Minor CP-Final (Print) - Less Anesthesia

PAHS MBBS CPs- Jr.
Clerkship (2nd Rotation)
Mouth Sore and Ulcers
Sore mouth
and mouth
ulcers
Acute (up to Chronic (>

2wks) 2wks)
Associated Associated
Non- Local to
Infectious systemic cutaneous
infectious mouth only
features disease
A mouth ulcer (an oral ulcer or a mucosal ulcer) is an ulcer that occurs on the mucous membrane of the oral cavity. It is a
sore or open lesion in the mouth.
An ulcer is a break in the skin or mucous membrane with loss of surface tissue. It is a tissue defect which has penetrated the
epithelial-connective tissue border, with its base at a deep level in the sub mucosa, or even within muscle or periosteum.
The two most common causes of oral ulceration are local trauma (e.g. rubbing from a sharp edge on a filling) and aphthous
stomatitis ("canker sores").
Mouth sore
and ulcer
Acute Chronic
(up to 2 weeks) (> 2 weeks)
Patients with a non-healing ulcer of over 3 weeks duration should be referred for biopsy or other investigations to exclude
malignancy.
As a general rule, a mouth ulcer that does not heal within 2 or 3 weeks should be examined by a health care professional
who is able to rule out oral cancer (e.g. a dentist, oral physician, oral surgeon/ maxillofacial surgeon).
15
PAHS MBBS CPs- Jr. Clerkship (2nd Rotation)
Clinical clues
Ask about:
Duration; Acute, Chronic
Fever, s/o infection
Pain most mouth ulcers are painful, but severe pain suggests a bacterial infection
History of local trauma or burn s/o non-infectious cause
Halitosis if severe s/o severe bacterial infection
Previous history of mouth ulcers (common in herpes simplex and apthous ulcers
Associated genital ulcers (Bechets disease)
Known suppressed immunity (HIV, long term oral steroid) prone to candida
Rash or ulcers on face s/o herpes zoster
Use of dentures s/o trauma or increases risk of candidiasis
Features of systemic illness (e.g. SLE, vasculitis)
Drug history many drugs can cause mouth ulcers (non-infectious cause)
Look for:
Lesion - site, number
Size of lesions
o Minor aphthous ulcers (80% of all aphthae) are less than 5 mm in diameter and heal in 7 to 14 days
o Major aphthous ulcers are large ulcers that heal slowly over weeks or months with scarring
o Herpetiform ulcers are multiple pinpoint ulcers that heal within about a month
Colour of lesions if white coated plaques, s/o candidiasis
Blistering s/o herpes simplex (cold sores) or herpes zoster
Small, round, or ovoid ulcers with circumscribed margins, erythematous haloes, and yellow or gray floors s/o
aphthous ulcer
necrosis and/or punched out ulceration of the interdental papillae ("punched-out papillae") s/o Acute necrotizing
ulcerative gingivitis (ANUG)
formation of a pseudo membrane (or "film") on the gingiva s/o ANUG
painful, bright red marginal gingiva that bleed upon gentle manipulation s/o ANUG
Associated Lymph nodes s/o ANUG
Associated skin rashes (e.g. SLE, vasculitis, Stevens Johnson syndrome, TEN)
History of altered bowel habit (inflammatory bowel disease may be associated with mouth ulcers)
History of genital ulcers associated with mouth ulcers (Behcets disease)
Investigations
Mostly acute mouth ulcers do not require further investigation. Diagnosis is based on the patients history and clinical
features because specific tests are unavailable.
In severe recurrent aphthous ulceration or in chronic ulcers, the following tests may be indicated to try and find an
underlying cause:
CBC (hemoglobin level, differential white cell count, and red cell indices),
iron levels, and possibly red cell folate and serum vitamin B12 measurements
Other investigations may help exclude systemic disorders.
Biopsy is rarely indicated.
Comments
Aphthous ulcers:
Recurrent aphthous stomatitis typically starts in childhood or adolescence and affects at least 20% of the population. Its
natural course is one of eventual remission.
Some cases have a familial and genetic basis; a minority involves etiologic factors that can be identified, including stress,
trauma, stopping smoking, menstruation, and food allergy. Most patients seem to be otherwise well.
Aphthae are seen in patients with hematinic deficiency (iron, folate, or vitamin B 12); celiac disease; Crohn's disease; HIV
infection, neutropenia, and other immunodeficiencies; Neumann's bipolar aphthosis, where genital ulcers may also be
present; and Behet's syndrome, where there may be genital, cutaneous, ocular, and other lesions. The mouth ulcers in
Behet's syndrome are often major aphthae with frequent episodes and long duration to healing
16
Herpes simplex:
A highly contagious virus, also known as the 'cold sore virus', which can cause cold sores on the mouth and the genitals.They
cause uncomfortable, fluid-filled blisters that typically appear outside the mouth, usually under the nose, around the lips or
under the chin, while mouth ulcers occur inside the mouth.
Primary herpetic ulceration can occur (most commonly HSV-1); these lesions are then prone to secondary bacterial
infection. Secondary nonspecific bacterial infection of chronic ulcers can delay the healing process.
Candida albicans :
Deep-rooted fungal infection should prompt enquiry as to possible systemic illness. Candida albicans is a normal
commensal but it tends to overwhelm other microbes when these are suppressed through long-term systemic
antimicrobial treatment or in the immunocompromised.
Acute Stomatitis : An acute inflammation of the mucous membrane of the mouth.
Acute necrotizing ulcerative gingivitis (ANUG):(Trench Mouth; Vincent's Stomatitis)
ANUG is a serious infection of the gums that causes ulcers, swelling, and dead tissues in the mouth. It may also be
associated with diseases in which the immune system is compromised, including HIV/AIDS.
Acute mouth ulcers

(up to 2 weeks)
Infectious Non-infectious
Trauma Burn Drugs

(check bite, toothbrush) (chemical, thermal) (causing SJS, TEN)
Most mouth ulcers that are not associated with recurrent aphthous stomatitis are caused by local trauma. The mucous
membrane lining of the mouth is thinner than the skin, and easily damaged by mechanical, thermal (heat/cold), chemical or
electrical means, or by irradiation.
Ask for:
History of trauma (chewing inside of mouth, tooth brush etc)
Use of dentures
Use of mouth washes or bleach cleaners
Pain - Chemical and thermal ulcers tend to be more painful than mechanical ulcers.
Drug history eg. alendronate (a bisphosphonate, commonly prescribed for osteoporosis) cytotoxic drugs (e.g.
methotrexate, i.e. chemotherapy), non steroidal anti-inflammatory drugs, and propylthiouracil (e.g. used for
hyperthyroidism).
Mucosal contact with hot food or liquids
Look for:
Distribution of ulcers look for obvious factor causing trauma in this area (e.g. broken tooth or dentures)In the case of
bleach associated with dentures, look for a line of ulceration along the gums.
Comments:
Mechanical trauma
This is the most common cause of oral mucosal ulceration.It may be acute or chronic and is characterised by a
shallow base and non-raised margins.
Factitious trauma occurs as a result of deliberate biting or scratching the mucosal surfaces with finger nails.
17
Suggestive features - history, ulcer size and location compatible with history and on removal of cause, signs of
healing appear within 10 days.
Chemical injury
Chemical injury can arise from direct contact of oral mucosa with aspirin (leaving white plaques which slough off) or
bleach, as may occur when improperly cleaned/rinsed dentures are worn. Recurrent use of phenols or silver nitrate
for aphthous ulcers can also give rise to these ulcers.
Thermal injury
The palate is the most commonly affected site but look for associated lip, tongue or oropharyngeal burns.
Diagnoses to consider in Acute mouth ulcers:

Viral: chickenpox, hand, foot and mouth disease, herpetic stomatitis, human immunodeficiency virus, infectious
mononucleosis, herpes zoster (if involvement of maxillary or mandibular division of CN V)
Bacterial: acute necrotizing ulcerative gingivitis, primary chancre of syphilis
Erythema marginatum
Stevens Johnson syndrome (SJS)
Toxic Epidermal Necrosis (TEN)
Burning mouth syndrome (due to deficiency states or associated with diabetes mellitis, drugs (e.g. ACE inhibitors),
psychogenic. This is relieved by eating. There are no actual ulcers visible usually.
Clinical Clues
Ask about:
Duration; Acute, Chronic
Fever s/o infective process
Known T.B or Syphilis or symptoms s/o this
Radiation
Painful or painless
Progression slow-growing non-healing ulcer should always suspect malignancy
Chewing Habit: Betel nut, Tobacco, Smoking increase risk of malignancy
Dietary habits deficiency of iron, folic acid and Vit B12 can all lead to glossitis and mouth ulcers.
Drug history especially cytotoxic drugs, NSAIDs.
Features of systemic illness e.g. joint swelling, fever, malaise (SLE, Behcetsvasculitis, IBD etc)
Known skin disorders associated with mouth ulcers e.g. lichenplanus, pemphigus, pemphigoid, erythema multiforme,
epidermolysisbullosa, and angina bullosahemorrhagica (blood-filled blisters that leave ulcerated areas after rupture),
discoid lupus erythematous, erosive lichen planus, dermatitis herpetiformis..
Look for:
Lesion site, size, shape, number
o Nonhealing ulcer with raised borders on lateral aspect of the tongue, floor of mouth or on the soft palate s/o
malignancy
o Blistering lesions if fragile blisters that easily break and have irregular ragged lesions s/o pemphigus. If tense
blisters which eventually rupture and heal slowly s/o pemphigoid.
Colour of lesion
o if red (erythroplakia) malignant until proven otherwise
o if white (leukoplakia) 6% risk of malignancy
Presence of induration (s/o malignancy)
Presence of discharge look for persistent discharge and sinus in skin over maxilla or mandible s/o osteomyelitis.
Nature of discharge
o Pus (osteomyelitis)
o Cheesy (actinomycosis)
Colour of teeth discoloured brown teeth suggests the tooth is dead and there may be infection in the underlying
bone.
Wickham's striae (= ring formation of white or violaceous fine, slightly raised thread-like lesions) on the buccal mucosa.
s/o lichen planus
Systemic features (involvement of eye, skin, joints, other body parts)
18
Investigation: As indicated by clinical history and examination

Routine Blood test, serology test (VDRL for syphilis), Cytology / Biopsy,X-ray, Direct immunofluorescence.
Comments
Neoplastic conditions
These are common and important

Squamous cell carcinoma (SCC) lesions account for 90% of all oral neoplasia . SCC may start as white (leukoplakia)
or red (erythroplakia) lesions: white patches carry a 6% risk of malignancy and red lesions are malignant until
proven otherwise. SCC may be found on the lip (lower>upper), tongue, gums or floor of mouth.
Basal cell carcinoma (BCC). These are usually found on the upper lip
Salivary gland tumour
Malignant melanoma
Kaposis sarcoma
Certain conditions are said to be pre-malignant and need to be monitored if found:

Erythoplakia
Leukoplakia
Lichen planus
Discoid lupus erythematosis
Submucous fibrosis
Epithelial dysplasia
These conditions may be precipitated by tobacco chewing, chewing of betel nut, alcohol use.
Lichen planus:
In addition to wickhamsstriae may find white papules or plaques (and less commonly, erosions and red atrophic areas). A
biopsy is often warranted to rule out systemic lupus erythematosus (SLE) and malignancy.
Irradiation ulcers:
Ulceration occurs either acutely (as a result of direct damage to epithelial cells) or more long-term, secondary to epithelial
atrophy and damage to underlying blood vessels.
Non ulcerative causes of oral soreness:
Erythema migrans (benign migratory glossitis, geographic tongue) is characterized by map-like red areas of atrophy of
filiform tongue papillae in patterns that change even within hours .The tongue is often fissured. Lesions can cause soreness
or may be asymptomatic.
Desquamative gingivitis, widespread erythema, particularly if associated with soreness, is usually caused by desquamative
gingivitis.
Diagnoses to consider:
Bacterial: Tuberculosis
Fungal: Blastomycosis, cryptococcosis, histoplasmosis, paracoccidiomycosis
Parasitic: Leishmaniasis
19
Orofacial Swelling and Pain

Orofacial swelling
and/or pain
Swelling without Pain without

Swelling with pain
pain swelling
Oral tumour Trauma Tooth sensitivity
Salivary gland Facial pain /

Infection
tumour neuromuscular
Temperomandibulr
Cyst
joint conditions
Swelling: This is an abnormal enlargement of a part of the body which may be due to inflammation, tumour or fluid
accumulation.
Pain: An unpleasant sensation occurring in varying degrees of severity as a consequence of injury, disease, or emotional
disorder.
Swelling without pain
Oral tumour Salivary gland tumour Cyst
Odontogenic Non-odontogenic
Tumor: A tumor is an abnormal growth of tissue resulting from uncontrolled progressive multiplication of cells and serving
no physiological function. It may be solid or fluid-filled. A tumor does not necessarily mean cancer. Tumours can be benign
(not cancerous), pre-malignant (pre-cancerous), or malignant (cancerous). There are many different types of tumours and a
variety of names for them - their names usually reflect their shape and the kind of tissue they appear in.Tumour sizes may
vary enormously.
Cyst: A cyst is a uni- or multilocular, epithelium-lined cavity of various etiologies that contains liquid or gaseous materials.
Non-epithelium-lined cavities are classified as "pseudocysts". In clinical practice, both pseudo cysts and cysts are generally
referred to as "cysts". Cysts may form in the alveolar bone, alveolar process or soft tissues; their growth is slow and
expansive, and they may lead to swelling of the bone and soft tissues.
20
Clinical clues
Ask about:
Pain
Fever
Duration of swelling
History of Trauma
Progression
Associated features of malaise or weight loss suggestive of malignancy
Functional impairment
Look for:
Swelling
Tenderness
Associated lymph nodes involved
Swelling Site, number, size, shape
Tissue origin (skin, soft tissue, bone)
Consistency:soft,firm, hard
Colour of swelling
Investigations
CBC
FNAC
X-ray
Biopsy
Oral
tumour
Non-
Odontoge
odontogen
nic
ic
Malignant Benign Malignant

Benign
e.g. e.g.exostos e.g. Ewings
e.g. is,
ameloblastic sarcoma,
ameloblastoma osteoma
carcinoma metastasis
Definitions:
Odontogenictumours: Tumours in the Jaws that arise from Odontogenic (tooth forming) tissues are referred to
asodontogenictumours.
A benign tumour (benign neoplasm) cannot metastasize. Most benign tumours are not harmful to human health. Even
though they are not cancerous, some may press against nerves or blood vessels leading to symptoms.
Ask for:
Age of patient different tumours common at different ages
Duration of swelling and nature of progression
History of pain, numbness and swelling s/o malignancy
Loose teeth
Failure of teeth to erupt
History of nasal or paranasal sinus obstruction s/o malignancy
Known history of malignancy that may have metastasized to bone (e.g. lung, breast, prostate, colon, kidney)
Look for:
Location of swelling different tumours common at different sites
Deformity of the face
Egg shell Crepitus s/o ameloblastoma
Alignment of teeth
Investigations
X-Ray is the most useful initial investigation as tumours have characteristic appearances.
Biopsy is needed to confirm the diagnosis
21
Comments:
ODONTOGENIC TUMORS OF THE JAWS
AMELOBLASTOMA
Ameloblastoma is the most common type of odontogenic lesion. Ameloblastoma (amel, meaning enamel + blastos,
meaning germ) is a rare, benign tumor of odontogenicepithelium much more commonly appearing in the lower jaw than the
upper jaw. Ameloblastomas are often associated with the presence of uneruptedteeth. Symptoms include painless
swelling(if severe pain), facial deformity, loose teeth, ulcers, and periodontal (gum) disease. The slow growth rate of the
lesion allows time for periosteum to develop thin shell of bone ahead of the expanding lesion. This shell of bone cracks
when palpated and this phenomenon is referred to as "Egg Shell Cracking" orcrepitus, an important diagnostic feature.
Ameloblastoma is tentatively diagnosed through radiographicexamination and must be confirmed by histological
examination (e.g., biopsy).
ADENOMATOID ODONTOGENIC TUMOR (AOT)

This is a tumour mostly of teenagers. It occurs in themiddle and anterior portions of the jaws in contrast toameloblastoma
which is found mostly in the posteriorsegment. This tumor is encapsulatedand is treated by curettage. The radiographic
appearance is a unilocular radiolucency,often around the crown of an uneruptedtooth in which case they resemble a
dentigerouscyst.
CALCIFYING EPITHELIAL ODONTOGENIC TUMOR (CEOT, Pindborgtumor)
This tumor calcifies in a concentrically lamellatedtree-ring pattern. This explains the name of calcifying
epithelialodontogenictumour.
CEOT lacks a capsule but apparently does not infiltrate as deeply into surrounding tissues as doesameloblastoma.
Radiographically, this tumour may appear as a radiolucenttumour but if sufficient calcifications are present,it becomes
dense.
AMELOBLASTIC FIBROMA
This is a tumour of childhood, the typical patient isabout 12 14 years old, seldom is it seen beyond age20. The posterior
segment of the mandible is the mostcommon location. Local swelling or failure of teeth toerupt on time or in proper
alignment may call attentionto the tumour. Ameloblastic fibromas are purelyradiolucent. This tumour is clearly benign.
ODONTOMA: COMPOUND AND COMPLEX TYPES

