. Mainly occurs in middle aged and elderly
of dental origin by careful history and examination. B. Pain lasts only for few seconds
12. Elective dental care should be deferred for 6 months in C. Ophthalamic division of trigeminal nerve is most
a patient with stroke since there is a risk of developing commonly involved
another stroke. D. Neurological examination is normal (no motor or
13. Stroke should be considered in patients who develop sensory deficit)
sudden loss of consciousness or neurological deficits 11. Probable site of lesion in Bell’s palsy is:
A. Within parotid gland
during dental surgery.
B. Brainstem
C. Cerbellopontine angle
SELF ASSESSMENT
D. Within facial canal
Multiple Choice Questions 12. Which one is not true about Bell’s palsy:
A. Presence of hyperacusis
1. Which is true in Bell’s palsy:
B. Taste sensation is impaired
A. Is lower motor neuron lesion
4. Commonest cause of facial nerve palsy, proximal to its A. Loss of nasolabial fold
branching in parotid is: B. Inability to blow or whistle
A. Bell’s palsy C. Loss of wrinkles over forehead
B. Ramsay-Hunt syndrome D. Dribbling of saliva on the side of palsy
C. Acoustic neuroma 15. Ramsay-Hunt syndrome is characterized by all except:
D. Brainstem diseases A. Presence of vesicles over external auditory canal
5. CSF glucose levels are normal in following type of meningitis: B. Ipsilateral facial nerve palsy
A. Tubercular B. Bacterial (pyogenic) C. Cause is herpes simplex of geniculate ganglion
C. Viral D. Fungal D. Lower motor type of lesion
6. Marked increase in polymorphs in CSF is a feature of which 16. Which of the following opportunistic meningeal infection is
type of meningitis: commonly seen in AIDS:
A. Pyogenic B. Tubercular A. Cryptococcus B. Candida
C. Viral D. Fungal C. Aspergillus D. Histoplasma
7. Which of the following is a cause of upper motor neuron 17. Drugs useful in treatment of status epilepticus are all except:
facial palsy: A. Phenytoin B. Phenobarbitone
A. Bell’s palsy C. Clonazepam D. Midazolam
B. Sarcoidosis
18. Tongue bite, incontinence of urine or stools, cry and D. Pain is associated with nasal congestion and
Nervous System
cyanosis are features of: lacrimation
A. Petit mal seizures B. Grand mal seizures 26. Which one is not effective in acute attack of migraine:
C. Myoclonic seizues D. Partial seizures A. Sumatriptan
19. Jacksonian march is seen in: B. Paracetamol
A. Simple partial seizures C. Amitriptyline
B. Petit mal seizures D. Ergotamine
C. Grand mal seizures 27. Most common cause of pyogenic meningitis in children is:
D. Complex partial seizures A. S. pneumonae
20. Neck rigidity, altered sensorium and skin rashes suggest: B. N. meningitides
A. Meningococcal meningitis C. H. influenzae
B. Pneumococcal meningitis D. Listeria monocytogenes
C. H. influenzae meningitis
D. Tubercular meningitis Fill in the Blanks
21. Neck rigidity is present in: 1. Weakness of the involved part following motor seizure
A. Posterior fossa tumor is called ________.
B. Meningitis 2. Tic doulourex is ________.
C. Subarachnoid hemorrhage 3. Anesthesia dolorosa is a complication of ________.
D. All the above 4. Most frequent type of migraine is ________.
22. Gum hypertrophy can occur with the use of: 5. The cell count in the normal CSF is ________.
A. Calcium channel blockers 6. Spider web is formed in the CSF of patients with
B. Phenytoin ________ meningitis.
C. Cyclosporine 7. India ink preparation is used to diagnose ________
D. All of the above infection.
23. The consciousness is not impaired in:
A. Grand mal seizures
8. Hyperacusis is due to paralysis of ________ muscle.
9. Taste sensation from anterior two-third of the tongue
187
B. Status epilepticus is carried by ________ nerve.
C. Simple partial seizures 10. Complex partial seizures generally arise from
D. Complex partial seizures ________ lobes.
24. All are features of common migraine except: 11. Rifampicin is used for the prophylaxis of ________.
A. Unilateral headache 12. Waterhouse-Friedreichsen syndrome is a
B. Visual symptoms complication of ________.
C. Vomiting 13. Most effective modality of treatment in cluster
D. Premonitory symptoms (Aura) headache is ________.
25. Which one is not true about “Cluster headache”: 14. Sumatriptan is contraindicated in patients with
A. It is common in males ________ and ________.
B. Pain occurs periodically at a specific time of the day 15. Recurrent meningitis can result from fracture of
C. Severe pain lasting about 24-48 hours ________.
Chapter
Endocrine and
8 Metabolic Disorders
THYROID DISORDERS
Anatomy of thyroid gland: The thyroid gland is situated in
the neck anterior to the thyroid cartilage. It weighs around
15-20g in the adult. The thyroid gland has two lobes, the
right and the left, joined by an isthmus.
Physiology: It secretes mainly thyroxin (T4) and a small
amount of triiodothyronine (T3).
• T3 is the active form of the hormone. Most of the T4 is
converted into T3 in peripheral tissues such as liver,
muscles and kidneys.
• Thyroid hormones are carried in plasma, predominantly
in the bound form with a plasma protein (thyroid binding
globulin, TBG), while only a small amount circulates
unbound (free hormone).
• Only the free form can enter cells and exerts its metabolic
action.
Regulation of thyroid hormone secretion: The production
of thyroid hormones is stimulated by the thyroid stimulating
hormone (thyrotropin, TSH), released by the anterior FIGURE 8.1: Feedback control of thyroid hormone
pituitary in response to the hypothalamic thyrotropin
TABLE 8.1: Causes of hypothyroidism
releasing hormone (TRH). There is a negative feedback
effect of thyroid hormone on the pituitary gland so that TSH Primary hypothyroidism
Spontaneous atrophic
secretion is suppressed if the level of thyroid hormone is Post-thyroidectomy
raised or vice versa (Fig. 8.1). Following 131I administration for hyperthyroidism
Congenital
Hypothyroidism Goitrous
Hoshimoto’s thyroiditis
Hypothyroidism is more common in females. It can be due Iodine deficiency
to either: Drug induced (lithium, amiodarone, methimazole)
a. Primary disorders of the thyroid gland (primary hypothy- Genetic enzyme defects (dyshormonogenesis)
Secondary hypothyroidism
roidism) or Destruction of pituitary gland
b. Decreased TSH secretion by the pituitary gland (secondary Post-surgery
hypothyroidism) Post-radiation
Causes are given in Table 8.1. The most common cause Tumor
Disorders of hypothalamus
of hypothyroidism worldwide is iodine deficiency. However,
Endocrine and Metabolic Disorders
in areas where iodine deficiency is not present, the important
causes are autoimmune thyroiditis and iatrogenic.
Autoimmune hypothyroidism is initially associated
with goiter (Hoshimoto’s thyroiditis) which later becomes
atrophic (atrophic thyroiditis). It is also associated with other
autoimmune disorders.
Clinical Features
Table 8.2 shows important symptoms and signs in hypothy-
roidism.
Common symptoms in hypothyroidism are a dry coarse
skin, weakness, tiredness, cold intolerance, puffy face,
edema in hands and feet, constipation, weight gain and a
hoarse voice (Fig. 8.2). Prolonged hypothyroidism results
FIGURE 8.2A: Enlarged tongue in hypothyroidism
in the deposition of hydrophilic mucopolysaccharides in
tissues. This causes non-pitting edema (myxedema).
General
Weakness, tiredness
Cold intolerance
Dry coarse skin
Pallor
189
Hair loss
Puffy face, hand, and feet
Myxedema
Weight gain, poor appetite
Hypothermia
Goiter
Hoarse voice
Gastrointestinal FIGURE 8.2B: Facial puffiness and pallor in hypothyroidism
Constipation
Large tongue Investigations
Reproductive a. Thyroid function tests:
Menorrhagia
Amenorrhea
• High serum TSH is the earliest and most sensitive
Infertility indicator of primary hypothyroidism.
Galactorrhea • The serum TSH level is low in secondary hypothy-
Nervous system roidism.
Poor memory
• Serum T4 is low.
Poor concentration
Carpal tunnel syndrome • Serum T3 levels is low but is not reliable for the
Delayed relaxation of deep reflexes diagnosis of hypothyroidism.
Cardiovascular • High serum TSH and normal serum T4 indicates
Bradycardia subclinical or mild hypothyroidism.
Hypertension
b. High titer of antibodies against thyroperoxidase (TPO)
Ischemic heart disease
Pericardial effusion and thyroglobulin are found in patients with Hashimoto’s
thyroiditis and atrophic thyroiditis.
c. Other findings are anemia (normocytic or macrocytic), TABLE 8.3: Clinical features of congenital hypothyroidism
high serum cholesterol and triglycerides, increased Feeding problems
serum creatine kinase and LDH, hyponatremia, and low Prolonged jaundice
voltage ECG. Hypotonia
Enlarged tongue
Delayed physical growth and development
Treatment Mental retardation
• Hypothyroidism should be treated with oral levothy- Short stature
roxine. The treatment is generally started with low dose Umbilical hernia
Other features as seen in adult patients with hypothyroidism
(50-100µg daily) and gradually increased.
• In elderly, a smaller starting dose (25 µg) is preferred to
avoid cardiac side effects.
• TSH is monitored periodically and the dosage adjustment
of thyroxine is made accordingly.
• The ideal goal is to maintain TSH at the lower half of
the reference range.
• Treatment is needed lifelong.
Myxedema Coma
This is a rare presentation of hypothyroidism. The clinical
features are altered sensorium, hypothermia, hypoglycemia,
hypoventilation, hypoxia, hypercapnia, hyponatremia, and
FIGURE 8.3: Cretinism
192
• ESR may be increased in subacute thyroiditis. thyroidism. This is also preferred in pregnant women.
• The uptake of radioactive iodine by thyroid is high in Before surgery, the patient is made euthyroid by
Graves’ disease and toxic nodular goiter whereas it is antithyroid drugs. Potassium iodide is then added 1-2
low in subacute thyroiditis. weeks before surgery. Both drugs are discontinued
• Ultrasonography of thyroid gland reveals diffuse after surgery. Complications of surgery are recurrent
enlargement of thyroid gland. It helps in differentiating laryngeal nerve palsy and hypoparathyroidism. However,
Graves’ disease from nodular goiter. recurrence of hyperthyroidism or development of
hypothyroidism may occur.
Essentials of Medicine for Dental Students
Treatment
The hyperthyroidism of Graves’ disease is treated by Thyroid Crisis
antithyroid drugs, radioactive iodine (131I) or subtotal This is a severe form of thyrotoxicosis which can occur
thyroidectomy. The choice of treatment depends on the cause during stressful illnesses, thyroid surgery or radioactive
and severity of hyperthyroidism, the patient’s age and clinical iodine administration. It manifests as delirium, tachycardia,
situation. vomiting, diarrhea, and high fever. In elderly, heart failure
a. Antithyroid Drugs: The most commonly used drugs are may occur. The mortality rate is high.
carbimazole, methimazole and propylthiouracil.
• These drugs reduce the synthesis of thyroid Treatment
hormones by inhibiting the iodination of tyrosine. • The patients should be rehydrated and given broad
These drugs also reduce the thyroid antibody levels. spectrum antibiotics.
• These are used in young adults and in patients with • Propranolol is given orally or intravenously.
mild thyrotoxicosis and small goiter. • Ipodate sodium (500 mg orally per day) is very effective
• The drugs are given (carbimazole 5-40 mg / day, in bringing the T3 levels to normal. This is a radiographic
propylthiouracil 100-200 mg every 6-8 h) for contrast medium which inhibits the release of thyroid
prolonged periods of about 1-2 years. Relapse occurs hormones and peripheral conversion of T4 toT3.
TABLE 8.6: Causes of hypocalcemia
194 •
nesemia.
The ECG may show prolongation of QT interval.
are given in Table 8.8.
• Primary hyperparathyroidism and malignancy account
Arrhythmias may occur. for 90 % of all the case of hypercalcemia.
• Hypercalcemia in malignancy may occur due to
Treatment (a) metastasis in bone, (b) increased bone resorption
Treatment of Severe Symptomatic Hypocalcemia: Calcium due to increased osteoclast activating factor (OAF), and
gluconate 2g, equivalent to 180 mg elemental calcium (20 (c) production of PTH related peptide (PTHrP).
ml of 10% calcium gluconate intravenously in 10-15 • Sarcoidosis may cause hypercalcemia by increased
Essentials of Medicine for Dental Students
minutes) should be given. This should be followed by production of vitamin D3 by granulomatous tissue.
infusion of 60 ml of 10% calcium gluconate in 500 ml TABLE 8.8: Important causes of hypercalcemia
dextrose water slowly in 4-6 hours. Subsequently the
infusion rate should be adjusted to maintain serum calcium Primary hyperparathyroidism
Adenoma
TABLE 8.7: Laboratory findings in hypocalcemia Hyperplasia
Carcinoma
Total Ionized Serum Serum Malignancy
serum serum phosphate PTH Tumors producing PTH related proteins (malignancy of lung,
calcium calcium ovary, kidney)
Hypoalbuminemia Low Normal Normal Normal Hematological malignancies (Myeloma, lymphoma, leukemia)
Alkalosis Normal Low Normal Normal Other causes
Osteomalacia (vit D Low Low Low High Sarcoidosis
deficiency) Vitamin D excess
Chronic renal failure Low Low High High Hyperthyroidism
Hypoparathyroidism Low Low High Low Lithium and thiazide use
Pseudohypoparathy- Low Low High High Milk alkali syndrome
roidism Immobilization
Endocrine and Metabolic Disorders
• Increased bone turn over in hyperthyroidism may lead e. Oral glucocorticoids are effective in hypercalcemia due
to hypercalcemia. to hematological malignancies, sarcoidosis and vitamin
• Prolonged immobilization may cause hypercalcemia due D toxicosis.
to continuing bone resorption in the absence of normal f. Hemodialysis may be needed in cases of renal failure
postural stimuli for bone formation. and heart failure.
• Milk alkali syndrome is due to ingestion of large amount g. The underlying cause should be treated. Para-
of calcium and absorbable antacids such as milk or thyroidectomy is done in primary hyperthyroidism.
calcium carbonate.
PARATHYROID DISORDERS
Clinical Features
There are four parathyroid glands situated posterior to the
The symptoms generally occur if serum calcium level is thyroid gland. These produce parathyroid hormone (PTH)
more than 12 mg/dL. Symptoms are more marked if which is a peptide comprising of 84 amino acids. The
hypercalcemia develops rapidly. secretion of PTH is regulated by the ionized calcium levels
• The gastrointestinal manifestations are anorexia, nausea, in serum. The important physiological roles of PTH are:
vomiting, peptic ulcer and constipation. a. It promotes resorption of calcium from bones
• Renal symptoms include polyuria, polydipsia, renal colic b. It promotes resorption of calcium from renal tubules
and nephrolithiasis. c. It stimulates the synthesis of 1, 25-dihydroxy-
• Neurological presentations are confusion, depression, cholecalciferol by the kidneys, thus indirectly promoting
drowsiness, stupor and coma. the absorption of calcium from the intestine.
• Ectopic calcification may occur in soft tissue if serum d. It inhibits the absorption of phosphate by the renal
calcium level is more than 13 mg/dL. tubules.
Investigations
195
Hypoparathyroidism
Serum calcium and serum PTH levels are measured.
Important causes of hypoparathyroidism are post-
• High PTH level is present in primary hyperpara-
thyroidectomy, after parathyroid gland surgery,
thyroidism while it is low in malignancies where
hemochromatosis and hypomagnesemia.
parathyroid related protein (PTHrP) is raised.
• Hypoparathyroidism can also be hereditary such as in
• Other tests are done to detect the presence of
Di George syndrome. This is characterized by
malignancies if suspected.
hypocalcemia, cardiovascular and facial anomalies.
• Measurement of thyroid hormones and vitamin D levels
• Hypoparathyroidism can be a manifestation of
may be required.
• ECG findings include short QT interval and ventricular polyglandular autoimmunity type I in which other
arrhythmias. features are candidiasis, Addison’s diseases and vitiligo.
• Pseudohypoparathyroidism is a condition in which the
Treatment production of PTH is normal, but there is tissue
a. Restoration of extracellular fluid volume is done with resistance to PTH. This is associated with structural
0.9 % saline. Three to four liters of fluid may be needed abnormalities such as short stature and short fourth
in the first 24 hours. metacarpal.
b. Saline diuresis is induced by giving an infusion of saline • Pseudohypoparathyroidism is characterized by the
which promotes the excretion of calcium. Frusemide presence of structural abnormalities as seen in
may be added in case of renal impairment or heart failure. pseudohypoparathyroidism but normal calcium and PTH
c. Bisphosphonate (60-90 mg pamidronate or zoledronate levels.
4 mg) is given intravenously. It inhibits bone resorption.
This is the drug of choice in malignancies. Clinical Features
d. Calcitonin (IM or SC) may be given particularly when
The manifestations of hypoparathyroidism are due to
there is renal failure. It inhibits bone resorption and
promotes calcium excretion. hypocalcemia (see hypocalcemia).
Investigations fibrosa cystica). This can also present as “brown tumors”
• The serum calcium is low, serum phosphate is high, and (cysts of the jaw).
serum alkaline phosphatase is normal.
• The PTH levels are low. It is normal or high in Investigations
pseudohypoparathyroidism. • In primary hyperparathyroidism serum PTH level is
• The magnesium level is measured to rule out elevated, serum calcium is high and phosphate is low. Serum
hypomagnesemia. alkaline phosphatase is raised if bone disease is present.
• In secondary hyperparathyroidism, PTH level is elevated.
Treatment Serum calcium is low and phosphate is high.
Treatment of hypoparathyroidism includes supplementation • Bone X-ray may show demineralization, subperiosteal
of calcium and vitamin D. erosions, resorption of terminal phalanges and loss of
lamina dura of the teeth. Skull X-ray may reveal pepper-
Hyperparathyroidism pot appearance.
Primary hyperparathyroidism is caused by hyper- • Radioimaging and ultrasound neck are needed to localize
secretion of PTH. In majority of cases, this is due to and diagnose parathyroid tumors.
autonomous hypersecretion of PTH. Primary hyper-
Treatment
parathyroidism (adenoma or hyperplasia) may be familial
and part of multiple endocrine neoplasia (MEN types Parathyroidectomy is recommended for patients with
1, 2a). symptomatic hyperparathyroidism. Medical management of
Secondary hyperparathyroidism is characterized hypercalcemia is described elsewhere (see hypercalcemia).
by the hypersecretion of PTH due to stimulation by
PITUITARY GLAND
196 hypocalcemia (Table 8.9). There is hyperplasia of all
parathyroid glands. Anatomy: The pituitary gland is situated in the sella turcica.
In tertiary hyperparathyroidism hyperplastic The gland is connected to the hypothalamus with pituitary
parathyroid glands (as in case of secondary hyper- stalk or infundibulum. The pituitary gland has two lobes,
parathyroidism) may result in adenoma formation and anterior and posterior. Portal vessels carry blood from the
autonomous PTH secretion. hypothalamus to the anterior lobe while the posterior lobe
receives nerve fibers from the hypothalamus.
Clinical Manifestations Physiology: The anterior lobe of pituitary gland secretes
Essentials of Medicine for Dental Students
Majority of patients may be asymptomatic. However, growth hormone (GH), prolactin (PRL), adrenocorticotropic
symptoms are generally due to hypercalcemia (see hormone (ACTH), thyroid stimulating hormone (TSH),
hypercalcemia). Bone resorption occurs due to excessive follicle stimulating hormone (FSH) and luteinizing hormone
PTH activity. This may lead to demineralization, pathological (LH). The secretion of these hormones is controlled by the
fractures and generalized cystic bone lesions (osteitis hypothalamus. The hypothalamus stimulates or inhibits the
secretion of anterior pituitary hormones through the release
TABLE 8.9: Types of hyperparathyroidism of substances in the portal vessels (Fig. 8.6).
Primary hyperparathyroidism Anti-diuretic hormone (ADH) and oxytocin are
Single adenoma (80%) synthesized in the hypothalamus and transported through
Hyperplasia of two or more glands the nerve axons to the posterior pituitary.
Carcinoma
Secondary hyperparathyroidism
Chronic renal failure
Hypopituitarism
Malabsorption Hypopituitarism may be caused by hypothalamic
Osteomalacia and rickets dysfunction or pituitary disease. There may be single or
Tertiary hyperparathyroidism
multiple hormonal deficiencies.
Endocrine and Metabolic Disorders
197
• Head size increases and mandible becomes more Adrenal insufficiency may result from either due to
prominent. It leads to prognathism and malocclusion. disease of adrenal glands (primary adrenal failure, Addison’s
• Tooth spacing is widened. disease) or due to adrenocorticotropic hormone (ACTH)
• The tongue is hypertrophied (macroglossia). deficiency caused by disorders of pituitary gland or
• Hands are enlarged and feet are widened. hypothalamus (secondary adrenal failure). Secondary adrenal
• There may be hypertension, cardiomegaly, and diabetes failure may also occur due to chronic glucorticoid therapy
mellitus. that suppresses ACTH secretion. In primary adrenal failure,
• The expansion of macroadenoma may lead to local there is inadequate secretion of both cortisol and aldosterone
complications including hypopituitarism. with increased level of ACTH, whereas in secondary adrenal
failure, there is deficiency of cortisol alone with decreased
Investigations
ACTH level.
• The serum GH is measured during oral glucose tolerance
test. In normal subjects, plasma GH is suppressed to Etiology
below 2 mU/L. Failure of suppression of GH level or The most common cause of Addison’s disease is auto-
paradoxical rise suggests acromegaly. immune adrenalitis. This may be associated with other
TABLE 8.11: Causes of Addison’s disease
Treatment
Diabetes Insipidus
a. DDAVP, an analogue of ADH is the drug of choice in
This disorder is characterized by increased thirst and the
central type of diabetes insipidus. This is usually given
passage of an increased amount of dilute urine. It is caused
intranasally.
by the deficiency of antidiuretic hormone (vasopressin,
b. Thiazide, amiloride and indomethacin are helpful in
ADH) or by resistance to the effects of ADH.
nephrogenic diabetes insipidus.
Diabetes insipidus can be classified into two types;
(a) central diabetes insipidus ( deficient ADH)
DIABETES MELLITUS
(b) nephrogenic diabetes insipidus where ADH secretion is
normal but renal tubules are unresponsive to ADH. Diabetes mellitus (DM) is a metabolic disorder characterized
Causes of diabetes insipidus are given in Table 8.12. by hyperglycemia due to absolute or relative deficiency of
insulin.
Clinical Manifestations
Classification
200
The patient has excessive thirst. The volume of ingested
Two broad categories of DM are type 1 and type 2. Other
fluid may reach upto 20 liters a day (polydipsia). The patients
types include gestational diabetes mellitus, and diabetes due
passes large amount of dilute urine (polyuria). If the fluid
to drugs, pancreatic diseases and genetic syndromes (Table
intake is not maintained as in an unconscious patient, the
8.13). The prevalence of DM has risen over past decades.
problems of hypernatremia and dehydration may occur.
Type 2 DM is more common.
