Everything You Need to Know (at least) for

NAME YEAR MATRIC NO ACADEMIC SESSION

EDITORIAL
(Al-Baqarah:117)

Apabila Ia mengkehendaki sesuatu urusan Ia katakan kepadanya: Jadilah, maka jadilah ia

Dengan nama ALLAH yang MAHA PEMURAH lagi MAHA PENYAYANG

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I know what I should love to do--to build a study; to write, and to think of nothing else. I want to bury myself in a den of books. I want to saturate myself with the elements of which they are made, and breathe their atmosphere until I am of it. Not a bookworm, being which is to give off no utterances; but a man in the world of writing--one with a pen that shall stop men to listen to it, whether they wish to or not. Dont give up, there is still time to study for the exam, GOOD LUCK! Onn Azli Puade Medic 4 20011/2012

I studied the lives of great men and famous women; and I found that the men and women who got to the top were those who did the jobs they had in hand, with everything they had of energy and enthusiasm and hard work. (Harry S Truman quotes-1884-1972)

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SYMPTOMS CHEST PAIN Definition Is a feeling of uncomfortable or pain at the chest area Causes Cardiovascular Myocardial infarction Acute aortic dissection Pericarditis Musculoskeletal Persistent cough Chest wall injuries Costochondritis Rib tumour, fracture Herpes Zoster Gastrointestinal Gastro-esophageal reflux Peptic ulcer disease Gastritis Oesophageal spasm Pulmonary Pneumonia Pulmonary embolisme Pneumothorax Central bronchial carcinoma Inhaled foreign body

Further history regarding Chest Pain 1. Location of the pain Retrosternally and radiates to jaw and left arm cardiac chest pain and oesophageal reflux Centrally located and radiates to shoulder pericarditis Radiates to back aortic dissection 2. Precipitating factor Effort, cold, food and emotion cardiac chest pain Inspiration (due to movement of thorax) pleuritic chest pain Posture gastro-oesophageal reflux 3. Relieving factor GTN oesophageal spasm and acute coronary syndrome Antacid gastro-esophageal reflux Aspirin pleuritic chest pain 4. Family and social history Any history of diabetes, hypercholesterolemia, smoking and dietary intake that mght become a risk factor for the cardiovascular disease 5. Associated symptom Dyspnoea, orthopnoea and easy fatigue all points towards cardiovascular disease
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Pathogenesis and pathophysiology

Atherosclerotic plaque obstructing coronary artery Reduce or diminished blood supply to region supply by the arteries distal to the obstruction Ischaemia of the myocardial cell Release substance to elicit vasodilation as a compensatory mechanism Still cannot receive adequate blood supply Production of more chemical mediator by ischaemic myocardial cell Histamine, serotonin and bradykinin released and entering vein of the hearts The mediators accepted by chemoreceptor located at the pericardial layer Sending Action Potential towards the lateral spinothalamic tract The signal is either converged or facilitated at the spinal cord (referred pain1 theory) RADIATING CHEST PAIN

Investigation 1. ECG To view the electrical profile of this patient heart. Elevated ST segment elevation seen in myocardial ischaemic, symmetrical T wave inversion in myocardial injury and abnormal Q wave in myocardial infarction. It can also detect Pulmonary embolisme 2. Cardiac Enzymes Look out for Troponin T presence, creatinine kinase and CK-MB enzyme elevation 3. Chest X-ray Observe heart as well as lung field to exclude any heart enlargement and disease that can cause pleuritic chest pain. Also to rule out the pain due to fracture or osteosarcoma 4. Blood cholesterol The number one factor contributes to ACS which is hyperlipidaemia. Poor diet habit also can cause elevation of total lipid in the blood

Referred pain also known as synalgia is pain felt in a part of the body other than where it might be expected due to sensory nerves from different parts of the body share common pathways when they reach spinal cord. For diagram, see Guyton pg 605 ONN0809