Both types of odontoma are found in the earlyyears, usually in the teens or early twenties. Compoundodontoma is more
common in the anterior jawsegment whereas the complex type is found morecommonly in the posterior jaws.
MYXOMA (ODONTOGENIC MYXOMA)

Myxoma is a tumour that occurs over a wide agerange but most occur in the second and third decades.It is an
unencapsulated, locally infiltrating tumour. If allowed to reach a large size, it takes a big operationto remove it.
NON ODONTOGENIC BENIGN TUMORS

Examples of benign tumours include:
Adenomas - tumours that arise from glandular epithelial tissue. Although adenomas are not cancerous, they can change and
become so; then they are called adenocarcinomas.
Fibromas - Benign tumours that grow on fibrous or connective tissue of any organ in the body.
Some fibromas can cause symptoms and may require surgical removal. Rarely, fibroids can change and eventually become
cancerous, they are then called fibro sarcomas.
Hemangiomas - benign tumours which consists of a collection of too many blood cells. The majorities of haemangioma
appear at birth and gradually go away after some months or years.
Lipomas - the most common form of soft-tissue tumour. Lipomas consist of adipose tissue (fat cells). Most of them are very
small, painless, soft to the touch, and generally movable.
22
NONODONTOGENIC BENIGN TUMORS OF THE JAWS

Exostoses and Tori
Osteoma
Osteoid Osteoma
Central Hemangioma
Arteriovenous Fistula
Neurogenic Tumors (neurilemmoma, neurofibroma)
Traumatic Neuroma
Chondroma
TUMOR-LIKE AND REACTIVE LESIONS
Central Giant Cell Granuloma
Fibrous Dysplasia
Histiocytosis X
EXOSTOSES AND TORI
Exostoses and tori are localized peripheral overgrowths of bone due to some unknown cause. They occur on any surface of
the jaw bones. Exostoses and tori are neither of pathological nor of clinical significance except that they interfere with
normal speech and other functions. On a radiograph, exostoses and tori appear as well-defined round or oval radiopacities
superimposed on the roots of teeth.
OSTEOMA
Osteoma is a benign tumor of bone which occurs most commonly on the skull and jawbones. The bony-hard discrete mass
extends from the cortex and produces asymmetry of the jaw. Osteomas can also occur in maxillary and fronto-ethmoidal
sinuses.
CENTRAL HEMANGIOMA
Central hemangioma is a benign vascular neoplasm within bone which produces aproliferation of blood vessels. It occurs
more often in the vertebrae and skull but rarely inthe jaws. The teeth in the vicinity of the tumour may be loosened and
bleeding may occur from the gingiva around the necks ofthe affected teeth.
ARTERIOVENOUS FISTULA (Arteriovenous shunt or malformation)
Arteriovenous fistula is a direct communication between an artery and a vein, and bypassing the intervening capillaries. The
most characteristic location for its occurrence is the ramus-retromolar area of the mandibleinvolving the mandibular canal.
NEUROGENIC TUMORS
Neurogenic tumors are rare benign intraosseous nerve tumours which occur mostly in the body and ramus of the mandible.
Neurilemmoma (Schwannoma)
The tongue is the favoured location, although lesions have been described in the palate, floor of the mouth, buccal mucosa,
gingiva, lips, vestibule and jaws.
Neurofibroma
Neurofibroma is a benign slow growing tumour composed of components of the peripheral nerves (including the axons) and
from the connective tissue of the sheath of Schwann.
TRAUMATIC NEUROMA (Amputation neuroma)
Traumatic neuroma is not a true tumour but is a proliferation produced by a damaged
nerve trunk. The trauma to the nerve is caused by tooth extraction, local anesthetic injection, jaw fracture, soft tissue
trauma, ill-fitting denture or accident.
CENTRAL GIANT CELL GRANULOMA
Central giant cell granuloma is a fairly common lesion which occurs almost exclusively in the jawbones, the mandible is more
frequently affected than the maxilla (3:1 ratio). The lesion occurs exclusively in the tooth-bearing areas of the jaws anterior
to the molar teeth.
FIBROUS DYSPLASIA
Fibrous dysplasia is a benign fibro-osseous lesion in which normal medullar bone is gradually replaced by an abnormal
fibrous connective tissue proliferation that contains fociof irregularly shaped trabeculae of immature bone. Fibrous
dysplasia may affect any bone in the skeleton but most often affects the skull and facial bones, or ribs. The swelling is bony
hard to palpation. The maxilla is more often involved than the mandible.
HISTIOCYTOSIS X (Reticuloendotheliosis, Langerhans' cell granulomatosis)
23
Histiocytosis X is a group of reticuloendothelial diseases that are not well understood; the etiology and pathogenesis are
unknown. It acts like a metabolic and a neoplastic disease.
NON ODONTOGENIC MALIGNANT TUMORS

EWINGS SARCOMA
Second most common bone tumour of children/adolescents.Highly malignant, 60% in males; over 95% in those under 20
years of age, Early complain of pain, numbness, and swelling. Diffuse, irregular bone lesion.
METASTATIC CANCER
Itisspread of a primary malignancy to the oral cavity structures orjaws (usually from lung, breast, prostate, colon, and
kidney).
OSTEOSARCOMA
It may present with pain paresthesia, trismus, nasal or paranasal sinus obstruction.It may be associated with pre-existing
bone disease such as; Pagets disease (10 to 15%), Fibrous dysplasia (0.5%).
Intraoral signs are: Tooth mobility (vertical), periapical radiolucency, distal displacement of terminal molar. Jaw mass may be
ulcerated.
Swelling without
pain
Salivary gland Cyst of oral

Oral tumour
tumour cavity
Major glands Minor
Parotid Submandibular Sublingual
Ask for:
Location of tumour
Rate of growth
Presence or absence of pain
Look for:
Location of swelling
Involvement of lymph nodes in neck
Consistency of swelling bony (torus), warty (papilloma), cystic, solid
Is the mass compressible - s/o haemangioma
Colour dark red (haemangioma), red and friable (pyogenic granuloma), bright yellow (lipoma), bluish
(Lymphangioma)
Comments:
SALIVARY GLAND TUMORS
Salivary gland tumours are abnormal cells growing in the ducts that drain the salivary glands. Tumours of the salivary glands
are uncommon and represent 2-4% of head and neck neoplasm. Most (70%) salivary gland tumours (SGTs) originate in the
parotid gland. Although 75% of parotid gland tumours are benign, slightly more than 50% of tumours of the submandibular
gland and 60-80% of minor salivary gland tumours (SGTs) are found to be malignant.
The incidence of salivary gland neoplasms peaks in the fifth decade of life. The most common benign tumour (85%) is the
pleomorphic adenoma. The classic presentation of a benign SGT is a painless, slow-growing mass on the face (parotid), angle
24
of the jaw (parotid tail (most commonly), submandibular), or neck (submandibular) or a swelling at the floor of the mouth
(sublingual).
Warthintumours are the second most common neoplasm of the parotid gland. It is a smooth, soft, well encapsulated when
located in the parotid gland and contains multiple cysts. It tends to be bilateral (10% of cases).
Papilloma: The papilloma, a benign epithelial neoplasm with little malignant potential,may occur as a single or multiple
growths. It appears as a small, warty elevation in the mucosa of the oral cavity, most frequently on the tongue.
Fibroma: This benign, soft tissue neoplasm of the oral cavity is often pedunculated and covered with normal mucous
membrane. The fibroma is found most often in the buccal mucosa where it is frequently bitten by the patient.
Denture Fibroma: The denture fibroma, a benign fibrous tissue hyperplasia due to impingement by a poorly fitting denture,
may become ulcerated and quite painful for the patient.
Pyogenic Granuloma: The pyogenic granuloma, most often found in a mouth with advanced dental caries, is a friable, red,
soft, easily bleeding mass which appears suddenly in the oral cavity and often follows trauma.
Torus:The torus is a benign exostosis-like overgrowth of bone most commonly seen as a lobulated bony mass in the midline
of the hard palate, covered by intact mucosa.
Benign nonepithelialtumours
Hemangioma
Hemangiomas are the most common SGTs in children and usually involve the parotid gland. Less often, they may involve
the submandibular gland. The typical presentation is an asymptomatic, unilateral, compressible mass.
Lymphangioma (cystic hygroma)

Lymphangiomas are most commonly located in the head and neck region of infants and children. They are spongy,
multiloculated masses with a yellowish or bluish surface and are formed by endothelial-lined spaces. Usually, they manifest
as painless masses that may involve parotid glands, submandibular glands, or both.
Lipoma
Lipomatumours are relatively uncommon in a major salivary gland. They appear grossly as smooth, well-demarcated, bright-
yellow masses. These tumours manifest as soft, mobile, painful masses and peak in the fifth and sixth decades of life, with a
male-to-female ratio of 10:1.
Swelling
without pain
Salivary gland
Oral tumour Cyst
tumour
Non- Traumatic/
Odontogenic Developmental
odontogenic inflammatory
25
Developmental cysts Inflammatory cysts
Odontogenic cysts Follicular cyst Radicular cyst:

Eruption cyst apical, lateral, residual
Gingival cyst Periodontal cyst
Lateral periodontal cyst
Glandular odontogenic cyst
Non-odontogenic cysts Cyst of the nasopalatine duct

Nasolabial cyst
Dental Lamina Cyst (Gingival Cyst of Newborn)

Cystic degeneration of residual dental lamina/odontogenic epithelium Small (12 mm), usually multiple, yellow-white
nodules over the alveolar crest in neonates.
Traumatic Bone Cyst

It may be due to traumatic injury producing intramedullary haemorrhage and subsequent clot resorption, usually in body of
mandible, painless in most cases.
Mucocele
It may be physical-traumatic injury to minor gland excretory duct or systemic (hormonal) etiology. The lower lip are most
common site; also occurs buccal mucosa, anteriorventral tongue. It is painless.
Mucus Retention Cyst

The mucocele, a retention cyst, duct obstruction may be due to a mucous plug or sialolith formation. Asymptomatic, soft
mucosal swelling can occur at any intraoral minor salivary gland site, especiallyupper lip.
Ranula
Obstruction of the sublingual (usually) or submandibular salivarygland by a sialolith or by trauma.Secondary to obstruction,
extravasations of saliva into the softtissue of the floor of the mouth. It is unilateral, fluctuant, soft tissue mass on the floor of
the mouth.Usually has a bluish, slightly translucent quality.
Radicularcysts
These form about the root of teeth,usuallyastheresult ofinfection
Swelling with Pain
Trauma Infection
Tooth #
Jaw # Spreading Localized
Avulsion of Tooth
viral
Cellulitis
Bacterial
Cavernous Sinus Thrombosis
Fungal
Ludwigs Angina
26
Clinical clues
Ask about:
History of Trauma
Pain
Fever s/o infection
Duration of swelling
Progression
Severe headache, Inability to move the eye, Pain or numbness around the face or eyes, deep retro-orbital pain.
Vision loss or double vision, seizures all symptoms of cavernous sinus thrombosis.
Drug history especially drugs that might increase the risk of blood clot (e.g. Oral contraceptive pill) risk for
cavernous sinus thrombosis.
Difficulty breathing, or neck pain s/o Ludwigs angina
Look for:
Tenderness
Associated lymph nodes involved
Site, size, Shape, number,
Consistency: soft, firm, hard
Colour
Fracture of teeth / jaw, Missing teeth (Avulsed); Check the Occlusion, if the teeth are not in occlusion(contact),
there may be fractured jaw or dislocation of the jaw.
Swelling, redness, or irritation around one or both eyes, drooping eyelids s/o cavernous sinus thrombosis
Investigations
CBC for evidence of infection
FNAC
Radiology
Biopsy
CT or MRI if suspect Cavernous sinus thrombosis
Comments:
Cavernous sinus thrombosis is typically caused by an infection that has spread beyond the face, sinuses, or teeth. Less
commonly, infections of the ears or eyes may cause cavernous sinus thrombosis. The body's immune system creates a
thrombus to prevent bacteria or other pathogens from spreading. The clot increases pressure inside the brain. This pressure
can damage the brain and may ultimately cause death.
Ludwigs Angina
Ludwigs angina is a subcutaneous tissue infection that occurs on the floor of the mouth, underneath the tongue. This
bacterial infection often follows a tooth abscess or other mouth infection or injury.
27
Localized Infection
Viral Bacterial Fungal
Apthous Ulcerations
Gingivitis Periodontitis Candidiasis
(Herpetic Infections)
Angular Chelitis
Others:
Pulpitis
Acute and Chronic -
Pulp Polyp
Periapical Abscess
Periodontal Abscess
Osteomyelitis
Pericoronitis
Dry Socket
Ask for:
Fever suggests bacterial or viral rather than fungal cause
Presence of ulcers (possible apthous ulcers or herpes)
Bleeding of gums during brushing (suggests gingivitis)
Last menstrual period pregnancy increases risk of gingivitis
Use of dentures, immunosuppressant drugs, HIV status/ risk factors for HIV, debilitating illness (all risk factors for
fungal infection)
Look for:
Condition of the gums (swelling, redness, grey colour)
Presence of ulcers (see CP on mouth ulcers)
Presence of white patches that lift off and leave a red base on scratching (s/o candida)
State of teeth (presence of caries, general oral hygiene, presence of loose teeth)
Cracking and bleeding at corners of mouth (angular chelitis)
Presence of lymph nodes, suggesting viral or bacterial infection
Comments:
Pericoronitis is a dental disorder in which the gum tissue around the molar teeth becomes swollen and infected. This
disorder usually occurs as a result of wisdom teeth, the third and final set of molars that most people get in their late teens
or early twenties.
Dry socket is a post-operative complication that interferes with the healing process that takes place after a tooth
extraction.Some people may be more likely to get dry socket after having a tooth pulled. That includes people who: smoke,
have poor oral hygiene, have wisdom teeth pulled, have greater-than-usual trauma during the tooth extraction surgery.
Discomfort from the extraction site starts to intensify 2 to 5 days after the tooth was initially removed.
Pulpitis result from an inflammatory reaction of the pulp inside the tooth. A tooth with acute pulpitis is very sensitive to
fluctuation of temperature range.
Gingivitis is inflammation of the gums. It is a form of periodontal disease. Gingivitis is due to the long-term effects of plaque
deposits on the teeth. If plaque is not removed, it turns into a hard deposit called tartar (or calculus) that becomes trapped
at the base of the tooth. Plaque and tartar irritate and inflame the gums. Bacteria and the toxins they produce cause the
gums to become infected, swollen, and tender. Risk factors for gingivitis include:
Certain infections and body-wide (systemic) diseases
Poor dental hygiene
Pregnancy (hormonal changes increase the sensitivity of the gums)
Uncontrolled diabetes
Misaligned teeth, rough edges of fillings, and ill-fitting or unclean mouth appliances (such as braces, dentures,
bridges, and crowns) Use of certain medications, including phenytoin, bismuth, and some birth control pills
28
The main symptoms of gingivitis are:

Bleeding gums (even after gentle brushing)
Bright red or red-purple appearance to gums
Gums that are tender when touched, but otherwise painless
Mouth sores
Swollen gums
Shiny appearance to gums
Periodontitis
Periodontitis is inflammation and infection of the ligaments and bones that support the teeth. It occurs when gingivitis is
untreated or treatment is delayed. Infection and inflammation spreads from the gums (gingiva) to the ligaments and bone
that support the teeth. Loss of support causes the teeth to become loose and eventually fall out. Periodontitis is the primary
cause of tooth loss in adults.
Plaque and tartar build up at the base of the teeth. Inflammation causes a pocket to develop between the gums and the
teeth, which fills with plaque and tartar. Soft tissue swelling traps the plaque in the pocket. Continued inflammation leads
to damage of the tissues and bone surrounding the tooth. Because plaque contains bacteria, infection is likely and a tooth
abscess may also develop, which increases the rate of bone destruction.
Symptoms early on resemble gingivitis. Later, get : loose teeth in addition.
Note: Aphthousulceration, Candidiasis and Osteomyelitis,are already mentioned in Mouth sore and ulcers CP.
Pain without
swelling
Tooth Facial pain & Temperomand

sensitivit neuromuscular ibular joint
y disorder conditions
e.g. Dental Chronic

caries, Oral
submucosal idiopathic
abrasion, facial pain
attrition fibrosis
Clinical clues
Ask about:
History of Trauma
Brushing habit
Eating habit, especially use of betel nut or ingestion of chilies - risk of oral submucosal fibrosis (OSMF)
Other habits; pipe smoking, tooth pick use, thread biting.
Bruxisum ( Night grinding of teeth )
Pain site, type, severity, duration, aggravating factor, radiating or not
Progression
Limitation in jaw movement
Symptoms suggestive of Tempero-mandibular joint disorders:
o Pain or tenderness in the face, jaw joint area, neck and shoulders, and in or around the ear when you chew, speak, or
open your mouth wide
o Limited ability to open the mouth very wide
o Jaws that get "stuck" or "lock" in the open- or closed-mouth position
o Clicking, popping, or grating sounds in the jaw joint when opening or closing the mouth (which may or may not be
accompanied by pain) or chewing
o A tired feeling in the face
o Difficulty chewing or a sudden uncomfortable bite as if the upper and lower teeth are not fitting together properly
o Swelling on the side of the face
29
Look for:
Dental caries
Fracture / Cracked teeth
Tenderness
Origin
lymph nodes
Features suggestive of OSMF
o Early lesions demonstrate blanching of the oral mucosa.
o Older lesions - palpable fibrous bands in the buccal mucosa and around the mouth opening or lips, resulting in a
mottled, marblelike appearance of the mucosa because of the vertical, thick, fibrous bands running in a blanching
mucosa.
o Reduction of the mouth opening (trismus)
o Stiff and small tongue
o Blanched and leathery floor of the mouth
o Fibrotic and depigmented gingiva
o Rubbery soft palate with decreased mobility
o Blanched and atrophic tonsils
o Shrunken budlike uvula
o Sinking of the cheeks, not commensurate with age or nutritional status
Investigations
o Radiology
o Biopsy
Comments:
Tooth erosionis the wearing away of tooth enamel by acid. The enamel is the hard calcified tissue that covers and protects
the outside of the tooth.Tooth erosion can also be caused by medical factors such as a decrease in saliva, acid reflux disease,
and certain gastrointestinal conditions.
Abfraction is the commonly seen condition of notching of the teeth near or even under the gum line.
Trigeminal Neuralgia, also known as Tic Douloureaux, is a nerve disorder that causes abrupt, searing, electric-shock-like
facial pains, most commonly the pain involves the lower face and jaw, but symptoms may appear near the nose, ears, eyes
or lips. Neuralgia is severe pain along the course of a nerve. The pain occurs because of a change in neurological structure or
function due to irritation or damage of a nerve.
Dental attrition is constant accumulated wear and deterioration of teeth as a result of contact with opposite teeth. Some
level of tooth attrition as a result of the usual process of chewing and eating is normal, resulting from physical pressure
opposing teeth locate on each other throughout the time of usual usage.
Abrasion is caused by the intraoral use of objects, such as tooth brush often in combination with abrasive substances. Other
habits include pipe smoking tooth pick use, thread biting.
Temperomandibular joint (TMJ) disorders

These occur as a result of problems with the jaw, jaw joint and surrounding facial muscles that control chewing and moving
the jaw. The cause of TMD is not clear, but dentists believe that symptoms arise from problems with the muscles of the jaw
or with the parts of the joint itself. It can be caused by:
Injury to jaw (e.g. whiplash, direct blow)
Grinding or clenching the teeth, which puts a lot of pressure on the TMJ
Dislocation of the soft cushion or disc between the ball and socket
Presence of osteoarthritis or rheumatoid arthritis in the TMJ
Stress, which can cause a person to tighten facial and jaw muscles or clench the teeth
Trismus reduced opening of jaw caused by spasm of the muscles of mastication. Many possible causes.
30
Oral submucosal fibrosis (OSMF) the main symptom in this condition is a progressive inability to open the mouth (trismus)
due to oral fibrosis and scarring. Many patients also complain of oral pain and a burning sensation upon consumption of
spicy foodstuffs. There may be associated hearing loss (due to stenosis of the eustachian tubes) or dysphagia to solids (if
the oesophagus is involved) or impaired mouth movements (e.g., eating, whistling, blowing, sucking).
It can be caused by: chewable agents, primarily betel nuts (Areca catechu), which contains substances that irritate the oral
mucosa, making it lose its elasticity. Nutritional deficiencies, ingestion of chilies, and immunologic processes may also have a
role in the development of oral submucous fibrosis
Chronic idiopathic/atypical facial pain.

The main features of AFP are: no objective signs, negative results with all investigations/ tests, no obvious explanation for
the cause of the pain, and a poor response to attempted treatments. AFP has been described variably as a medically
unexplained symptom, a diagnosis of exclusion, a psychogenic cause of pain, and as a neuropathy. AFP is usually burning
and continuous in nature, and may last for many years. Depression and anxiety are often associated with AFP, which are
either described as a contributing cause of the pain, or the emotional consequences of suffering with unrelieved, chronic
pain. For unknown reasons, AFP is significantly more common in middle aged or elderly people, and in females.
31
DISORDERS OF PIGMENTATION
Normal color of skin is dependent on melanin pigment, the major color determinant along withhemoglobin (both
oxygenated and reduced state) and carotenoids. Melanin pigment is synthesized and distributed to adjacent keratinocytes
by cutaneous melanocyte normally found in basal layer of epidermis. The racial and ethnicvariations in skin color are related
to number, size, shape and distribution of melanin-laden organelles called melanosomes produced in melanocytes.
Disorders of
Pigmentation
Hypopigmentaion Depigmentation Hyperpigmentation
Localized Generalized
Pigmentary changes on the skin can be hyperpigmentation, hypopigmentation or depigmentation. Patients with abnormal
pigmentation seek advice primarily for cosmetic reasons. Pigment changes are usually asymptomatic and of no medical
consequence, however they may signify underlying systemic disease.
Hyperpigmentation: Darker than normal skin, increased amount of melanin in the skin
Hypopigmentation: Lighter than normal skin color, decreased production of melanin by normal number of
melanocytes in the skin
Depigmentation: Loss of preexisting pigment in skin, total lack of melanin in the skin
HYPERPIGMENTATION
Hyperpigmentation
Localized Generalised
See below
Congenital Acquired
Dark brown Light brown,

single/few/isolated multiple
Multiple Irregular shape, brown,
Cafe-au-lait large patches
Congenital macules
melanocytic nevi
Upper Sun exposed
trunk sites Female Previous
face inflammatory
skin condition
Oval, scaly Appear after No change after Melasma

sun exposure sun exposure
Post
inflammatory
Pityriasis hyperpigmen-
Freckles tation
versicolar
Lentigens
32
Hyperpigmentation is usually caused by:

Overproduction of melanin by normal number of melanocytes (e.g. freckles)
Increasednumber and altered distribution of melanocytes (e.g. melanocytic nevus)
Malignanttransformation of melanocytes (e.g. melanoma)
Clinical clues: Think whether this is primary skin disease or secondary to systemic illness
Ask for:
1. Time of onset:
a. Melanocytic nevi usually appear at birth
b. Caf-au-lait macules, freckles commonly present in childhood
c. Post inflammatory hyperpigmentation and melasma in adults
2. Distribution of lesions: single, multiple or diffuse
3. Associated symptoms: mostly asymptomatic except for cosmetic concern
4. Exposure to sun light increase freckles
5. Pregnancy:melasma, prescribe safe drug
6. Past history of inflammatory skin conditions: post inflammatory hyperpigmentation
7. Drug ingestion: OCPs, chloroquine, hydroxychloroquine, minocycline, clofazimine, bleomycin can cause
hyperpigmentation
8. Associated illness mostly inquire for other autoimmune and systemic illness i.e. systemic review
Look for:
1. Entire skin surface in natural light: color, shape, size and distribution of lesion
2. Palms, soles, oral mucosa, skin creases
3. Features of other systemic conditions as suggested by history
Hyperpigmentation:
Diagnosis to consider
A. Generalized hyperpigmentation: Mainly secondary to systemic illness except scleroderma
Endocrine:hyperthyroidism, Addisons disease, Nelsons syndrome
Primary haemochromatosis
Biliary cirrhosis (primary)
Chronic renal failure
Chronic infection: malaria, kalazar
Neoplastic: oat cell carcinoma of bronchus, lymphoma
Immunologic: rheumatoid arthritis, Stills disease, systemic sclerosis, scleroderma
Drugs/chemicals: OCPs, chloroquine,hydroxychloroquine, clofazimine,cyclophosphamide, phenytoin,
minocycline, amiodaroneproduce hyperpigmentation on exposed areas
B. Localized hyperpigmentation:
Freckles, lentigens, melasma
Neurofibromatosis (Caf au lait macules)
Post inflammatory hyperpigmentation
Peutz-Jegherssyndrome
33
Comments:
Hyperpigmented lesions
1. Freckles: Autosomal disorder, small light brown pigmented macules, usually <3mm in diameter which appear
on sun exposed sites (face, trunk, arms), increase in number and size during summer months and become
smaller, lighter and fewer in the winter.
2. Lentigens: Brown or brown-black macules,(more darker than freckles) circular or oval, with or without slight
scaling, scattered in distribution; no seasonal variation
3. Melasma: Blotchy brownish, macules with poorly defined border on centrofacial (cheeks,forehead and chin)
region usually appear during/after pregnancy
4. Pityriasisversicolor: Multiple round/oval, brownish, coalescing macules with furfuraceous scales, mainly on
upper trunk which later become hypopigmented
5. Pellagra: Hyperpigmentation (copper colored) following erythema, brown scaling and crusts confined to sun-
exposed sites.
6. Post-inflammatory hyperpigmentation: Hypermelanosis commonly following acute or chronic inflammatory
process in the skin that is more marked in dark skinned people.
Hyperpigmentation in systemic disorders:

1. Systemic sclerosis, Scleroderma: Generalized mixed pigmentation (salt and pepper) or of addisonian type but
without mucosal involvement and predominantly on face and limbs
2. Neurofibromatosis: Round or oval patches of light-brown pigmentation (caf-au-lait macules)with a diameter
of 5mm or more and six or more in number along with axillary freckling, lisch nodules etc.
3. Puetz-Jeghers syndrome: Autosomal dominant disorder, lentigens on oral mucosa
(lips/buccal/gingival/palatal), around the nose and mouth, on fingers and toes in association with intestinal
polyps
4. Xerodermapigmentosum: Freckle like pigmentation on the face and other exposed skin begins in infancy or
early childhood, may be associated with telangiectasias, small white atrophic spots and later with tumors and
severe photosensitivity
5. Renal failure: Brown pigmentation most intense on palms and soles (patchy or diffuse)
6. Primary biliary cirrhosis: Diffuse hypermelanosis
7. Haemochromatosis: Autosomal recessive, bronze or slate gray mucocutaneous pigmentation, initially on sun-
exposed sites later generalized
8. Amyloidosis: Localized, often symmetrical,bluish macule on upper back with distinctive ripple pattern
9. Addisons disease: Diffuse but more intense on light exposed areas, accentuated in the flexures, at the sites
of pressure and friction areas,over the creases of palms and soles, including conjunctival and vaginal mucous
membrane
10. Hyperthyroidism: Diffuse and addisonian patternwith less mucosal involvement
11. Chronic infections: Diffuse light brown pigmentation
12. Vitamin A deficiency: Generalized hyperpigmentation with dryness and desquamation
Drug induced hyperpigmentation:

1. Fixed drug eruption: Slate-brown pigmentation commonly following erythematous or bullous stage of fixed
drug eruption
2. Hydantoin: Pigmentation on face and neck resembling melasma
3. Antimalarial drugs: Bluish-grey pigmentation on face and neck and more intense on light exposed areas,
transverse band or diffuse pigmentation in nail and associated with bleaching of hair color
4. Minocycline: A local well demarcated blue black pigmentation at previous site of inflammation as in acne
scars
5. Clofazimine: Initially reddish later violaceous brown color most noticeable in lesional skin
34
HYPOPIGMENTATION
Face/child Pityriasis
Maculosquamous alba
lesions
Pityriasis
Upper trunk
versicolor
Acquired Papulosqua- Tuberculoid

Anaesthetic
mous lesion leprosy
Hypo- Prior inflammatory Post inflammatory

Localized
pigmentation skin lesion hypopigmentation
Wrinkled atrophic
surface Morphea
Decreased
pigmentation
Congenital Ash leaf macule
Generalized Congenital Albinism
Depigmentation
Vitiligo
Chemical leukoderma
Localized Acquired Localized
Halo nevus
Hypopigmentation usually results from

Loss of melanocytes (vitiligo)
Inabilityof melanocytes to produce melanin (albinism)
Depigmented lesions can either be localized or generalized whereas hypopigmented lesions are mostly localized
Clinical clues:
Ask for:
1. Time of onset (birth, childhood, later): albinism, piebaldism, ash leaf macules are congenital; pityriasis alba
commonly present in childhood, vitiligo is acquired and often there is history of trauma (Koebnersphenomenon)
2. Distribution of lesions: localized or generalized
3. Associated symptoms in lesions: mostly asymptomatic except forcosmetic concern (depigmented lesions easily
burn by long exposure to UV rays)
4. Occupation & chemical exposure:leukoderma
5. Past history of inflammatory skin conditions: post inflammatory hypopigmentation
6. Family history: possibility of vitiligo, piebaldism; vitiligo is found to have increased frequency in patients with
endocrinopathies and autoimmune diseases (poor prognosis)
7. Associated illness: mostly inquire for other autoimmune and systemic illness e.g. hypothyroidism in vitiligo
Look for:
1. Entire skin surface in natural light: color, shape, size and distribution of lesion
2. Other systemic conditions as suggested by history
35
Depigmentation: Diagnosis to consider

A. Generalized Depigmentation
Albinism
Generalized vitiligo
B. Localized depigmentation:
Vitiligo
Halo nevus
Ash leaf macules of tuberous sclerosis
Chemical leukoderma: in workers of rubber industry exposed to paratertiary-benzyltoulene
Piebaldism
Conditions that can give rise to hypopigmentation:
Pityriasisversicolor
Pityriasis alba
Leprosy (tuberculoid)
Post inflammatory hypopigmentation
Morphea
Steroid induced hypopigmentation
Nevus anemicus
Nevus depigmentosus
Investigations:
Mainly clinical features make diagnosis and investigation is required in few confusing cases only.
Woods lamp: distinguishes depigmentation from hypopigmentation and also differentiatesepidermal and dermal
melanosis
o Hyperpigmented lesions:
Accentuation of dark color: epidermal melanosis
No change: dermal melanosis
o Hypopigmented lesions:
Milky white accentuation: vitiligo (complete pigment loss)
No change: partial pigment loss (hypopigmentation)
Yellow: Pityriasisversicolor
o Coral red: erythrasma
Other investigations as per the clinical manifestations of systemic disease
Skin biopsy in selected cases
Comments:
Depigmented lesions
1. Ash leaf macules of tuberous sclerosis:Hypomelanotic macules, usually multiple, irregularly scattered, frequently have
lance-ovate shape, a configuration of an ash leaf. Earliest manifestation of tuberous sclerosis and are of diagnostic
significance in babies with seizures.
2. Albinism: Partial or complete congenital absence of melanin in the skin, hair and eyes resulting into light skin, hair and
eyes with photophobia, nystagmus, refractive error etc.
3. Piebaldism:Autosomal dominant disorder,stable areas of vitiligo like amelanotic skin lesions associated with white
forelock
4. Vitiligo: Depigmented macules noted in sun exposed/pressure areas, usually symmetrically distributed, gradually
progressive and sometimes associated with grey hair within the macule. Usually associated with other autoimmune
disorders like thyroid disease(hyperthyroidism & hypothyroidism), type 1 diabetes mellitus, alopecia areata etc.
5. Chemical leukoderma: In workers coming in contact with rubber, tar, phenolic compounds, monobenzylether of
hydroquinone (examples are: phenolic antiseptic detergents; glues &adhesives;rubber used in brassiers,girdles,
pantiesor condoms;sticking bindis and ECG electrodes)
6. Halo nevus: Halo of hypomelanosisaround a central cutaneous tumor, usually around a benign melanocytic nevus
Hypopigmented lesions
1. Pityriasis alba: dry, white and ill-defined macules usually on face in children
2. Tuberculoid leprosy: dry hypopigmented plaque with raised border and slight or total loss of sensations (touch,
temperature and pain)
3. Post-inflammatoryhypopigmentation:hypopigmentation that occurs after inflammatory skin diseases, resolution
of eczema, psoriasis, P.versicolor, etc.
36
DISORDERS OF HAIR AND NAIL

DIORDERS OF HAIR
Hair
Disorders
Alopecia Increased Hair shaft

growth abnormality
Non- Cicatricial Hypertrichosis

cicatricial Hirsuitism
Patchy Diffuse
Scaly Non-scaly Recent Gradual

excess loss loss
Tinea Alopecia All over

Patterned
capitis areata Anagen scalp
hair loss
Androgenic effluvium
alopecia Telogen Alopecia
effluvium Androgenic totalis
alopecia
Drugs
Old age
Hair is found only in mammals. During the course of evolution its primary purpose was for insulation and protection from
elements however in the present world it has profound role in social interaction.
Though medical importance of hair is not documented, loss of hair or excessive hair growth in unwanted areas can lead to
significant psychological and emotional disturbances. Some hair disorders may reflect internal health conditions like
malnutrition, stress, thyroid disorders, etc.
Like human life hair also grow and shed off cyclically. There are three phases of hair growth:anagen, catagen and telogen.
Anagen hairs are growing hairs; they grow for about 2 to 6 years. Catagen hairs are in transitional phase, lasting for about 1
to 2 weeks, in which all growth activity ceases. Telogen hairs are the resting hairs which continue to rest for 3 to 5 months
before they fall out. In a normal human scalp, 85% to 90% hairs are in anagen phase, 10 to 15 % hairs are in telogen phase
and catagen phase of hairs comprise less than 1% of scalp hairs. Normally around 100 hairs shed in a day.
Types of hair in human:

Lanugo: fine, long, nonmedulatedandnonpigmentedfoundon the body of fetus
Vellus: soft, fine, nonmedulated,lightcoloured and thin found on forehead, ears and trunk
Terminal: coarse, thick, medulated and pigmented found on scalp,beard area, axillae,pubis, eyebrows
Hair occurs in all skin surfaces except the palms, soles, labia minora, lips, nails, glans and prepuce.
Disorders of hair can be classified as alopecia (thinning or loss of hair), excessive unwanted growth of hair
(hypertrichosis) and hair shaft abnormality.
Causes of alopecia is generally divided into broad categories of cicatricial and noncicatricial alopecia
Cicatricial alopecia: scarring alopecia

Non-cicatricial alopecia: non scarring alopecia
37
Non-cicatricial alopecia: Clinical clues

Ask for:
Sudden or gradual hair loss (sudden hair loss is noticed in alopecia areata where as it is gradual in other)
Presence of skin symptoms: pain, itching, scaling
Presence of systemic disease or high fever:telogen effluvium
Recent psychological or physical stress: telogen effluvium
Weight loss or change in diet
Medication or chemical exposure (ACE inhibitors, allopurinol,azathioprine, anticoagulants,chloroquine, lithium,
contraceptives, carbamazepine, metoprolol, cytotoxic drugs)
Use of chemicals, dyes for various cosmetic purposes
Family history: density of hair, pattern of hair loss
History of hair pulling during stress
Look for:
Localized vs generalized (site, size, pattern of hair loss including length of lost hair)
Signs of inflammation
Density of hair: normal or decreased
Recession of hair line: not seen in female pattern androgenic alopecia
Exclamation hair in alopecia areata
Surrounding skin atrophy
Hair loss from other body parts in alopecia totalis or universalis
Skin disease in other areas (see below)
Hair shaft: normal or damaged
Easily pluckable hair: tineacaptis, alopecia areata
Investigations:
Hair shedding count
Hair pull test
Hair shaft microscopy
KOH and fungal culture to rule out fungal infection
Skin biopsy from scalp
Lab: CBC, TFT, serum ferritin/iron binding capacity
Additional test as suggested by history and physical finding: testosterone/DHEA, prolactin, ANA, ds DNA, CRP, ESR,
VDRL/TPHA
Hair pluck (trichogram):anagen to telogen ratio
Non-cicatricial:Patchy type
Alopecia areata: smooth and shiny, round or oval patches of hair loss with exclamation mark hairs (tapered fractures)
Androgenic alopecia: androgen dependent hair loss tends to follow family pattern. hair loss pattern is different in males &
females
Infection induced:
o Tineacapitis non inflammatory type
o Secondary syphilis (typical moth-eaten appearance)
Trichotilomania: irregular patches of hair loss with varying length of terminal hairs due to chronic pulling out of hair, seen in
persons with deficient mental condition
Traction alopecia: hair loss resulting by repeated pulling and tugging of hair shaft e.g. tight hair band, rolling; seen in girls &
young women, bald area show short broken hairs, folliculitis and sometimes scarring; site depends on type of traction used
Non-cicatricial: Diffuse type
Telogen effluvium: stress related conditions (post partum, post operation, post typhoid, post natal period for new born,
debilitated case) causea large percentage of hairs suddenly stop growing and enter the resting or 'telogen' phase resulting
into diffuse fall about 3 months later
Anagen effluvium: growth period is arrested and hair falls e.g. after cytotoxic drugs, methotrexate, leflunomide
Androgenic alopecia: patterned baldness in male, female: often diffuse alopecia mainly frontal region of scalp
Alopecia totalis/universalis
Systemic disease: SLE, syphilis, thyroid disease, diabetes, malignancy
SLE: coarse, brittle, short hair of varying length known as lupus hair commonly seen on frontal scalp.
Hypothyroidism: hair become coarse, brittle, dry and sparse
Hyperthyroidism: fine and sparse hairs
Diabetes: loss of hair in lower extremities
Nutritional deficiency:Fe, Cu, Zn deficiency
38
Ectodermal dysplasia: A group of rare inherited disorders characterized by sparse hair, scanty sweat glands, and poor
development of the nails and teeth.
Cicatricial alopecia: Scarring type of alopecia, from where hair does not grow due to permanent damage to hair follicles,
and obvious loss of tissue or atrophy by inflammatory (infectious or noninfectious) or other pathologic processes and
healing occurs with scarring.
Hair loss
Non-cicatricial Cicatricial
Congenital/ Acquired
developmental
Aplasia cutis Multipl

Single
Nevus e
sebaceous
Injury/ Lichen planus
Linear
infection Discoid lupus
erythematosus
Burn Cicatricial
Trauma Morphea pemphigoid
Herpes zoster
Inflammatory
tinea capitis
Clinical clues:
Ask for:
Previous skin lesion on scalp
History of trauma/burn
Known systemic disease e.g. SLE
Look for:
Evidence of tissue destruction (inflammation, atrophy,scarring)
Presence of follicular opening
Evidence of systemic disease e.g. for SLE
Causes of scarring alopecia

a) Congenital or developmental defects: aplasia cutis(congenital loss of hair due to loss of skin), mother on
carbimazole may deliver baby with congenital aplasia cutis
b) Cutaneous disease: deep fungal infections,inflammatory tineacapitis (kerion,favus),TB of skin, carbuncle, deep
foliculitis, DLE, lichen planus, morphea, lichen sclerosus, dermatomyositis, cictricialpemphigoid, acne keloidalis
c) Neoplasms: BCC, SCC, metastatic tumours
d) Systemic disease: SLE, scleroderma, dermatomyositis
e) Physical or chemical agent:burn, trauma, radiation, acid, alkali
Hypertrichosis: Excessive hair growth in non sexual distribution that may involve vellus, terminal or lanugo type hair is called
hypertrichosis. It can be congenital or acquired. For details see CP on Hirsutism.
Hirsutism: Excessive growth of hair in a female, distributed in a male secondary sexual pattern is called hirsuitism. A search
for more serious causes is indicated if the changes are of rapid onset.
Hair shaft abnormality:
Seen in genetic syndromes and can be acquired usually due to excessive use of chemicals and mechanical trauma
39
DISORDERS OF NAIL
Yellow
White
Colour Red streaks
Longitudional
streaks
Infection/
Paronychia
Inflammation
Nail fold
Telangiectasia SLE
Psoriais
Eczema
Chonic paronychia
Thyrotoxicosis
Attachment Onycholysis
Nail Pseudomonas infection
disorders Trauma
Shedding
Lichen planus
Plate
Surface Ridging
Grooving
Thickening & Pitting
Subungal hyperkeratosis Onychomycosis Lichen planus
Clubbing
Shape
Koilonychia
The nail apparatus composed of the nail plate and surrounding soft tissue structures, adds function(especially fingernails)
and protects terminal digits. Nail structures can be altered by primary skin diseases, infections, trauma, internal diseases,
congenital syndromes, and tumors.
Terminology: -
1. Onycholysis: detachment of nail from its bed at distal and/or lateral attachments
2. Onychogryphosis: hypertrophy of nail plate and subungual hyperkeratosis mainly seen in elderly
Ask for:
Occupation: minor, subtle trauma to nail matrix in manual workers may mainfest as splinter haemorrhages,
subungual hematoma may be confused with subungual melanoma, chronic trauma from sports and ill fitting shoes:
gross thickening of toe nails (onychogryphosis), ingrowing nails, separation of nail plate from nail bed (onycholysis)
Frequent exposure to moisture (immersion in water): chronic paronychia
Pain, pus discharge
Known skin disease e.g. psoriasis, alopecia areata
Drug history
History of trauma: even subtle trauma like nail biting or vigorous manicure
40
Look for:
All nails both finger and toe (toe nails are affected more commonly in onychomycosis whereas finger nails are affected
commonly in candidal paronychia)
Nail plate: colour, thickening, pitting
Yellow: psoriasis, onychomycosis, jaundice
White: hypoalbuminemia (liver cirrhosis)
Red streaks: endocarditis, vasculitis
Brown: half &half nail (CRF)
Longitudional streaks: melanocytic naevi, Addison's disease, subungual melanoma
Subungal hyperkeratosis: psoriasis, onychomycosis
Pitting: psoriasis, alopecia areata, chronic hand eczema
Ridges and grooves:lichen planus, chronic eczema of hand, elderly hand
Ladder pattern of transverse ridges and furrows at centre of thumb nail plate: due to habit tic nail dystrophy
Nail fold:
Inflammation of nail fold (oedema, erythema, pus): paronychia, ingrown nail
Telangiectasias (dilated capillaries) in nail fold: dermatomyositis, SLE
Nail in multisystem diseases:
Apparent leukonychia (terrys nail): hypoalbuminaemeia (cirrhosis of liver)
Half and half nail: uremia (chronic renal failure)
Yellow nail syndrome: bronchiactasis, chronic bronchitis
Onycholysis/photo-onycholysis: thyroid disease,iron deficiency anaemia, tetracycline, retinoids,psoralens,
chemotherapeutic agents
Periungal fibroma: tuberous sclerosis
Splinter haemorrhages: arterial emboli, vasculitis, scurvy, endocarditis
Nail fold telangiectasia and erythema: dermatomyositis, lupus erythematosus, systemic sclerosis, secondary
Raynauds phnomenon
Transverse grooves (Beaus lines): appear few weeks after sudden, severe, acute particularly febrile illness,
chemotherapeutic agents
Koilonychia: iron deficiency anaemia, rarely congenital
Clubbing: chronic lung and heart disease, familial
Drugs:
o Onycholysis: minocycline, antimalarials, gold
o Beaus line: chemotherapeutic agents
Investigations:
Nail clipping and scrapping of subungal debris for KOH and fungal culture
Pus for culture and sensitivity
Nail plate and nail bed biopsy
Other as suggested by history and physical examination
Comments:
Components of nail apparatus: Nail plate, proximal nail fold, cuticle, lateral fold, lunula, free margin, nailmatrix, nail bed,
hyponychium
Nail disorders associated with skin disease:

Psoriasis
Lichen planus
Alopecia areata
Bacterial and viral infections: acute and chronic paronychia, pseudomonas infection, herpetic whitlow
Fungal nail infections
Trauma: onycholysis, nail and cuticle biting, ingrown nail, subungual hematoma, nail hypertrophy, white spots,
brittle nails
Tumors:
o Benign: warts, pyogenic granuloma, periungual fibroma, myxoid cyst, nevi
o Malignant: melanoma
41
SKIN LESIONS
Patients may present with varieties of skin lesions.Different people may use different termsfor the same skin condition
depending upon place and language, andsometimes evenuse wrong terminology to describe a particular lesion, which may
mislead the physician. So over the years, a method has been evolved to facilitate recording of signs of skin disease. Because
the lesions are available for inspection and palpation, and normal skin is also available for comparison, it is easy to describe
the lesions using these unique terms. A good description of skin lesions enables the listener to formulate a series of
differential diagnoses.
Skin lesions are broadly divided into primary and secondary lesions.
Primary lesion: It is the initial lesion that has not been altered by trauma or manipulation (scratching, scrubbing) or natural
regression over time.
Secondary lesion:These are created by scratching, scrubbing or infection. They may also develop normally with time, e.g.
macular erythema is a primary lesion in sunburn but on resolution scaling and hyperpigmentation become prominent as
secondary changes.
Skin lesions
Primary Secondary
Flat Raised Broken Raised
Macule Solid Fluid filled

Patch Excoriation
Scale
Erosion
Clear Purulent Crust
Papule Fissure
Lichenification
Plaque Ulceration
Nodule Pustule
Vesicle
Tumour
Bulla
For the sake of simplicity, the common dermatological diseases are divided into acute and chronic erythematous
and non-erythematous conditions.
Skin conditions
Acute erythematous conditions Chronic erythematous conditions Non-erythematous conditions
42
ACUTE ERYTHEMATOUS CONDITIONS

Eczema
Pruritic Candidiasis
Papular
urticaria
Papules/vesicles/
Furunculosis
pustules/plaques
Abscess
Discrete
Carbuncle
Localized Chicken pox
Painful
Herpes simplex
Grouped
Herpes zoster
Nodule Erythema nodosum
Acute
erythematous
conditions
Photoexposed Photodermatitis
areas SSSS* SLE
Skin peeling
TEN#
Dermatomyositi
s
Viral exanthem Pellagra

Maculopapular
Drug rash
Generalized Porphyria
Papulovesicular Chicken pox
Transient itchy
papules/plaques Urticaria
*SSSS: Staphylococcal Scalded Skin Syndrome

#TEN: Toxic Epidermal Necrolysis
1
Photo exposed areas: forehead, nasal bridge, malar area, lower lip, rim of pinnae, V- area of neck, extensor
surface of forearms, and dorsum of the hands and feet.
Ask for:
Pain: usually indicates infection, erythema nodosum
Itching:mainly seen in eczema, urticaria, and drug rashes
Duration: transient itchy wheals which resolve within 24 hours isurticaria,wheals with pain/burning
sensation that persist beyond 24 hours indicatesurticarial vasculitis
Aggravating factors like sunlight, heat, exercise, cold etc.
Drug ingestion:drug rash may manifest in various ways like maculopapular, bullous, urticarial form etc.,
some drugs (NSAIDs, quinolones, tetracyclines,etc) can bephototoxic
Family history: chicken pox
Systemic features: fever, cold, cough, malaise, sore throat etc with generalized lesions suggestsviral
exanthems like measles, chicken pox or a drug eruption
Irritation or burning sensation prior to vesicular eruptionsuggest herpes simplex/zoster
Exposure to pets/garden (bushes/plants) indicates insect bite
Sun exposure: swimming/ hiking may cause sunburn, polymorphic light eruption
Contact with allergen like nickel, rubber, cosmetics, plants,etc prior to itchy skin rashsuggest allergic
contact dermatitis
Change in the pre-existing lesions (increase in size, color) in type I lepra reaction
43
Look for:
Type of lesion: macule/papule/plaque which gives clue to possible diagnosis
Site: erythema or telangiectasia on photo exposed areas suggest SLE, dermatomyositis
Size: vesicle or bulla, nodule or tumour
Shape: malar rash in SLE is seen in butterfly shape
Colour: erythema indicates inflammatory process is going on the lesion
Number: single lesions are seen in furunculosis, lesions are seen in groups in herpes simplex/zoster
Border: eczema usually has ill defined border
Arrangement: linear arrangement is seen in herpes zoster
Distribution of lesions along with change in surface
Palpate lesions for temperature, texture and tenderness
Regional lymph nodes whether enlarged, tender
Vitals and systemic examination where indicatede.g. in measles, chickenpox, SLE
Peeling of skin with foci of a staphylococcal skin infection indicates SSSS, and after ingestion of drug suggest TEN
Mucosal involvement: oral, ocular, genital in SJS,TEN and other dermatosis
Involvement of palms, soles (differentiate drug rash from viral exanthem)
Do not forget to examine nails, hairs and scalp
Investigation:usually not required as most conditions can be diagnosed clinically

Pus swab for culture and sensitivity
Cytological smear of the vesicle (Tzanck smear) to look for large multinucleated giant cells and inclusion bodies in
viral vesicular lesions or acantholytic cells in immunobullous diseases
Anti HSV antibody IgM and IgG for both HSV-1 and HSV-2
Viral culture from vesicle fluid
Hematology, biochemistry and others as indicated by history and physical examination
Diagnosis to consider:
Impetigo: group of papules and pustules with honey colored crust around mouth or nose in a child
Varicella zoster (chicken pox):discrete, polymorphic lesions (consisting of macule papule, umbilicated vesicles,
crusted papules) in centripetal distribution with URTI and fever
Herpes zoster: grouped vesicleson erythematous bed inunilateral dermatomal distribution
Herpes simplex: recurrent grouped vesicles with burning sensation
Contact dermatitis: weepy, eczematous lesions at the site of contact with allergen/irritant
Viral exanthem: generalized maculopapular eruption with fever and features of URTI
Drug eruption: generalized itchy maculopapular eruption involving palms and soles with history of drug ingestion,
Type I lepra reaction: erythematous, shiny,indurated,tender, annular plaques, which were non-
inflammedpreviously
Comment:
SLE &dermatomyositis affect multiple organs. Skin is one of the organs they manifest either solely, before or after they
involve other organs. If typical lesions on the skin are visualized,a complete work up should be done to rule out these
diseases.
Pellagra should be considered in alcoholics presenting with lesions over photoexposed areas and work up should be
done for chronic alcoholic liver disease.
CHRONIC ERYTHEMATOUS CONDITIONS