Investigations
• The plasma osmolality is increased and the urine is dilute TABLE 8.13: Classification of diabetes mellitus
Essentials of Medicine for Dental Students
204
and management of electrolytes especially potassium and may manifest as polyneuropathy or mononeuropathy.
phosphates. The requirement for insulin is less in HHS than Neuropathy occurs in 50% cases with long standing DM.
in DKA. The presence of neuropathy is a risk factor for foot trauma,
ulceration and arthropathy. Cranial nerves may also be
Chronic Complications
involved. The most commonly affected nerves are 3rd and
Ocular Complications 6th cranial nerves. Autonomic neuropathy may manifest as
These are important causes of blindness in the diabetics in postural hypotension, resting tachycardia, nocturnal
developed countries. Diabetic retinopathy is an important diarrhea, impotency and urinary bladder dysfunctions.
Essentials of Medicine for Dental Students
ocular complication of DM. This generally develops after Hyperhidrosis or anhidrosis may occur.
10 years of the disease and almost all patients have The neuropathy may be asymptomatic. Annual
retinopathy after 20 years of the disease. Duration of the examination of lower extremities for the touch and vibration
disease and degree of the glycemic control are important sensations is recommended.
predictors of this complication. Painful neuropathy is treated with tricyclic anti-
The diabetic retinopathy has two stages non-prolife- depressant (amitriptyline) or anticonvulsants (carbamazapine,
rative (background or simple retinopathy) and proliferative gabapentin, and phenytoin). Blood glucose should be
retinopathy. Simple retinopathy is characterized by controlled strictly. Alcohol should be avoided and vitamins
microaneurysms, retinal hemorrhages, exudates and cotton (B12, B6, and folate) are replaced if deficient.
wool spots. New vessel formation occurs in proliferative
retinopathy. Macrovascular Complications\
Other ocular complications are macular edema, Various risk factors for the macrovascular disease include
premature cataract and glaucoma. insulin resistance, hyperglycemia, micro-albuminuria,
Prevention is the most desired way to control the hypertension, hyper-lipidemia, smoking, and obesity. Optimal
complications. Strict control of blood sugar and blood glycemic control, control of blood pressure to less than
Endocrine and Metabolic Disorders
130/80 mmHg (125/75 mmHg in patients with proteinuria), exercise, self monitoring of blood glucose and urinary
treatment of dyslipidemia (target LDL level <100 mg/dL, glucose and ketones. Patients should be warned about the
Triglyceride <150 mg/dL), cessation of smoking and weight symptoms and dangers of hypoglycemia. They are trained
reduction are ways to minimize the macrovascular in foot and skin care and about insulin injections.
complications.
Pharmacological Management
Management of Diabetes If glycemic control is not achieved by non-pharmacological
This includes diet modification, exercise, education and means such as diet control, and increased physical activities
medications. in 3-4 weeks, pharmocological therapy is indicated.
Ideal goals of the glycemic control in patients with DM Pharmocological therapy consists of oral glucose lowering
are as follows. However, these goals are individualized. agents and insulin.
1. Average preprandial glucose values 90-130 mg/dL
Glucose Lowering Agents
2. Bedtime glucose value of 100-140 mg/dL
3. Peak postprandial glucose less than 180 mg/dL Oral glucose lowering agents are generally indicated in type
4. The level of HbA1C less than 7% 2 DM since residual pancreatic function is required for their
The management of patients with DM includes: glucose lowering effects. Insulin is ultimately required in
a. Glycemic control advanced stage of type 2 DM. Oral glucose lowering agents
b. Treatment of associated conditions like hyper- are classified into various groups (Table 8.16).
tension, dyslipidemia, obesity and cardiovascular The treatment should be started with lower dosage and
disease increased slowly to the optimal dose in several days or
c. Detection and management of diabetes related weeks.
Some of these agents are available in extended release
complications.
Diet Modification
forms. Hence, these need to be administered less frequently.
Insulin secretogogues: These agents stimulate insulin
205
The diet is modified in such a way that it helps in maintenance secretion by pancreatic beta cells. Important side effects
of ideal body weight and provides essential nutrients. The are weight gain and hypoglycemia. Sulfonylurea should be
caloric intake is optimized. Protein and fat should provide given 30 to 60 minutes before meals. Non-sulfonylureas
15-20% and less than 30% of the total caloric intake are given with each meal to reduce meal related increase in
respectively. Saturated fat should provide less than 10 % of blood glucose. These should not be given if a patient is
the total caloric intake. Cholesterol intake is restricted to observing fast.
less than 300 mg per day. Intake of dietary fibers is Biguanides: Biguanides reduce hepatic glucose production
increased. Carbohydrate intake is individualized based on and improve glucose utilization in peripheral tissues. These
glycemic control, plasma lipids and body weight. Use of are taken with food. They also improve lipid profile and
sweeteners is acceptable. promote weight loss. Side effects are diarrhea, anorexia,
nausea and lactic acidosis. They do not result in
Exercise hypoglycemia. Metformin is contra-indicated in renal
It provides multiple benefits. It improves insulin sensitivity, insufficiency, heart failure, liver disease, severe hypoxia and
lowers plasma glucose, reduces blood pressure and lowers other conditions associated with the acidosis.
cardiovascular risk. Other benefits are weight reduction and Alpha glucosidase inhibitors: They reduce post-prandial
maintenance of muscle mass. hyperglycemia by delaying glucose absorption. These are
given with the first bite during meal. Side effects are diarrhea
Education and flatulence. These agents can also be used in type 1 DM.
The education of patients on different aspects of the disease Thiazolidinediones: Thiazolidinediones enhance insulin
is very important. They should be educated about the diet, sensitivity in muscle, adipose tissue and liver, hence reduce
TABLE 8.16: Glucose lowering agents (Anti-diabetic drugs) They mediate their actions by binding and activation of
Drugs Daily dose receptors (GLP-1R and GIP-R) located in several tissues,
ORAL including alpha and beta cells in the pancreas.
Insulin secretogogues GIP and GLP-1 stimulate glucose dependent insulin
Sulfonylureas release from beta cells. They contribute 60-70% of the total
a. First generation:
Chlorpropamide 100-500 mg, single dose post-prandial insulin response in healthy individuals (Incretin
Tolbutamide 500-2000 mg in 2-3 divided doses effect). This incretin effect is markedly decreased in diabetic
Tolazamide 100-1000, in 1 or 2 divided doses patients due to low levels of post-parandial incretin
b. Second generation:
hormones.GLP-1 also suppresses hepatic glucose output by
Glyburide 1.25-20 mg in 1 or 2 divided doses
Glipizide 2.5-40 mg in 1 or 2 divided doses inhibiting glucagon response from alpha cells in a glucose
Gliclazide 40-320 mg in 2 divided doses dependent manner.
Glimepiride 1-8 mg, single dose After secretion these are rapidly metabolized by the
Glibenclamide 2.5-10 mg in 1 or 2 divided doses
Non-sulfonylureas:
enzyme dipeptidyl peptidase (DPP-IV). The plasma half-
Repaglinide 1-16 mg in 2-4 divided doses life of these incretins is short (2-5 minutes). Following
Natiglinide 180-360 mg in 3 divided doses degradation, the metabolites are eliminated from the kidneys.
Biguanides: Agents that either have similar action as GLP-1 or
Metformin 500-2000 mg in 2-3 divided doses
Alpha glucosidase inhibitors increase GLP-1 activity are now available for use in diabetes.
Acarbose 75-300 mg in 3 divided doses Two major strategies have been developed to increase the
Miglitol 75-300 mg in 3 divided doses effects of incretins:
Thiazolidinediones
1. Incretin mimetics (GLP-1 analogues, GLP-1 receptor
Rosiglitazone 2-8 mg in 1 or 2 divided doses
Pioglitazone 15-45 mg, single dose antagonists): These are injectable agents that mimic
206
Incretins the action of GLP-1 on glucose control. Exenatide
DDP-IV inhibitors is a 39 amino acid peptide and exhibits same
Sitagliptin 100 mg OD
Vildagliptin 50 mg BD
glucoregulatory effects as the human incretin
PARENTERAL
hormone GLP-1. It is resistant to endogenous
Insulin (see Table 8.16) DDP-IV, thus have prolonged GLP-1 like action. It
Incretins improves glycemic control by reducing glucose
GLP-1 receptor agonist concentration by following mechanisms:
Exenatide 5-10 mcg BD
Amylin agonist a. Beta cell effect-enhancement of glucose
Essentials of Medicine for Dental Students
209
needed to stop bleeding in such cases. Patients may be
A. Hematuria
difficult to deal as they may be anxious and irritable. B. Raised serum creatinine
11. Deposition of subcutaneous mucopolysaccharides in C. Microalbuminuria
hypothyroidism may lead to impaired ability of small D. Overt proteinuria
vessels to contract when cut. This may result in excessive 8. All of the following hormones are secreted by anterior
bleeding. Hence, local pressure is required for longer pituitary except:
period to control bleeding. A. ACTH B. TSH
C. ADH D. FSH
12. There is also a delayed wound healing and increased
9. Bone pain, bone cysts, fracture and renal stones are found
risk of infection due to poor healing in hypothyroidism.
in:
13. Use of sedatives, opioid analgesics and tranquillizers may A. Multiple myeloma B. Hyperparathyroidism
precipitate myxedema coma in patients with C. Osteomalacia D. Marfan’s syndrome
hypothyroidism. 10. In alkalosis, following is true:
14. Well controlled hyperthyroidism and hypothyroidism do A. Normal total serum and normal ionic calcium
not pose any additional risk for dental procedures. B. Low total serum and normal ionic calcium
15. Dryness of the mouth may be present in diabetes C. Normal total serum and low ionic calcium
insipidus. D. Low total serum and low ionic calcium
11. Tetany may occur in:
16. Brown tumor of the jaw should be differentiated from
A. Alkalosis B. Hyperparathyroidism
giant cell granuloma of the jaw. C. Myxedema D. Hyperglycemia
17. Enamel hypoplasia, delayed eruption and chronic 12. Following are features of diabetes insipidus except:
mucocutaneous candidiasis may occur in idiopathic A. Polyurea
congenital hypoparathyroidism. B. Polydipsia
C. Polyphagia C. High incidence of thromboembolic complications
D. High plasma osmolality D. Presence of ketosis
13. Most common cause of thyrotoxicosis is: 23. Which of the following drug is not a insulin secretogogue:
A. Graves’ disease A. Glipizide B. Glimperide
B. Multinodular goiter C. Repaglinide D. Rosiglitazone
C. TSH secreting pituitary tumor 24. Hypoglycemia is not a complication of:
D. Toxic adenoma A. Glipizide B. Glimperide
14. Pretibial myxedema is seen in: C. Metformin D. Repaglinide
A. Hypothyroidism B. Graves’ disease 25. Drug which inhibits absorption of glucose from intestine is:
C. Hoshimoto’s disease D. All of above
A. Gliclazide B. Pioglitazone
15. Which one of the following is the early feature of
C. Acarbose D. Natiglinide
hypothyroidism:
A. Low T3 B. High TSH
Fill in the Blanks
C. Low T4 D. Low TSH
16. In hypoalbuminemia, following is true: 1. Moon face and buffalo hump are seen in _________.
A. Low total serum calcium 2. Active form of thyroid hormone is called_________.
B. Low ionized calcium 3. Trousseau’s sign is present in_________.
C. Low total serum calcium and low ionized calcium 4. Normal level of total serum calcium is_________.
D. Low total serum calcium and normal ionized calcium 5. Carpopedal spasm (main d’ accoucheur) is a feature
17. Following is seen in hypocalcemia: of_________.
A. Convulsions B. Laryngeal spasm 6. Goiter, bruit over thyroid gland, ophthalmopathy and
C. Perioral parasthesia D. All of the above dermapathy is seen in thyrotoxicosis due to
18. The common causes of hypocalcemia include all except: _________.
A. Chronic renal failure B. Hypoparathyroidism 7. Condition when the production of PTH is normal but
Infections
• Incubation period is 14-21 days.
Unilateral • Patients are infective from up to a week before to two
Parotid cyst weeks after the onset of the rash.
Parotid tumor • Skin, joint and placenta are mainly involved.
Stone in the parotid duct
Bilateral
Infectious
Clinical Features
Viral: mumps, Coxsackie, HIV, influenza, EBV The main presenting features are fever, lymphadenopathy
Bacterial: S. aureus, Streptococci, Gram-negative bacteria and rash. In many, the infection is subclinical.
Non-infectious
Sarcoidosis • The fever is mild and occurs on the first day of the rash.
Sjögren’s syndrome • There may be coryza and conjunctivitis.
Diabetes mellitus • Rash is maculopapular and nonconfluent which begins
Cirrhosis
on the face and then spreads downwards. Petechial rash
Drugs (propyl thiouracil, phenothiazines)
may appear on the soft palate (Forschheimer’s spots).
• Posterior auricular, cervical and suboccipital lympha-
Differential Diagnosis denopathy are typically present.
The most devastating effect of rubella is on the fetus if
The parotitis in mumps should be differentiated from other
infection occurs in pregnant women during first trimester
causes of parotid swelling. The Table 9.3 shows other causes
and early second trimester.
of parotid enlargement.
• Spontaneous abortion may occur.
• Congenital rubella: Classical signs of congenital rubella
Treatment
are cataract, heart disease (patent ductus arteriosus,
The patient should be isolated until the swelling subsides.
The patient needs bedrest during the febrile period. The
treatment of parotitis, meningitis and pancreatitis is purely
pulmonic stenosis), deafness and other defects such
as mental retardation, autism, microcephaly and 213
retinopathy.
symptomatic. Analgesics and cold or warm compresses are
helpful in relieving parotid pain. Complications
The role of prednisolone in the management of orchitis
Polyarthritis occurs in about 25% adult female patients.
is not fully established. However, it may reduce the
Other complications are bleeding due to thrombocytopenia
discomfort of orchitis. Interferon alpha has been shown to
and vascular damage, encephalitis and hepatitis.
be helpful in some cases of orchitis.
Investigations
Prevention
The diagnosis is made by the demonstration of virus or
The infection confers life long immunity. The primary
specific antibodies. The presence of IgM antibody or four-
prevention of mumps is done by the administration of live
fold rise in IgG antibodies in paired acute and convalescent
attenuated vaccine. MMR vaccine is given during 12-15
sera is diagnostic.
month of age (Table 9.1). The vaccine provides life long
immunity. The vaccine can also be given to susceptible adults Treatment
who have not had mumps. However, this is contraindicated
There is no specific therapy. The fever and joint pain are
in pregnant women and immunocompromised individuals.
managed symptomatically.
RUBELLA (GERMAN MEASLES)
Prevention
Rubella or German measles is a systemic viral infection
The rubella vaccine (in form of MMR) is given to children
caused by togavirus.
at 12-15 months of age (Table 9.1). A second dose is given
• The infection spreads through droplets.
at 4 years.
CHICKENPOX (VARICELLA) AND
HERPES ZOSTER (SHINGLES)
Varicella-zoster virus is a human herpes virus 3. It causes
two important clinical entities in humans chickenpox
(varicella) and herpes zoster (shingles).
Chickenpox
It is a highly contagious disease. The spread of infection is
through inhalation of infected droplets (aerosol) or through
contact with the skin lesions. Incubation period is 10-21
days.
Clinical Features
Chickenpox is generally a disease of children, although it
can also occur in adults. The disease is mild in children
and more severe in adults, pregnant women and immuno-
compromised individuals.
• The initial manifestations are fever and malaise followed
by the appearance of rash. Rashes appear first over
mucous membrane and then spread in centripetal
distribution over skin (more in the trunk, sparse in limbs).
• Intense itching leads to infection due to scratching of FIGURES 9.1A and B: (A) Pleomorphic rash over abdomen
lesions. in chickenpox (B) Rash over face
• After the primary infection, the virus remains dormant
in nervous tissue. Reactivation later in life may lead to women and immunocompromised patients. It manifests
herpes zoster, more common in elderly. as tachypnea, cough, dyspnea and fever.
d. Hepatitis can occur in small number of patients.
Complications e. Other complications include myocarditis, nephritis and
a. The most common complication of chickenpox is arthritis.
secondary infection of the skin lesions by Streptococcus f. Infection in females during first trimester of pregnancy
pyogenes or Staphylococcus arueus. can lead to congenital malformations in fetus (congenital
b. Acute cerebellar ataxia and meningitis may occur after varicella). Mortality rate in neonates is high if they
3 weeks of onset of rash. It is generally self-limiting. get infection within five days of delivery (perinatal
Encephalitis, Guillain-Barré syndrome are other rare varicella).
neurological complications. g. Reye’s syndrome (fatty liver with encephalopathy)
c. Varicella pneumonia is a serious complication of may complicate children with varicella who receive
varicella. It is more common in adults especially pregnant aspirin.
Diagnosis
Infections
Diagnosis is usually clinical from the typical appearance of
the lesions.
• The confirmation of infection is made by isolation of
varicella on tissue culture or by detection of viral DNA
by PCR.
• Serological diagnosis by the demonstration of rising
titers of antibody is also helpful.
• Multinucleated giant cells can be demonstrated by
Tzanck smear.
Treatment
1. General:
a. The patient is isolated till the complete sloughing of
crusts.
b. Personal hygiene should be maintained to prevent
skin infection. Nails should be closely cropped.
c. Antipruritic agents, tepid water baths and wet
compresses can be used to ease pruritus.
d. Aspirin should be avoided in children.
2. Antiviral Therapy: Acyclovir, 800 mg orally five times
a day for 5-7 days is given within 24 hours of onset of
rashes and is of benefit particularly in immunocom- 215
promised host and complicated varicella.
HERPES SIMPLEX
Herpes viruses are associated with various human diseases.
Eight types of herpes viruses may cause disease in humans
(Table 9.4). Primary infection with herpes virus may be
subclinical and is followed by latent stage. Each type of
virus may affect particular organ. Immunodeficiency or
FIGURE 9.3: Rashes over thoracic and lumbar roots impaired immunity later in life is associated with recurrences
or relapses due to reactivation of virus.
Source of Infection
Clinical Presentation
Primary infection may be asymptomatic or may cause
FIGURE 9.4: Multidermatomal herpes zoster in an immunocom-
Essentials of Medicine for Dental Students
Infections
Bell’s palsy: HSV-1 has also been associated with Bell’s
palsy (infranuclear VII nerve palsy). See chapter 7.
Genital herpes: HSV-1 may also cause vulvovaginitis
and cervicitis in females, balanitis in males. Bilateral lesions
of external genitalia occur. HSV may also cause rectal
infection (proctitis) and perianal infection.
• Primary genital herpes may be associated with
systemic manifestations like fever, headache,
weakness, myalgia and inguinal adenopathy.
• Lesions occur in form of painful grouped vesicles
or pustules in the genital and perianal regions that
ulcerate. Discharge (vaginal, urethteral), dysuria and
FIGURE 9.5: Herpes simplex labialis itching may occur.
• First episode of HSV-1 and HSV-2 are similar clinically,
and oral cavity (herpes labialis, Fig.9.5 ). Lesions may occur however, recurrent genital herpes is more common
on gingiva, soft palate, tongue and lips. Lesions in oral area with HSV-2 infection. HSV-2 infection increases the
are characterized by vesicles, which occur in groups. risk of acquiring HIV infection. In HIV infection
Vesicles later ulcerate and epithealize in few weeks. recurrences of HSV-2 occur more frequently.
Recurrence: After primary infection, virus remains in Eye involvement: HSV infection can cause keratitis,
latent stage in ganglion of sensory nerves. Stress, infection, keratoconjuctivitis and chorioretinitis. Keratitis presents as
217
radiotherapy, chemotherapy, sunlight, drugs and impaired acute pain, blurred vision, chemosis and dendritic ulcers of
immunity may lead to reactivation of virus and recurrences. cornea. HSV infection of eye can lead to blindness.
• Recurrences usually are associated with milder Congenital herpes: Transmission of infection occurs
disease, few lesions and heal more rapidly as during delivery or during intrauterine stage. Disseminated
compared to primary infection. and potentially fatal infection may occur in neonates
• Recurrent herpes labialis is more commonly a (congenital herpes). It is characterized by visceral and CNS
manifestation of reactivation. involvement. Maternal infection during pregnancy is
• Ulcerations on lips, oral mucosa or facial skin may associated with highest risk of transmission.
occur due to reactivation of HSV from the trigeminal Skin: HSV infection in patients with eczema may result
ganglia. in severe infection involving large areas of skin and oral
• Patient may develop oral-labial lesions few days after lesions may spread to visceral organs (eczema herpeticum).
procedures like trigeminal root decompression and Infection of the finger (herpetic whitlow) may occur as a
dental extraction. complication of HSV oral or genital infection or through
• Ulceration in oral mucosa is difficult to differentiate occupational infection. Vesicular or pustular lesion of
from aphthous ulcers, traumatic ulcers and drug- fingertip occurs with edema, redness and tenderness. Lesion
induced ulcers. may be difficult to differentiate from pyogenic bacterial
In immunosuppressed individuals, infection is more infection.
severe and extends into deeper tissues. Lesions are Nervous system: HSV infection can cause encephalitis,
characterized by severe pain, inability to eat, bleeding and the most serious complication of herpes simplex infection.
necrosis. Differential diagnosis includes bacterial infections, Recurrent benign lymphocytic meningitis (Mollaret’s
fungal infections, drug-induced ulcers and trauma. meningitis) is another CNS complication of HSV infection.
Diagnosis TABLE 9.5: Treatment of herpes simplex infection
Diagnosis is usually clinical but to differentiate from other Primary HSV
vesicular eruptions laboratory tests may be needed. • Acyclovir 200 mg five times daily for 7-14 days
a. Multinucleated giant cells or intranuclear inclusion • Valacyclovir 1 g twice daily for 7-14 days
• Famciclovir 250 mg three times daily for 7-14 days
bodies can be demonstrated in scrapings from the lesion • Acyclovir IV 5 mg/kg 8 h for 5 days in Severe
and staining with Giemsa’s stain (Tzanck preparation) primary infection
or Papnicolaou’s stain. These findings may be present Recurrent HSV
in other viral infection like VZV infection. Oro-labial
• Famciclovir 1500 mg single dose or 750 mg b.d. for
b. Confirmation of HSV can be done by detection of HSV
1 day
DNA by PCR, culture from vesicular fluid and direct • Valacyclovir 2 g single dose or 2 g b.d. for 1 day
fluorescent antibody staining of scraped lesions. Genital
c. Serology is useful in primary infections. • Acyclovir 800 mg tid for 2 days or 200 mg five
d. CSF-PCR is useful in HSV encephalitis. times for 5 days
• Valacyclovir 500 mg b.d. for 3 days
• Famciclovir 1500 mg single dose or 750 mg bid for
Treatment 1 day or 125 mg b.d. for 5 days
In immunocompetent persons, therapy is usually not required Disease suppression
but if initiated early it may ameliorate or shorten the duration • Acyclovir 400 mg b.d.
• Valacyclovir 500 mg –1 g daily
of symptoms. Antiviral treatment is effective if started in
• Famciclovir 250 mg b.d. or 500 mg once daily
initial stages (first 48 hours). Severe manifestations require
antiviral therapy irrespective of time of presentation. characterized by fever, lymphadenopathy, pharyngeal
Serious manifestations (CNS infections, visceral HSV inflammation, and atypical lymphocytes on peripheral blood
(idoxuridine, vidarabine and cidofovir). secretions of patients or asymptomatic carriers. About 90%
of asymptomatic seropositive persons have virus in their
Prevention saliva. It is also transmitted through blood transfusion and
• Use of barrier contraception during sexual activity bone marrow transplantation. The incubation period is 4-6
(condoms) decreases the rate of transmission of HSV weeks.
infection.