DYSPNOEA, ORTHOPNOEA2, PAROXYSMAL NOCTURNAL DYSPNOEA3 Definition Dyspnoea - Is an uncomfortable awareness of breathing or can be described as breathlessness Causes Cardiac failure left heart failure or congestive cardiac failure Arrhythmia Valvular Heart Disease Pulmonary Hypertension Further history regarding these symptoms 1. History or family history of hypertension? Systemic hypertension can leads to congestive cardiac failure but it occurs more likely to the left heart before affecting right heart 2. Surgical history History of chest surgery as well as tooth debridement and any invasive procedure will increase tendency of getting systemic infection which likely to be affecting heart valve 3. Associated signs and symptoms Cyanosis indicating heart failure Cough with pink frothy sputum indicating pulmonary oedema, secondary to pulmonary hypertension Fever indicating infective endocardiis 4. Drug used Certain drugs can cause arrhythmia such as beta blockers 5. Medical history Any pulmonary disease such as obstructive, fibrosis and vascular disease can cause pulmonary hypertension and in long standing case, it can leads to congestive cardiac failure

Orthopnoea is breathlessness the prevents the patient from lying down so that the patient has to sleep propped up in bed (by pillows) or sitting on the chair
3

Paroxysmal Nocturnal Dyspnoea is severe dyspnoea that wakes the patient from sleep that the patient is to forced to get up gasping for breath ONN0809

Pathogenesis and pathophysiology

Recumbent position Increase venous return to the right heart Increase afterload of the right heart Pulmonary congestion Pulmonary hypertension Exudation of fluid to the alveolar space (pulmonary oedema) Lung is ventilated but not perfuse V/Q mismatch Respiratory acidosis Increase carbon dioxide (indirectly) and reduce oxygen (directly) level below 30 mmHg Stimulate the chemoreceptor mainly the aortic and carotid body Ascend via vagus and glossopharyngeal nerve Terminates at the nucleus of the tractus sollitarius Stimulate the medullary respiratory area In recumbent position ORTHOPNOEA Increase the respiratory effort as a compensatory mechanism of respiratory acidosis DYSPNOEA PAROXYSMAL NOCTURNAL DYSPNOEA Further investigation regarding dyspnoea 1. Arterial Blood Gas To recognize the respiratory failure and the metabolic profile of the patient 2. Peak expiratory flow rate Reduce in peak flow may indicates asthma or chronic airflow limitation 3. ECG Eliminates probability of cardiac disease related to the symptoms. Look out for axis deviation to rule out left or right ventricular enlargement 4. FBC To rule out any pulmonary infection as well as anemia When sleeping Woke up and gasping for air

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ANKLE SWELLING Definition Swelling of the lower limb may be unilateral or bilateral. Causes Local Swelling Acute swelling Trauma DVT4 Cellulitis Allergy Rheumatoid arthritis Chronic swelling Varicose vein Obstruction to venous return Lymphoedema Caongenital malformations Paralysis Dependency General Swelling Congestive cardiac failure Hypoproteinaemia Renal failure Fluid overload Myxoedema

Further history regarding ankle swelling 1. Swelling location Bilateral swelling cardiac, renal and hepatic failure Unilateral swelling trauma, venous disease, lymphatic disease 2. Associated and signs symptoms Pain trauma, DVT, infection or complication of varicose veins Red, swollen, hot and tender cellulitis Wasting neurological damage Frozen pelvis varicose vein, pelvic tumour Dyspnoea, orthopnoea, PND, ankle oedema cardiac failure Weight loss, diarrhea, steatorrhoea malabsorption 3. Past medical history Trauma to the limb, recent pregnancy (DVT), abdominal or pelvic malignancy

DVT or deep vein thrombosis is an obstruction of a vein by a clot within the deep veins of the calf of the leg. May be caused by prolonged immobility, heart failure, pregnancy, injury and surgery predispose to thrombosis by encouraging sluggish blood flow ONN0809

Pathogenesis and pathophysiology

Right heart failure Reduce afterload of the right heart Blood congested in the right heart Backflow of the blood in the Inferior Vena Cava, precipated by gravity Blood become congested in the lower limb, precipated by left heart pumping Increase hydrostatic pressure Exudation of interstitial fluid to extravascular space ANKLE SWELLING Further investigation regarding ankle sweling 1. FBC Low Hb indicating trauma or fracture secondary to large haematoma. Large haematoma also associated with reduced platelet count 2. Chest X-ray Finding suggestive cardiomegaly, pulmonary oedema and pleural effusions 3. Limb X-ray May show fracture, tumour or gas in the tissues associated with gas gangrene 4. Venography Will confirm Deep Vein Thrombosis 5. Lymphangiography May demonstrate the cause lymphoedema, e.g hypoplasia or obstruction