Chronic erythematous conditions
Eczema/ dermatitis Papulo-pustular Papulo-squamous Vesiculo-bullous Ulcerative
44
Eczema/Dermatitis
Plaque/erosion Atopic dermatitis
Flexures
Greasy, yellow
Seborrhoeic dermatitis
scales erythema
Contact with allergen Contact dermatitis
Exposed parts
Photoallergic contact
Photo exposed areas
Eczematous dermatitis
plaque
Palms/soles Sagograin like deep

vesicles Pompholyx
Extremities Coin shaped Numular eczema
Thickened,
Lichen simplex
Accessesible areas hyperpigmented
chronicus
lichenified plaque
Clinical clues
Ask for:
Itching:
o Intensity, timing, precipitating factors (synthetic clothing, wool, fragrances, food,oils, soaps &detergent)
atopic dermatitis
o Predominant symptom in eczema is itching. This often leads to a vicious cycle (itch- scratch cycle) which
causes other secondary changes on the surface of the lesion leading to lichenification, or secondary
infection due to scratch
Working/ living environment, hobbies, clothing, cosmetics: contact dermatitis
Psychological component like stress, family conflict: lichen simplex chronicus
Past history: chronic or relapsing courses
Asthma/hay fever: atopic dermatitis
Family history: atopic dermatitis, asthma
Previous treatment: secondary sensitization to topical therapeutic agents
Systemic symptoms
45
Look for:
Eczematous changes:
o Acute stage:erythematous, oozy plaque consisting of erythematous papulesand vesicles, crusts with ill
defined margin, often without scale
o Chronic stage: dry plaque with scales and lichenification
Xerosis: atopic dermatitis, eczema craquele
Secondary bacterial infection
Age: atopic dermatitis is usually seen in infants and children; eczema craquele is often seen in elderly and neglected
people
Involved sites:
o Atopic Dermatitis usually affects flexures in children and adolescent whereas scalp, face and extensor
surface of upper and lower limbs are affected in infants
o Exposed or contact areas with sharp margin suggest contact dermatitis
o Yellowish, greasy scales on scalp, retroauricular fold, eye brows/lashes,nasolabial fold,interscapular region
indicateseborrhoeic dermatitis
o Small, tiny deep seated, vesicleson sides of fingers, palms and soles suggestpompholyx
o Dry to papulovesicular, exudative, and /or crusted, coin like plaques symmetrically distributed over upper
and lower limbs- nummular eczema
o Itchy eczematous lesions over photo exposed areas indicate photodermatitis
Entire skin to explore other lesions missed by patient
Investigation:
Skin swab for pus culture from infected lesion
Patch test in suspected contact dermatitis
Prick test in atopic dermatitis
Skin biopsy in confusing cases
Exogenous eczemas:
Allergic contact eczema
Irritant eczema
Photoallergic contact eczema
Eczematous polymorphic light eruption
Infective eczema
Endogenous eczemas:
Atopic eczema
Seborrhoic eczema
Asteatotic eczema
Nummular (discoid) eczema
Eyelid eczema
Pityriasis alba
Hand eczema
Venous eczema
Juvenile planter dermatosis
46
Papulopustular lesions
Papulopustular lesions
Face Trunk Generalised

excoriated papules
Comedones Pityrosporum
Comedones present absent Scabies
folliculitis
Pediculosis
Miliaria
Rosacea Acne vulgaris
Acne Folliculitis Drug induced
Perioral acneiform
dermatitis eruption
Ask for:
Age of onset: acne (teenage), rosacea (middle age)
Itching/pain: deep folliculitis is painful, itching in scabies worsens at night
Scabies and pediculosis and insect bite are noted for severe itching
Aggravating factors: sun light, spicy food, stress aggravates rosacea
Treatment/other drugsbeing used for other problems
Family history/symptoms in close contacts: scabies/pediculosis
History of travel: scabies
Look for:(refer acute erythematous conditions)
Site, distribution and arrangement
Regional lymphadenopathy in suspected bacterial infection
Acne vulgaris: teenage, papules with or without pustules on face, upper back and chest with comedones
Rosacea: middle aged women>man, papules and pustules mainly centrofacial area with flushing and
telangiectasia aggravated by sun light, alcohol,hot and spicy food without comedones
Impetigocontagiosa:fragile vesiculopustules that break and leave red oozy erosion covered with thick golden
yellow crusts with satellite lesions mostly seen around nasal and oral orifices in young children
Scabies:
o Excoriated tiny erythematous papules, burrows with typical distribution (wrist, elbow, finger web spaces,
lower abdomen, thigh in adult, and sides of feet, heels and scalp in infant)
o Indurated erythematous nodules on male genitalia: characteristic finding.
o Crusted scabies: a variant of scabies is seen in immunocompromised and neglected elderly
Insect bite: itchy papule consists of typical central vesicle surrounded by erythema usually on exposed areas
esp. extremities, wheals
Pediculosis: nits attachedon hairs, scales, furunculosis, adult lice on scalp and in the seams of clothing,
eczematous changes, scratch marks, erythematous papules in body lice
Folliculitis: papules and pustules located at the openings of hair follicle
Furunculosis: deep folliculitis with central necrosis, red tender nodule with pus point at centre
Perioral dermatitis
Pustular psoriasis
Drug induced acne e.g. steroid
Investigations:usually clinical diagnosis; in doubtful condition can perform:

A superficial epidermal shave biopsyfrom a burrow/papule and see under microscope covered with
immersion oil: for presence of adult mite, scybella
Pus for culture and sensitivity in furunculosis and any other secondary pyodermas
Random blood sugar in case of recurrent furunculosis
47
Papulosquamous Lesions (drypapules or plaques with scaling on surface)

Papulosquamous lesions
Anular Pink,disoid Oval scaly Discoid, atrophic

plaque, on Plaque with
plaque with plaque with Purple,pruritic plaque with warty surface
central loose silvery flat topped trunk herald adherent scale &
clearing scales papules patch follicular
plugging
Dermatophytosis Pityriasis Tuberculosis

Psoriasis Discoid lupus
(tinea infection) Lichen rosea erythematosus verrucosa cutis
planus
Chromoblastomycosis
Ask for:
Pruritus: most cases of psoriasis and pityriasisrosea are asymptomatic, most papules and plaques of lichen planusare
intenselyitchy
Initial lesion: herald patch is noticed 1-2 weeks prior to eruption, in most cases of pityriasisrosea
Aggravating factors: alcohol aggravates psoriasis, sun light aggravates discoid lupus, humidity aggravates dermatophyte
infection
History of trauma by thorn or twigs suggest deep fungal infection like chromoblastomycosis or sporotrichosis
Contact with tuberculosis, leprosy in past
Joint pain: possibility of psoriatic arthritis or other connective tissue diseases
Drugs:
o ACE inhibitors,isotretinoin, BCG vaccination etc are implicated for pityriasisrosea like eruption
o Recent use of systemic steroidprecipitates generalizedpustularpsoriasis, whichrequires hospitalization
o Lithium, beta-blockers, hydralazine, NSAIDs, antimalarials, progesterone are implicated in aggravating psoriasis
o Immunosuppresives may be the reason for recurrent bacterial or fungal infections
Look for:
Shape: annular dermatophyte infection, circular psoriasis
Distribution: extensor surface esp. knees, elbows, sacral region for psoriasis, wrist & ankles for lichen planus, warm &
moist place like groin fordermatophyte infection, pityriasisrosea presents with fine scaly, circular or oval lesion in
covered areas
Scales: small, loose and silvery in psoriasis,along with Auspitz sign
Distribution of lesions along with palms, soles, scalp and nail changes
Involvement of mucosa in lichen planus, drug eruption
Investigation:
Skin scrapping for KOH smear and fungal culture
VDRL: secondary syphilis closely mimics pityriasisrosea
Slit skin smear for identification of M. leprae in suspected leprosy
Punch biopsy in confusing cases for histopathology, AFB stain, fungal stain and culture
CBC, ESR, Chest X-Ray, Mantoux test in suspected tuberculosis
Blood sugar and HIV in extensive or recurrenttineacorporis
Psoriasis
Lichen planus
Pityriasisrosea
Pityriasisrubrapilaris
Dermatophyte infection (tinea)
Discoid lupus erythematosus
Lupus vulgaris
Tuberculosis verrucosa cutis
Leprosy
Secondary syphilis
Dermatomyositis
Comment:
Auspitz sign: Psoriasis
Wickhams stria: Lichen planus
Koebner phenomenon
48
Vesiculobullous Lesions
Vesicobullous
lesions
Hereditory Acquired
Epdermolysis Intraepidermal Subepidermal

bullosa (flaccid) (tense)
Adult
Neonate/children Bullous pemphigoid
Pemphigus vulgaris
Bullous impetigo Dermatitis herpetiformis
Pemphigus
foliaceous Linear IgA diseae
Friction blister
Clinical clues
Ask for:
Pruritus:bullous pemphigoid is itchy
Pain: pemphigus vulgaris is painful
th th
Age: pemphigus vulgaris is disease of 4 to 5 decades, bullous pemphigoid usually appears in the elderly
Involvement of oral mucosa: pemphigus vulgaris affects oral mucosa whereas bullous pemphigoid usually not
Type of bulla: flaccid bullae rupture early or sometime patient does not notice them, whereas tense bullae are
noticed by patient and ruptures in 2-3 days
Malabsorption, gluten sensitive enteropathy in dermatitis herpetiformis
Burning/tingling/pain/discomfort prior to herpetic eruption
Recurrence: recurrent herpes simplex infections are less painful compared to primary infection
Sexual history:genital herpes is transmitted by sexual contact
Family history:epidermolysisbullosa
Look for:
Size: vesicle or bulla
Arrangement:
o Painful vesicles in group surrounded by erythematous halo: herpes simplex
o Annular polycyclic lesions with blisters around the edge (string of pearls): linear IgA disease
Site:
o Pemphigus vulgaris affects scalp, face, neck and upper trunk
o Bullous pemphigoid is seen mostly onflexures of limbs
o Dermatitis herpetiformis is seen on extensor surface of extremities
o Chronic bullous disease of childhood commonly manifests around natural orifices & limbs
o Epidermolysisbullosaacqusita in pressure prone areas
Bacterial super infection: presence of yellow or golden crust on older lesion
Tense or flaccid bulla: flaccid in pemphigus vulgaris tense inbullous pemphigoid
Nikolskys sign and bulla spread sign +ve in pemphigus vulgaris, -ve in bullous pemphigoid
Regional lymphadenitis
Mucosal involvement: small and circular in apthous ulcer, large and irregular in pemphigus vulgaris, whitish thick
plaque-leukoplakia
Investigation:
Cytological smear of the vesicle (Tzanck smear) to look for large multinucleated giant cells and inclusion bodies in
viral infection or acantholytic cells in auto immune bullous disease like pemphigus
Skin biopsy of a typical vesicle for level of cleavage, acantholytic cells
Immunofluorescence
ELISA
Anti HSV antibody IgM and IgG for both HSV-1 and HSV-2
Virus culture from vesicle fluid
49
Comment:
The most common sites for lesions in herpes simplex are on the face (lips, perioral area, cheeks, and nose) and neck,
which is caused by HSV-1. The next common site is anogenital area, then the sacrum and buttocks caused by HSV-2,
which is considered as sexually transmitted. However, due to change in peoples sexual behavior either strain can infect
anywhere. It is uncommon for recurrent lesions to be located inside the oral cavity except in immunocompromised
individuals.
Depending upon the location, the pre-eruptive pain of herpes zoster may be confused with that of pleural or cardiac
disease, cholecystitis or other acute abdomen pain, renal or ureteric colic, sciatica, or other ailments. In ophthalmic
zoster (V1), if the tip of nose is involved there is possibility of concomitant kertoconjunctivitis (Hutchinsons sign).
Multiple dermatomesare affected in immunocompromised individuals and can present with atypical lesions
Post-herpetic neuralgia common in elderly people
IMMUNOBULLOUS DISEASE, BURN, DM, ECZEMA, INFECTION, DRUG ERUPTION, MECHANICAL BULLA
Common Uncommon
Infancy Bullous Impetigo Congenital porphyrias
Epidermolysisbullosa
Childhood Impetigo contagiosa Chronic bullous disease of childhood
Insect bite hypersensitivity Bullous drug eruption
Bullous papularurticaria
Pemphigus vulgaris
Dermatitis herpetiformis
Adult Bullous eczematous eruption Bullous SLE
Bullous drug eruption Porphyria
Erythema multiforme Neuropathic bulla(DM, leprosy)
Stevens-Johnson syndrome
Toxic epidermal necrolysis
Old age Bullous pemphigoid
50
Ulceration
Ulceration
Head & neck Mouth Lower leg/ Genital

trunk ankle/feet
BCC Solitary Multiple

Painful Painless
SCC Arterial ulcer
Trauma Herpes Primary
Melanoma Venous ulcer genitalis syphilis
Dental ulcer Vasculitis (chancre)
Chancroid
Mycetoma Granuloma
Bechet's inguinale
Actinomycosis syndrome
Chronic Recurrent Lymphogra
Neuropathic Erosive lichen
Mucosal nuloma
Herpes Neoplastic planus venerum
lichen planus simplex Pemphigus
Pemphigus Bechet's vulgaris
vulgaris Syndrome Stevens
Discoid lupus Apthous ulcer johnson
syndrome
Clinical clues
Ask for:
Site of ulcer: see in schema for significance
Initial lesion: how the ulcer developed from which primary lesion
Sexual history including, no of partner, last exposure, use of condom in any type of genital lesion
Painful or painless
Duration and growth of ulcer
Chronic non healing or recurrent: r/o malignant or benign
Skin lesions: mucosal pemphigus/lichen planus
Drug usedfor present condition and for other disease: fixed drug eruption, SJS, chemotherapy (methotrexate)
Systemic diseases like DM, HTN, rheumatoid arthritis
Look for:
Type and site of ulcer:
o Superficial or deep, mucosal or cutaneous
o Venous leg ulcer: medial malleolus
o Arterial leg ulcer: lateral malleolus and over tibia
Palpate for tenderness, induration, mobility
Regional lymph nodes
Mucosa and skin both
Investigations:
Smear from base of ulcer for dark ground microscopy, Giemsa stain for genital ulcer suspected to be sexually
acquired
VDRL, TPHA (if VDRL +ve) HIV
Skin/mucosal biopsy for histopathology and fungal stain and culture
As indicated by history and examination
Comments:
Venous leg ulcers: surrounding skin is pigmented due to haemosiderindeposition; there may be fibrosis and
woodiness. Ulcers usually are shallow with flat margins and moderate exudates.
Arterial leg ulcers: skin is pale, cool, decreased capillary refill and reduced peripheral pulses. Ulcers are deep, punched
out with clear margins.
51
NON ERYTHEMATOUS CONDITIONS
Non erythematous lesions
Papule Macule
(see disorders of pigmentation)
Umbilicated Pedunculated Dome Verrucous

Flat topped shaped Follicular
skin coloured surface
white/skin white
coloured
Verruca plana Verruca Keratosis

Acrochordon Milia vulgaris
Xanthelasma pilaris
Molluscum Neurofibrom Comedone Seborrhoic
Syringoma a Phrynoderma
contagiosum keratosis
Clinical clues
Ask for:
Duration of lesions: warts often persists several years if not treated, MC start to regress usually after 6 months
Distribution of lesions: involvement of other areas of body apart from what is shown to you
Associated symptoms: planter wart can be quite painful during walking if located over pressure points
st
Family history: viral infections like wart, molloscumcontagiosum (MC) is contagious, 1 degree relatives are
affected in neurofibromatosis, keratosis pilaris
Look for: distribution, number, color, surface