• Valacyclovir 500 mg once daily reduces chances of Pathogenesis
transmission of infection between sexual partners. The virus infects epithelial cells of the oral cavity and
• Isolation and use of gloves, gowns and handwashing salivary glands and is shed in salivary secretions.
decrease spread of infection from patients with Lymphocytes in tonsils may be infected directly or B
mucocutaneous, genital and disseminated infection to lymphocytes may get infected after contact with epithelial
hospital staff and other patients cells. The virus then spreads through blood stream.
Lymphoid tissue is enlarged because of proliferation and
INFECTIOUS MONONUCLEOSIS expansion of B cells and reactive T cells. Activated B cells
Infectious mononucleosis is mostly caused by Epstein- produce antibodies against EBV antigens and host cells.CD4
Barr virus (EBV), a human herpes virus (HHV-4) and is + T cells decrease in number and CD8+ T cells increase
TABLE 9.6: Complications of Infectious mononucleosis
Infections
leading to inverse CD4+/CD8+ cells ratio. B cells form the
reservoir for EBV in the body. Central nervous system complications
• Meningitis
Clinical Features • Encephalitis
• Cranial nerve palsies
Infection may occur at any age. • Acute transverse myelitis
a. In developing countries infection occurs most commonly • Polyneuritis
in early childhood. Infection is usually subclinical and Airway obstruction
Splenic rupture
most patients are asymptomatic. By adulthood majority Bacterial superinfection
of population has antibodies against EBV. Hematological complications
b. In developed countries infection occurs during • Autoimmune hemolytic anemia
• Granulocytopenia
adolescence and young adults (10-36 years). In this • Thrombocytopenia
situation many patients have typical infectious mono- • Red cell aplasia
nucleosis (IM). • Pancytopenia
Rare complications
• It presents with nonspecific symptoms like fever, • Hepatitis
myalgia, weakness and malaise. • Myocarditis
• Pharyngitis with or without tonsillitis is usually • Pericardtis
• Interstitial nephritis
present. • Interstitial pneumonia
• Lymphadenopathy, mainly posterior cervical group
of lymph nodes are involved but generalized peripheral lymphocytes must be atypical. Granu-
lymphadenopathy may also be seen. Lymph nodes locytopenia, thrombocytopenia may be seen.
are tender, mobile and discrete. b. Serum levels of aminotransferases and alkaline
• Splenomegaly may be seen in second or third week
of illness. Maculopapular rash is present in 5-15%
phosphatase are usually elevated. Bilirubin levels may
be raised in some cases. 219
of cases. If ampicillin is given, most patients (>90%) c. Presence of heterophile antibodies in serum is an
will develop rash. important test for the diagnosis. Tests for heterophile
antibodies are positive in about 40% of patients in first
Complications week of illness but they become positive in almost 90%
Most cases are self-limiting but complications may be seen of cases during the third week. Heterophile antibodies
in some patients (Table 9.6). when adsorbed in guinea pig kidney, agglutinate
• Complications may be due to CNS involvement erythrocytes of other species e.g. sheep, horse or cow.
(meningitis, encephalitis, cranial nerve palsies mostly Paul-Bunnell test or slide test (Monospot test) is used to
VII nerve, transverse myelitis and polyneuritis). demonstrate presence of heterophile antibodies.
• Upper airway obstruction occurs because of enlargement d. Elevation in other antibodies directed at various EBV
of lymphoid tissue in tonsils and adenoids and is an antigens may also be useful in diagnosis patients who
indication for hospitalization. don’t have heterophile antibodies and patients with
• Coombs positive hemolytic anemia may occur because atypical presentation. These include
of formation of antibodies against the red cell antigen. • IgM and IgG antibodies against viral caspid antigen
Granulocytopenia and thrombocytopenia may also occur. (anti-VCA)
• Antibodies to early antigen (anti-EA-D and anti-
Laboratory Findings EA-R)
a. After a week of illness, WBC count is elevated with • Antibodies to EBV nuclear antigen (anti-EBNA)
lymphocytosis and atypical lymphocytes. Atypical e. Detection of EBV DNA by polymerase chain reaction
lymphocytes are larger than normal lymphocytes with is useful in demonstrating virus in EBV-associated
plenty of cytoplasm, vacuoles and dark chromatin with malignancies and for diagnosis in immunocompromised
indented cell membrane. For diagnosis at least 20% of individuals when serology is not helpful.
Differential Diagnosis d. It is associated with Burkitt’s lymphoma (90% of cases
Most of the cases of IM are due to EBV. Few percentages in Africa and about 15% of cases in USA). EBV-DNA
of cases may be caused by cytomegalovirus (CMV). IM can be detected from tumor tissue and these patients
caused by CMV is less severe and heterophile antibody test have high titre of antibodies to EBV.
is negative. Other less common causes of IM are acute e. Nasopharyngeal carcinoma is also associated with EBV
Toxoplasmosis, acute HIV infection, HHV-6, hepatitis virus infection. EBV-DNA levels in plasma correlates with
and hypersensitivity drug reactions. Exudative pharyngitis poor prognosis and EBV-DNA levels in such patients
and heterophile antibodies are not seen in other causes are used to monitor patients.
of IM. f. EBV infection is also associated with Hodgkin’s
lymphoma (especially mixed cellularity type). Viral
Treatment antigen and EBV-DNA can be demonstrated in Reed-
Treatment is usually symptomatic as majority of patients Sternberg cells in such patients and patients have high
will recover. levels of antibodies to EBV.
• Rest and avoidance of excessive exertion are helpful.
DIPHTHERIA
• Acetominophen and other nonsteroidal anti-
inflammatory drugs (NSAIDS) are used for symptomatic Diphtheria although eradicated from most of the developed
relief. Warm saline gargles and throat irrigation also world still occurs in developing countries.
provides relief. • This is caused by aerobic gram-positive bacteria
• Acyclovir therapy is not effective and is not recommended. Corynebacterium diphtheriae.
• Glucocorticoids (prednisolone) are used in airway • The infection occurs mostly in the upper respiratory tract
obstruction, autoimmune hemolytic anemia, and severe via droplets which spread from the cases or carriers.
• Patients should avoid sports activities for few weeks until Clinical Manifestations
splenomegaly has resolved because of the danger of
The presentations may be predominantly nasal, laryngeal,
splenic rupture.
pharyngeal or cutaneous.
• The pharyngeal form is the most common one. The initial
Other EBV-Associated Diseases
presentations are usually mild fever, sore throat and
a. EBV-associated lymphoproliferative disease may occur membrane formation over tonsils. The membrane is
in immunodeficient patients including AIDS patients, grayish, firm and adherent, surrounded by a zone of
post-transplant patients and patients with severe inflammation. The membrane often extends beyond the
combined immunodeficiency. In such patients it may margin of tonsils unlike the exudates in staphylococcal
cause B cell hyperplasia or B cell lymphoma. pharyngitis. Swelling of neck may occur along with
b. Duncan’s disease is a X-linked recessive lympho- tender lymphadenopathy (bull-neck).
proliferative syndrome seen in young boys who develop • Husky voice, high-pitched cough and respiratory
fatal lymphoproliferative syndrome after EBV infection. obstruction may occur due to laryngeal involvement.
c. Oral hairy leukoplakia is seen in HIV infection and is • Patients may have epistaxis and nasal obstruction.
characterized by raised, corrugated lesions on tongue; • Death may occur due to acute circulatory failure
EBV-DNA can be detected from these lesions. (Table 9.7).
TABLE 9.7: Clinical manifestations of diphtheria TABLE 9.8: Dose of diphtheria antitoxin
Infections
Mild fever, sore throat Mild cases 4000-8000 units IM
Tachycardia Moderate cases 16000-40000 units IM
“Pseudomembrane” over tonsils, larynx, nasal cavity Severe cases up to 100000 units IV
Hoarseness of voice
Respiratory obstruction
Acute circulatory failure • An urgent tracheostomy may be needed in case of
Complications respiratory obstruction.
Myocarditis • Following recovery, the patient should be immunized
Palatal and laryngeal paralysis
Peripheral neuropathy
with diphtheria toxoid.
• The patient is isolated till three daily consecutive cultures
Complications are negative for the organism.
222
abdominal pain and tenderness, dark or fresh blood in stool indicated in severe cases (altered sensorium or shock)
and leukocytosis suggest these complications. Other as a single dose of 3 mg/kg followed by 8 doses of 1 mg/kg
complications are shown in Table 9.9. every 6 hourly.
Carriers are treated with oral antibiotics (amoxycillin,
Investigations ciprofloxacin, TMP-SMX) for 6 weeks.
a. Blood culture is positive for S. typhi or S. paratyphi. The
yield is higher in first week of illness (90% in untreated Prevention
Essentials of Medicine for Dental Students
cases) but decreases to 50% by third week. • Immunization is indicated in close household contacts,
• Culture of bone marrow may be positive when blood travelers to endemic area and during epidemics. Multiple
cultures are negative. dose oral vaccines or single dose parenteral vaccines
• Stool, urine, rose spots and gastrointestinal secretions are available. These provide protection for 5 and 3 years
can also reveal positive culture. Stool culture is respectively.
positive during the third week of infection. • Other preventive measures are proper waste
TABLE 9.9: Complications of enteric fever disposal and protection of food and water from
contamination.
Intestinal perforation • Carriers should not work as food handlers.
Intestinal hemorrhage
Others
Osteomyelitis TABLE 9.10: Usual antibiotics for enteric fever
Arthritis
Cholecystitis Drug Dose Duration
Meningitis Ciprofloxacin 500-750 mg twice daily 10-14 days
Myocarditis Ofloxacin 300-400 mg twice daily 10-14 days
Nephritis Levofloxacin 500 mg daily 10-14 days
Parotitis Ceftriaxone 1-2 g IV or IM daily 10-14 days
Psychosis Azithromycin 1 g once daily 5 days
Differential Diagnosis
Infections
GONORRHEA
Gonorrhea is caused by Neisseria gonorrhoeae, a gram- Gonorrhea should be differentiated from non-gonococcal
negative diplococcus. It is transmitted through sexual activity urethritis or vaginitis due to Chlamydia trachomatis,
(vaginal, oral, anal sex). Sexually active young population trichomoniasis, candidiasis, bacterial vaginosis.
is the most commonly affected one. The incubation period
is 2-10 days. Investigations
• Smear examination of the discharge may show gram-
Clinical Features negative diplococci in polymorphonuclear leukocytes.
Infection may be asymptomatic, or they may present as the • Diagnosis is confirmed by culture.
following: • Ligase chain reaction (LCR) assay may detect both N.
a. In males, urethra is most commonly involved. Dysuria gonorrhoeae and Chlamydia trachomatis in urethral or
and purulent urethral discharge are initial symptoms. It cervical swab and urine.
may progress to involve the prostrate, epididymis and
periurethral glands. Chronic infection may lead to Treatment
urethral stricture and prostatitis. In homosexual men, a. Antimicrobial is started as soon as possible. A single
rectal infection may occur which is either asymptomatic dose is curative in uncomplicated infection (Table 9.11).
or presents with discharge, discomfort or rectal bleeding. Cefixime and ceftriaxone are first line agents because
b. In females, the infection may be asymptomatic in 50% of fluoroquinolones resistance. In patients with
cases. Urethral infection may present as dysuria, sensitivity to beta lactams, spectinomycin should be
discharge or increased frequency. Vaginitis or cervicitis used. Doxycycline (100 mg twice daily for 7 days) or
may occur and present as vaginal discharge. Infection azithromycin (1 g orally) is generally added to cover
of Bartholin’s glands and periurethral glands is also
common. Rectum may be involved due to anal sex or
other coinfections like Chlamydia.
b. Complicated infection requires prolonged therapy.
223
spread from urogenital infection. Uterus and fallopian PID is treated with antimicrobials effective against
tubes may be involved resulting into salpingitis. Chronic gonococci, chlamydia and anaerobes. Complicated
salpingitis may lead to scarring of fallopian tubes gonorrhea (salpingitis, prostatitis, arthritis, bacteremia)
and sterility. Pelvic inflammatory disease (PID) refers is treated by any of the following:
to mixed infection with gonococci, chlamydia and • Penicillin G (10 million units intravenously daily for
anaerobes. It may present as lower abdominal pain, 5 days)
discharge, pain during coitus and vaginal bleeding. • Ceftriaxone (1 g intravenously daily for 5 days)
c. Pharyngeal gonorrhea may be asymptomatic or present • Fluoroquinolones (ciprofloxacin 500 mg twice daily
as sore throat and occurs due to oral sex. orally for 5 days or levofloxacin 500 mg daily for 5
d. Eye involvement occurs in the form of conjunctivitis days).
due to direct inoculation of gonococci. The purulent c. All sexual partners and patient should be treated and
conjunctivitis and edema of eyelids are found in neonates tested for syphilis and human immunodeficiency virus
(ophthalmia neonatorum). It may lead to panophthalmitis. (HIV).
Urgent treatment is required to prevent corneal damage
and loss of vision. TABLE 9.11: Treatment of uncomplicated gonorrhea
e. Dissemination of gonococci through bloodstream from
Cefixime 400 mg Orally
primary site may cause bacteremia and systemic Ceftriaxone 125 mg Intramuscularly
infection. Intermittent fever, arthritis, tenosynovitis and Ciprofloxacin 500 mg Orally
skin involvement are common. Rash may be Ofloxacin 400 mg Orally
Levofloxacin 250 mg Orally
maculopapular or hemorrhagic. Endocarditis and Spectinomycin 2g Intramuscularly
meningitis are rare presentations.
Prevention The differential diagnosis of primary chancre is
The preventive methods include education, and adoption chanchroid (painful nonindurated ulcer), lymphogranuloma
of mechanical measures like condoms. Sexual partners of venereum, genital herpes and neoplasm.
the patient should be treated. The patient is advised to abstain Secondary Syphilis
from sex until therapy is completed. Effective drugs in
Secondary stage occurs 6-8 weeks after the development of
therapeutic dosage if taken within 24 hours of exposure may
chancre. The manifestations are due to the dissemination of
abort an infection.
Treponema pallidum to distant sites. Main features are fever,
SYPHILIS rash and lymphadenopathy.
• Rashes are non-pruritic and symmetrical. The palm and
Syphilis is sexually transmitted chronic systemic infection
soles are generally involved. Rashes may be in the
caused by Treponema pallidum. It is transmitted during
form of macular, papular, pustular or follicular or a
sexual contact through abrasions in skin or mucous
combination of these but not vesicular.
membranes. It can be transferred from mother to fetus via
• Mucosal patches and ulcers may occur in the oral cavity,
placenta (congenital syphilis).
and genitalia. These are highly infectious. In the oral
Transmission may also occur by blood transfusion,
cavity the lips, oral mucosa, tongue, palate and pharynx
kissing and percutaneous injury.
may be involved. Differential diagnosis of oral ulcers in
secondary syphilis is given in Table 9.12.
Clinical Manifestations
• “Weeping” papules over warm and moist areas like vulva
The clinical features of syphilis are broadly classified as and perianal region are called candyloma lata.
early and late syphilis. • Lymphadenopathy is generalized, non-tender, discrete
a. Early syphilis includes primary syphilis, secondary and rubbery.
224 syphilis and latent syphilis.
b. Late syphilis includes ‘Late’ latent syphilis and tertiary
• Other features are meningitis, cranial nerve palsies,
uveitis, hepatitis, gastritis, periosteitis, glomerulonephritis.
syphilis (benign tertiary syphilis, cardiovascular and alopecia (moth-eaten appearance) may also occur.
neurosyphilis).
Latent Syphilis
Early Syphilis Latent syphilis is characterized by positive serological tests
for syphilis, absence of clinical manifestations and normal
Essentials of Medicine for Dental Students
Primary Syphilis
CSF.
Primary syphilis is the first stage in the natural history of a. The latent phase during first year of infection is known
the disease. as early latent syphilis when the patient is sexually
• The incubation period is 10-90 days (average 2-4 weeks). infectious.
• Typical lesion is a chancre, which develops at the site of b. Late latent syphilis begins after 1 year of infection in
the inoculation, usually located on the penis in untreated patients. This stage is sexually non-infectious.
heterosexual males. It begins as a painless papule that
TABLE 9.12: Differential diagnosis of oral lesions
ulcerates and becomes indurated. in secondary syphilis
• The inguinal lymph nodes are enlarged, rubbery, discrete
Aphthous ulcers
and non-tender. It heals without treatment in 2-6 weeks; Ulcerative stomatitis
a scar may form, particularly if secondary bacterial Herpes simplex
infection has occurred. Infectious mononucleosis
Primary HIV infection
• In homosexual male, lesion can occur in rectum or anal Agranulocytosis
canal. In female patients, cervix and labia are common Stevens-Johnson syndrome
primary sites. Atypical primary sites of chancre include Behcet syndrome
Reiter’s syndrome
tongue, tonsils, nipple and fingertips.
Infections
However, transmission of infection through blood or maternal syphilis can lead to still birth, premature birth and
placenta may occur in both early and late latent syphilis. neonatal death. A child may be born with syphilitic features,
Latent syphilis may persist throughout life or could end in same as in secondary syphilis, or may develop manifestations
the development of late syphilis (tertiary syphilis) in 30 to during first few weeks of life.
40% cases. • The features of early syphilis are rhinitis (snuffles),
maculopapular rash, condyloma lata, mucous patches,
Tertiary Syphilis periosteitis, lymphadenopathy, hepatosplenomegly,
Benign Tertiary Syphilis anemia and thrombocytopenia. This stage is infectious.
• Some children remain in latent phase and develop
Benign Tertiary Syphilis may develop between 3-10 years
features of congenital syphilis or residual stigmata after
of infection and can involve skin, mucous membrane, bone,
2 years. Late congenital syphilis presents as benign
muscle or viscera. Chronic granulomatous lesion (gumma)
tertiary syphilis, interstitial keratitis, deafness, neuro-
is the characteristic feature. Gumma can be single or multiple
syphilis, and Clutton’s joint (bilateral knee effusion).
and most commonly involved sites are the skin, bone,
• Stigmata include Hutchinson’s teeth, mulberry molars,
mouth, upper respiratory tract, liver and the stomach. Upper
frontal bossing, saddle nose, maxillary hypoplasia, high
respiratory gumma can lead to perforation of the palate or
arched palate, rhagades and saber tibia.
nasal septum. Gummatous tongue may heal to develop
a. Hutchinson’s teeth are widely spaced peg-shaped
leukoplakia which is premalignant.
notched upper central incisors.
Other causes of granulomatous lesions such as
b. Mulberry molars are sixth year molars with poorly
tuberculosis, sarcoidosis, leprosy and fungal infection must
developed cusps.
be considered in the differential diagnosis of gumma.
c. Rhagades are linear scars at angle of the mouth, nose
225
Cardiovascular Syphilis and anus following secondary bacterial infection of
the rashes.
Cardiovascular Syphilis may present after many years of
infection. Aorta, coronary ostia and aortic valve may be
Investigations
affected leading to aortic aneurysm, angina and aortic
regurgitation. T. pallidum cannot be cultured in vitro hence diagnosis
depends on (a) Microscopic examination, (b) serological
Neurosyphilis tests and (c) other tests.
Neurosyphilis takes years to develop. Neurosyphilis may be a. Dark-field microscopic examination may show motile
asymptomatic or symptomatic. spirochaetes from lesions in infectious syphilis. Fluid
• Asymptomatic neurosyphilis is characterized by CSF from chancre or moist cutaneous lesions in secondary
abnormalities in the absence of clinical signs. syphilis or congenital syphilis is used for this purpose.
• Symptomatic neurosyphilis may present as: Organism is not found in late syphilis.
a. Meningovascular syphilis The direct fluorescent antibody T. pallidum test
b. General paresis of insane (DFA-TP) is also used to detect the pallidum in fixed
c. Tabes dorsalis smears prepared from lesions. PCR test is also used in
Some important clinical features are Argyll Robertson some centers.
pupils and Charcoat’s joints. Argyll Robertson pupil is small b. Serological tests: Tests used in the diagnosis of syphilis
irregular pupil which reacts to accommodation but not to are given in Table 9.13.
light. Non-treponemal tests measure the ability of serum
to flocculate cardiolipin-lecithin-cholesterol antigen
Congenital Syphilis complex. These tests are used for primary screening and
Transmission of infection from untreated mother to fetus are positive 4 weeks after the primary infection,
transplacentally can lead to congenital syphilis. Untreated secondary syphilis and at birth in congenital syphilis.
TABLE 9.13: Serological tests for syphilis b. Treatment of late syphilis (late latent, cardiovascular,
Non-treponemal tests benign tertiary): Lumbar puncture is done to examine
Venereal diseases research laboratory test (VDRL) CSF. If CSF is abnormal, patient is treated for
Rapid plasma reagin test (RPR) Neurosyphilis.
Treponemal antibody tests (specific)
• Patients with normal CSF are treated with benzathine
Fluorescent treponemal antibody-absorbed test (FTA-ABS)
T. pallidum hemagglutination test (TPHA) penicillin weekly for 3 weeks. Alternatively, doxycy-
Agglutination assays for antibodies to T. pallidum. line or tetracycline is given for 4 weeks.
• Neurosyphilis (asymptomatic or symptomatic) is
treated with aqueous penicillin G for 10-14 days.
False positive reactions may occur in other diseases and Probenecid is added if procaine penicillin G is given.
diagnosis must be confirmed by specific treponemal c. The only drug indicated in neurosyphilis, pregnancy with
antibody test. The titer correlates with disease activity syphilis and HIV coinfected with syphilis is aqueous
and can be used to monitor the response to therapy. penicillin G. Patients allergic to penicillin are treated
Specific tests are used to confirm the diagnosis as after desensitization.
these are negative in non-treponemal infections. These d. Jarisch Herxheimer reaction: This is a mild acute febrile
are positive in primary and secondary syphilis. reaction which occurs following initiation of treatment.
c. Other tests: CSF examination is required in late syphilis The features are fever, chills, myalgia, headache,
such as in benign tertiary syphilis, cardiovascular syphilis tachycardia and hypotension. The reaction occurs due
and neurosyphilis. It should also be examined in to release of toxic products after massive destruction of
seropositive patients with neurological signs. Biopsy spirochaetes. Treatment is symptomatic. The symptoms
may be required to diagnose gumma. Chest X-ray, ECG generally resolve within 24 hours.
and echocardiography are done to detect cardiovascular
226 syphilis. Prevention
Use of condom is helpful in prevention. Following exposure
Treatment
to infectious syphilis, azithromycin 1 gm single dose or
Penicillin G is the drug of choice in all stages of syphilis. procaine penicillin G 2.4 million units IM may be used to
Alternatively tetracycline, doxycycline, cephalosporin, and prevent infection.
azithromycin can be used in penicillin allergic patients
(Table 9.14).
Essentials of Medicine for Dental Students
AMOEBIASIS
a. Treatment of early syphilis (primary, secondary and
Amoebiasis is an infection caused by the intestinal protozoan
early latent) Single dose of benzathine penicillin G is
Entamoeba histolytica. The infection is spread by cysts
the drug of choice. Alternatively, two weeks course of
which are present in water and uncooked food contaminated
tetracycline or doxycycline can be given in penicillin
by human feces. About 90% of infections are asymptomatic.
sensitive patients. Ceftriaxone (for 8-10 days) or
azithromycin (single dose) are also effective. Pathogenesis
• The trophozoites are released from cysts in the intestine
TABLE 9.14: Drugs used in syphilis
and invade the mucous membrane of the large bowel,
Benzathine penicillin G 2.4 million units IM, single dose chiefly the cecum. They can produce flask-shaped ulcers
Aquous penicillin G 18-24 million unit daily IV, divided doses surrounded by healthy mucosa. These ulcers can bleed
Procaine penicillin G 2.4 million unit daily IM, divided doses
Probenecid 500 mg q.i.d. Oral
or lead to perforation.