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EASY FATIGUE, INTERMITTENT CLAUDICATION5, SYNCOPE6 Definition

Is a state of increased discomfort and decreased efficiency due to prolonged or excessive exertion Causes Cardiac Failure Lack of Sleep Anemia Depression Hypoglycemia Peripheral vascular disease Pathogenesis and pathophysiology Cardiac failure Low cardiac output Poor blood supply (oxygen) to the skeletal muscle Exercise/strenuous work Anaerobic respiration produces energy and lactic acid Increase level of lactic acid Lactic acidosis
Walking Pain in the thigh and calves INTERMITTENT CLAUDICATION Poor blood supply to the carotid artery Poor blood supply to the cerebral artery Transient loss of consciousness SYNCOPE

Discomfort and hurt at the skeletal muscle FATIGUE

Intermittent claudication is related to the claudication distance which is the distance the patient walk until the pain in one or both calves, thighs and buttocks can be felt 6 Syncope is a transient loss of consciousness due to the reduce blood supply to the cerebral artery ONN0809

PALPITATION Definition Awareness of the heartbeat Causes Cardiac arrhythmia Premature ventricular contraction Premature atrial contraction Atrial fibrillation Supraventricular tachycardia Pathogenesis and pathophysiology

Sinus tachycardia Anxiety/emotional stress Caffeine Nicotine Alcohol Ventricular tachycardia

Cardiac failure Inadequate cardiac output Reduced blood supply (Oxygen) to the body tissue Ischaemic tissue release substance Stimulate the sympathetic activity as a compensatory mechanism Increase heart rate to increase cardiac output Hyperdynamic circulation Ventricular tachycardia Awareness of the heart beat due to the hyperdynamic circulation PALPITATION

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SIGNS CACHEXIA, POOR WEIGHT GAINED Definition Is a condition of abnormally low weight, weakness and general bodily decline associated with chronic disease Causes Systemic disease Malignancy Cardiac failure Chronic respiratory disease Malabsorption Renal failure Liver failure Infective Infective endocarditis Tuberculosis HIV Helminth infection

Endocrine Hyperthyroidism Diabetes mellitus Addisons Disease

Psychiatric Anorexia Nervosa Depression

Systemic Infection Cardiac failure Inflammatory reaction Release of TNF- Stimulate the release of the cachectin factor Cachectin factor enters blood circulation Suppress appetite center of the hypothalamus Lost of appetite CACHEXIA Reduced blood supply to the body Compensatory mechanism Stimulate the sympathetic nervous system Long standing sympathetic stimulation Growth retardation POOR WEIGHT GAINED/CARDIAC CACHEXIA

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ANAEMIA AND PALLOR7 Definition Is defined as a haemoglobin concentration of less than 13.5 g/dl in adult males and 11.5 g/dl in adult females Causes Microcytic (MCV <80 fl) Iron deficiency Anaemia of chronic disease Thalassaemia

Normocytic (MCV 80 95 fl) Acute blood loss Haemolytic Anaemia Mixed deficiencies Secondary anaemia* Bone marrow failure Pregnancy

Macrocytic (MCV >95 fl) Megaloblastic anaemia Alcoholism Liver disease Hypothyroidism Addisons disease Hyperthyroidism Marrow infiltration

Pathogenesis and pathophysiology

Systemic Infection (infective endocarditis) Inflammatory reaction Release of TNF- Suppress the bone marrow Reduce production of red blood cell Reduce total haemoglobin in the blood Normocytic nomochromic anaemia PALLOR

Pallor is an abnormal paleness of the skin due to the deficiency of haemoglobin especially in the mucous membrane of the sclerae