Look and feel for surface of lesion:
o Rough, hyperkeratotic with digitations and loss of normal skin creases (lines of finger print): verruca
vulgaris (common warts)
o Flat surface, 1-2 mm thick, skin colored often on face, dorsa of hands: verruca plane (flat warts)
Soft, yellowish papules and plaques localized to upper eyelids and around inner canthus: xanthelasma
Skin colored or yellow firm papules, often multiple frequently around eyelids, on face, axillae, upper chest and
vulva:syringoma
Pearly white or skin coloured, isolated, single/multiple, scattered papules with centralumbilication (keratotic
plug):molluscumcontagiosum
Skin coloured or brownish; flat, dome- shaped or pedunculated; soft or firm with or without button-hole sign
neurofibroma. If suspected look for other physical findings such as: eyes (lisch nodules),plexiformneurofibroma,
caf-au-lait lesions, freckles (axilla), kyphoscoliosis, tibial bowing
Soft, skin coloured, pedunculatedpapilimatousgrowth aroundneck inintertriginous areas (axilla, inframammary,
groin): acrochordon (skin tag)
Small,spiny, hyperkeratotic follicular papules of normal skin color appear mainly on extensor surface of upper arms,
shoulders and thighs: keratosis pilaris
Phrynoderma: mostly seen in children and present with follicular papules little larger than keratosis pilaris on
elbows and knees, look for signs of vitamin A deficiency
Investigation:usuallyclinical diagnosis
Excisional or wedge biopsy if doubt in diagnosis
Serology for HIV if large and generalized warts, MC
Serum cholesterol if xanthelasma is suspected
Smear of keratotic plug: for molluscum bodies (inclusion bodies)
52
PRURITUS
Pruritus, one of the most common dermatological symptoms is an unpleasant cutaneous sensation that elicits the desire to
scratch. Itching may be localized, or generalized. It serves as a protective mechanism against external agents such as plants
and parasites. it may be caused by primary cutaneous disorder, but it may signal an underlying systemic disease in a large
number of people.
Sensation of itch is carried by afferent, fine, unmyelinated C fibers to the dorsal root ganglia and lateral spinothalamic tract
to the thalamus and somatosensory cortex of the postcentralgyrus. Itch sensations that arise in these nerve fiber endings in
the subepidermal area are often due to inflammation, dryness or other skin damage. Itching may be elicited by different
stimuli such as light touch, temperature change, and emotional stress. Chemical, mechanical, thermal, and electrical stimuli
also elicit itching. Pruritus is mediated by the release of chemical substances such as histamine, serotonin and tryptase.
Pruritus
Primary to skin lesion Secondary to systemic

conditions
Specific lesions Non- specific lesions Internal malignancy

(see below) Xerosis Hypothyroidism
Old age Renal disease
Excessive washing Liver disease
Iron deficiency anaemia
Ask for:
Nature, onset, duration and severity (sleep affected or not)
Localized or generalized
Preceding skin lesions present or not
Medications, foods, soaps, occupational, environmental, sun exposure and over-the-counter remedies (history of
previous treatments may clarify altered natural progression of skin disorders)
Underlying medical problems: constitutional symptoms (fever, malaise, weight loss, fatigue), gastrointestinalor
upper respiratory symptoms
Rash accompanied by fever is common with disseminated infections (viral or bacterial), drug reactions, collagen
vascular diseases, vasculitis, history of renal/ liver disease
Psychogenic pruritus does not usually disturb sleep
LMP in female
Look for:
Entire skin and mucosal surfaces. Natural light exposure is preferable
Types of skin lesions primary or secondary lesions, morphology, distribution and location, color, border, type, and
arrangement including any spared areas.
Palpation can help appreciate texture of the lesions, depth, and tenderness
Thorough physical examination to detect any possible underlying malignancy/disease- pallor, icterus, lymph node,
liver, spleen, thyroid gland, stigmata of renal/ liver disease, failure to thrive in children/short stature
In generalized persistent pruritus of unknown etiology two levels of screening laboratory tests are recommended
53
Initial screening
Complete blood count with differentials, eosinophils (increase in allergic conditions) and ESR (increased in
malignancy)
Chemistry profile:blood sugar,liver and renal
Urinalysis (renal disease)
Stool for ova and parasite
Occult blood in stool in patients over 40 years (GI malignancy)
Chest X-ray (malignancy)
Thyroid panel
Skin biopsy for routine histology and special stains for mast cells and immunofluorescence
Second level screening

Ferritin levels
Calcium and phosphate levels
Hepatitis panel
HIV
5-Hydroxyindolacid and mast cell metabolites in the urine
Other radiologic studies as necessary
Primary skin lesions that are so intensely itchy that person is unable to stop himself from damaging his skin (bleeding)
are:
Eczema: Lichen Simplex Chronicus, atopic dermatitis, nummular eczema
Prurigonodularis
Dermatitis herpetiformis
Urticaria
Polymorphic light eruption
Insect bite
Lichen planus
Scabies
Drug rash
Pruritus due to systemic conditions:

Drug reactions or drug effects (e.g. opiates)
Endocrine:
o Hyperthyroidism/hypothyroidism
o Diabetes mellitus
Iron deficiency
Obstructive biliary diseases: primary biliary cirrhosis, obstructive jaundice
Pregnancy
Uremia
Visceral malignancies: Hodgkins disease, Lymphoma/leukemia, CNS tumours
Psychogenic: delusions of parasitosis, psychogenic pruritus
Senile pruritus
With the increased prevalence, chronic renal failure associated pruritus contributes for a significant cause of pruritus. One
fourth to one third of uremic patients treated without dialysis exhibit pruritus and with maintenance hemodialysis the
number even increases.
54
URETHRAL DISCHARGE
Fluid passing out through urethra is urethral discharge. Considering the length of urethra, it usuallyis not appreciated in
female. Females mostly complaint of vaginal discharge (refer to the respective CP).
Urethral discharge may be physiological that is not associated with urethritis or it may be pathological discharge due to the
presence of urethritis (inflammation of the urethra).
Prosemen
Physiological
Prostatorrhea
Male
Nocturnal emission
Pathological Gonococcal
Infectious urethritis
Urethral Traumatic Non gonococcal

discharge urethritis
Neoplastic
Urethral
Urethritis
Interstitial cystitis
Urethral diverticulum
Female Infection of skene's gland
Physiological
Vaginal
(see PV discharge in Gynae)
Pathological
Clinical clues:
Ask for:
Onset of urethral discharge: The incubation period is short and symptoms typically have their onset 15 days after
sexual contact with an infective person in gonococcal urethritis; it is gradual in non-gonococcal urethritis whereas it
appears 1-3 wks in chlamydial infection
Amount and colour of discharge: yellow and profuse in gonococcal;mucopurulent and scanty in nongonococcal
urethritis
Pain and dysuria: marked in gonococcal urethritis; less significant in nongonococcal urethritis or may be due to
acute swelling of prostate or glans penis
Genital itching: discharge, erythematous moist macular lesion on glans and prepuce suggests balanoprosthitis
Previous similar history or other STIs, type and numbers of sexual partners(A majority of women with early
infections report no symptoms)
55
Timing of discharge: some men present with extreme anxiety about nocturnal emissions due to a health belief that
this causes weakness, in fact this is normal ejaculatory function
Sexual behavior and unsafe contact: always think of an STI when a man comes with urethral discharge unless
another diagnosis is clear.
Extragenital manifestations of infection e.g. proctitis,pharyngitis, conjunctivitis, skin rashes, arthritis, tenosynovitis
in extragenital manifestation of gonorrhea. Arthritis, conjunctivitis and urethritis constitute Reiters triad.
Anxiety/worryabout the problem. Some people feel so guilty/ worried that they visit doctor to doctor thinking that
they have acquired an STI even though they dont have any: venereophobia
Rarely tuberculosis of prostate and seminal vesicles present with urethral discharge.
Prostatorrhoea (urethrorrhea): physiologic prostatorrhoea means the few drops of prostatic secretion that comes
out during conditions of strainig as with urination, defecation or cough. It is a physiologic phenomenon that occurs
commonly in young adults
Prosemen: few drops of mucoid fluid that come out from the male urethra during the foreplay or excitation stage
of sexual response cycle.
Use of detergents, soaps, antiseptic solutions to try clean the urethra actually lead to chronic irritation and
further discharge. Use of latex condoms may cause contact dermatitis
Look for:
Fever, pulse, BP: systemically unwell patient suggests acute prostatitis
Urethral meatus and surrounding area: colour, consistency and amount of the discharge, other skin lesions
(erosions, ulcers, vesicles)
Genital hygiene (retract foreskin): poor hygiene can be cause of balanoprosthitis
Scarring and phimosis: chronic balanoprosthitis, balanitisxeroticaobliterans
Milking of urethra if discharge is not visible (ask patient to come back in 2-3 hour(prior to voiding))
Palpate for tenderness and inguinal lymphadenopathy
Testicles and epididymis:epididymo-orchitis
Abrasions and irritations in the urethra: due to repeated manipulations (physical or chemical) of the urethra mainly
by anxious people with an STI
Per rectal examination to look for tender boggy prostate suggests acute prostatitis
Investigations:
Endourethral smear
o Gram stain: gram negative intracellular diplococciwithin phagocytes in gonorrhea (presumptive diagnosis)
o Culture of the organism and differentiation from other Neisseriaspecies by antigenic or biochemical
testing (confirmation)
o Polymorphonuclear cells per oil emersion field (>5) and negative gram stain suggests nongonococcal
urethritis
o KOH mount: candida
o Saline wet mount: trichomonasvaginalis
Urine routine and culture as necessary
VDRL and HIV (for other STIs)
NAAT (nucleic acid amplification test)
Gonococcal urethritis
Non-gonococcal urethritis( nonspecific urethritis)
Chlamydia trachomatis infection
Trichomonasvaginalis infection
Intraurethral herpes or wart
Candidiasis
Prostatitis
Foreign body
Carcinoma of the urethra
56
Comments:
Neoplastic: Carcinoma of the urethra or the penis may present as ulcer or by stricture formation. Both forms may
lead to necrosis and secondary infection of the urethra producing purulent discharge that is resistant to treatment.
Accordingly any old male presenting with recent onset of urethral discharge that did not respond to treatment for 2
weeks should be investigated for carcinoma of urethra especially in the uncircumcised men with blood tinged
discharge.
Discharge may be spontaneous if not the urethra may be milked 3 or 4 times from the base to the meatus to
attempt to express the discharge. Symptomatic men without apparent discharge should be re-evaluated after
longer interval preferably prior to their voiding.
To take an endourethral swab discharge may be expressed from urethra or a fineswab or loop can be gently
inserted at least 2 cm into the urethra and rotated 360. The swab is then rolled across a clean microscope slide, let
it air dry then evaluate by Gram stain.
Most of the time both gonococcal and chlamydial infectionoccurs simultaneously so patient should be treated for
both.
4Cs in STI: Compliance to treatment,Counseling/education,Contact tracing and Condom
Balanoprosthitis is inflammation of the glans penis and foreskin in uncircumcised males. It is common in children.
The discharge is actually preputial rather than utethral- so careful physical examination can distinguish it from
gonococcal or chlamydial urethritis. In adults always milk urethra to look for concomitant urethritis. In children
commonest cause is poor hygiene or irritant contact balanoprosthitis. In adolescents and adults consider Group A
streptococcus, candida and STIs.
National guidelines on STI case management (syndromic management) is available at National Centre for AIDS and
STD Control (NCASC),Teku
GENITAL LESIONS
Genital Problems
Discharge Pruritus Lesions
Primary skin
disease
Urethral Vaginal Papule Vesicle Ulcer
Verroucous Flat topped Herpes

Painful Painless
genitalis
Condyloma Condyloma
accuminata lata
Herpes genitalis Primary syphilis
(chancre)
Chancroid
Granuma
Bachet's syndrome inguinale
Erosive lichen Lympho-
planus granuloma
Pemphigus venerum
vulgaris
Steven Johnson'
syndrome
57
Sore Throat and Hoarseness
Sore throat/
Hoarseness
Sore Throat Hoarseness
Acute Chronic Acute Chronic
Inflammatory
Inflammatory Inflammatory Traumatic Neuromusculat/
Inflammatory Structural/
Muscle tension
Neoplastic imbalance
Neoplastic
/Structural Infective Infective Non
Foreign body
Infective
Benign
Miscellaneous
Non Infective Primary
Premalignant/
Malignant
Secondary
Sore throat and Hoarseness are common clinical presentations. A clear understanding of the causes of sore throat as well as
hoarseness and an appreciation that it may represent a serious underlying pathology are therefore vitally important.
Painful, irritation or itchy condition in oropharynx is called sore throat.
Hoarseness refers to a raspy or harsh-sounding voice, which is produced by lesions that involve vocal cords. It impairs
communication or reduces voice-related quality of life (QOL). Same lesions that produce hoarseness may sometimes
produce stridor, depending on size and location of lesion and age of child.
Sore throat suggests pathology of pharynx whereas hoarseness suggests pathology in the larynx.
In some instances, patient may complain of sore throat as well as hoarseness if pathology involves both pharynx and larynx
e.g. carcinoma of supraglottis/hypopharynx extending to glottis, LPR (laryngopharyngeal reflux) etc. Although a detailed
history may point to the diagnosis, in many cases it is impossible to exclude malignancy and other physical abnormalities
without a laryngeal examination.
58
Acute sore throat
Sore throat
Acute Chronic
(< 3 weeks) (> 3 weeks)
Inflammatory Inflammatory
Neoplastic/
Foreign body Structural
Miscellaneous
Normally acute sore throat(pharyngitis) lasts from few days to weeks and chronic pharyngitis lasts from weeks to months or
years. Arbitarily for descriptive purpose,less than 3 weeks is called acute pharyngitis and more than 3 weeks chronic
pharyngitis.It may be intermittent as well.
However,time course of the pain may be critical factor in establishing the diagnosis because acute pain tends to be
associated with infectious etiologies or trauma, whereas chronic pain may be associated with chronic inflammation or
neoplasm.
Clinical clues
Ask for:
1. Age: Pharyngitis in adults is caused by a bacterial infection in approximately 5% to 10% of patients. This is different
than in children, in whom bacterial pharyngitis accounts for 30% to 40% of cases. Croup, epiglottitis are more
common in children than in adults.
2. Presence of fever is suggestive of infection. High grade fever likely bacterial, low grade viral. Localised deep neck
space abscess may not be associated with fever.
3. Onset, duration, progression: Very acute onset and rapid progression in a child suggestive of epiglottitis or in an
older children/adult with submental swelling suggestive of ludwigs angina.
4. History of ingestion of foreign body or choking episode.
common in children and old age (edentulous).
Sometimes history of ingestion may not be clear.
5. Associated drooling, dysphagia and distress s/o epiglottitis
6. Associated rhinorrhoea, cough, sore throat s/o croup prodrome or viral pharyngitis
7. Barking cough s/o croup
8. Stridor or respiratory distress s/o croup or epiglottitis
9. Neck pain and neck swelling s/o retropharyngeal or parapharyngeal abscess
10. Constitutional symptoms such as weight loss or night sweats may point towards tuberculosis, lymphoma etc.
11. Systemic review: Behcets syndrome is characterised by aphthous-like ulcer, genital ulcerations & uveitis.
Esophageal candidiasis is the common cause of dysphagia in HIV infected patients.
12. Drugs & allergy hisotry: Immunosuppressive therapy, corticosteroids
13. Personal history: Smoking, alcohol increases the risk of oropharyngeal malignancy. Bettel nut, Parag, Gutkha are
associated with submucous fibrosis of oral cavity and also risk factor for oral cancer.
59
Look for:
Examination of oral cavity (as a part of routine examination)
Lips
Buccal mucosa
Gums and teeth
Hard palate
Tongue (anterior two-third): movement, bulk, power, lump, ulcer, induration
Floor of mouth is raised in case of Ludwigs angina. Plunging ranula is seen as bluish thin walled cystic swelling in
floor of mouth and bimanually palpable soft swelling in neck.
Retromolar trigone area potential site for malignancy
Use of instruments should be avoided in suspected case of epiglottitis in children as respiratory obstruction may increase
and spread of the swelling in pre-epiglottic space or from vagal stimulation.
Examination of oropharynx
Tonsils and pillars: In acute tonsillitis, hyperaemia of pillars, soft palate and uvula. Bilateral tonsils are red and
swollen with yellowish spots of purulent material or covered with whitish membrane. White patches/membranes
over tonsils/posterior pharyngeal wall (PPW) may also be seen in diphtheria, Vincent angina, candidiasis, infectious
mononucleosis, leukaemia etc.
o In Peritonsillitis, tonsil is buried under the congested anterior pillar and it is generally unilateral.
o Pseudo enlargement of tonsil is seen in case of parapharyngeal space tumour, where tonsil is pushed
medially but without signs of inflammation.
Soft palate: gag reflex, movement
Base of tongue
Posterior pharyngeal wall: Bulging of PPW is seen in retropharyngeal abscess, unilateral in acute and bilateral in
chronic.
Examination of larynx
External examination of larynx
Indirect laryngoscopy:
o The diagnosis of supraglottitis/epiglottitis can be missed if laryngeal examination is not performed in
adults with acute odynophagia and a normal oropharynx
Examination of the neck