Doxycycline 100 mg b.d. Oral • Rarely, intestinal infection may lead to formation of mass
Tetracycline 500 mg q.i.d. Oral lesion (amoeboma).
Azithromycin 2g Oral single dose • The trophozoites may reach the liver through the portal
Ceftriaxone 1 g daily IM/IV
vein and cause parenchymal destruction leading to the
Infections
formation of amoebic liver abscess. The abscess is 5. Aspiration of abscess: The aspitated fluid is pink to
usually found in right lobe of the liver. chocolate brown color (anchovy sauce) and may contain
• Other extraintestinal sites such as genitourinary tract, free amoebae.
skin and cerebrum may become involved rarely. 6. Immunofluorescence techniques show the presence of
antibodies in the serum of about 95% patients with
Clinical Manifestations amoebic liver abscess and 60% with amoebic dysentery.
• In endemic areas, around one-third of the population is 7. Blood tests reveal mild leukocytosis, normal liver
asymptomatic passers of amoebic cysts. transaminases and raised alkaline phosphatase.
• The usual symptom is frequent loose stools containing
mucus with or without blood. The stool has an offensive Management
odor. This is known as amoebic dysentery. There may • The drug of choice is metronidazole in dosage of 750-
also be mild abdominal pain. 800 mg 8 hourly for 5-10 days. The common side effects
• On palpation, the colon particularly cecum is tender. of metronidazole are metallic taste and disulfiram like
Cecal involvement may mimic acute appendicitis. reaction. Longer acting nitroimidazoles (tinidazole,
• The acute diarrheal presentation with blood in stool
mimics bacillary dysentery or ulcerative colitis.
• The presentation may be severe in elderly and in
immunocompromised individuals.
•
right upper abdomen and right shoulder.
The liver is enlarged and tender. Jaundice is rare. 227
• The large abscess may rupture through the diaphragm
into the lung. The contents of the abscess thus may be
coughed out. Occasionally the abscess may rupture into
the pleural cavity, peritoneal cavity or pericardial sac.
• The diagnosis is suspected on clinical grounds and FIGURE 9.6: Ultrasound showing solitary abscess
confirmed by ultrasonography. (Amoebic liver abscess)
Investigations
1. Fresh stool examination reveals the presence of
trophozoites or amoebic cysts. Trophozoites are
diagnostic of acute dysentery. The stool is positive for
heme (occult blood).
2. Sigmoidoscopy may reveal typical flask-shaped ulcers.
Biopsy of the margin of the ulcer may show the presence
of trophozoites.
3. X-ray chest may reveal raised diaphragm in cases of
liver abscess.
4. Ultrasonography confirms the diagnosis of liver abscess
(Figs 9.6 and 9.7). Amoebic liver abscess is generally
solitary. Presence of multiple abscesses indicates FIGURE 9.7: Ultrasound showing multiple abscesses
pyogenic liver abscess. (pyogenic liver abscess)
ornidazole) are equally effective. Tinidazole is given as Transmission of Malaria
daily single dose of 2 g for 3 days. This is followed by Malaria is transmitted from human to human through bite
administration of diloxanide furoate 500 mg 8 hrly for of infected female Anopheles mosquitoes. There is no animal
10 days to eliminate luminal parasites. Chloroquine and reservoir for human malaria. Other rare routes of transmis-
emetine used previously should preferably be avoided sion are transplacental and through blood transfusion.
because of their significant side effects.
• Asymptomatic cyst passers or carriers can be given Life Cycle
luminal agents like diloxanide furoate (500 mg 8 hourly The mosquito is infected with the sexual form of parasite
for 10 days) or iodoquinol (650 mg 8 hourly for 20 days). (gametocyte) when it feeds on human blood. These
• The amoebic liver abscess is treated with medications gametocytes develop into sporozoites in the salivary gland
as mentioned above. The aspiration of the amoebic liver of the mosquito within 7-20 days.
abscess is indicated if it is large and threatens to burst or When the infected mosquito bites an uninfected human,
does not respond promptly (within 72 hr) to drug therapy. inoculated sporozoites travel to the liver within half an hour.
Aspiration may also be needed to differentiate it from In the hepatic cells, the sporozoites transform into merozoites
pyogenic liver abscess especially in case of multiple (exoerythrocytic stage). However, in cases of P. vivax and
abscesses. P. ovale infections, some sporozoites remain in dormant
form in liver (hypnozoites) for a period of upto a year or
MALARIA
more. Hypnozoites can reactivate later and cause delayed
Malaria is a parasitic infection caused by Plasmodium vivax, primary infection or relapses. Relapse can also occur if
P. falciparum, P. ovale and P. malariae. Globally around treatment is not given to eradicate hypnozoites.
1.5-3 million people die each year due to malaria, mostly Merozoites leave the liver and infect erythrocytes. In
230
infection. Primaquine is added in the case of P. vivax nausea, diarrhea, methemoglobinemia
and P. ovale infection to destroy the hypnozoites and to Artesunate Oral : 4 mg/kg followed by 2 mg/kg per day for 4
days
prevent relapse. Parenteral: 2.4 mg/kg IV followed by 1.2 mg/kg at 12
• In severe attacks, parenteral therapy with quinine is and 24 hours then once daily
started and switched to oral as soon as possible. Side effects: Anaphylaxis, urticaria, fever, lowers
reticulocyte count
Primaquine is added in case of P. vivax and P. ovale
Artemether Oral dose same as artesunate
infections. Parenteral artesunate, artemether or Parenteral: 3.2 mg/kg IM followed by 1.6 mg/kg daily
Essentials of Medicine for Dental Students
chloroquine are other alternatives and can be used in Side effects same as artesunate
place of quinine.
231
Mode of Transmission
lentivirus family (Fig. 9.9). It is a RNA virus. HIV 1 is
• The most common mode of transmission of HIV in India subdivided into three groups, M (major), O (outlier) and N.
as well as worldwide is heterosexual contact. In India, The most common group is M, which is further classified
around 85-90% patients have received infection through into nine subtypes or clades, lettered A, B, C, D, F, G, H, J,
unsafe sex with commercial sex workers (CSW), mostly and K. Subtype C is prevalent in India whereas subtype B
in metropolitan cities. In Mumbai, about half of the CSW is common in North America and Europe.
are HIV positive.
• Other modes of transmission are through contaminated Pathogenesis
blood or blood products, contaminated syringes (as in HIV infects CD4 positive immune cells chiefly T helper
IV drug abusers) and from infected mother to fetus/ lymphocytes, but other cells like B lymphocytes, monocytes,
newborn baby (Table 9.17). dendritic cells and microglial cells are also infected. A
• The transmission of HIV from mother to child occurs glycoprotein gp 120 present on the surface membrane of
mostly during labour although it can happen during any the virus has high affinity with the CD4 molecule present
time in pregnancy or after birth, through breastfeed. on the surface of immune cells. Certain coreceptors such
• Stool, saliva, sweat, urine have not shown to transmit as CXCR4 (on lymphocytes) and CCR5 (on monocytes)
infection although viral particles have been demonstrated are also needed for the binding of the virus over cell
in these fluids. surface. Following binding with the lymphocytes, HIV
TABLE 9.17: Modes of transmission of HIV enters the cell (Fig. 9.10). Its genomic RNA is released in
the cytoplasm and converted into viral DNA by a unique
1. Sexual route (heterosexual, homosexual)
2. Parenteral route enzyme reverse transcriptase. Viral DNA is integrated into
a. blood and blood products the host cell DNA and captures the genetic machinery of
b. injection drug users the host cell. This leads to the rapid production of viral genome
c. occupational injury
3. Mother to child transmission
which attains the shape of full virus with the help of protease
enzymes.
Asymptomatic Stage
Following resolution of the acute HIV syndrome, infected
individuals remain asymptomatic (clinical latency) for 2-8
years, although HIV continues to multiply and damage the
immune system of the patient. There is a progressive decline
in the CD4 count.
Diagnosis
• The diagnosis of HIV infection is generally based on
the detection of antibodies against viral proteins in the
serum of the patients. The tests are ELISA and western FIGURE 9.13: Molluscum contagiosum
blot. The former is more sensitive and is used for the
screening whereas the later is more specific and is needed • ELISA test may be negative during the first 3-6 weeks
to confirm the diagnosis if the ELISA test is inconclusive. of infection when detectable amount of antibodies may
• According to NACO guidelines, two different ELISA not have formed. During this ‘window period’ tests based
in symptomatic and three different ELISA in asym- on detection of antigens (p24) or viral RNA through RT-
ptomatic are required to be positive for the diagnosis of PCR (reverse transcriptase-polymerase chain reaction)
HIV infection.
•
are recommended.
The CD4 count, measured by flow cytometry tells about 233
the current immune status of the patient and guides us
to start prophylactic therapy and anti-retroviral treatment.
Viral RNA load suggests the prognosis of the patient.
• Patients are investigated for the evidence of co-infection
with hepatitis B, and hepatitis C and positivity for
syphilis (VDRL test).
• Investigations are also performed, if need be, to detect
the presence of opportunistic infections.
• Besides these, complete blood count, liver function tests,
blood urea, serum amylase, blood sugar and lipid profile
are done as the baseline before initiation of anti-retroviral
therapy.
234
improved survival of HIV patients. The control of OI initiated if patient has CD4 count between 250-350
also retards the progression of HIV. Some infections are and WHO clinical stage II or III. (see NACO
to be treated lifelong. website).
The co-infection of tuberculosis with HIV poses
special problem in India and other developing countries. Limitations of ART
The presence of tuberculosis adversely affects the • ART is not curative. Only 70-80% patients respond to
prognosis of HIV infection and the presence of HIV ART.
Essentials of Medicine for Dental Students
infection in tuberculosis leads to problem in the diagnosis • The treatment needs to be given life long.
as the manifestations are more commonly atypical. HIV • There is also the problem of drug resistance.
positive patients are 15 times more prone to have • The anti-retroviral drugs are not free from toxic effects.
reactivation of tuberculosis than their HIV negative These can lead to significant complications like
counterparts. gastrointestinal intolerance, bone marrow failure,
pancreatitis, lipodystrophy (Fig. 9.14), myopathy,
TABLE 9.19: Primary prophylaxis of opportunistic infections neuropathy and increased cardiovascular mortality.
Infections Indications Medications Anemia is a common side effect of zidovudine (AZT)
Pneumocystis carinii CD4 count Cotrimoxazole, while neuropathy may occur with stavudine therapy.
<200/mm3 dapsone, pentamidine
Toxoplasmosis CD4 count Co-trimoxazole, Anti-retroviral Drugs and Regimens
<100/mm3 pyrimethamine plus
dapsone More than 20 drugs are approved for therapy. Most drugs
Cytomegalovirus CD4 count Gancyclovir are directed against viral enzymes such as reverse
<50/mm3 transcriptase and protease. Recent drugs like entry inhibitors
Mycobacterium avium CD4 count Azithromycin,
and integrase inhibitors are also being tried. Anti-retroviral
complex (MAC) <50/mm3 clarithromycin, rifabutin
drugs are listed in Table 9.20.
Infections
The response to therapy is monitored clinically,
immunologically and by viral load reduction. In patients
who respond, there is a rise in CD4 count and decrease in
the plasma viral load.
236
Essentials of Medicine for Dental Students
b. Use of sterilized syringes and needles and instruments hopes. The zidovudine (300 mg twice a day) is given to
for every injection, immunization and surgery. HIV positive pregnant mothers from the 10th to 12th week
c. Screening of all blood and blood products for HIV of pregnancy or immediately after the diagnosis, if done
infection. later. During labor, AZT is given intravenously. The newborn
is given syrup AZT 1mg/kg three times a day for 6 weeks.
Mother to Child Transmission of HIV Infection As a result of this, the chances of transmission are reduced
The success story of ART in the prevention of transmission by one-third, from 26-30% to 8%. Recent trials have reported
of HIV infection from mother to fetus/newborn has instilled the efficacy of single dose of nevirapine (200 mg) given at
the time of labor.
TABLE 9.22: Oral manifestations in HIV infection
Infections
Infections
Fungal
Candidiasis
Histoplasmosis
Cryptococcosis
Viral
Oral hairy leukoplakia (EBV)
Herpes simplex
Cytomegalovirus
Varicella zoster
Papilloma virus
Bacterial
Periodontal infections
Necrotizing ulcerative gingivitis
Necrotizing stomatitis
Neoplasms
Kaposi sarcoma
Lymphoma
Idiopathic oral aphthous ulcers
HIV salivary gland disease (DILS)
FIGURE 9.16: Diffuse infiltrative lymphocytosis syndrome in Cervical lymphadenopathy
HIV patient
238
j. Diffuse infiltrative CD8 lymphocytosis syndrome (DILS) A. Antigen B. Antibody
may present as bilateral salivary gland enlargement, C. Viral RNA D. Viral particles
usually parotid (Fig. 9.16) and xerostomia. Xerophthalmia 3. Estimated number of HIV infected people in the world:
A. 4 million B. 40 million
can also occur. Sjögren syndrome and lymphoma may
C. 10 billion D. 1 billion
develop in these patients.
4. Universal work precaution is needed while caring for:
A. Symptomatic AIDS patients
IMPLICATIONS ON DENTAL PRACTICE B. All patients with HIV/AIDS
Essentials of Medicine for Dental Students
1. HIV patients are usually able to tolerate all types of dental C. All patients whether HIV positive or negative
procedures. No dental modification is needed for patients D. Only during surgery
based on their HIV status. Patients with HIV are not 5. HIV can infect:
A. CD4 T lymphocytes only
more susceptible to complications after dental treatment
B. CD4 and CD8 T lymphocytes
regardless of CD4 cell count. Routine use of antibiotic
C. All CD4 bearing cells
prophylaxis is not recommended in HIV patients. D. All cells arising from bone marrow
However antibiotics are added in case of neutropenia 6. Most common opportunistic infection in AIDS patients in
(count <750/mm3) India is:
2. HIV patients may have xerostomia particularly due to A. Candidiasis B. Amoebiasis
anti-retroviral medications. Xerostomia may also occur C. Tuberculosis D. Hepatitis
due to HIV associated disease of salivary glands. Hence, 7. Mother to child transmission of HIV occur mostly:
this should be taken into consideration while planning A. During labor
B. During throughout pregnancy
dental procedures like restorative procedures and
C. Through breastfeeding
fabricating fixed or removable prosthodontics. D. During last trimester of pregnancy
3. The drug interactions are common with anti-retroviral 8. The risk of transmission of HIV through needle injury is:
agents. This should be considered when prescribing any A. 2-10%
medicines to such patients. B. 0.3%
C. 10-30% 19. In resource poor settings, if CD4 facility is not available,
Infections
D. 0.09% following can be used as parameter for starting ART:
9. Following malignancies are increasingly associated with HIV A. Eosinophilia
infection except: B. Total lymphocyte count
A. Kaposi sarcoma C. ESR
B. Hodgkin’s disease D. PPD test
C. Carcinoma breast 20. Following is true during latent period of HIV disease:
D. Primary CNS lymphoma Elisa p24 Symptoms
10. Following are at increased risk of getting HIV except: A. + +++ –
A. Truck driver B. – – +
B. IV drug abuser C. + +/– –
C. Who frequently donate blood D. – ++ –
D. Those having STD 21. Following drugs are used in herpes zoster except:
11. Following are anti-HIV drugs except: A. Acyclovir B. Valacyclovir
A. Ritonavir B. Acyclovir C. Indinavir D. Famcyclovir
C. Saquinavir D. Efavirenz 22. Which one of the following is the most common complication
12. Following test is used for diagnosis of HIV infection during of mumps in postpubertal males?
window period: A. Myocarditis B. Orchitis
A. Western blot B. p24 C. Nephritis D. Parotid abscess
C. B2 microglobulin D. CD4 23. Koplik’s spots are seen in:
13. Diagnosis of tuberculosis in HIV positive patients may be A. Mumps B. Measles
difficult because: C. Rubella D. Chickenpox
A. Tuberculosis is not common in HIV patients 24. Following are features of rashes in chickenpox except:
B. Presentation of tuberculosis may be atypical A. Pleomorphic rash
C.
D.
Bacterial strain is different
All the above
B.
C.
Rashes are pruritic
First appears in extremities 239
D. Rashes are infective till crusts slough
14. Following drug is contraindicated in pregnancy:
25. Most common complication of chickenpox is:
A. AZT (Zidovudine)
A. Encephalitis
B. Stavudine
B. Meningitis
C. Efavirenz
C. Viral pneumonia
D. All the above
D. Secondary infection of skin lesion
15. Following percentage of HIV patients respond to ART:
26. Subacute sclerosing panencephalitis (SSPE) is associated
A. 10-20% B. 60-70%
with:
C. >90% D. 30-40%
A. Mumps B. Measles
16. Anemia is important side effect of:
C. HIV D. Japanese encephalitis
A. Lamivudine B. Efavirenz
27. Following are features of congenital syphilis except:
C. AZT (Zidovudine) D. All of the above
A. Mulberry molars
17. Which is true for ART:
B. Maxillary hyperplasia
A. ART is least effective
C. High arched palate
B. ART is very effective in all patients D. Rhagades
C. ART is accompanied with increased cardiovascular 28. Following drugs are used in syphilis except:
mortality A. Penicillin B. Doxycycline
D. All the above C. Azithromycin D. Cotrimoxazole
18. Following opportunistic infection may occur even at CD4 29. Jarisch Herxheimer reaction can occur following initiation
count >500/cmm: of treatment of:
A. CMV A. Plasmodium falciparum
B. Herpes zoster B. HIV disease
C. Mycobacterium avium intercellulare C. Syphilis
D. PCP D. Gonorrhea
30. The longest incubation period is found in which type of 35. Palatal palsy is a complication of:
malaria: A. Mumps
A. P. falciparum B. P. ovale B. Diphtheria
C. P. vivax D. P. malariae C. Syphilis
31. Primaquin is given for radical cure in: D. Rubella
A. P. vivax and P. falciparum 36. Following may occur through blood transfusion except:
B. P. falciparum and P. ovale A. Syphilis B. HIV
C. P. vivax and P. ovale C. Gonorrhea D. Malaria
D. P. malariae and P. ovale
32. Following agents can be used for chemoprophylaxis of Fill in the Blanks
malaria except: 1. Forschheimer’s spots are seen in ________ infection.
A. Chloroquine B. Mefloquine 2. Hutchinson’s teeth are seen in ________.
C. Doxycycline D. Quinine 3. Gumma occurs in ________ stage of syphilis.
33. Most common site involved in amoebiasis is: 4. Drug of choice in primary syphilis is________.
A. Jejunum B. Rectum 5. Syphilis is caused by________.
C. Caecum D. Gastro-esophageal junction 6. Cerebral malaria is caused by Plasmodium________.
34. Most common organ involved in extra-intestinal amoebiasis 7. Tropical splenomegaly is associated with________.
is: 8. Amoebiasis is caused by________.
A. Brain B. Lung 9. Anchovy sauce pus is a feature of________.
C. Liver D. Pancreas 10. “Bull neck” may occur in ________infection.
240
Essentials of Medicine for Dental Students
Chapter
Medical Emergencies
10 in Dental Practice
Patients who come for treatment for their problems to dental The dental clinic should be well equipped in order to
surgeon may also be suffering from other systemic disorders. deal with any emergency. A list of paraphernalia and drugs
Some of these disorders may have direct relevance to the which must be available in the clinic is given in Table 10.3.
dental illness while others may not. However patients may History: A quick but discrete history must be taken to
develop serious life threatening problems during or just after know about the past and present illness in the patient and
the dental treatment. Emergency situations may arise more also about the medication he/she is taking. In addition to
commonly when invasive or painful procedures are this, a proper counseling is needed so that the patient
performed or medically compromised patients are treated. understands the nature of treatment he is going to receive
Hence the knowledge of these disorders is necessary in order and the side effects expected if any. This will allay fear from
to avoid or manage emergency situations. A list of important the mind of the patient and build trust and confidence. This
medical emergencies that may occur during dental treatment/ will also ensure full cooperation on the part of the patient.
procedure is given in the Table 10.1. A general guideline Such steps are very helpful in avoiding complications like
should be followed (Table 10.2). TABLE 10.3: List of drugs and equipments to deal
with medical emergencies
TABLE 10.1: Important medical emergencies in dental practice Drugs
• Inj adrenaline (0.5 ml ampules of 1:1000 solution)
• General: syncope, postural hypotension • Inj chlorphenramine
• Cardiovascular: angina, myocardial infarction, cardiac arrest, heart • Inj hydrocortisone sodium succinate (100-200 mg)
failure, severe hypertension • Inj glucagon 1 mg
• Respiratory: asthmatic attack, hyperventilation, airways obstruction • Inj diazepam
• Neurological: seizures, stroke • IV dextrose (20%, 50%)
• Allergic: anaphylaxis • glucose powder
• Endocrinal: hypoglycemia, adrenal crisis • glyceryl trinitrate 0.3-1 mg,
• Hematological: excessive bleeding • aspirin
• salbutamol solution for nubulizing
Equipments
TABLE 10.2: General precautions and guidelines • oropharyngeal airway
• oxygen supply kit
• Patient should lay supine while receiving local anesthesia • suction machine
• Ensure that diabetic patient has taken meal timely • ambubag and airways
• Always have an assistant • tourniquet
• Assistant should be well versed with techniques such as • laryngoscope
venepuncture, CPR, monitoring vitals and maintaining airways • sphygmomanometer
• Emergency kit should be readily accessible and periodically • stethoscope
checked • IV cannula
• Watch carefully for any change in behaviour, breathing pattern, • disposable syringes and needles
wheeze, sensorium in patient while on procedure • IV drip sets and DNS bottles
• Contact phone number of physician/emergency department/ • nebulizer
ambulance Contact numbers of physician/emergency department/ambulance
TABLE 10.4: History taking before dental TABLE 10.6: Important causes of postural hypotension
treatment/procedure
• Defective postural reflexes: Diabetes, aging, parkinsonism
• Any problem during previous dental treatment • Drugs: vasodilators, beta blockers, diuretics, antidepressants
• History of hypertension, angina or any heart disease, seizures, • Hypovolemia: diarrhea, excessive sweating, hemorrhage, diuretics
fainting, asthma, syncope, drug allergy, renal disease, diabetes,
peptic ulcer, chronic bronchitis, bleeding diathesis, anemia, jaundice,
pregnancy, risk factors for HIV, TABLE 10.7: Measures to avoid Postural Hypotension
• Details of present medications
• To avoid prolonged standing
• To avoid sudden change in posture to sitting or standing
TABLE 10.5: Clinical examination • Movement of legs prior to standing
General • Plenty of fluids and salt intake prior to the procedure
• Pallor
• Pulse causes precipitating hypovolemia must be obtained
• blood pressure
before the procedure (Table 10.6)
• jaundice
• edema
• goiter Management
• lymphadenopathy
• temperature a. Patients who have underlying causes of postural
• skin hypotension should be advised to attain upright position
Systemic slowly. Preferably they may be asked to sit down first
• higher functions for sometimes before standing (Table 10.7).
• heart sounds b. Plenty of fluids should be given to prevent hypovolemia.
• respiratory
c. These patients should not be made to remain in standing
• liver
• spleen position for long.