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ARTERIAL PULSE NORMAL AND ABNORMAL PULSE Definition Is a series of pressure waves within an artery caused by contractions of the left ventricle corresponding with the heart rate which is usually palpated at the radial artery Normal heart rate 60 100 bit/minute Abnormal pulse 1. Rate and rhythm Rhythm\Rate Regular Tachycardia Congestive cardiac failure Constrictive pericarditis Hypovolaemic shock Myocardial ischaemia Sick sinus syndrome Atrial fibrillation Pulmonary embolisme Myocardial ischaemia Left atrial enlargement Mitral valve disease Bradycardia 3rd degree AV block 2nd degree AV block Myocardial infarction Hypothyroidism Drugs (-blockers, digoxin) Atrial fibrillation 2nd degree AV block type I

Irregular

2. Volume Type Thready pulse Weak pulse Description Difficult to be felt and are not palpable e.g. hypovolaemic shock Is not palpable when slight pressure applied e.g. hypovolemc shock, atherosclerotic plaque, congestive cardiac failure Feels full and spring like even under moderate pressure e.g. aortic regurgitation

Bounding pulse

3. a) b) c) d)

Character Pulsus alternans alternating weak and strong pulse due to left ventricular failure Pulsus parvus et tardus slow uprising of the carotid upstroke in Aortic stenosis Pulsus bisferiens a double waveform due to aortic stenosis/regurgitation Spike and dome pulse double carotid impulse due to hypertrophic obstructive cardiomyopathy
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HYPERTENSION Definition Hypertension is elevation of blood pressure8 above the normal range expected in a particular age group Classification characteristic Benign Malignant

aetiology usually primary* primary or secondary* blood pressure diastolic 90-120, very slow rise diastolic >120, very rapid rise age middle age, elderly young, middle age course very slow (years) rapid (months) incidence common uncommon *Primary hypertension/essential hypertension is due to unknown causes *Secondary hypertension is due to certain disease that leads to rise in blood pressure Complication of hypertension 1. Congestive cardiac failure/left ventricular failure 2. Hypertensive retinopathy 3. Atherosclerosis The goal of antihypertensive drugs is to reduce or 4. Hypertensive nephropathy inhibit both factors that are increasing TPR as well 5. Cerebral haemorrhage as CO 6. Artery berry aneurysm 7. Abdominar aorta aneurysm The goal of antifailure drugs is to reduce the TPR as 8. Aortic aneurysm well as increasing cardiac output. 9. Ischaemic heart disease Regulation of Blood Pressure
Humoral Factor Vasoconstrictor Vasodilator Cardiac Factor Heart rate Contractility

Total Peripheral Resistance

Neural Factor Vasoconstrictor Vasodilator
8

Cardiac Output
Blood volume Mineralocorticoids Sodium

Blood pressure can be define as the pressure of the blood against the arterial wall or total peripheral resistance times cardiac output ONN0809

HEART FAILURE9 LEFT HEART FAILURE Failure of the left heart to pump oxygenated blood to meet up body blood requirement Causes 1. Ischaemic heart disease 2. Systemic hypertension 3. Aortic or mitral valve disease 4. Non ischaemic myocardial disease Pathogenesis
Valvular heart disease (pressure or volume overload) Systemic hypertension (pressure overload) Increase cardiac workload Increase wall stress Cell stretch (Frank Starling mechanism) Hypertrophy/dilation Contraction of the heart become less efficient due to thicken wall LEFT HEART FAILURE Symptoms Exertional dyspnoea Orthopnoea Paroxysmal nocturnal dyspnoea Syncope Intermittent claudication Easy fatigue Signs Tachypnoea Central cyanosis Hypotension Cardiac cachexia Sinus tachycardia Displaced apex beat Left ventricular S3 sound Sign of pulmonary oedema Ischaemic heart disease (volume overload)

Can be define as failure of the heart pumping out the blood to all over the body to meet adequate tissue perfusion

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RIGHT HEART FAILURE Failure of the right heart to drain deoxygenated blood and to pump the blood to the pulmonary circulation Causes Severe pulmonary hypertension Atrial Septal Defect Tricuspid regurgitation Pulmonary stenosis Pulmonary regurgitation Myocardial disease of the right heart Causes of left heart failure