Laryngeal framework
Laryngeal crepitus
Neck nodes: Lymphatic drainage follows a specific pattern in head and neck. It will guide to locating primary site of
lesion in case of infections, malignancies. Enlarged tender LNs s/o acute inflammation, whereas in chronic
conditions LNs are non-tender. Matted LNs seen in Tuberculosis. Rubbery LNs found in lymphoma. Malignant LNs
are hard, with extracapsular extension becomes fixed.
Any other swellings
Systemic examination
Fever, tachycardia, respiratory distress
Investigations:
CBC
Throat swab in case of acute tonsillitis is not recommended routinely.
X-ray soft tissue neck
o Thumb sign (lateral view) in acute epiglottitis
o Steeple sign (AP view) in croup
o In suspected foreign body increased prevertebral space shadow, radioopacity s/o FB, air-gas shadow.
FNAC neck nodes
Biopsy
CT scan/MRI neck
60
Comments
Bacterial tonsillitis/tonsillopharyngitis presents with acute onset, significant throat pain with otalgia, dysphagia,
odynophagia, cervical adenitis, and high fevers. On oral examination, tonsillar and posterior pharyngeal erythema with
exudates may be seen. Most common bacterial cause is group A -hemolytic streptococcus.
Peritonsillar abscess presents with "Hot potato" voice, trismus, soft palate edema/erythema with uvular deviation, drooling,
odynophagia and otalgia.
Ludwigs angina presents with rapidly spreading, firmly indurated cellulitis in floor of mouth that originates intraorally
,usually bilateral and involves supramylohyoid and inframylohyoid compartments resulting in rapidly progressing upper
airway obstruction.
Retropharyngeal abscess tends to be acute in children which is due to suppuration of nodes of rouviere whereas in adults it
is commonly chronic. In adults tubeculosis of cervical spine is the common cause. Children with retropharyngeal infections
often present with neck pain, neck swelling, fever, irritability, dysphagia, excessive drooling, and dyspnoea or noisy
breathing suggestive of upper airway compromise. Adults tend to present with neck pain, fever, anorexia, nasal obstruction,
snoring, and dyspnoea. Careful oropharyngeal examination often reveals unilateral bulging of the posterior pharynx, which
is localized in retropharyngeal lymphadenitis and may extend the length of the pharynx when cellulitis or an abscess is
present. In cases of chronic retropharyngeal abscess, bulging tends to be bilateral.
Epiglottitis typically presents with acute onset of sore throat and fever. Rapid progression to difficulty swallowing, drooling,
restlessness, and stridor or air hunger ensues. The clinical triad of the three Ds (drooling, dysphagia, and distress) is a
classic presentation. A viral prodrome and cough are seldom observed with acute epiglottitis and are more often witnessed
in association with croup that may include rhinorrhea, cough, and sore throat for 1 to 2 days before the onset of the classic
croup symptoms. The patient who has croup typically presents with a hoarse voice, a barking cough, a low-grade fever,
and variable degrees of stridor and respiratory distress.
Laryngitis may present with both sore throat and hoarseness. It may result from infection by an invading microorganism or
from irritative, traumatic, metabolic, allergic, autoimmune, or idiopathic causes. Acute and chronic laryngitis are very
common in otolaryngologic practice, and the causes in pediatric and in adult patients are different. In infants and children,
for example, the most common cause of laryngitis is acute infection, whereas in adults, laryngitis generally tends to have a
chronic, noninfectious cause. Laryngopharyngeal reflux has been implicated to be a far more important cause of laryngeal
inflammation than was previously recognized.
Recurrent Aphthous ulcer anywhere in the oral cavity is painful, and is one of the most common oral ailments. The disease
is characterized by recurring painful ulcers of the mouth that are round or ovoid and are surrounded by inflammatory halos.
These ulcers typically appear first in childhood. Aphthous ulcer may present as small ulcers 2 to 8 mm in diameter (minor
aphthous ulcers) or larger ulcers, often 1 cm or more in diameter (major aphthous ulcers) and may heal spontaneously in 10
to 14 days.
Plummer Vinson syndrome presents with dysphagia, glossitis, anemia, koilonychia.
Tonsillitis
Peritonsillitis
Ludwig's angina
Epi/Supraglottitis
Croup
Retropharyngeal/Parapharyngeal abscess
Laryngitis (Acute or chronic)
Aphthous ulcer (Recurrent)
Foreign bodies( eg.fish bone,wires etc)
61
Chronic sore throat
Sore throat
Acute Chronic
(< 3 weeks) (> 3 weeks)
Inflammatory Inflammatory
Neoplastic/
Foreign body Structural
Miscellaneous
Chronic Inflammatory
Clinical Clues
Ask for:
Fever s/o inflammation, but neck abscess may not be associated with fever.
Nature of pain
sharp lancinating pain s/o neuralgia,
throbbing pain s/o inflammation,
deep dull pain due to mechanical pressure of tumor.
Age malignancy is more common in the elderly
Systemic features weight loss, decreased appetite s/o malignancy, tuberculosis
Look for:
Fever s/o inflammation
Associated LN commonly tender in inflammation, non-tender swelling in malignancy
Diffuse redness or swelling of tonsils and pillars s/o inflammation
Medial displacement of oropharyngeal wall without erythema s/o parapharyngeal space tumour.
62
Neoplastic/Structural
Chronic
(>3 weeks)
Neoplastic/
Inflammation Miscellaneous
structural
Benign Malignant
Lingual thyroid Oropharyngeal Cancer
Epiglottic cyst Hypopharyngeal cancer
Laryngocele Laryngeal Cancer
Pharyngocele Parapharyngeal space tumour

Parapharyngeal space tumour
Clinical clues
Ask for:
1. Age: Laryngocele presents in middle age and rarely in infancy when it can cause respiratory distress which typically
becomes worse on crying due to increased distension of the laryngocele with air. Pharyngocele also presents in
middle age.
2. Sex: Post cricoid cancer is common in females. Pharyngocele is more common in male.
3. Pain: nature of pain, timing of onset.
4. Presence of lump or swelling:
a. If swelling increases with crying, straining s/o laryngocele.
b. Associated features: Hoarseness, cough, & respiratory obstruction s/o laryngocele. Snoring, sleep apnoea, & mild
dysphagia s/o parapharyngeal tumor. Neck swelling, regurgitation of 1-2 days old food s/o pharyngocele.
5. Foul smelling breath s/o recurrent tonsillitis, vincents angina, pharyngocele.
6. Systemic review: weight loss, fatigue, decreased appetite s/o malignancy, chronic infection.
7. Family history: some malignancies run in family like nasopharyngeal cancer.
8. Personal history: smoking, alcohol
Look for:
Examination of oral cavity- as before
Examination of oropharynx
Tonsils and pillars: Medial displacement of oropharyngeal wall without erythema is suggestive of parapharyngeal
space tumour.
Soft palate: gag reflex may be absent in IX CN palsy/NPC
Base of tongue: lingual thyroid, vallecular cyst
Posterior pharyngeal wall: enlarged lymphoid follicles in chronic granular pharyngitis, allergic pharyngitis.
External examination of larynx: External framework of larynx may be distorted in case of laryngeal malignancies
with extralaryngeal extension. Laryngeal crepitus may be absent in postcricoid carcinoma.
Indirect laryngoscopy: On laryngeal examination, globular swelling in the base of tongue may be the ectopic
thyroid and sometimes the only thyroid tissue. Cystic swelling in the epiglottis (epiglottic cyst) may also present
with something stuck in throat. Malignant growth may be seen in the larynx, hypopharynx, base of tongue.

Laryngeal framework
Laryngeal crepitus
Neck nodes
Any other swellings: Soft cystic swelling with cough impulse adjacent to thyroid cartilage is due to laryngocele, and
size increases with valsalva. On palpation, hissing sound may be heard (Bryces sign). Soft doughy swelling adjacent
to aerodigestive tract with gurgling sound on palpation is due to pharyngocele.
Systemic examination
63
Comments
On laryngeal examination, globular swelling in the base of tongue may be the ectopic thyroid and sometimes the only
thyroid tissue. Cystic swelling in the epiglottis/vallecula may also present with something stuck in throat. Laryngocele can be
internal, external or mixed type. Laryngocele presents in middle age and rarely in infancy when it can cause respiratory
distress which typically becomes worse on crying due to increased distension of the laryngocele with air.
Parapharyngeal space tumour presents with upper neck swelling and tonsil may be seen pushed medially. Malignancy of
oropharynx and hypopharynx generally presents in advanced stage with neck swelling, dysphagia, globus like sensation,
referred otalgia and lesion in the specific site whereas glottis cancer presents early with hoarseness.
Investigations
Flexible Nasopharyngolaryngoscopy
Oesophagogastroduodenoscopy (UGI endoscopy)
Radiology: X-ray, Ba swallow, USG, CECT, MRI, Thyroid scan
FNAC, Biopsy
Panendscopy: multicentricity of the aerodigestive tract malignancy.
24-h dual-site pH monitoring with impedance
Miscellaneous
Neuromuscular Functional
Glossopharyngeal Globus
neuralgia pharyngeus/FOSSIT
Styalgia
Vertebral osteophytes
Comments
In Glossopharyngeal neuralgia, there is severe lancinating pain from the pharynx to the ear, neck, and head that is short
lived (lasts seconds). The pain can be triggered by swallowing, chewing, or coughing. Eagle syndrome is due to elongated
styloid process or calcified stylohyoid ligament which can be felt on palpation of tonsillar fossa. The symptoms include pain
in the peritonsillar region and base of the tongue area posterior to the angle of the mandible, dysphagia and otalgia.
Globus pharyngeus is feeling of something stuck or sensation(FOSSIT) of a lump in throat. It is a diagnosis of exclusion and
the symptoms are variable within and between subjects and objective clinical findings are absent. It may be one of the
presenting symptoms of somatization disorder.
Acute thyroid inflammation as well as large masses or goitres may cause pain referred to throat. Other symptoms include
tender thyroid mass or enlargement, hoarseness, swallowing difficulties, neck mass, and symptoms of hyper or
hypothyroidism.
64
Annex- important differential diagnosises
S.N. White patches in throat Midline neck swelling Lateral neck swelling
1. Acute membranous tonsillitis Submental lymphadenitis Parotid swelling

(particularly tail)
2. Candidiasis Thyroglossasl Cyst Lymph nodes
3. Vincent Angina Subhyoid bursitis Cystic hygroma
4. Acute Leukemia Pyramidal lobe of thyroid Thyroglossal cyst
5. Diptheria Isthmus goitre Branchial cyst
6. Infectious mononeucleosis Lipoma Thyroid swelling
7. Sebaceous cyst Pharyngocele
8. Dermoid Lipoma
9. Sebaceous cyst
10. Dermoid
65
Hoarseness
Hoarseness
Acute Chronic
< 3 wks >3 wks
Structural/
Inflammatory Traumatic Inflammatory
Neoplastic Neuromusculat/
Muscle tension
Infective imbalance
Infective Non Infective Benign
Primary
Non Infective Premalignant/
Malignant
Secondary
Patients with persistent hoarseness or a change in their voice for 2-3 weeks, who are smokers, aged 50 years or older and
heavy drinkers, should have an urgent chest X-ray to exclude recurrent laryngeal nerve palsy secondary to lung cancer.
Those with positive findings on X-ray should be referred urgently to a lung cancer specialist team. Those with negative
findings or with other upper aerodigestive tract symptoms should be referred to ENT specialist.
66
Acute Hoarseness
Hoarseness
Acute Chronic
Inflammatory Traumatic
Infective
Non Infective
Clinical clues
Ask for
Sudden onset hoarseness is seen in case of vocal cord paralysis, haemorrhage in the True vocal cord (TVC) etc.
Hoarseness may gradually improve due to compensation by contralateral TVC in TVC palsy.
Fever s/o infection
Associated cough & rhinosinusitis s/o URTI or LRTI or viral laryngitis
Associated respiratory distress , stridor and sore throat in a child s/o croup or epiglottitis
Exposures to irritants e.g. smoke, chemicals/fumes s/o non-infective inflammatory cause.
Trauma to neck
Recent excessive use of voice s/o phonotrauma
Look for
Examination of oral cavity/oropharynx- as before
External examination of larynx
Indirect laryngoscopy-when needed
Flexible Nasopharyngolaryngoscopy-when needed
o Edematous, congested vocal cords is seen in laryngitis.
o Epiglottis may be swollen/congested/edematous.
o There may be TVC paresis/palsy.
Laryngeal framework
Laryngeal crepitus
Neck nodes
Comments
Simple physical trauma due to increased friction between poorly lubricated vocal folds from prolonged shouting, inadequate
fluid intake, dehydrating agents or exposure to irritants such as smoke and chemicals can also cause laryngitis.
Diagnosis to Consider
Ac. Laryngitis
Due to irritant/chemicals/fumes
Croup
Foreign bodies/trauma
67
Chronic Hoarseness
Hoarseness
Acute Chronic
(<3 weeks) (>3 weeks)
Neuromuscular/
Structural or
Inflammatory Muscle tension
Neoplastic
imbalance
Infective Non-infective Benign
Premalignant/
Primary Malignant
Secondary
Clinical clues
Ask for:
Age: Certain congenital anomalies like laryngomalacia, laryngeal web, laryngeal cyst, laryngeal cleft, and laryngocele
may produce hoarseness as well as stridor in children.
Recurrent respiratory papillomatosis (RRP) presents with hoarseness as well as stridor in children.
Adult onset respiratory papillomatosis usually does not recur but there is risk of turning into malignancy.
The child, particularly from ages 3 to 7 years, who is hoarse, may have epiglottitis or croup, a life-threatening
condition characterized by trouble breathing, drooling, sore throat, and respiratory stridor.
Hoarseness in older age group who are smoker, malignancy has to be ruled out.
Sex: Puberphonia may affect the adolescent male if they dont tend to adapt to the physical changes occurring during
the adolescence.
Occupation: Screamers nodule is common in children. Similarly teachers/singers may be affected by vocal nodules.
Onset, duration, progression: In old-aged patients with hoarseness of more than 2-3 weeks duration, malignancy has
to be ruled out.
Hoarseness due to LPR has waxing and waning periods.
Chronic abuse of the voice during speaking and/or singing commonly causes hoarseness that improves at least
partially during periods of relative voice rest.
Associated symptoms, aggravating and relieving factors: LPR, though not always, is associated with water brash,
heart burn, regurgitation of food.
Hoarseness along with odynophagia is caused by hypopharyngeal carcinoma.
Hoarseness is associated with perilaryngeal pain in cases of secondary causes of muscle tension imbalance (e.g.
vocal nodules, polyps, LPR, laryngitis etc.)
Unilateral otalgia in the absence of ear disease may indicate an underlying malignancy.
Constitutional symptoms such as weight loss or night sweats may point towards tuberculosis, lymphoma etc.
Laryngocele may present with hoarseness, cough, respiratory obstruction and neck swelling which increases on
crying or straining or valsalva manoeuvre.
Systemic review: Previous history of pulmonary tuberculosis with scarring of left upper lobe of lung, lung cancer of
left upper lobe causes the left RLN palsy.
Neurological evaluation is necessary in cases suspected vocal cord paralysis associated with aspiration,
dysphagia, and hemiparesis.
Puberphonia, conversion dysphonia/aphonia is thought to have psychological basis.
Past history & surgical history: Surgery of the skull-base, neck region (e.g., thyroidectomy, anterior cervical fusion),
or thorax (e.g., thoracic aortic aneurysm repair, oesophagectomy) can damage the superior or recurrent laryngeal
nerves supplying the intrinsic laryngeal muscles.
Previous intubation may result in granuloma formation, post-intubation phonatory insufficiency, and vocal fold
paresis.
68
Laryngopharyngeal reflux has been implicated in the pathogenesis of acute and chronic laryngitis, benign vocal
fold lesions, and muscle tension dysphonia.
Drugs & allergy history: Drugs like fluticasone/salmeterol inhaler (secondary to fungal laryngitis), alendronic acid
(secondary to increased reflux), and ACE inhibitors (secondary to chronic cough) may cause hoarseness.
Family history: Some conditions known to be associated with hoarseness like laryngopharyngeal reflux, essential
tremor, Parkinson's disease, spasmodic dysphonia, and some cancers - can be hereditary.
The triad of risk factors identified for RRP are first born child, vaginal delivery & mother younger than 20 years.
This does not apply for adult onset RP and so the reactivation of latent infection is refuted.
Personal history: Past and present tobacco use history, amount of alcohol and caffeine consumed, and any
recreational drug use should be assessed.
Look for:
Quality of voice
Weak with reduced pitch range s/o neuromuscular
Staccato s/o spasmodic dysphonia
Rough s/o structural lesion or inflammation
Examination of oral cavity/oropharynx
External examination
Indirect laryngoscopy
o Vocal cord mobility when restricted/absent, it could be either adductor or abductor paralysis, unilateral or
bilateral.
o Edematous, congested and thickened vocal cords is seen in laryngitis.
o Vocal nodule appears as a small sessile lesion, usually less than 3 mm, which occurs between the anterior and
middle third of the true vocal cord. It is typically bilateral, symmetrical, and immobile during phonation. A
polyp, in contrast, may be sessile or pedunculated, usually larger than 3 mm, and it occurs on the free edge of
the anterior third of the true vocal cord. It is generally unilateral and, if pedunculated, mobile on phonation.
o TB laryngitis may typically have-swelling in the interarytenoid area(mamillated appearance),ulceration of vocal
cords/arytenoids, diffuse granulation tisssues, eaten up or pseudoedema of epiglottis(turban epiglottis)
o Posterior laryngitis demonstrating red arytenoids with interarytenoid mucosal hypertrophy is commonly seen
with LPR. Infraglottic edema is seen frequently resulting in pseudo sulcus vocalis.
o In Reinkes edema the vocal cords become extremely oedematous and filled with a thin jelly-like fluid. The
oedema fails to resolve due to poor lymph drainage of the vocal cord.
o In RRP cauliflower like warty growths may be seen arising from the vocal cords on laryngoscopy.
o Ulceroproliferative, sometimes infiltrative type of growth may be seen involving the various sites/subsites of
larynx depending on the extent of Carcinoma larynx.
- Laryngeal framework: External framework of larynx may be distorted in case of laryngeal malignancies with
extralaryngeal extension.
Laryngeal crepitus: Absent in postcricoid involvement, retropharyngeal abscess etc.
Neck nodes: Generally enlarged LNs due to acute infection are firm in consistency, whereas malignant LNs are hard
and fixed. Matted LNs are found in Tuberculosis. LNs of lymphoma are rubbery in consistency. Lesion of midline
structures like epiglottis, base of tongue, nasopharynx etc. metastasize to bilateral LNs.
Any other swellings
Systemic examination: To rule out systemic causes e.g. amyloidosis, sarcoidosis, Tuberculosis, central causes etc.
Metastases form head and neck malignancies have to be screened for, rarely vice versa. Left RLN palsy is commonly due
to pathology in chest.
Investigations
Assessment of voice
Oesophagogastroduodenoscopy (UGI endoscopy)
Radiology: X-ray, Ba swallow, USG, CECT, MRI, Thyroid scan
FNAC, Biopsy
Panendscopy: multicentricity of the aerodigestive tract malignancy.
Videolaryngostroboscopy
24-h dual-site pH monitoring with impedance
69
Chronic Inflammatory Hoarseness