242 exacerbations of bronchial asthma, vasovagal syncope, surge
d. Medications that aggravate the problem should be
discontinued.
in blood pressure, intense tachycardia or excessive bleeding. e. Movement of legs prior to rising may facilitate the
A scheme of history taking is given in Table 10.4. venous return and help avoid OH.
Examination: A quick but thorough clinical examination f. Upon development of initial symptoms of OH, patient
should be performed before any dental treatment/procedure. should immediately be laid supine. He is given water to
This includes general and important systemic examination. drink and advised to attain sitting posture slowly as
Essentials of Medicine for Dental Students
243
myocardial ischemia or hypertensive crisis.
• Assure and calm the patient
An adequate medical history about the presence of
• Ensure that patient has taken medicines for asthma as
cardiac disease should be taken. One should make sure that
prescribed
patient is regularly taking medications. The patient should
• Avoid numerous dental products which may exacerbate
be properly counseled prior to the procedure. The procedure
asthma such as some toothpastes, tooth enamel dust and
is done in cordial and comfortable environment. The
methacrylate.
management is done as mentioned in Table 10.8. (see also
The patient is urgently managed as discussed in Table 10.10.
chapter 4). However, if recovery does not occur, he should be shifted
TABLE 10.8: Management of acute pulmonary edema to medical emergency department.
• Patient is put in sitting posture
AIRWAYS OBSTRUCTION
• Stoppage of dental procedure
• Reassurance During dental procedures, objects such as fragments of
• Oxygen is administered to improve hypoxia tooth, filling materials or segments of bone may find their
• IV frusemide (20-80 mg) gives rapid relief
• Call for medical help way into the posterior part of the oral cavity, pharynx and
• Monitor vital signs
• IV morphine (2-4 mg) can be given TABLE 10.10: Management of acute asthmatic attack
• If no relief, shift the patient to medical emergency
Stop the procedure
All dental materials removed from patient’s mouth
CHEST PAIN Reassure the patient
Do not lay patient supine, place in comfortable posture
Patients with ischemic heart disease may develop Administer oxygen
retrosternal chest pain due to angina. Occasionally it may Nebulize with salbutamol (2.5-5 mg)
Inject hydrocortisone IV 200 mg
develop for the first time during procedure in patient not
Call an ambulance in case the condition does not settle
previously known to be a cardiac patient. Hence, a history
TABLE 10.11: Prevention of airways obstruction central nervous system neurons. Precipitating factors for
seizures are given in Table 10.14. (see also Chapter 7)
Use of rubber dams wherever possible
Adequate use of oral packings
Proper positioning of patient Management
Effective uses of dental assistance and suction The patient should be shifted to a safe place, away from
danger (water, fire, machine). The patient is made to lie in
larynx. In conscious patient, airway obstruction is less semi-prone position in order to prevent aspiration (Table
common due to cough reflex. The symptoms are violent 10.15). Nothing should be given orally until patient has
respiratory efforts, feel of choking and deepening cyanosis. fully recovered. Oral cavity and airways are cleaned and
Preventive measures should be taken to avoid such events cleared preferably with a piece of gauge (finger should not
(Table 10.11). be inserted into mouth to avoid bite injury).
If the foreign body is swallowed, its location should be Proper history of any seizure disorder must be asked
confirmed with the help of radiologists. Tips of broken from the patient. If patient has seizure disorder, one should
instruments, burs or dental restorations may have pointed make sure he is taking the medication regularly. Precipitating
or jagged edges that might injure the gut mucosa. The patient factors for seizures must be avoided.
is advised to eat soft bulk diet and to keep watch for
evacuation of foreign body. A follow-up X-ray must be done TABLE 10.12: Causes of hyperventilation
to ensure its elimination. • Psychogenic or anxiety
If the foreign body has been aspirated, certain maneuvers • Pulmonary diseases (pneumonia, asthma, embolism)
are performed and patient is referred to thoracic surgeon. • Cardiac diseases (CHF, hypotension)
• Metabolic acidosis (diabetic, renal, lactic)
Different maneuvers are: • Drug induced (salicylates, methylxanthines)
• Make patient stand up and use abdominal thrusts until • Fever, pain, sepsis
244 foreign body is expelled (Heimlich maneuver).
• A Trendelenberg position (legs raised) can allow the
TABLE 10.13: Management of hyperventilation
gravity to move the object close to the oral cavity • Stop the procedure
wherefrom it can be easily removed. • Assure the patient
• Put the patient in comfortable position
• Use laryngoscope and pharyngeal suction. • Generally the problem is self-limiting
• If obstruction persists, insert a cannula of 10-12 IV size • Patients may be asked to breathe in a paper bag
through cricothyroid ligament (cricothyrotomy). • May give mild sedative in case of intense anxiety
Essentials of Medicine for Dental Students
• Arrange transfer to hospital for specialized care. • Exclude other causes of hyperventilation
246
for the investigations must be drawn before administration may be used
of any drug/factors. Initial investigations include tests listed
in Table 10.23. Other tests can be done later. TABLE 10.23: Initial investigations in patients
For detailed description of hemostatic disorders, readers with excessive bleeding
are advised to see chapter on hematological disorders • Complete blood count (including platelet count)
(Chapter 3). • Prothrombin time
• Activated partial thromboplastin time
DENTAL PROCEDURES IN PREGNANT WOMEN • Bleeding time
Essentials of Medicine for Dental Students
Critical Care
• SIRS caused by inflammation due to non-infectious
Steriod therapy (chronic administration of high dose steroids) causes like pancreatitis, crush injuries and drugs
Atrophy of adrenal glands (salicylates) may also lead to shock.
Tuberculosis, amyloidosis, metastasic disease of adrenal glands
Bilateral hemorrhage in adrenal glands Clinical Presentation
Patients present with fever, chills, hypotension, altered
surgery. This response is impaired in certain clinical settings mental status and features of end organ failure due to
leading to deceased secretion of cortisol from adrenal gland
hypoperfusion. Systolic blood pressure is 90 mmHg or
and impaired host response to stress. Causes of adrenal
mean arterial blood pressure <70 mmHg. In some patients
insufficiency are given in Table 11.4.
clinical features may point toward specific etiology.
Shock due to hypoadrenal state is characterized by
Generalized erythroderma may be present in toxic shock
hypovolemia, decreased systemic vascular resistance and
syndrome, Staph. aureus or Strep. pyogenes infection.
reduced cardiac output.
N. meningitides infection causes hemorrhagic or petechial
Diagnosis rahes over skin.
Adrenal insufficiency can be diagnosed by ACTH Septic shock is also characterized by hypoperfusion of
stimulation test. organs and may lead to dysfunction or failure of many organs
if not treated promptly.
Treatment • Restlessness, confusion, delirium and coma may result
Hydrocortisone (100 mg every 4-6h) or dexamethasone from encephalopathy as a result of hypoperfusion of the
(4 mg) is given intravenously, along with volume replacement brain.
and intravenous vasopressors. • ARDS may result from increased permeability of
Septic Shock
pulmonary capillaries and pulmonary edema.
• Acute renal failure may occur due to renal hypo-
249
Septic shock and anaphylactic shock are classified under perfusion. Prolonged hypoperfusion or toxic injury may
distributive shock. Sepsis is the most common cause of cause acute tubular necrosis.
distributive shock. It is characterized by hypotension due • Increased levels of serum bilirubin and hepatic enzymes
to decreased vascular tone (reduced systemic vascular (AST, ALT) suggest hepatic dysfunction.
resistance), inadequate cardiac output and normal circulatory • DIC is frequently present in severe septicemia.
volume.
• Sepsis is defined as SIRS (systemic inflammatory
response syndrome) with proven or suspected infectious
etiology. TABLE 11.5: Causes of septic shock/SIRS
• SIRS may be due to infectious or non-infectious etiology Septic
and is characterized by fever or hypothermia, Infection
Gram negative bacteria
leukocytosis or leucopenia, tachypnea and tachycardia.
• E. coli
• Severe sepsis is sepsis with one or more organ • Klebsiella
dysfunction. • Proteus
• Pseudomonas
• Septic shock is defined as sepsis with hypotension i.e.
Gram positive cocci
mean arterial blood pressure <70 mmHg or Arterial Gram negative anaerobes
systolic blood pressure <90 mmHg for at least 1 hour • Bacteriodes
despite adequate fluid resuscitation. Septic shock is SIRS (systemic inflammatory response syndrome)
usually caused by inflammation due to bacterial Pancreatitis
infection. It is caused mainly by gram negative bacteria Crush injuries
Drugs (salicylates)
(Table 11.5).
Investigations consists of one antibiotic from group 1 or group 2 plus
• Blood culture may reveal causative organism. one from group 3 (e.g. Ceftriaxone plus gentamycin,
• Culture of material from local infected foci should also Meropenem plus tobramycin). If the patient is allergic
be performed to know causative organism and antibiotic to betalactam antibiotics, one antibiotic from group 3
sensitivity. plus clindamycin is given. Vancomycin is added if
• TLC reveals increased WBC count and DLC reveals infection due to methicillin resistant (Staph. aureus)
polymorphonuclear leukocytosis. (MRSA) is suspected. Antibiotics are changed, if
required, after culture and sensitivity reports are
• Increased levels of serum urea and creatinine suggest
available. Maximum recommended does of antimicrobial
renal dysfunction.
agents are given intravenously.
• Increased bilirubin levels and hepatic enzymes (AST,
• Fluid administration is usually required for correction
ALT) are usually found.
of hypotension and it is monitored by measuring central
• Low platelet count, increased prothombin time (PT) and
venous pressure (CVP). Ionotropic or vasopressor agents
partial thromboplastin time (aPTT) suggest DIC.
are given if hypotension does not respond to fluid
• Arterial blood gas analysis may show hypoxia and
therapy.
metabolic acidosis.
• Septic shock may be associated with relative adrenal
• Chest X-ray may show features of ARDS.
insufficiency and corticosteroids like hydrocortisone
(50 mg 6 h for 5-7 days) are associated with improved
Management
survival.
As in all types of shock, initial treatment consists of basic • Drotrecogin alfa (activated human protein C)
life support (airway, breathing and circulation). Airway administration has been shown to reduce mortality in
maintenance, oxygen inhalation, ventilatory support, severe sepsis and shock. It has anti-inflammatory,
250 intravenous access and fluid resuscitation are important
measures in management.
antithrombotic properties and is given as continuous
infusion of 24 mcg/kg body weight/hr for 96 hours.
• Antimicrobial therapy should be started as soon as
possible after sending blood sample and other specimen Cardiogenic Shock
for culture. Empirical therapy is started with broad Shock as a result of impaired cardiac function is known as
spectrum antibiotics to cover gram negative and gram cardiogenic shock (CS). It is most commonly seen after acute
positive organisms (Table 11.6). Empirical therapy myocardial infarction causing pump failure. Other causes
Essentials of Medicine for Dental Students
TABLE 11.6: Antimicrobial regimens used in septic shock of cardiogenic shock are given in Table 11.7.
Group 1 CS secondary to acute myocardial infarction is
• Ceftriaxone 2g od characterized by
• Ticarcillin-clavulanate 3.1g q 4-6h • Hypotension (systolic blood pressure < 90 mmHg, mean
• Piperacillin-tazobactum 3.375g q 4-6 h arterial pressure <60 mmHg),
Group 2
• Imepenem-cilastatin 0.5g q6h TABLE 11.7: Causes of cardiogenic shock
• Meropenem 1g q8h
• Cefipime 2g q 12 h Pump failure
Group 3 • Acute myocardial infarction
• Cardiomyopathy
• Gentamycin 5-7 mg/kg q 24 h
• Tobramycin 5-7 mg/kg q 24 h Acute myocarditis
Arrhythmias
Group 4
Valvular lesions
• Ciprofloxacin 400 mg q 12h • Acute severe aortic or mitral regurgitation
• Levofloxacin 500-750 mg q 12 h • Critical mitral or aortic stenosis
• Clindamycin 600 mg q 8h
Rupture of ventricular septum or free ventricular wall
Group 5 Pericardial tamponade
Vancomycin 15 mg/kg q 12 h Right ventricular failure due to pulmonary embolism
Management
Critical Care
• Decreased cardiac index
• Elevated intracardiac pressure (pulmonary capillary a. The aim of therapy is to increase blood pressure
wedge pressure >18 mmHg) and sufficient to maintain systemic and coronary perfusion
• Increased peripheral vascular resistance. and maintain volume status to ensure proper ventricular
In cardiogenic shock, CVP is usually raised (it is low in function and preventing volume overload.
hypovolemic shock). Depressed myocardial contractility, b. Oxygen inhalation is given to maintain PaO2 of >60
usually due to ischemia, results in low cardiac output and mmHg. Endotracheal intubation and mechanical
hypotension. A vicious cycle is formed as hypotension ventilation may be required. It reduces work of breathing
results in hypoperfusion and ischemia of myocardium and and increases cardiac pressure which may improve
further depression of myocardial contractility. Compensatory cardiac output.
reflux arteriolar vasoconstriction leads to reduced blood flow c. Hematocrit is maintained >30%, fluid replacement is
to kidneys, muscle, abdominal viscera and skin while done to maintain adequate preload and ventricular
vasodilatation of cerebral and coronary arteries occurs in function. Excessive fluids may cause pulmonary edema.
order to maintain circulation in these territories. d. Pressors are administered only after adequate fluid
Vasoconstriction not only helps in elevating blood pressure resuscitation.
but also causes tissue hypoxia and acidosis. e. Drugs are used to increase blood pressure and cardiac
output in patients of CS. The dose is titrated to maintain
Clinical Features blood pressure of >90 mmHg or mean arterial pressure
Shock (acute circulatory failure, low output state) is a clinical of >60 mmHg.
syndrome characterized by • Dopamine is usually used in CS. It has variable
• Arterial hypotension (systolic blood pressure <90 effects according to dosage. At low dose (2 mcg/kg/
mmHg, mean arterial pressure <60 mmHg)
• Weak and rapid pulse
min) it dilates renal vascular bed and increases
glomerular filtration rate because of dopaminergic 251
• Cold extremities and cyanosis effects. At moderate dosage (2-10 mcg/kg/min) it
• Oliguria (low urine output <30 ml/h) and stimulates beta adrenergic receptors and increases
• Features of altered mentation (agitation, confusion, myocardial contractility (positive ionotropic effect)
drowsiness and coma). and heart rate (positive chronotropic effect). At
In addition, features of underlying cardiac disease are higher dosage (10 mcg/kg/min) it produces
present. vasoconstriction because of alpha adrenergic
Most patients with acute myocardial infarction present stimulation.
with severe chest pain, dyspnea, anxiety and sweating. • Dobutamine produces greater ionotropic effects
Cardiac findings include S3 gallop (third heart sound) and as compared to dopamine. It is a synthetic
systolic murmurs. Raised jugular venous pressure (JVP) and sympathomimetic amine and is given in dosage of
pulmonary rales are audible in patients with left ventricular 2-20 mcg/kg/min. It also reduces afterload because
failure and cardiogenic shock. of its vasodilating effects. Amrinone or milrinone is
given with dobutamine.
Investigations • Norepinephrine is a potent vasoconstrictor and
Chest X-ray, electrocardiogram and echocardiography are ionotropic agent and is given in dosage of 2-10 mcg/
investigations which help in diagnosis. Echocardiogram min. It is reserved for patients with CS and refractory
should be done to find etiology of CS. Pulmonary artery hypotension. It is also useful in distributive or
catheterization helps in measurement of filling pressures neurogenic shock.
and cardiac output and helps in diagnosis and proper f. Aortic counterpulsation: Intraaortic balloon pumping, a
management (volume replacement and use of pressor mechanical circulatory assist device, augments arterial
agents). diastolic pressure and cardiac output. It is used in patients
not responding to medical treatment or in acute valvular alveolar epithelial cells as well as capillary endothelial cells.
insufficiency/VSD. It is inserted percutaneously and This causes increased vascular permeability and decreased
the balloon inflates during diastole and deflates during production of surfactant. There is accumulation of protein
systole, reducing afterload and improving cardiac output. rich fluid and inflammatory cells in the alveoli and
It also increases coronary blood flow during diastole. interstitium leading to pulmonary edema, alveolar collapse
g. Definitive treatment is directed toward underlying cause. and hypoxemia.
This can be in form of angioplasty, coronary artery
bypass grafting, valvular replacement or cardiac trans- Clinical Features
plantation. The rapid establishment of bloodflow in The usual symptom is rapid onset dyspnea which follows
infarct-related artery is essential in acute myocardial the underlying causative event within 12-48 hours.
infarction. Examination reveals tachypnea, labored breathing and
intercostal retraction. Auscultation of lungs shows bilateral
ACUTE RESPIRATORY DISTRESS crackes (crepts). Most patients with ARDS have multiorgan
SYNDROME (ARDS) failure involving kidneys, liver, gut, CNS and cardiovascular
ARDS is most severe form of acute lung injury (ALI) system.
characterized by acute hypoxemic respiratory failure
following systemic or pulmonary insult without heart failure. Diagnosis
ARDS is a physiological and radiographic syndrome rather Diagnosis is based on following criteria:
than a specific disease. a. Acute onset of severe dyspnea
b. PaO2/ FiO2 <200 mmHg
Causes c. Bilateral infiltrates on chest X-ray
Investigations
TABLE 11.8: Causes of ARDS Important investigations include:
Systemic insult (Indirect lung injury) • X-ray chest PA view
• Sepsis • Arterial blood gases
• Multiple blood transfusions • Hemogram
• Severe trauma
• Blood sugar
• Burns
• Pancreatitis • Blood urea/Serum creatinine
Pulmonary insult (Direct lung injury) • Liver function tests, serum amylase/lipase
• Pneumonia
• Aspiration of gastric contents Treatment
• Miliary tuberculosis
General measures include:
• Oxygen toxicity
• Pulmonary contusion 1. Recognition and treatment of underlying cause
• Near drowning 2. Minimizing invasive procedures
• Toxic inhalation
3. Prophylaxis for venous thromboembolism
• High altitute
4. Management of nosocomial infection
Mechanical Ventilation TABLE 11. 9: Causes of sudden cardiac death/cardiac arrest
Critical Care
Mechanical ventilation may be needed in patient with Coronary artery disease
respiratory failure. Positive pressure mechanical ventilation Hypertrophic cardiomyopathy
Aortic stenosis and pulmonary stenosis
with lowest level of PEEP and supplemental oxygen required
Cyanotic congenital heart disease
to maintain the PaO2 above 60 mmHg or SaO2 above 90% Atrial myxoma
is used. Volume cycle ventilation with small tidal volumes WPW syndrome
have been shown to reduce mortality over standard forms Electrolyte abnormalities
Hypoxia
of mechanical ventilation. Acidosis
Currently, use of corticosteroids is not recommended Prolonged QT interval
as no mortality benefit has been demonstrated with Brugada syndrome
steroids. Surfactants and inhaled nitric oxide have also been
tried. Sudden Cardiac Death (SCD)
SCD is defined as unexpected non-traumatic death in
Prognosis clinically well or stable patient who dies within 1 hour of
Mortality is 40-60% on treatment. It is around 90% if ARDS onset of symptoms. The causative rhythm in most cases is
is accompanied by sepsis. VF.
Causes of cardiac arrest and are given in Table 11.9.
CARDIOVASCULAR COLLAPSE
Cardiovascular collapse is defined as a loss of effective Management of Cardiac Arrest
blood flow due to acute dysfunction of heart or peripheral Following are important steps in the management of cardiac
arrest. (see cardiopulmonary resuscitation below)
253
vasculature. Cardiovascular collapse may be caused by:
a. Cardiac arrest: which requires intervention to prevent a. The initial response and basic life support
death. b. Defibrillation
b. Other causes which are transient and non-life-threatening c. Advanced life support
with spontaneous return of consciousness. These include d. Postresuscitation care
e. Long-term management
syncope (vasovagal, postural hypotension, neurocar-
diogenic syncope) oratransient severe bradycardia.
CARDIOPULMONARY RESUSCITATION
CARDIAC ARREST All health care providers must know the procedures of basic
life support (BLS) and advanced cardiac life support
Cardiac arrest is defined as abrupt cessation of cardiac pump
(ACLS). When cardiac arrest occurs, BLS must be started
function. This may be reversible by prompt intervention or
immediately. The goal of resuscitation is to maintain cerebral
can lead to death if no intervention is done. There is
perfusion until cardiopulmonary function is restored. The
aberration in the underlying electrical activity leading to longer the period of cardiopulmonary arrest, the lower is
following conditions. Any of these conditions may be the chance of restoring healthy life. Irreversible cerebral
responsible for cardiac arrest. damage may occur after 3 minutes of anoxia. Ventricular
a. Ventricular fibrillation (VF) –responsible for 50-80% arrhythmias are responsible for majority of cardiac arrests,
of arrests hence defibrillation facilities should be available.
b. Asystole Following sequence should be followed during adult
c. Persistent bradyarrhythmias resuscitation:
d. Pulseless electrical activity (PEA) 1. Assessment of unresponsiveness
e. Pulseless sustained ventricular tachycardia (VT) 2. Activation of emergency medical services
3. BLS until defibrillation is available 6. Circulation: Cardiac arrest is accompanied by circulatory
4. Defibrillation if indicated collapse. Assess circulation by palpating for pulses and
5. Intubation checking for signs of perfusion including swallowing
6. Administration of appropriate medications or breathing for more than occasional gasps. Absence
of carotid pulse for 10 seconds confirms circulatory
BLS collapse.
Airway, breathing and circulation are the essentials of BLS. a. External chest compressions should be initiated at a
In an unconscious patient, the following is recommended: rate of 80-100 per minute in the absence of carotid
1. Determine the responsiveness by gently shaking the pulse .
patient and shouting into ear. Shaking of patient’s head b. The patients should be lying on firm surface.
and neck should be avoided if trauma to these areas is c. The heel of one hand is placed over the lower half
suspected. of the victim’s sternum and the heel of the second
2. If no response is obtained, activate the emergency hand is placed over the first with fingers interlocked.
medical services system. If breathing problem is the Chest compressions are performed with the heel of
likely cause of unconsciousness (drowning, choking, one hand on the back of the other hand. Hand
alcohol intoxication, trauma), resuscitation should be position should be one inch cephalad to the patient’s
performed before going for help. xiphoid process. With shoulder directly above the
3. Patient should be laid on firm, flat surface. If the patient hands and elbows in locked position, the patient’s
is moved, he should be moved as a single unit so that sternum should be compressed below to 1.5 to 2
head, neck and body moves simultaneously. inches.
4. Airway: The patient’s mouth should be opened, debris
d. The adequacy of compressions should be assessed
254
(e.g. mucus and blood ) should be removed and dentures
periodically by having another rescuer palpate the
should be left in place. Loose or ill-fitting dentures
carotid pulse.
should be removed. Open the patient’s airway by flexing
e. Respiratory and circulatory support is continued by
the neck and extending the head. The head tilt-chin lift
providing two effective breaths for every 15 cardiac
should be performed if neck injury is not suspected. If a
compressions. Fifteen chest compressions should be
cervical injury is suspected, use the jaw thrust maneuver
performed followed by two ventilations. Once the
to limit the potential for spinal cord injury.
patient is intubated, ventilation can be performed at
Essentials of Medicine for Dental Students
255
history including current medications and treatments, and • Pulseless electrical activity may be due to several
obtain appropriate tests (electrolytes, hematocrit, arterial potential reversible causes (Table 11.11). It carries a very
blood gas analysis, ECG, radiographs, etc.) to determine poor prognosis. Effective treatment involves addressing
and treat the cause of the arrest. The patient’s rhythm the underlying cause.
and pulse should be assessed after every intervention. The
team leader also should determine when termination of
TABLE 11.10: Causes of unexpected cardiac arrest
resuscitative efforts is warranted.
a. ACLS consists of ECG monitoring, endotracheal Cardiac arrhythmias (e.g. ventricular fibrillation)
intubation and setting up an intravenous line in a large Sudden pump failure (e.g. acute myocardial infarction)
Acute circulatory obstruction(e.g. acute pulmonary embolism)
peripheral vein or central vein.