Pathogenesis
Pulmonary hypertension, pulmonary stenosis (pressure overload) Stronger contraction of the right heart to overcome the pressure/volume Increase cardiac workload Increase wall stress Cell stretch (Frank Starling mechanism) Hypertrophy Contraction of the heart become less efficient due to thicken wall RIGHT HEART FAILURE Symptoms Peripheral swelling Abdominal distension Anorexia Nausea Signs Raised Jugular Venous Pressure Right ventricular heave Right ventricular S3 Pansystolic murmur Hepatomegaly Pulsatile liver Oedema Atrial Septal Defect, tricuspid regurgitation (volume overload)

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CONGENITAL HEART DISEASE Definition Is an abnormality of the heart or great vessel that is present from birth Causes Can be divided to 3 different causes 1. Genetic factor I. Chromosomal aberrations Down Syndrome or Robersonian translocation II. Mendelian inheritance single gene mutation that is passes generation to generation 2. Maternal factor i. Maternal or placental infection Toxoplasma gondii, rubella virus or cytomegalovirus are the most common ii. Insulin dependant diabetes exposed the fetus to the high level of glucose and induced fetal hyperinsulinaemia which can leads to cardiac defect or neural tube defect (diabetic embyopathy) iii. Hypertension hypertensive embryopathy iv. Lifestyle intake of alcohol, drugs and smoking 3. Environmental factor i. Chemical exposure inhalation of corrosive chemical substance ii. Radiation hazardous and non-hazardous radiation such as X ray, uv ray etc prove to cause anomalies such as microcephaly, blindness 4. Multifactorial any collection of above symptoms Classification
Congenital Heart Disease

Acyanotic Without shunt - Coarctation of aorta (5%) - Congenital aortic stenosis (4%) - Pulmonary stenosis (8%) - Bicuspid aortic valve - Dextocardia With shunt

Cyanotic

- Atrial Septal defect (10%) - Ventricular Septal Defect (42%) - Patent Ductus Arteriosus (7%)

- Tetralogy of Fallot (5%) - Eisenmenger Syndrome - Pulmonary Atresia - Transposition of Great Arteries (4%)

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Normal fetal circulation due to the rudimentary structure of the lung and liver, blood has to bypass both of this organs receives blood supply mainly from umbilical vein from maternal blood via placenta blood will go directly to the IVC via ductus venosus and 50% more will enters the liver sinusoids blood will enters the heart through IVC directly to the right atrium and then some to the left atrium via foramen ovale which opens the structure interatrial septum, some to the right ventricle, left ventricle and some to the lung (approx. 10%) from the left ventricle, blood is pumped to the aorta from the right ventricle, blood will be pumped to the pulmonary trunk and straight to the aorta via ductus arteriosus From aorta, blood will drains to the umbilical artery and lastly back to placenta into maternal circulation. * For pathological point of view of Congenital Heart Disease, simply imagine the circulation in adult is same as above Atrial septal defect a congenital defect of the heart in which there is a hole in the partition separating the two atria Ventricular septal defect a congenital defect of the heart which there is a hole between the 2 ventricles Patent Ductus Arteriosus a condition in which the ductus arteriosus is failed to close Coarctation of aorta10 a congenital narrowing of the short segment of the aorta which commonly occurs just beyond the origin of the subclavian artery from the aorta Tetralogy of Fallot Characterized by 1. Pulmonary stenosis 2. VSD 3. Overriding of Aorta 4. Right Ventricular Hypertrophy

10

Sorry for unable to list all the signs, symptoms, pathogenesis and investigation for congenital heart disease details. Kindly refer to the pathology book ONN0809