Cardiovascular rupture (e.g. myocardial rupture, aortic dissection)
b. Immediate therapy includes defibrillation, oxygen and Vasomotor collapse (e.g. pulmonary hypertension)
administration of cardioactive drugs.
c. As soon as possible the cardiac rhythm should be TABLE 11.11: Most frequent causes of pulseless
established. If the ECG reveals ventricular arrhythmia electrical activity
or there is doubt to the nature of the rhythm (e.g. Fine Hypovolemia
VF may be confused with asystole) immediate Hypoxemia
defibrillation is performed. Hypokalemia/hyperkalemia
Hypothermia
d. If initial defibrillation attempts are unsuccessful, victim
Metabolic acidosis
is intubated and setting of intravenous line is performed Cardiac tamponade
while the circulation is supported by external chest Tension pneumothorax
compressions. If there is any difficulty in intubating the Pulmonary thromboembolism
Acute coronary syndrome (coronary thrombosis)
patient, ventilation should be continued by means of an Toxins
airway, a ventilating bag and oxygen.
Chapter
Anaphylaxis and
12 Drug Allergy
ANAPHYLAXIS
Anaphylaxis is a type I IgE mediated rapidly developing
systemic allergic reaction. Exposure to an antigen results in
the formation of specific IgE which binds with the mast
cells. Once IgE is bound to the surface of mast cells, the
individual is primed to develop type I hypersensitivity
reaction. Repeat exposure to same antigen in the sensitized
individual can lead to the activation of IgE bound mast cells
and release of a number of mediators such as histamine,
serotonin, leukotriens and prostaglandins (Fig. 12.1). These
mediators cause bronchoconstriction, vasodilatation, fluid
exudation and smooth muscle contraction which are
responsible for clinical features of the anaphylactic reaction
(Table 12.1).
Anaphylactoid reaction: Certain substances can cause
activation of mast cells directly (non-IgE mediated) and lead
to similar clinical picture. This is known as anaphylactoid
reaction. Radio-contrast media are the most common cause
of anaphylactoid reaction.
TABLE 12.1: Mediators and their actions in anaphylaxis
Primary mediators
Histamine Vasodilatation, increased vascular FIGURE 12.1: Mechanism of anaphylaxis
permeability, bronchospasm,
increased mucus secretions
Causes
Chemotactic factors Chemotaxis of eosinophils and
(ECF-A, NCF-A) neutrophils Important causes of anaphylactic reaction are drugs,
Proteases Generate other inflammatory mediators foodstuffs and insect venoms. These are listed in Table
12.2.
Secondary mediators
Leukotrienes (LT) Clinical Manifestations
LTC4 and LTD4 Vasoactive and spasmogenic
LTB4 Chemotaxis of neutrophils, eosinophils The manifestation may be mild, very severe or life
and monocytes threatening. Type I reaction can occur as systemic disorder
Prostaglandins (PGD2) Bronchospasm and increased mucus (anaphylaxis) or local reaction (urticaria and/or
productions angioedema). Serious manifestations occur within seconds
Platelet activating Platelet aggregation, histamine
factor (PAF) release
to minutes after exposure to antigen. Sometimes, the reaction
is delayed be few hours. Important clinical features are given
TABLE 12.2: Causes of anaphylactic reaction TABLE 12.3: Clinical features of anaphylaxis
257
• Urticaria is a raised flat-topped well demarcated skin The diagnosis of anaphylactic reaction is clinical, based on
lesion with surrounding erythema (Figs 2A and B). the history of exposure to the triggering agent and
Individual lesions usually last from minutes to appearance of symptoms and signs within minutes of
hours.They are localized or disseminated and are exposure. An elevated serum tryptase during an episode
pruritic. confirms the diagnosis of anaphylactic reaction.
A B
FIGURES 12.2A and B: Urticaria
FIGURES 12.3A and B: Angioedema
Treatment
1. Discontinuation of suspected drugs
FIGURE 12.5: Toxic epidermal necrolysis 2. If the reaction is mild (skin rash) and the offending drug
needs to be given essentially, the drug may not be
discontinued. The reaction is treated symptomatically.
occurs in SJS, (<10% of total body surface area involved) 3. For treatment of anaphylaxis, urticaria and angioedema,
and TEN (if >30% body surface is involved). Involvement see page 258.
of 10-30% of the body surface area is known as SJS-TEN
overlap. The offending drug which has resulted in the above IMPLICATIONS ON DENTAL PRACTICE
reactions should not be given again. Future skin testing with
1. Swelling of the lips and floor of the mouth may occur in
the offending drug is absolutely contraindicated.
angioedema.
260
2. Dry mouth and drowsiness may occur in patients taking
Hepatic Syndromes
antihistaminics.
Hepatic syndromes can present as hepatocellular 3. Emergency kit should always be available in order to
damage (phenytoin, halothane) and cholestatic jaundice deal with any allergic reactions during dental procedures.
(phenothiazine, erythromycin and azathioprime). 4. Latex and rubber products can cause allergic reactions.
These are now increasingly seen as the use of gloves
Renal Syndromes has become more common with the advent of HIV/
Renal syndromes may present as interstitial nephritis (fever,
Essentials of Medicine for Dental Students
AIDS.
pyuria, hematuria, proteinuria, rash and eosinophilia). Drugs 5. Patients should be in supine position when injections
implicated are methicillin, sulfonamides, and cephalosporins. are given. Fainting after injection is common and can
be confused with anaphylaxis.
Pulmonary Syndromes
Pulmonary syndromes presents as pulmonary infiltration SELF ASSESSMENT
(nitrofurantoin, gold) and bronchospasm (aspirin, NSAIDs). Multiple Choice Questions
1. The drug of choice in a patient with an acute allergic reaction
Management of Drug Allergy involving bronchospasm and hypotension is:
A careful history is taken for any drug allergy. In case of A. Aminophylline
history of drug reaction, the name of the offending drug B. Epinephrine
and the date of the reaction should be noted. Patients may C. Dexamethasone
D. Chlorphenaramine maleate
loose their sensitivity to a drug over time. Prompt appearance
2. The blood cell, responsible for humoral immunity are:
of symptoms of drug reaction suggests IgE-mediated
A. T-cells
anaphylactic reaction. In other types of immune-mediated B. B-cells
reactions, symptoms may develop several days after the C. Both T and B cells
completion of course of therapy. D. No cells only antibodies
3. Type I hypersensitivity is mediated by which of the following 7. Which of the following is not true about urticaria:
261
Chapter
13 Nutrition
Nutrition
PROTEIN ENERGY MALNUTRITION (PEM)
(RDA) of vitamins
PEM is still a major health problem in the developing
Vitamin Adult Adult Pregnancy Lactation
Male Female
countries including India. It occurs mainly in childhood and
is an important cause of morbidity and mortality.
Vitamin A ( g/d) 900 700 750 1200
Vitamin C (mg/d) 90 75 85 120 PEM occurs due to absolute or relative deficiency of
Vitamin D ( g/d)* 5 5 10 10 energy and protein. It may be due to inadequate food intake
Vitamin E (ng/d) 15 15 15 19 or secondary to illnesses such as diarrhea, respiratory
Vitamin K ( g/d) 120 90 90 90
Thiamine (mg/d) 1.2 1.2 1.4 1.5
infections, measles and intestinal worms. Factor contributing
Riboflavin (mg/d) 1.6 1.4 1.6 1.6 to PEM are poverty, poor environmental conditions, large
Niacin (mg/d) 18 16 18 18 family size, poor maternal health, failure of lactation,
Vitamin B6 (mg/d) 2.0 2.0 2.5 2.5 premature termination of breastfeeding and adverse customs.
Folate ( g/d) 200 200 400 300
Vitamin B12 ( g/d) 1 1 1.5 1.5
Pantothenic acid Classification
(mg/d) 5 5 6 7 PEM is classified in various ways depending on weight,
Biotin ( g/d) 30 30 30 35
Choline (mg/d) 550 425 450 550
height , severity and relative contribution of energy or protein
deficit. The commonly used classification is Wellcome Trust
*as calciferol (1 g is equal to 40 IU)
Classification which is given in Table 13.2. Another
as water soluble and fat soluble vitamins. Fat soluble classification (WHO classification) describes PEM under
vitamins are vitamin A, D, E and K. Water soluble vitamins different nomenclature normal, stunting and wasting.
are thiamin (B1), riboflavin (B2), niacin (B3), pyridoxine
(B6), cobalamin (B12), folate, pantothenic acid, biotin and Clinical Manifestations
L-ascorbic acid (vitamin C). Recommended dietary
allowances (RDA) of vitamins are given in Table 13.1.
The clinical manifestations of PEM range from mild growth
retardation and weight loss to distinct clinical forms like
263
kwashiorkor and marasmus. The weight to height ratio is
Minerals
low. There is loss of subcutaneous fat, wasting of muscles
Body requires major minerals, electrolytes and trace and edema. Features of specific vitamin deficiency may also
elements. These are needed for growth, repair and vital body be found. Oral manifestations of malnutrition are given in
functions. Major minerals are calcium, magnesium and Table 13.3.
phosphorus. Electrolytes include sodium, potassium and
TABLE 13.2: Classification of PEM
chloride. Trace elements are iron, zinc, copper, manganese,
molybdenum, fluoride, iodide, cobalt, chromium and Kwashiorkor 60-80% of expected weight with edema
selenium. Under nutrition 60-80% of expected weight without edema
Marasmus Less than 60% of expected weight without
edema
Balanced Diet Marasmic Kwashiorkor Less than 60% of expected weight with
A balanced diet is defined as a diet which provides adequate edema
amount of energy, amino acids, carbohydrates, fats, vitamins
and minerals to maintain health and general wellbeing. The TABLE 13.3: Oral manifestations in malnutrition
diet should also provide extra amount of nutrients to meet Findings Deficiency of nutrients
the demands during short periods of deficiency. Glossitis Niacin, riboflavin, Vitamin B12,
folate, pyridoxine
Recommended Dietary Allowance (RDA) Bleeding gums Vitamin C, riboflavin
Cheilosis and angular stomatitis Riboflavin, niacin
Nutritional requirements are generally expressed in the form Atrophic lingual papillae Niacin, riboflavin, iron, folate,
of RDA. This is the average daily dietary intake that meets Vitamin B12
the nutrient requirements in healthy persons of a specific Hypogeusia Vitamin A, zinc
Tongue fissuring Niacin
sex, age and physiological condition (pregnancy, lactation).
Kwashiorkor occurs due to protein deficiency while the common than single vitamin deficiency. Body stores for
energy intake is adequate. The child develops dependant vitamins B12 and vitamin A are large and persist for more
edema, ascites, anasarca, ‘flaky paint’ dermatosis and fatty than an year after being on a deficient diet while folate and
liver. Marasmus is caused by the deficiency of both, energy thiamine stores are short lived and deplete within weeks.
and proteins. Patient typically develops weight loss, wasting Daily requirement of vitamins are given in Table 13.1.
and cachexia. Body fat stores are depleted and muscle mass Most deficiencies are associated with malnutrition,
decreases. There may be intermediate clinical forms having malabsorption, alcoholism, medications, total parenteral
features of both kwashiorkor and marasmus. nutrition, hemodialysis, food faddism or inborn errors of
Kwashiorkor like PEM may develop in adults following metabolism.
trauma, burn and sepsis. Marasmus like PEM may result Vitamin deficiency develops gradually and the symptoms
from chronic obstructive pulmonary disease, congestive are nonspecific in the early stages. The physical findings
heart failure, cancer and AIDS. appear late. Subclinical deficiency of vitamins is common
particularly in the geriatric age group and can be recognized
Laboratory Assessments by laboratory testing.
a. Laboratory assessment includes anthropometric measur- Excess vitamins can also cause disease. Some vitamins
ements for subcutaneous fat and skeletal muscles (mid- are also used as drugs, e.g. niacin for hyperlipidemia and
arm circumference and thickness of the triceps skin fold vitamin A for cystic acne and skin wrinkles.
of the posterior mid-upper arm).
b. Serum levels of protein, minerals, vitamins and assessment Thiamine (Vitamin B1)
of immune functions are important laboratory tests. Functions
1. Thiamine pyrophosphate (TPP) acts as a coenzyme in
264
Treatment the decarboxylation of alpha-ketoacids and branched-
Treatment of PEM is a slow process. Patients fed rapidly chain amino acids and thus is a source of energy
may develop complications like hypokalemia, hypopho- production.
sphatemia and congestive heart failure due to volume 2. Thiamine pyrophosphate acts as a coenzyme for a
overload. transketolase reaction that mediates conversion of
• Fluid and electrolyte abnormalities and infections are hexose and pentose phosphates.
controlled. 3. It plays a role in peripheral nerve conduction.
Essentials of Medicine for Dental Students
• The treatment is directed toward repletion of protein, 4. It is a coenzyme for the enzyme alcohol dehydrogenase.
energy, vitamins and micronutrients.
• The supple mentation can be done orally or parenterally. Sources
Important sources of thiamine are yeast, pork, legumes,
VITAMINS beef, whole grains and nuts. Milled and polished rice is a
Vitamins are organic compounds required by the body for poor source of vitamin B1. Hence, deficiency of vitamin B1
variety of essential metabolic functions. These are grouped is more commonly seen in those with polished rice based
as water soluble and fat soluble vitamins. Fat soluble diet. Tea and coffee contain thiaminases that destroy the
vitamins are vitamin A, D, E and K. Water soluble vitamins thiamine.
are thiamin (B1), riboflavin (B2), niacin (B3), pyridoxine
(B6), cobalamin (B12), folate, pantothenic acid, biotin and Deficiency
L-ascorbic acid (vitamin C). The deficiency of thiamine most commonly occurs due to
Vitamins are not synthesized at all or are inadequately poor intake and alcoholism. The deficiency presents with
synthesized in the body; hence they are required in the diet. nonspecific symptoms in the early stages such as anorexia
They are generally needed in very small quantities for and irritability. Prolonged deficiency of thiamine causes
essential functions. Multiple vitamin deficiency is more beriberi. Beriberi may be wet or dry.
Nutrition
a. Wet beriberi is characterized by the presence of deficiencies. People who consume rice as staple diet
cardiomegaly, tachycardia, congestive heart failure and are more prone to riboflavin deficiency. The clinical
peripheral edema. manifestations are mucocutaneous lesions of the mouth and
b. Dry beriberi presents with symmetrical sensorimotor skin such as chelosis, angular stomatitis, magenta tongue
neuropathy. and seborrhic dermatitis. Corneal vascularization and
Alcoholics with chronic thiamine deficiency may also have anemia may also occur.
central nervous system manifestations. These include
Wernicke’s encephalopathy (nystagmus, ophthalmoplagia, Diagnosis
cerebellar ataxia and mental impairment) and Korsakoff’s The treatment is usually started empirically. However, the
syndrome (amnesia, confabulation and impaired learning). diagnosis can be confirmed by measurement of red blood
cell and urinary riboflavin concentrations or red blood cell
Diagnosis glutathione reductase activity.
In most cases, the clinical response to thiamine therapy
supports the diagnosis. However, biochemical tests can also Treatment
be performed to confirm the deficiency. These include an Riboflavin deficiency is easily treated with oral preparations
assay of transketolase activity before and after addition of of the vitamin with the dosage of 5-15 mg/day. It is given
thiamine pyrophosphate and measurement of thiamine levels till the clinical findings are resolved.
in blood and serum.
Niacin (Vitamin B3)
Treatment Functions
Thiamine in a dose of 100 mg/day parenterally is given for Niacin refers to nicotinic acid, nicotinamide and their
7 days in acute cases. This is followed by 10 mg/day orally
till complete recovery. Anaphylaxis has been reported with
derivatives. It serves as a precursor of nicotinamide adenine
dinucleotide (NAD) and nicotinamide adenine dinucleotide
265
the parenteral use of thiamine. phosphate (NADP) which are involved in many oxidation-
Benfotiamine is a newer derivative of thiamine. It is lipid reduction reactions. Unlike other vitamins, niacin is
soluble and hence is absorbed much better than water soluble synthesized in the body from the amino acid tryptophan,
thiamine hydrochloride. It activates the enzyme transketolase but to a very small extent.
ten times more than thiamine.
Sources
Riboflavin (Vitamin B2)
Important sources of niacin are milk, eggs, beans and meat.
Functions The bioavailability of niacin from cereals especially maize
Riboflavin plays an important role in the oxidation-reduction is low.
reactions and is a cofactor in a number of enzymes involved
in energy metabolism. Deficiency
The deficiency of niacin leads to pellagra. This is more
Sources common in people who eat corn-based diet. Pellagra can
Milk and other dairy products, eggs and green leafy also occur in alcoholics and in inborn errors of tryptophan
vegetables are important sources. Other sources are cereals, metabolism (Hartnup’s disease).
legumes, broccoli and fish. Pellagra is characterized by dermatitis, diarrhea and
dementia. There are dark, dry and scaly lesions in sun
Deficiency exposed areas such as back of the hands, lower legs, face
Riboflavin deficiency is usually due to poor dietary intake and neck (Casal’s necklace). Other features are anorexia,
and is commonly associated with multiple vitamin irritability, bright red glossitis, stomatitis and weight loss.
Depression, seizures and psychosis may also occur. Treatment
Advanced pellagra can result in death. Vitamin B6 is given orally in a dosage of 10-20 mg/day.
However, higher doses (100-200 mg/day) are needed in
Diagnosis cases with medication-related vitamin deficiency. It is also
Pellagra is generally diagnosed clinically. However, indicated in the prevention of isoniazid-induced neuropathy.
measurement of niacin metabolites in the urine can be
performed to confirm the diagnosis. Toxicity
High doses of vitamin B6 can cause sensory neuro-pathy
Treatment and dermatitis.
Oral nicotinamide or nicotinic acid (10-150 mg daily)
effectively treats pellagra. Folate and Vitamin B12
These vitamins are discussed in Chapter 3.
Toxicity
Toxicity may occur at high dosage of nicotinic acid used to Biotin
treat hyperlipidemia. Symptoms include flushing, skin This is a water soluble vitamin which plays a role in
dryness and itching. Others are gastric irritation, gluconeogenesis and fatty acid synthesis. Dietary sources
hepatotoxicity, hyperglycemia, gout and macular edema. of biotin are liver, beans, yeast and egg yolk. Significant
amounts are also formed by the bacteria of the gut. In adults,
Vitamin B6 (Pyridoxine) the deficiency of biotin results into depression, hallucination,
Functions paresthesia, anorexia. Seborrhic rash may occur over face.
Vitamin B6 refers to a group of closely associated substances The deficiency of biotin in infants can lead to lethargicness,
Deficiency Choline
Deficiency of vitamin B6 may occur in association with Choline is a precursor of acetylcholine, phospholipids and
various drugs (isoniazid, cycloserine, oral contraceptives) betane. It is also necessary for the integrity of cell membrane.
or alcoholism. Glossitis, cheilosis, weakness are usual Deficiency can lead to fatty liver and elevated transaminases
features of the vitamin B6 deficiency. Severe deficiency levels.
results in the peripheral neuropathy and personality
changes including depression and irritability. Microcytic Vitamin C (L-ascorbic Acid)
hypochromic anemia and seizures may also occur. Functions
Vitamin C is a potent antioxidant which is involved in many
Diagnosis oxidation-reduction reactions. It is also required for the
A low level of pyridoxal phosphate in blood is diagnostic synthesis of collagen and conversion of dopamine to
of vitamin B6 deficiency. norepinephrine. Vitamin C promotes iron absorption because
Sources
Nutrition
it reduces ferric iron in diet to ferrous form which is better
absorbed. It is also involved in drug metabolism, wound Rich sources of vitamin E are sunflower oil, safflower oil
healing and carnitine biosynthesis. and wheat germ oil. It is also found in meat, nuts, cereals,
fruits and vegetables.
Sources
Amla, citrus fruits, guava, green vegetables, potatoes and Deficiency
tomatoes are good sources of vitamin C. The requirement Dietary deficiency of vitamin E is rare. Deficiency can occur
for vitamin C increases under stress, smoking and in those in chronic and severe malabsorption, abetalipoproteinemia,
on hemodialysis.
and in children with chronic cholestatic liver disease or cystic
fibrosis.
Deficiency
Manifestations of vitamin E deficiency include hemolytic
Deficiency may occur in poor, elderly and chronic
anemia, areflexia, gait disturbances, decreased vibration and
alcoholics. Vitamin C deficiency causes scurvy in which
position sense and ophthalmoplegia. Myopathy and
there is impaired formation of mature connective tissue. The
retinopathy may also occur. It also causes posterior column
patients may have petechiae, ecchymosis, swollen and
and spinocerebellar symptoms.
bleeding gums, hemarthrosis, anemia and poor wound
healing. In children bone growth is impaired. Periodontal Diagnosis
signs do not develop in edentulous patients.
Low blood levels of α tocopherol is diagnostic of vitamin E
Diagnosis deficiency.
Diagnosis is made clinically and confirmed by the low level
Treatment
267
of ascorbic acid in plasma and leukocytes.
Symptomatic vitamin E deficiency is treated with 800-1200
Treatment mg of α tocopherol daily. Higher doses are required in
The usual dose of vitamin C is 200-500 mg/day orally. abetalipoproteinemia. In higher doses, vitamin E protects
Studies have reported that high intake of vitamin C may from intraventricular hemorrhage of prematurity and oxygen-
protect against certain cancers. Vitamin C in the dosage of induced retrolental fibroplasias and bronchopulmonary
1-2 g/day may decrease the duration and symptoms of upper dysplasia.
respiratory infection.
Toxicity
Toxicity High dose of vitamin E (>800 mg/day) may interfere with
More than 2 g/day can cause gastric irritation and diarrhea. vitamin K metabolism, hence it should not be given to
Higher doses can lead to hyperuricemia and raised levels of patients taking warfarin. Higher doses can also cause nausea,
alanine amino transferase (ALT) and lactate dehydrogenase flatulence and diarrhea.
(LDH). It can also lead to false negative test for fecal occult
blood and disturbs the urinary glucose estimation. Vitamin A
Vitamin A (retinol) is a high molecular weight alcohol,
Vitamin E synthesized from plant carotenoids. The oxidized
Functions metabolites of retinol, retinaldehyde and retinoic acid are
Vitamin E is a collective name for naturally occurring also biologically active compounds. Retinaldehyde is
tocopherols. α tocopherol is the most potent of all toco- required for normal vision and retinoic acid is necessary
pherols. It is a powerful antioxidant. Vitamin C, glutathione for growth and cell differentiation. Vitamin A also plays a
and various enzymes maintain vitamin E in the reduced state. role in iron metabolism and humoral and cellular immunity.
Sources Vitamin K
Liver and fish have preformed vitamin A. Green leafy Vitamin K exists in two natural forms, vitamin K I
vegetable, green and yellow fruits (papaya, mango, (phylloquinone) and vitamin K II (menaquinone). Vitamin
pumpkin) and carrots are good sources of β-carotene also K II is synthesized by intestinal bacteria and vitamin K I is
known as provitamin A. Milk is a poor source of vitamin A. found in animal and plant sources. Menadione (K III) is a
Fortified food (vanaspati and milk) are also sources for synthetic provitamin which is converted to vitamin K II by
vitamin A. the liver.