ISCHAEMIC HEART DISEASE Definition Defined clinically as Acute Coronary Syndrome (ACS) is a collections of syndromes due to imbalance of Oxygen supply and Oxygen requirement Syndromes 1. Angina pectoris refer to the chest pain in which are divided to 3 different types as stated below; i. Typical or Stable Angina ii. Prinzmetal or Variant Angina iii. Cresendo or Unstable Angina 2. Myocardial infarction Due to the long standing myocardial tissue ischemic which leads to tissue injury before infarction 3. Chronic ischaemic heart disease Develops slowly as a progression of coronary artery narrowing but not completely occluded 4. Sudden Cardiac death Due to the tissue hypoxic and failure to remove the metabolites Causes 1. Role of acute plaque change 2. Role of inflammation 3. Role of arterial thrombosis 4. Role of vasoconstriction Risk factors 1. Age (40-60 increase risk of getting IHD up to 5 folds) 2. Sex (oestrogen proven to be protecting endothelial layer, female has lower risk) 3. Genetic (hypertension and primary hyperlipidemia is the major cause) 4. Secondary hyperlipidemia (increase circulating triglycerides contributes to the role of thrombosis) 5. Smoking (contributes to the endothelial injury as well as role of inflammation) 6. DM (decrease liver removal of LDL from circulation) 7. Hypothyroidism (decrease the formation of LDL receptor in the liver) 8. Nephrotic syndrome (increase hepatic production of lipids and lipoprotein)

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Pathogenesis and pathophysiology

Hypertension Increase afterload Increase myocardial demand Oxygen supply/requirement imbalance Chronic ischaemia of myocardial cell Release pain producing substance Shear stress to the endothelial Arterial damage Accelerated atherosclerosis Atheroma Progressive gradual narrowing of lumen Exposure of the subendothelial layer Platelet aggregation Fissuring or ulceration of the platelet plaque Platelet rupture Embolisme Angina Pectoris Coronary artery involves Ischemia of the myocardial cell Coronary spasm Prinzmetal angina Neuroendocrine imbalance (catecholamines, prostaglandin) Sudden cardiac death Injury of myocardial cell Recovery with scarring or fibrosis Hyperlipidaemia LDL deposits at the site of injury

Myocardial Infarction Chronic IHD IHD

Chronic heart failure

Acute heart failure

Cardiac arrhythmia

Cardiac rupture Cardiac tamponade

Cardiogenic shock

Cardiac arrest

DEATH

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RHEUMATIC HEART DISEASE Definition Is an acute, immunological mediated, multisystem inflammatory disease that occurs a few weeks after an episode of Group A (-haemolytic) streptococcus pharyngitis that involves the heart Causes 1. Chronic valvular disease mitral valve stenosis 2. -haemolytic Group A streptococci 3. Hypersensitivity reaction type II and III Major and Minor Criteria for Diagnosing Rheumatic fever Major Subcutaneous nodules Polyathritis Erythema Marginatum Carditis Sydenhams Chorea

Minor Fever Athralgia Previous Rheumatic Fever Raised ESR or C-reactive protein Leukocytosis Prolonged PR nterval

Pathogenesis (the exact pathogenesis is still unknown) Streptococcus pyogenes Infection of the throat (pharyngitis) Immune response involving monocytes and macrophage M-proteins combine with HLA class II molecules Presented to the CD4+ T cell Travels in blood vessels and reaching heart tissue Cross reaction occurs between M peptides, myocardium and valvar tissue with the CD4+ T cell Hypersensitivity reaction to the myocardium and valvar tissue Formation of Aschoff Body (characterized by granular fibrinoid material, Aschoff giant cells, lymphocytes, plasma cell, fibroblast and collagen) Pancarditis/mitral valve stenosis Chronic RHD ONN0809

Major Signs and their Pathophysiology Cross reaction with host tissue To skin To cardiac tissue Formation of Aschoff body Pancarditis (pericardium, myocardium or endocardium) To valvar tissue (mainly mitral valve) Formation of Aschoff body fish mouth appearance Vegetation or fissuring endocarditis Slowly affecting myocardium Myocarditis Tachycardia and dilation Cardiac failure Mitral stenosis To joint cartilage Inflammation Polyathritis Maculopapular rash Erythema Marginatum

Large Aschoff body Subcutaneous nodules

To subthalamic and caudate nuclei Sydenhams chorea

Pericarditis Inflammation of the pericardial cavity bread and butter appearance Chest pain and fever

For better understanding The streptococcus may share the same antigen with human tissues, particularly cardiac cell and valves. ONN0809