Vitamin K plays an important role in the coagulation
Deficiency process by acting as a cofactor for the post translational
gamma carboxylation of factor II, VII, IX and X, protein C
Vitamin A deficiency is one of the most common vitamin
and S. These modified proteins are able to bind with platelets
deficiency syndromes and is a common cause of blindness.
in a calcium dependent reaction and participate in the
Night blindness is the earliest symptom. Conjuctival
coagulation process more efficiently. Without gamma
xerosis, Bitot’s spots, corneal xerosis and keratomalacia are
corboxylation, these factors do not function efficiently.
other ocular signs of vitamin A deficiency. Xerophthalmia
Warfarin type drugs prevent the conversion of vitamin K to
refers to all ocular manifestations of vitamin A deficiency. its active hydroquinone form.
Keratomalacia is ulceration and necrosis of cornea which
may perforate. Sources
Extraocular manifestations include hyperkeratotic skin Dietary source of vitamin K are green leafy vegetables, fruits,
lesions, anorexia and growth retardation. milk, butter, liver and coffee. It is also present in olive oil
and soyabean oil. Vitamin K II is endogenously produced
Diagnosis
268 Measurement of serum retinol is diagnostic. Abnormalities
by gut bacteria.
A intramuscularly or 60 mg (200,000 IU) orally. The dose are particularly susceptible to vitamin K deficiency because
of low stores, low levels of vitamin K in the breast milk,
is repeated every six months in endemic areas.
lack of intestinal flora and liver immaturity.
Toxicity Deficiency of vitamin K may present as bleeding from
any site.
Acute toxicity has been reported after excess consumption
of polar bear liver or intake of more than 150 mg vitamin A. Diagnosis
Presentations include increased intracranial pressure, Prothrombin time (PT) is prolonged in mild deficiency. PT
vertigo, diplopia, seizures and exfoliative dermatitis. and APTT both are elevated in advanced cases; however,
Chronic toxicity (ingestion of 15 mg/day for several PT is elevated to a greater extent. The vitamin K level can
months) manifests as dry skin, cheilosis, glossitis, alopecia, be measured by chromatography.
bone pain, hypercalcemia and increased intracranial
pressure. Treatment
High dose of carotenoids may cause yellowing of skin The deficiency is treated with 10 mg vitamin K parenterally.
(palm and soles) but not the sclera. Patients with chronic malabsorption should receive 1-2 mg
Nutrition
parenterally every week. Newborns are given 1 mg vitamin vitamin D activation (in renal disorders) and resistance to
K intramuscularly at the time of birth as a prophylaxis. the effects of vitamin D (defective receptors). Drugs such
as phenytoin, rifampicin and barbiturates can lead to
Toxicity increased metabolism of vitamin D in liver, thus they can
Toxic effects of vitamin K are hemolysis and hyper- cause vitamin D deficiency.
bilirubinemia which are reported after parenteral use of Vitamin D deficiency leads to rickets in children and
menadione. osteomalacia in adults. Rickets is characterized by growth
failure, bony deformities, muscular hypotonia, tetany and
Vitamin D convulsion. Bony deformities include curved legs, pigeon
Vitamin D exists in two forms: ergocalciferol (vitamin D2) chest, Harrison sulcus, rickety rosary, kyphoscoliosis
and cholecalciferol (vitamin D3). Ergocalciferol is derived and deformed pelvis. Defective skeleton mineralization,
from plants (the ergot fungus found especially on rye) bone fractures and proximal myopathy are found in
and cholecalciferol is synthesized in the skin from 7- osteomalacia.
dehydrocholesterol under the influence of ultraviolet rays
present in sunlight or is synthetically produced. Vitamin D Diagnosis
is stored largely in fat depots. Cholecalciferol is converted Serum calcium and phosphate levels are low. There is a
to active forms by hydroxylation in the liver and compensatory increase in PTH level. Serum concentration
subsequently in kidneys. In the liver, it is converted to 25- of vitamin D is low.
hydroxycholecal-ciferol (25[OH] D3) and in kidney, to
most potent metabolite 1, 25-dihydroxycholecalciferol Treatment
269
(1,25[OH]2 D3) or calcitriol. Treatment involves replacement of vitamin D and calcium.
The main function of vitamin D is to increase absorption Vitamin D can be replaced in various forms like ergocalciferol,
of calcium and phosphate from the intestine. It also increases 1-α-hydroxy vitamin D3 (α-calcidol) and 1,25-dihydroxy
the renal tubular resorption of phosphate. Vitamin D vitamin D3 (calcitriol). The dose of calcitriol is 0.25 to 0.5
promotes bone mineralization. It may also have other µg daily.
systemic effects since vitamin D receptors are found in many
body tissues. Toxicity
Vitamin D is actually a hormone and if sufficient Excessive intake of vitamin D may cause hypercalcemia
exposure of sunlight is given to the skin it is not required in which present as anorexia, nausea, vomiting, thirst, polyurea
the diet. It was classified as vitamins when much was not and drowsiness. Cardiac arrhythmias, renal failure and coma
known about it. may occur.
270 A. Kidney
C. Bone
B. Liver
D. Skin
A.
B.
Provitamin A
Vitamin K
6. Glossitis and angular stomatitis are features of all the C. Vitamin D
vitamins except: D. Vitamin C
A. Niacin B. Pyridoxine
C. Riboflavin D. Ascorbic acid Fill in the Blanks
7. All the following are causes of bleeding gums except:
1. Diarrhea, dementia and dermatitis are due to
A. Acute myeloblastic leukemia
_________ deficiency.
Essentials of Medicine for Dental Students
B. Phenytoin therapy
2. Wernicke’s encephalopathy is due to the deficiency
C. Scurvy
of _________ vitamin.
D. Candidiasis
3. Night blindness is a feature of _________ deficiency.
8. Deficiency of vitamin D can lead to:
4. Bitot’s spot is seen in _________.
A. Hypercalcemia
5. Osteomalcia is due to deficiency of _________.
B. Decreased absorption of calcium from intestine
6. Vitamin _________ is required for synthesis of clotting
C. Decreased renal excretion of calcium
factors.
D. Increased renal calcium excretion
7. Subacute combined degeneration of spinal cord can
9. The syndrome of angular oral fissure, corneal vascularization
occur in _________ deficiency.
and glossitis is due to:
8. Deficiency of vitamin B 1 is more common with
A. Pyridoxine deficiency
_________ based diet.
B. Niacin deficiency
9. Corneal vascularization can occur in _________
C. Riboflavin deficiency
deficiency.
D. Xerophthalmia (vitamin A deficiency)
10. _________ is used to prevent isoniazid induced
10. Sensory neuropathy can occur with high doses of which of
neuropathy.
the following vitamin:
11. People who eat corn based diet are prone to develop
A. Thiamine B. Pyridoxine
_________ deficiency.
C. Niacin D. Vitamin B12
Chapter
14 Preoperative Evaluation
Patients must be thoroughly assessed preoperatively for Blood pressure should be well controlled before
their fitness for anesthesia and surgery. This is important surgery.
because there is a risk of morbidity and mortality in patients
undergoing surgery. The mortality increases with age as PULMONARY EVALUATION
geriatric population is at increased risk of cardiac events. Pulmonary complications in the postoperative period include
Cardiac causes are major causes of death in postoperative pneumonia, hypoventilation and atelectasis. Perioperative
period (First 48 hours). Death in the later period is mainly pulmonary function tests such as FEV1 are indicated in
due to sepsis, pneumonia, cardiac arrest, pulmonary patients with suspected lung disease, COPD and in smokers.
embolism and renal failure. FEV1 is the best predictor of the surgical risk. Chest X-
Identification of high risk patients requires a proper ray is also recommended in suspected lung disease. Arterial
history taking and a focused clinical examination. Evaluation blood gas analysis is generally not needed, however, it is
of such patients is important so that their suitability recommended in patients with severe COPD. Patient should
for surgery may be ascertained. American Society of
be advised to stop smoking weeks before the surgery. The
Anesthesiologists (ASA) have classified the surgical risk
dose of bronchodilators must be optimized.
on the basis of patient’s functional status, comorbid
diseases and the type of surgery. Head and neck surgery is HEMATOLOGICAL EVALUATION
stratified as intermediate risk (<5% mortality) and superficial
Patients should be evaluated for the presence of hemorrhagic
procedures as low risk surgery (<1% mortality).
diastheses. A history of use of aspirin and other NSAIDs,
CARDIOVASCULAR EVALUATION warfarin or heparin must be obtained. Aspirin should be
discontinued one week prior to elective procedure. Warfarin
Cardiac risks of surgery include myocardial infarction and
is advised to be discontinued at least five days before the
other cardiac events which may be fatal. The risk for cardiac
surgery. However, if anticoagulation is required, low
complications depends upon functional capacity, age
molecular weight heparin (LMWH) may be given. This is
of the patient, type of surgery and presence of comorbid
discontinued 12-24 hours prior to surgery and restarted
conditions. The predictor of cardiac ischemia in
postoperative period include left ventricular hypertrophy on postoperatively. An INR of <1.5 is considered safe for most
ECG, history of hypertension, definite coronary artery surgeries. Patients with risk of venous thromboembolism
disease, diabetes mellitus and use of digoxin. require prophylactic administration of LMWH and early
During preoperative cardiac evaluation one should mobilization.
particularly look for the evidence of ischemic heart disease,
ENDOCRINAL EVALUATION
valvular heart disease, congestive heart failure, arrhythmias
and hypertension. A moderate control of blood sugar (<150 mg/dL) is desirable
Routine surgery must be delayed for at least 6 months in perioperative period. Patient on oral hypoglycemic agent
after a myocardial infarction. (OHA) should hold the medication on the morning of
surgery (48 hours before in case of metformin). risks of drug-induced nephro-toxicity. Patient with end-stage
Subsequently, if needed, insulin is given to control blood renal disease may need hemodialysis prior to surgery and
sugar. in postoperative period.
Surgery is contraindicated in uncontrolled hyper- Elective surgery is absolutely contraindicated in patients
thyroidism until the patient is euthyroid. with severe acute infections.
Adrenal insufficiency may occur in patients who have
received long-term steroid therapy. These patients require PREOPERATIVE LABORATORY EVALUATION
corticosteroids in perioperative period. Certain routine tests are recommended before elective
surgery (Table 14.1). However, specific tests may be required
NUTRITIONAL EVALUATION based on the clinical conditions of the patient.
Patients with malnutrition and hypoalbuminemia have higher
postoperative morbidity and mortality. They require TABLE 14.1: Preoperative laboratory tests
preoperative nutritional intervention. • Complete blood count (Hb, TLC, DLC, and Platelet
count)
EVALUATION OF OTHER ORGANS • Prothrombin time (PT) and activated partial thrombo-
plastin time (APTT)
Patients with chronic liver disease have high risk for • Urine analysis
anesthesia (delayed clearance of anesthesia and prolonged • Electrolytes
intubation). PT and APTT tests are mandatory prior to • Biochemistry (Blood sugar, blood urea, serum
surgery. creatinine, liver function tests)
• Chest radiograph
Patients with renal failure should be monitored for fluid • Electrocardiagraphy
and electrolyte imbalance, hypertension, hypotension and
272
Essentials of Medicine for Dental Students
Test Paper
1. Which of the following clinical features is indicative of left 8. Match the following:
ventricular failure: A. Pulsus alternans 1. Cardiac tamponade
A. Neck vein distension B. Pulsus paradoxus 2. LVF
B. Ascites C. Water-Hammer pulse 3. AF
C. Orthopnea D. Irregularly irregular pulse 4. AR
D. Edema 9. Following are the features of iron deficiency anemia except:
2. Which of the following is a sign of aortic stenosis: A. Low serum ferritin
A. Diastolic rumble B. Hypochromic microcytic
B. An opening snap C. Absent marrow iron on biopsy stain
C. Loud second heart sound D. Decreased total iron binding capacity
D. Harsh systolic murmur 10. All are true regarding idiopathic thrombocytopenic purpura
3. All the following are cardiac risk factors except: except:
A. Hypertension A. Steroids are used in treatment
B. Family history of CAD B. Splenomegaly is usually present
C. High levels of HDL C. Bone marrow reveals increased megakaryocytes
D. Diabetes mellitus D. Splenectomy can be effective therapy
4. All of the following features are seen in patients with 11. All of the following patients may have DIC except:
pulmonary embolism except: A. Patients with gram negative infections
A. Cyanosis B. Hypoxia B. Patients with multiple trauma
C. Bradycardia D. Right heart failure C. Patients with administered thrombolytic agents
5. A reduced one second forced expiratory volume to forced D. Patients with retained dead fetus
vital capacity is present in all the following except: 12. Hemolysis is indicated by all of the following except:
A. Allergic asthma B. Chronic bronchitis A. Increased LDH levels
C. Emphysema D. Lung abscess B. Shortened red blood cell survival
6. Match the following: C. Decreased number of reticulocytes
A. VSD 1. Absent femoral pulses D. Reduced serum haptoglobin
B. ASD 2. Continuous murmur 13. All the following can cause inflammatory bloody diarrhea
C. PDA 3. Fixed, wide second except:
heart sound A. Entamoeba histolytica
D. Co-arctation of aorta 4. Holosystolic murmur B. Giardia lamblia
7. Match the following: C. Campylobacter jejuni
A. AS 1. Loud first heart sound D. Shigella species
B. MS 2. Parvus et tardus 14. Following is not true regarding Plummer-Vinson syndrome:
C. MR 3. Austin Flint murmur A. Esophageal webs are present
D. AR 4. Pansystolic murmur B. Webs may be associated with iron deficiency anemia
C. Also known as Paterson-Kelly syndrome 24. Which of the following should be avoided in treatment of
D. Lesions are not premalignant tuberculosis in mild to moderate renal failure:
15. Therapy of ascites includes all the following except: A. Rifampicin B. Pyrazinamide
A. Diuretics C. Isoniazid D. Streptomycin
B. Paracentesis 25. All the following can cause hypercalcemia except:
C. Unrestricted salt intake A. Sarcoidosis
D. Bedrest B. Multiple myeloma
16. Rifampicin is used in: C. Tumor lysis syndrome
A. Treatment of tuberculosis D. Prolonged immobilization
B. Prevention of meningococcal meningitis 26. A 52-year-old female with type 2 diabetes is found
C. Treatment of staphylococcal endocarditis to have 24-hr urinary proteinuria of 280 mg. Which
D. All the above of the following drug should be used to retard progression
17. Match the following: of renal disease:
A. Cough 1. Calcium channel A. Aspirin B. Thiazide
blockers C. Ramipril D. Amiloride
B. Gingival hyperplasia 2. Beta blockers 27. In a patient of Listeria meningitis who is allergic to penicillin,
C. Precipitation of 3. ACE inhibitors the antimicrobial of choice is:
asthma A. Gentamicin
D. Hypokalemia 4. Diuretics B. Ceftriaxone
18. Limb edema can occur with the use of following drug: C. Trimethoprim-sulphamethoxazole
A. Beta blockers D. Vancomycin
B. Calcium channel blockers 28. All the following can cause megakaryocytic thrombocytopenia
C. Diuretics except:
Test Paper
except: D. Gastric atrophy
A. Hyperuricemia is a side effect of pyrazinamide 39. All the following diseases cause massive splenomegaly
B. Red-green color impairment is a sign of ethambutol except:
toxicity A. Malaria
C. Ethambutol accumulates in renal failure B. Kala azar
D. ‘Flu like syndrome’ is usually seen in people taking C. Idiopathic myelofibrosis
rifampicin on daily basis D. Infective endocarditis
33. Which of the following organisms, when isolated in blood, 40. A 10-day-old neonate is posted for pyloric stenosis surgery.
requires the synergistic activity of penicillin plus an The investigations report shows a serum calcium level of
aminoglycoside for appropriate therapy: 6.0 mg /dL. What information would you like to know before
A. Enterococcus faecalis you supplement calcium to this neonate:
B. S. aureus A. Blood glucose B. Serum bilirubin
C. Streptococcus pneumoniae C. Serum albumin D. Oxygen saturation
D. Bacteriodes fragilis
41. All the following drugs are used in the management of status
34. All the following can cause DIC except: epilepticus except:
A. Amniotic fluid embolism A. Phenytoin B. Thiopentone sodium
B. Intrauterine fetal death C. Carbamazepine D. Diazepam
C. Diabetes mellitus
42. Urgent reversal of warfarin therapy can be done by
D. Abruptio placentae
administration of:
35. Ebstein-Barr virus is associated with: A. Platelet concentrates B. Cryoprecipitate
A. Carcinoma larynx C. Fresh frozen plasma D. Packed red blood cell
B. Carcinoma bladder
43. Which of the following is generally not seen in idiopathic
C. Carcinoma nasopharynx
D. Carcinoma maxilla
36. A 12-year-old girl has history of recurrent bulky stools and
thrombocytopenic purpura (ITP):
A. Petechiae, ecchymosis and bleeding 275
B. Palpable splenomegaly
abdominal pain since 3 years of age. She has pallor and her C. More common in females
weight and height are below the third percentile. Which of D. Increased megakaryocytes in the bone marrow
the following is the most appropriate investigation to make
44. A young patient presenting with massive hematemesis was
a specific diagnosis
found to have splenomegaly. In this case the most likely
A. barium studies
source of bleeding is:
B. D-xylose test
A. Duodenal ulcer B. Esophageal varices
C. 24-hr fecal fat estimation
C. Erosive gastritis D. Gastric ulcer
D. Endoscopy and small intestinal biopsy
45. Following resuscitation, a patient with bleeding esophageal
37. A child underwent a tonsillectomy at 6 years of age with no
varices should be treated initially with:
complications. He underwent a preoperative screening for
A. Sclerotherapy B. Sagstaken Blackmore tube
bleeding at the age of 12 years before an elective laparotomy,
C. Propanolol D. Surgery
and was found to have a prolonged partial thromboplastin
time but normal Prothrombin time. There was no family 46. In which of the states in India the maximum number of AIDS
history of bleeding. The patient is likely to have: cases have been reported till now:
A. Acquired liver disease A. Delhi B. Kerala
B. Acquired vitamin K deficiency C. Tamil Nadu D. Bihar
C. Mild hemophilia A 47. Most sensitive test to detect hypothyroidism is:
D. Factor XII deficiency A. T3 B. T4
38. Endosopic biopsy from a case of H. pylori related early C. TSH D. Radioactive iodine uptake
chronic gastritis is most likely to reveal: 48. Following is not an anterior pituitary hormone:
A. Multifocal atrophic gastritis A. FSH B. TSH
B. Erosive gastritis C. ACTH D. ADH
49. HIV positive patients usually have: 58. Chronic type A gastritis is characterized by all the following
A. Low CD4, low CD8 clinical findings except:
B. High CD4, low CD8 A. Pernicious anemia
C. Low CD4, high CD8 B. Presence of parietal cell antibody
D. High CD4, high CD8 C. Antral involvement
50. Which of the following mediators is released during late D. Associated other autoimmune disorder
phase reaction of anaphylactic reaction: 59. A person vaccinated against hepatitis B will have following
A. Eosinophil chemotactic factor (ECF-A) serologic finding:
B. Histamine A. Hepatitis B surface antigen (HBsAg)
C. Leukotriene B4 B. Hepatitis B surface antibody (anti-HBs)
D. Angiotensinogen C. Both HBsAg and anti-HBs
51. IgE-mediated hypersensitivity is implicated in all of the D. Hepatitis Be antibody
following reactions except: 60. All the following can precipitate hepatic encephalopathy in
A. Serum sickness patients of cirrhosis:
B. Latex anaphylaxis A. Gastrointestinal bleeding
C. Systemic reaction to insect sting B. SBP
D. Asthma C. Ampicillin therapy
52. Following are indications of surgery in endocarditis except: D. Sedatives
A. Congestive heart failure 61. A positive Chovstek’s sign is found in:
B. Fungal endocarditis A. Hyperkalemia B. Hypocalcemia
C. History of injection drug use C. Acidosis D. Hypoglycemia
D. Failure to respond to antibiotic therapy 62. In Pseudohypoparathyroidism the lab test reveal:
53. Generalized lymphadenopathy is found in all except: A. Low calcium and high PTH (parathyroid hormone)
276
A. Infectious mononucleosis B. High calcium and low PTH
B. HIV-1 C. High calcium and high PTH
C. Malaria D. Low calcium and low PTH
D. Syphilis 63. All the following features may be in hyperthyroidism except:
54. Bacterial and viral meningitis are characterized by all except: A. Atrial fibrillation B. Pretibial myxedema
A. Neck rigidity C. Constipation D. Lid lag
B. Increased protein in CSF 64. Crackles are present in which of the following condition:
C. Increased cells in CSF A. Pleural effusion B. Pneumothorax
Essentials of Medicine for Dental Students
Test Paper
by: A. All coagulation factors
A. ABG analysis B. All coagulation factors and platelets
B. Chest X-ray C. Factor VIII, vWF and fibrinogen
C. Ventilation perfusion scan D. Platelets and leukocytes
D. Pulmonary angiography 78. Serum creatinine is generally normal in:
69. Clubbing may be seen in all the following conditions except: A. Acute renal failure
A. Fallot’s tetralogy B. Eisenmenger syndrome B. Nephrotic syndrome
C. Infective endocarditis D. Constrictive pericarditis C. End-stage renal disease
D. Nephritic syndrome
70. A female patient has presented with a history of menorrhagia
and easy bruising. Lab studies show a normal PT, a 79. Following is true in Gilbert’s syndrome:
prolonged APTT and prolonged bleeding time. The most A. Raised alkaline phosphates
likely diagnosis is: B. Unconjugated hyperbilirubinemia
A. Hemophilia C. High ALT and AST
B. Factor IX deficiency D. Tender hepatomegaly
C. von Willebrand’s disease 80. Which of the following is not an oral manifestation of HIV:
D. Severe hepatic dysfunction A. Hairy leukoplakia B. Papilloma virus (warts)
C. Candidiasis D. P. cranii
71. A patient has serum calcium of 13.5 mg% on routine
examination. Which of the following would be most 81. Which of the following is not matched properly?
appropriate test to diagnose primary hyperparathy- roidism: A. Primary syphilis – chancre
A. Serum phosphate B. Tertiary syphilis – gumma
B. Ultrasound of the neck C. Secondary syphilis – mulberry molars
C. Serum parathyroid levels D. Congenital syphilis – Hutchinson’s teeth
277
D. Serum ionized calcium 82. HIV can be confirmed and detected by:
A. Polymerase chain reaction (PCR)
72. The side effects of thiazide diuretic therapy is:
B. Reverse transcriptase – PCR ( RT-PCR)
A. Hypoglycemia B. Hyperuricemia
C. Real time PCR
C. Cough D. Bronchospasm
D. Mimic PCR
73. All the following are causes of eosinophilia except:
83. Patients infected with HIV may have:
A. Ascaris infestation
A. Elevated blastogenesis
B. Nitrofurantoin therapy
B. Depressed serum immunoglobulin levels
C. Enteric fever
C. High T4-T8 ratio
D. Allergic bronchopulmonary aspergilosis (ABPA)
D. Thrombocytopenia
74. Following are features of enteric fever except: 84. AIDS is associated with depletion of:
A. Splenomegaly B. Rose spots A. T4 lymphocytes B. T8 Lymphocytes
C. Relative tachycardia D. Leukopenia C. B lymphocytes D. Monocytes
75. A patient has fasting blood sugar level of 98 mg/dL and has 85. AIDS is frequently complicated by opportunistic infections,
182 mg% blood sugar level 2 hr after glucose load (GTT). A notably pneumonia due to:
patient is having: A. Klebsiella pneumoniae
A. Diabetes mellitus B. Pneumocystis cranii
B. Impaired fasting glucose C. Streptococcus pneumoniae
C. Impaired glucose tolerance D. Mycoplasma pneumoniae
D. Diabetic ketoacidosis 86. Diagnosis of typhoid fever in the first week is made by
76. A patient has purpura with a platelet count of 2 lacs/ mm3. following test:
Following may be the possibilities except: A. Widal test B. Stool culture
A. Henoch-Schönlein purpura C. Urine culture D. Blood culture
B. Uremia 87. Causes of chest pain include all except:
C. ITP A. Prinzmetal’s angina B. Pericarditis
D. Vasculitis C. Aortic stenosis D. Mitral stenosis
88. Which of the following is used in hypertensive crisis: 102. Carbamazepine is used to treatthe following except:
A. Atenolol A. Partial seizures
B. Thiazides B. Trigeminal neuralgia
C. Enalapril C. Postherpetic neuralgia
D. Nitroglycerine or nitroprusside D. Tension headache
89. Multiple myeloma is commonly associated with all except: 103. Déjà vu phenomenon is associated with:
A. Anemia A. Absence seizures
B. High serum calcium B. Grand mal seizures
C. High serum alkaline phosphatase C. Simple partial seizures
D. High ESR D. Complex partial seizures
90. Following type of insulin has longest duration of action: 104. Recently identified liver protein which regulates iron
A. Regular B. Lispro metabolism is:
C. Aspart D. Glargine A. Hepadna B. Haptoglobin
91. Hypoglycemia may occur in: C. Hepcidin D. Transferrin receptor
A. Insulin overdose B. Insulinoma 105. Iron therapy is not indicated in:
C. Severe hepatitis D. All the above A. Chronic blood loss B. Pregnancy
92. Polyurea is seen with: C. CRF D. Thalassemia minor
A. Diabetes mellitus B. Diabetes insipidus
106. Anemia of chronic inflammation has following features
C. Hyperparathyroidism D. All the above
except:
93. Earliest indication of diabetic nephropathy is: A. Low ferritin
A. Hematuria B. Oliguria B. Normal bone marrow iron
C. Proteinuria D. Raised serum creatinine C. Low serum iron
94. Hypovolemic shock occurs when intravenous volume is D. Low TIBC
Test Paper
A. Atrial flutter components, except:
B. Atrial fibrillation A. Serosurveillance.
C. Complete heart block B. Health education and information
D. Second degree heart block C. Screening of blood and blood products
115. Indicator of active replication of hepatitis B virus is: D. Banning of sexual contact with foreigners
A. HBsAg B. HBcAg 129. The antibiotic cover is mandatory before extraction in the
C. HBeAg D. Anti-HBe following condition of the heart:
116. Austin Flint murmur may be mistaken for: A. Ischemic heart disease (IHD).
A. MR B. MS B. Hypertension
C. TS D. PR C. Congestive cardiac failure
D. Congenital heart disease
117. Match the following:
A. Graham Steel murmur 1. AR 130. Blue sclera is characteristic of:
B. Mid-diastolic murmur 2. VSD A. Amelogenesis imperfecta
C. Pansystolic murmur 3. PR B. Tetracycline hypoplasia
D. Early diastolic murmur 4. MS C. Fluorosis
D. Osteogenesis imperfecta
118. Collapsing pulse may be present in all the following except:
A. AR B. PDA 131. Bence Jones protein found in the urine may be suggestive
C. Severe anemia D. AS of:
A. Hyperparathyroidim B. Hodgkin’s disease
119. Following drugs cause bronchodilatation except:
C. Multiple myeloma D. Christian’s syndrome.
A. Salbutamol B. Terbutaline
C. Corticosteroids D. Iptratropium bromide 132. The syndrome which is associated with predisposition to
the development of carcinoma of oral mucous membrane
120. Clopidogrel is a following agent:
is:
A. Antiplatelet
C. Fibrinolytic
B. Throbolytic
D. Anticoagulant
A.
B.
Gardner’s syndrome
Osler-Rendu-Weber syndrome
279
121. Following are causes of hypocalcemia except: C. Sturge-Weber syndrome
A. Hypomagnesemia B. Acute pacreatitis D. Plummer-Vinson syndrome
C. Milk alkali syndrome D. Hypoparathyroidism
133. The most preferred approach for pituitary surgery at
122. Following is associated with high mortality if it occurs present is:
during pregnancy: A. Transcranial B. Transethmoidal
A. Hepatitis A B. Hepatitis B C. Transphenoidal D. Transcallosal
C. Hepatitis C D. Hepatitis E
134. The normal range of serum osmolality (in mOsm/kg H2O) is:
123. Drug of choice in trigeminal neuralgia is: A. 275 to 295 B. 310 to 330
A. Carbamazepine B. Phenobarbitone C. 350 to 375 D. 200 to 250
C. Beta blockers D. Verapamil
135. Afferent component of corneal reflex is mediated by:
124. Pulmonary oligemia is characteristically seen in: A. Vagus nerve
A. ASD B. VSD B. Facial nerve
C. PDA D. Fallot’s tetralogy C. Trigeminal nerve
125. All the following are associated with infranuclear facial D. Glossopharyngeal nerve
palsy except: 136. Ground glass appearance in bone is seen in:
A. Bell’s palsy B. Acoustic neuroma A. Hyperparathyroidism B. Fibrous dysplasia
C. Cerebral infarction D. Middle ear disease C. Condensing osteitis D. Osteopetrosis
126. In adults, the spinal cord normally ends at: 137. An affected male infant born to normal parents could be
A. Lower border of L1 B. Lower border of L3 an example of all the following except:
C. Lower border of S1 D. Lower border of L5 A. An autosomal dominant disorder
127. Iron is present in all the following except: B. An autosomal recessive disorder
A. Myoglobin B. Cytochrome. C. A polygenic disorder
C. Catalase. D. Pyruvate kinase D. A vertically transmitted disorder
138. Nevirapine is a: C. Decreasing the osteoclast-mediated resorption of
A. Protease inhibitor bone
B. Nucleoside reverse transcriptase inhibitor D. Decreasing the parathyroid hormone secretion
C. Non-nucleoside reverse transcriptase inhibitor 145. Brown tumors are seen in:
D. Fusion inhibitor A. Hyperparathyroidism
139. All the following are the known causes of osteoporosis B. Pigmented villonodular synovitis
except: C. Osteomalacia
A. Fluorosis B. Hypogonadism D. Neurofibromatosis
C. Hyperthyroidism D. Hyperparathyroidism
146. Megaloblastic anemia due to folic acid deficiency is
140. All the following are risk factors for atherosclerosis except: commonly due to:
A. Increased waist-hip ratio A. Inadequate dietary intake
B. Hyperhomocysteinemia B. Defective intestinal absorption
C. Decreased fibrinogen levels
C. Absence of folic acid binding protein in serum
D. Decreased HDL levels
D. Absence of glutamic acid in the intestine
141. All the following antibacterial agents act by inhibiting cell
147. Which one of the following drugs is an antipseudomonal
wall synthesis except?
penicillin?
A. Carbapenems B. Monobactams
A. Cephalexin B. Cloxacillin
C. Cephamycins D. Nitrofurantoin
C. Piperacillin D. Dicloxacillin
142. A diabetic patient developed cellutitis due to
148. All of the following are therapeutic uses of penicillin G,
Staphylococcus aureus, which was found to be methicillin
resistant on the antibiotic sensitivity testing. All the except in:
following antibiotics will be appropriate except: A. Bacterial meningitis B. Rickettsial infection
A. Vancomycin B. Imipenem C. Syphillis D. Anthrax
C. Teichoplanin D. Linezolid 149. Which the following organs is not involved in calcium
280 143. Calcitonin is secreted by:
A. Thyroid gland B. Parathyroid gland
homeostasis?
A. Kidneys B. Skin
C. Adrenal glands D. Ovaries C. Intestines D. Lungs
144. Bisphosphonates act by: 150. Mycotic aneurysm is due to:
A. Increasing the osteoid formation. A. Bacterial infection B. Fungal infection
B. Increasing the mineralization of osteoid. C. Viral infection D. Mixed infection
Essentials of Medicine for Dental Students
Reference Laboratory Values
282
Troponin T (s) 0-0.1 ng/mL
Urea Nitrogen (s) 10-20 mg/dL
Urea (s) 20-40 mg/dL
Uric acid (s)
Male 2.5-8.0 mg/dL
Female 1.5-6.0 mg/dL
Vitamin B12 250-900 ng/mL
Essentials of Medicine for Dental Students
HEMATOLOGICAL EVALUATION
Hemoglobin (p)
Male 13-16 g/dL
Female 12-15 g/dL
Hematocrit (p)
Male 42-52%
Female 37-48%
TLC 4000-11000/mm³
DLC
- Neutrophils 45-74%
- Lymphocytes 16-45%
- Monocytes 4-10%
- Eosinophils 0-7%
- Basophils 0-2%
Platelets 1.5-4.0 lacs/mm³
Reference Laboratory Values
ESR
Westergren <50 yrs
– Male 0-15 mm for 1st hr
– Female 0-20 mm for 1st hr
Westergren >50 yrs
– Male 0-20 mm for 1st hr
– Female 0-30 mm for 1st hr
Bleeding Time < 7 min
Prothombin Time (PT) control ± 1 sec
Partial Thromboplastin Time comparable to control (Activated PTT)
Thrombin Time control ± 3 secs.
Mean Corpuscular Hb (MCH) 27-33 pg
Mean Corpuscular Hb Concentration (MCHC) 31-35 %
Mean Corpuscular Volume (MCV) 82-98 fL
Osmotic Fragility
– Slight hemolysis 0.45-0.39%
– Complete hemolysis 0.33-0.3%
Reticulocyte
– adults 0.5-1.5 %
– children 2.5-6.5 %
283
CEREBROSPINAL FLUID
CSF Pressure 50-180 mm H2O
CSF Volume ~150 ml
Glucose 40-70 mg/dL
Protein 20-50 mg/dL
Cells total < 5 per mm3
DLC
-Lymphocyte 60-70%
-Monocyte 30-50%
-Neutrophils None
TOTAL CHOLESTEROL
Desirable <200
Borderline high 200-234
High > 240
HDL CHOLESTEROL
Low <40
High >60
TRIGLYCERIDES
Normal < 150 mg/dL
Borderline high 150-199 mg/dL
High 200-499 mg/dL
Very high > 500 mg/dL
290
pain 78, 122, 243 Endoscopic
precipitating factors 108 retrograde cholangiopancreatography
X-ray 82
reticulocyte count 51 32
Chickenpox 214
Cough 120 therapy 22
Cholestatic jaundice 34
Crigler-Najjar syndromes 34 Energy 262
Choline 266
CT scan and MRI 32 Enteric fever 221
Chorea 83 Cushing’s disease 199 Epilepsy 169
Chronic Cutaneous reactions 259 Epstein-Barr virus 63
complications of malaria 229 Cyanosis 8, 79 Eradication of streptococci 84
diarrhea 27
Erythema marginatum 83
Essentials of Medicine for Dental Students
gastritis 22
heart failure 104 D Esophageal
disease 16
hepatitis 39 Decline in glomerular filtration rate 154 dysphagia 21
B 40 Delerium 3 transection 44
C 40 Dementia 3 Essential hypertension 93
lymphocytic leukemia 61 Dense proteins 11 Estimation of glomerular filtration rate 154
meningitis 177 Dental Etiology of lung cancers 148
myeloid leukemia 60 procedures in pregnant women 246 Examination of
obstructive pulmonary disease 134 trauma 179 comatose patient 167
renal failure 159 Di George syndrome 195 cranial nerves 162
viral hepatitis 40 Diabetes Excessive bleeding 246
Chvostek’s sign 193 insipidus 200 Extra-abdominal diseases 15
Cirrhosis of liver 41 mellitus 200
Classical migraine 178 Diabetic
F
Clinical features of acute hepatitis 37 ketoacidosis 203
Clot lysis 65 nephropathy 204 Facial
Clubbing 7, 0 neuropathy 204 migraine 179
Cluster headache 180 Diarrhea 25 nerve 165
Coagulation Diet and nutrition 262 palsy 181
disorders 69 Diphtheria 220 pain 180
Index
Fat 262 D 37 Interstitial
Fat soluble vitamins 264 E 37 lung disease 147
Fatigue 78, 79 Hepatocellular pneumonia 127
Fecal fat estimation 29 carcinoma 45 Intestinal obstruction 15
Folate and vitamin B12 266 diseases 34 Investigations in renal disorders 154
Folic acid 54 Hepatorenal syndrome 45 Iron deficiency anemia 51, 52
Food poisoning 26 Herpes Ischemic heart disease 96
Forced labialis 20
expiratory volume 125 simplex virus 20 J
vital capacity 125 zoster 15, 214, 215
Functional platelet disorders 68 Herpesvirus hominis 216 Jacksonian march 170
Fungal meningitis 177 Herpetic stomatitis 20 Jarisch Herxheimer reaction 226
HIV and tuberculosis 140 Jaundice 7, 15, 16, 32
Hodgkin’s disease 61 Jugular venous
G pressure 6
Horner’s syndrome 163, 180
Gallstones 15 Hoshimoto’s thyroiditis 189 pulse 6, 81
Gastritis 22 Hospital acquired pneumonia 126 Junctional tachycardia 116
Gastrointestinal and hepatobiliary system 15 Human immunodeficiency syndrome 231
German measles 213 Hydrothorax 9 K
GI bleeding 16 Hyperbilirubinemia 7 Kernig’s sign 174
Gilbert’s syndrome 34 Hypercalcemia 194 Kidneys 17
Gingival hyperplasia 20 Hypereosinophilic syndrome 137 Kussmaul’s sign 6
Glossitis 52 Hyperglycemic hyperosmolar state 204 Kwashiorkor 264
Glassopharyngeal nerve 166 Hyperkinetic pulse 5
Glossopharyngeal neuralgia 181 Hyperparathyroidism 196
Glucose lowering agents 205 Hyperpyrexia 4
L
Glycated hemoglobin measurement 202 Lactate dehydrogenase 54
Hypertension 92
Gonorrhea 223 Laryngeal paralysis 167
Hypertensive crisis 96, 242
Graves’ disease 191
Gum hyperplasia 58
Gynecological diseases 15
Hyperthyroidism 190
Hypertrophic osteoarthropathy 8
Late latent syphilis 224
Latent syphilis 224 291
Hyperventilation 244 Left ventricle 108
Hypoadrenal shock 248 Leukemia 58
H Hypocalcemia 193 Liver 30
Halitophobia 11 Hypoglossal nerve 167 abscess 15
Halitosis 11 Hypoglycemia 208, 245 biopsy 32
Headache 178 Hypoparathyroidism 195 disease 9
Health care associated pneumonia 126 Hypopituitarism 3, 196 function tests 30
Heart Hypothyroidism 3, 188 Lobar pneumonia 126
burn 15 Hypovolemic shock 247 Low output heart failure 105
failure 103 Lower
Helicobacter pylori 63 I half headache 179
Hematemesis 16 limbs 12
Hematological Idiopathic thrombocytopenic purpura 67 Lung
diseases 20 Immunosuppressive therapy 55 abscess 128
evaluation 271 Impaired cancers 148
system 50 fasting glucose 202 Lutembacher’s syndrome 109
Hemoglobinopathy 56 glucose tolerance 202 Lymph nodes 10
Hemolytic anemia 56 hepatic metabolism 33 Lymphadenopathy 74
Hemophilia 69 Implications on dental practice 47, 118, Lymphomas 61
Hemoptysis 79, 121 160, 208, 238, 260, 269
Hepatic Infections 211
Infectious mononucleosis 218
M
encephalopathy 44
syndromes 260 Infective endocarditis 89 Malabsorption 28
Hepatitis Inferior vena caval filters 139 Malaria 228
A 35, 39 Inherited coagulation disorders 69 Management of
B 35, 39 Insulin 207 cardiac arrest 253
C 36 Intermittent fever 4 cardiogenic pulmonary edema 107
diabetes 205 hemostasis 64 Pelvic
drug allergy 260 Nutrition 262 inflammatory disease 223
hemorrhagic tendency in liver disease Nutritional ulcer 15, 23
44 deficiency 20 Percutaneous transluminal coronary
HIV infection 233 evaluation 272 angioplasty 99
Management steps in diabetic patients 207 Peripheral
Marfan’s syndrome 3 O cyanosis 8
Measles 211 signs of infective endocarditis 80
Medical emergencies in dental practice 241 Obstructive Physiologic bad breath 11
Medulla 169 jaundice 34 Pituitary gland 196
Megaloblastic anemia 53 shock 248 Platelet
Melena 16 Oculomotor nerve 164 disorders 67
Meningitis 174 Odynophagia 21 plug formation 65
Mental and emotional status 3 Olfactory nerve 162 Pleural
Methimazole 192 Ophthalmoplegic migraine 179 diseases 145
Migraine 178 Optic nerve 162 effusion 146
equivalent 178 Oral Pleurisy 145
Migrainous neuralgia 180 candidiasis 20 Pneumonia 15, 126
Miliary cavity 12 Pneumothorax 146
pneumonia 127 iron therapy 53 Portal
tuberculosis 140 manifestations in HIV disease 237 hypertension 42
Milk products 11 ulcers 18 venous pressure 43
Minerals 263 Oropharyngeal dysphagia 21 Post-herpetic neuralgia 181
Mitral Orthopnea 78 Post-primary pulmonary tuberculosis 140
regurgitation 86 Orthostatic hypotension 242 Postural
stenosis 84 Osmotic diarrhea 27, 29 hypotension 111, 242
valve Osteitis fibrosa cystica 196 syncope 111
repair 87 Osteum Preoperative
Pallor 7
Mumps 212 hyperparathyroidism 196
Palpitation 78
Myocardial infarction 15 pulmonary tuberculosis 139
Pancreatic exocrine functions 30
Myth about halitosis 12 syphilis 224
Pancreatitis 15
tuberculosis 139
Pantothenic acid 266
N Prominent veins 17
Paracentesis 45
Prophylactic therapy 179
Nausea and vomiting 15 Parathyroid disorders 195
Prophylaxis 91, 230
Neck rigidity 174 Parenteral iron therapy 53
Propranolol 192
Necrotizing ulcerative stomatitis 19 Paroxysmal nocturnal dyspnea 78
Propylthiouracil 192
Nephritic syndrome 156 Partial seizures 170
Protein 262
Nervous system 162 Patent ductus arteriosus 109
energy malnutrition 263
Neurogenic shock 248 Pathogenesis of coronary atherosclerosis 97
Proteinuria 153
Neurosyphilis 225 Pathologic bad breath 11
Pulmonary
Niacin 265 Pathological basis of headache 178
angiography 125, 138
Nodular lymphocyte predominant Pathophysiology of
embolism 137
Hodgkin’s disease 63 coma 167
eosinophilia 136
Non-Hodgkin’s lymphoma 63 halitosis 11
evaluation 271
Nonsteroidal anti-inflammatory drugs 220 unstable angina 99
function tests 134
Normal Patterson Kelly syndrome 52
secretion examination 128
hematopoiesis 50 Peak expiratory flow rate 126
stenosis 110
Index
syndromes 260 Shape of abdomen 16 Tonic
tuberculosis 139 Shock 247 clonic seizures 170
Pulse 4 Sick sinus syndrome 114 pupil 163
rate 4 Sickle cell Transitory bad breath 11
Pulsus alternans 5 anemia 56 Transmission of malaria 228
Pupillary examination 163 disease 57 Treatment of
Pyridoxine 266 Sinus acute attack 179
bradycardia 113 bad breath 12
R venosus 109 high grade lymphoma 64
Skin 17 low grade lymphoma 63
Radio-femoral delay 5 Sleep 167 resistant malaria 230
Recommended dietary allowance 263 Spinal diseases 15 urticaria and angioedema 258
Red blood cells 50 Spleen 17 variceal hemorrhage 43
transfusion 53 Spontaneous bacterial peritonitis 46 Trench mouth 19
Reed-Sternberg cells 62 Sputum 121 Tricuspid stenosis 6
Regulation of calcium metabolism 193 Stable angina 97 Trigeminal
Renal Staphylococcus aureus 90 nerve 164
diseases 68, 153 Starling forces 9 neuralgia 180
stones 15 Status epilepticus 173 Trochlear nerve 164
syndromes 153, 260 Steroids 84 Tropical eosinophilia 136
Respiratory Trousseau’s sign 193
Stokes-Adams attacks 114
diseases 120 Tuberculosis 139
Stomatitis 18
failure 144 Tuberculous meningitis 177
Stress testing 98
system examination 123 Types of
Stroke 245
Rheumatic valvular heart disease 84 breath sound 123
Stupor 3, 167
Rhythm 4 heart failure 104
Subcutaneous nodules 83
Riboflavin 265 jaundice 33
Sudden cardiac death 253
Right atrium 108 pneumothorax 146
293
Sugars 11
Right ventricular hypertrophy 110 Typhoid fever 221
Supraventricular tachycardias 116
Route of infection 126
Symptoms and signs of
Rubella 213
cardiovascular diseases 78 U
gastrointestinal diseases 15
S Ulcerative stomatitis 19
Syncope 78, 79, 110, 111
Ultrasonography 31
Salicylates 84 Syphilis 224
Umbilicus 16
Schamroth’s window test 8 Systolic or diastolic heart failure 105
Uncommon types of gastritis 23
Scheme of general examination 12 Unconjugated hyperbilirubinemia 33
Schilling test 29 T Unstable angina 99
Secondary Upper
hemostasis 65 Tachyarrhythmias 114
gastrointestinal bleeding 43
hyperparathyroidism 196 Takayasu’s disease 110
GI endoscopy 30
hypertension 93 Tension headache 180
Urine
syphilis 224 Tertiary
bilirubin 30
Secretory diarrhea 27, 29 hyperparathyroidism 196
test 202
Seizures 111, 244 syphilis 225
Using
Septic shock 249 Tetralogy of Fallot 110
bad breath detective 11
Serological Thalassemias 56
halimeter 11
studies 30 Thiamine 264
tests 128 pyrophosphate 264
Serum Thyroid V
albumin 31 crisis 192 Vaccination 144
bilirubin 30 disorders 188 Vagal tone 116
biochemistry 154 function tests 169 Vagus nerve 166
enzymes 31 Thyrotropin releasing hormone 188 Valsalva maneuver 116
fructosamine measurement 202 Todd’s paralysis 170 Variants of migraine 179
Severe falciparum malaria 229 Tongue and bad breath 12 Varicella 214
Vascular disorders 111 Visual Volatile sulphur compounds 12
Vasovagal syncope 111 acuity 163 von Willebrand’s disease 69
Ventilator associated pneumonia 126 field 163
Ventricular Vitamin 262, 264
fibrillation 117 A 267
W
premature beats 117 B1 264 Water soluble vitamins 264
septal defect 108, 110 B2 265 Waterhouse Friderichsen syndrome 174
tachyarrhythmias 117 B3 265 Weight loss 16
tachycardia 117 B6 266 Wheezing 122
Vessel wall abnormalities 67 C 266
Vestibulocochlear nerve 165 D 269
Vincent’s infection 19 E 267
X
Viral meningitis 177 K 268 Xylitol chewing gums 12
294
Essentials of Medicine for Dental Students