INFECTIVE ENDOCARDITIS Definition Is a disease of the heart valves particularly: the mural endocardium is only occasionally affected by late spread from the valves Causes 1. Gram positive bacteria Streptococcus viridans Streptococcus pyogenes Streptococcus pneumonia Staphylococcus aureus Staphylococcus epidemidis 2. Gram negative bacteria Eischerichia coli Pseudomonas sp. Klebsiella pneumonia Haemophilus influenza 3. Fungus Candida albicans Aspergillus sp. Signs and symptoms Symptoms Fever Dyspnoea Easy fatiguability

Signs Splinter haemorrhage Osler Nodes Janeway lesion Clubbing Roths spots Splenomegaly Haematuria

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Pathogenesis and pathophysiology Deposition of immune complex (SLE ad RHD) Endothelial damage Exposure of subendothelial collagen High altitude Platelets deposition Development of thrombi Tooth extraction Endoscopy I/V drug abuse Nonbacterial thrombotic endocarditis Clinical procedure Provide bacterial entry to the blood stream Genitourinary instrumentation Cardiac surgery Blood stasis Valvular dysfunction Cardiac catheterization

Hypertension

Virulent pyogenic bacteria (staphylococcus aureus) Acute Bacterial Endocarditis Vegetation large and crumbling Loose mixture of organisms and fibrin mainly, with cellular debris Rapid destruction of cusps and chordae and spread of suppuration to adjacent heart muscle Acute heart failure

Low grade bacteria (streptococcus viridians) Subacute bacterial endocarditis Large firm vegetation, fairly dense fibrin and platelet aggregation with bacterial colonies, few leukocytes Gradually increasing damage to valve cusps Minimal spread to adjacent structures Gradual heart failure

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NORMAL VALUES OF THE INVESTIGATION Haematology RBC White cell count Adult Infant (full term at birth) Infant (1 year) Basophil Eosinophil Neutrophil Monocyte Lymphocyte Fat Cholesterol HDL

Male (4.6 - 6.5 x 1012 /L) Female (3.9 5.6 x 1012 /L) 4 11 x 109 /L 10 25 x 109 /L 4 18 x 109 / L 0 0.1 x 109 /L 0.01 0.44 x 109 /L 2 7.5 x 109 /L 0.2 0.8 x 109 /L 1.3 3.5 x 109 /L 3.6-6.3 mmol/L Male (0.78-1.81 mmol/L) Female (0.78-2.2 mmol/L) Male (2.3-5.57 mmol/L) Female (2.3-5.7 mmol/L)

(0 1%) (1 6%) (40 75%) (2 10%) (20 45%)

LDL

Cardiac enzymes Creatinine Kinase CK-MB Lactate Dehydrogenase Others ESR Male (<195 IU/L) Female (<170 IU/L) Male (<25 IU/L) Female (<31 IU/L) 230-460 IU/L

male (3 -5 mm/hr) Female (4 7 mm/hr) <250 Todd Units

ASOT

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THANK YOU FOR ALL THE LECTURES OF PPSP USMKK FOR ESPECIALLY AS STATED BELOW FOR CHECKING, CORRECTING ALL THE FACTS WHICH WERE PUBLISHED AND FOR TEACHING MEDICAL STUDENT BATCH 2008/2009 2ND YEAR WITH HARDWORKING AND GREAT DEDICATION 1. ASSOCIATES PROF OTHMAN MANSOR 2. DR THIN THIN WIN @ SAFIYA 3. DR SAMARENDA S MUTUM 4. DR ISKANDAR ZULKARNAIN ALIAS 5. DR MOHD ASNIZAM ASARI REFERENCE 1. PPSP lectures Lecture notes 2nd year 2008/2009 2. Oxford Concise Medical Dictionary, 6th edition definition 3. Clinical Examination, 5th edition, Nicholas J Talley and Simmon OConnor clinical signs 4. Differential diagnosis, 2nd edition, Andrew T Raftery and Eric Lim clinical signs and symptoms 5. Pathology Basis f Disease, 7th Edition, Robbins and Cotran pathogenesis of diseases 6. MIMS respiratory guide, Malaysia Edition 2004/2005

SPECIAL THANKS TO KH CHEONG BASIC PRINCIPLE OF ECG ROBIATUL AIDAWIYAH CARDIAC CYCLE

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