Chronic
(>3 weeks)
Inflammatory
Infective Non-infective
Primary
Secondary
Ask for
Fever +/- prolonged cough s/o chronic infection e.g. TB
Associated with persistent nasal discharge clear s/o allergy, purulent s/o rhinosinusitis
Laryngopharyngeal reflux (LPR) is more likely if the hoarseness is worse in the morning and when it is associated with other
symptoms, such as chronic cough, phlegm in the throat, throat clearing, globus sensation and difficulty swallowing liquids
and tablets.
Occupation Employment history is important to evaluate the importance and pattern of vocal use in the patient's
profession and to assess exposure to environmental irritants and noise.
Drugs and allergy history - Fungal infections from Candida albicans can result from the incorrect use of steroid inhalers or in
cases of immunosuppression.
Look for as before
Inflammatory causes
Infective Non-infective
Primary - laryngeal Laryngopharyngeal reflux

Viral
Allergy
Bacterial (including tuberculosis)
Fungal Trauma/Irritation
Phonotrauma
Chemical/Fumes/Smoke
Secondary Drugs
Pulmonary infections Asthma inhalers, antimuscarinics
Rhinosinusitis
Autoimmune e.g. Sjogrens syndrome
70
Structural /Neoplastic
Chronic
(>3 weeks)
Structural or
Neoplastic
Benign Premalignant/
Malignant
Systemic
Vocal Reinke's Papillomatosis Granuloma Laryngocele
cause
nodules/polyps edema
Amyloid/
Rheumatoid
deposits
Hypothyroidism
Excess
androgens in
female
Ask for
Features s/o systemic illness e.g. associated weight gain and slowness s/o hypothyroidism, joint swelling s/o RA,
masculinisation in female s/o androgen excess.
Occupation e.g. singers or teachers prone to vocal nodules
Weight loss, anorexia s/o malignancy
Look for- as before
Comments
Structural or neoplastic conditions are where there is a structural abnormality or mass lesion involving part of the
larynx. This type of condition may involve any layer from the inner mucosal surface to the outer cartilage of the
larynx. The effect on the voice will depend on the effects of the lesion on vocal fold vibration and glottic closure.
If the vocal fold vibration is disorganised, this will tend to cause a rough voice, whereas if glottic closure is
incomplete, the voice may have a more breathy quality.
Androgens can cause the female larynx to irreversibly enlarge and severe hypothyroidism can cause the vocal folds
to become thickened.
The anatomical structure of the vocal fold and false cords can become distorted by benign and malignant
neoplasms or from deformities of the laryngeal skeleton from external trauma.
Neoplastic or structural causes
Benign Malignant/Premalignant
Nodules Epithelial origin
Polypoid nodules Hyperkeratosis
Reinkes edema Dysplasia
Pseudocyst Squamous cell Carcinoma
Cysts
Haemorrhagic polyp/Angioma
Sulcus vocalis
Papillomatosis
Granuloma Arytenoid, Pyogenic Minor salivary gland origin
Hypothyroidism
Amyloid, Rheumatoid deposits
Laryngeal framework trauma
Laryngocoele
71
Neuromuscular conditions/muscle tension imbalance
Ask for
Quality of voice
Features s/o central cause e.g.
o Resting tremor, shuffling gait Parkinsonism
o Progressive weakness all muscle groups + fasciculations motor neurone disease(MND)
o Diplopia + drooping eyelids, tiring with use Myasthenia Gravis
Associated cough + smoking history suspect left recurrent nerve palsy due to lung cancer.
Look for- as above
Comments
Neuromuscular conditions arise when any part of the neural pathway or function of the vocal muscles is impaired. True
hypofunctional conditions occur when there is global reduction in vocal muscular activity. The voice is generally weak, the
pitch range reduced and the voice tires with use. Hyperfunction of vocal muscles associated with speech tasks is seen in
spasmodic dysphonia which is a focal dystonia and gives a staccato quality to the voice.
Vocal cord paralysis occurs commonly due to malignancy, surgical trauma, nonsurgical trauma, neurological causes,
inflammatory causes, idiopathic etc. Unilateral vocal cord palsy or paresis is so far the commonest neuromuscular cause of
hoarseness. Left recurrent laryngeal nerve (RLN) palsy is more common than right RLN. Right RLN is at more risk than left
RLN during surgery because of its variable course.
Primary muscle tension imbalance is when there is inefficient use of the vocal apparatus causing either episodic dysphonia
or aphonia. Ineffective vocal fold vibration can result from poor posture and breathing patterns, too much inappropriate
muscular effort or failure of relaxation of the laryngeal muscles. Primary muscle tension imbalance can also lead to
structural abnormalities such as vocal fold nodules.
Symptoms of muscle tension imbalance due to psychological conditions include inappropriate voice pitch for age and sex,
bizarre, whispery or strained voice qualities
Neuromuscular conditions/ Muscle tension imbalance
Vocal cord palsy/paresis
Spasmodic dysphonia
Conversion dysphonia/aphonia
Puberphonia
Central causes - Parkinsons disease, Myasthenia gravis, Bulbar palsy, Pseudobulbar/spastic dysphonia,
Motor neurone disease, Multiple sclerosis etc.
72
EAR DISCHARGE
Ear discharge
External ear Middle ear Miscellenous
Furunculosis
Chronic CSF Otorrhea Hemorrhagic Serosanguinous
Acute Otitis Otitis Media
Media
(COM)
Diffuse otitis externa
trauma trauma
Tuberculosis
e.g. temporal
COM-mucosal bone #
Otomycosis foreign body
(Tubotympanic)
Granulomatous
COM-Squamous Tumors Tumors diseases
Otitis externa
hemorrhagica (Atticoantral) e.g.Wagner's
Congenital granulomatosis
( bullous myringitis)
Herpes zoster oticus
Malignant
(necrotising)
otitis externa
Seborrohoeic otitis
externa
Eczematous Otitis externa
Ear discharge(otorrhea) is a common presenting symptom to the outpatient clinics. Common causes of otorrhea differ
between adults and children. In children, the most common cause of otorrhea is either acute otitis media with tympanic
membrane rupture or chronic otitis media through tympanic membrane perforation. In adults, otorrhea most commonly
results from either otitis externa or chronic otitis media with a perforation.
Ear discharge is associated with pain in cases of otitis externa, acute otitis media, foreign bodies, complicated cases of
CSOM, trauma, tumors etc.
73
Ear discharge
External Middle Miscellaneous
Clinical clues
Ask for:
Fever with ear ache (suggests middle ear)
Pain on movement of pinna or pressing over the tragus
History of trauma
Look for:
Tragal tenderness
Discharge, swelling or presence of foreign body or mass in external canal
Tympanic membrane (intact, perforated or inflamed)
Evidence of trauma around head and neck
Nature of discharge (blood, CSF, pus)
EXTERNAL EAR
Clinical clues
Ask for
Pain- severe pain on movements of the pinna and jaw in furunculosis. It is milder in other conditions.
History of trivial trauma/or habit of ear picking - common in furunculosis
Itching- Intense in otomycosis and milder in diffuse and seborrhoeic otitis externa
Nature of discharge-purulent in burst furuncle, curd like or dark with musty odour in otomycosis, clear in allergic
conditions
Ear fullness- due to furuncle, diffuse edema, discharge, otomycotic debris
History of dandruff or eczema
History of medication (especially topical drops which may lead to an allergic reaction)
Reduced hearing
Look for
Tragal/Pinna tenderness(positive circumduction test)
Swelling in the external auditory canal(EAC)
Laceration with clotted/fresh blood in case of trauma
Lymph nodes (preauricular, postauricular, jugulodigastric) may also be enlarged.
Oedema/tenderness over the mastoid with obliteration of the retroauricular groove - furuncle of posterior meatal
wall.
Discharge- In burst furuncle, discharge is purulent. Candidiasis appear as white or creamy, Aspergillous niger looks
as blackish while Aspergillous fumigates is pale blue or green in appearance.
Vesicles on the tympanic membrane or meatus (Herpes zoster)
Facial asymmetry may be present in malignant otitis externa.
Mastoid tenderness due to extension of infection (malignant otitis externa)
Investigations
Pus for Gram stain and culture
Fungal stains
Blood sugar-in case of recurrent or bilateral otitis externa
CT scan-in malignant otitis externa
74
Comments
Furunculosis,Diffuse otitis externa and otomycosis are the common conditions.
A. Furunculosis. A furuncle is a staphylococcal infection of the hair follicle. As the hair is confined only to the
cartilaginous part of the meatus, furuncle is seen only in this part of meatus. Usually single, the furuncles may be
multiple.
B. Otomycosis or diffuse otitis externa are common in hot and humid climate and in wet ears. Trauma to meatal skin
and invasion by staph aureus or Gram ve organisms like pseudomonas, proteus, E.Coli is common predisposing
factor for diffuse otitis externa.
C. Otitis externa haemorrhagica- It is characterised by formation of haemorrhagic bullae on the tympanic membrane
and deep meatus. It is probably viral in origin and may be seen in influenza epidemics. The condition causes severe
pain in the ear and blood-stained discharge when the bullae rupture.
D. Herpes zoster oticus- It is characterised by formation of vesicles on the tympanic membrane, meatal skin, concha
and postauricular groove. The seventh and eighth cranial nerves may be involved.
E. Malignant (necrotising) otitis externa- It is an inflammatory condition caused by pseudomonas infection usually in
the elderly diabetics, or in those on immunosuppressive drugs. Its early manifestations resemble diffuse otitis externa
but there is excruciating pain and appearance of granulations in the meatus. Facial paralysis is common. Infection
may spread to the skull base and jugular foramen causing multiple cranial nerve palsies. Anteriorly, infection spreads
to temporomandibular fossa, posteriorly to the mastoid and medially into the middle ear and petrous bone. CT scan
is useful, to know the extent of disease.
F. Eczematous otitis externa- It is the result of hypersensitivity to infective organisms or topical ear drops such
chloramphenicol or neomycin, etc. It is marked by intense irritation, vesicle formation, oozing and crusting in the
canal.
G. Seborrhoeic otitis externa - It is associated with seborrhoeic dermatitis of the scalp. Itching is the main complaint.
Greasy yellow scales are seen in the external canal, over the lobule and postauricular sulcus.
MIDDLE EAR DISCHARGE
Otitis media is an inflammation of the middle ear. Middle ear implies middle ear cleft, i.e. eustachian tube, middle ear, attic,
aditus, antrum and mastoid air cells. Otitis media can be classified as following types based on duration (Senturia et
al:1980)
1. Acute otitis media-up to 3 weeks duration
2. Subacute otitis media- lasting from 3 weeks to 3 months duration
3. Chronic otitis media (CSOM/COM) - more than 3 months duration
75
Types of CSOM
Clinically, it is divided into two types:
1. CSOM, tubotympaanic (COM, mucosal type). Also called the safe or benign type; it involves anteroinferior part of
middle ear cleft and is associated with a central tympanic membrane perforation.
2. CSOM, atticoantral (COM, squamous type). Also called unsafe or dangerous type; it involves posterosuperior part of
the cleft (i.e. attic, antrum and mastoid) and is associated with an attic or a marginal perforation. The disease is
often associated with a bone-eroding process such as cholesteatoma, granulations or osteitis. Risk of complications
is high in this variety.
Clinical clues
Ask for
1. History of upper respiratory tract infection , nasal allergy, cleft palate or nasal obstruction- predisposing factors for
ASOM or cause for persistent/recurrent discharge in case of CSOM.
2. Fever: High grade fever may be seen in the stage of suppuration of ASOM often associated with vomiting and convulsion
at times in children. Fever may also be present in complicated cases of CSOM(squamous) e.g. meningitis
3. Ear discharge: Amount, nature, colour, odour, whether blood mixed, duration should be noted.
It is purulent often mixed with blood in case of ASOM
In tuberculosis,Wegeners granulomatsis, discharge may be serosanguinous.
4. Hearing loss: In all stages of Acute otitis media, there is mild conductive hearing loss/ear fullness
Hearing loss may be out of proportion to the progression of disease in case of tubercular otitis media
5. Pain: Excruciating pain is the hallmark of suppurative stage of ASOM. Patient feels relieved once the tympanic membrane
bursts and ear discharge ensues. Pain may also be the feature of impending complication of atticoantral CSOM. E.g .
extradural abscess, trauma and malignancy.
6. Bleeding: May occur from granulations or polyps when cleaning ears especially in atticoantral type and or in cases of
trauma and tumor.
7. Any history of vertigo, tinnitus, facial asymmetry, severe headache, double vision, loss of consciousness, vomiting, neck
rigidity, fever should be asked for to rule out complications (common in atticoantral type).
Look For
Tympanic membrane (TM) may appear dull and retracted with foreshortening of handle of malleus and loss of
cone of light in early stage of acute otitis media (stage of tubal occlusion)which later (stage of suppuration) may be
congested and bulged finally before perforating during stage of resolution
Tubotympanic Atticoantral
Perforation of TM* Anterior, posterior or inferior to handle Attic or marginal (usually posterosuperior)
of malleus (central perforation)
Small, medium or large or extending up
to the annulus.
Nature of discharge Non-offensive, mucoid or Scanty, continuous, purulent, sometimes mixed
mucopurulent, copious, intermittent with blood and foul smelling
Retraction pockets Not present Present in attic or posterior superior quadrant**

Middle ear mucosa Pale pink or if there is inflammation, red Red oedematous and swollen. May be covered
and oedematous. by cholesteatoma and granulation tissue
Polyps/granulation tissue Pale polyps may be present Usually granulation tissue rather than polyp
Ossicular chain Usually intact and mobile Destruction is common
Hearing loss Usually conductive and no worse than Can be conductive, sensorineural or mixed. No
55dB limit to severity of hearing loss, or there may be
no hearing loss at all (when cholesteatoma
bridges the destructed ossicles)
Complications Rare Frequent
76
*Perforation of TM - It is Irregular with fresh margins in case of traumatic tympanic membrane perforations. There
may be multiple perforations in case of Tubercular otitis media
**Cholesteatoma - Pearly white flakes of choleasteatoma can be sucked from retraction pockets/ perforations.
Tympanosclerosis(Chalky white patches)/fibrosis/adhesions- are more common in tubotympanic type-they are the
result of healing process and may result in some hearing loss.
Presence of any periauricular abscess/fistula or facial paresis are the signs of intratemporal and intracranial
complications. Facial paralysis is a common complication in tubercular otitis media and may come unexpectedly.
This may be the presenting feature in a child.
Nystagmus may be present in labyrinthitis, labyrinthine fistula, vestibulitis etc. in complicated cases of CSOM or
due to trauma.
Investigations
1. Examination under microscope- to see the presence of granulations, in-growth of squamous epithelium from the edges of
perforation, status of ossicular chain, tympanosclerosis and adhesions.
2. Audiogram. It gives an assessment of degree of hearing loss and its type. Usually, the loss is conductive but a
sensorineural element may be present.
3. Culture and sensitivity of ear discharge. It helps to select proper antibiotic ear drops.
4. Mastoid X-rays. Mastoid is usually sclerotic but may be pneumatised with clouding of air cells in case of tubotympanic
type and evidence of bone destruction/cavity is seen in atticoantral disease. CT scan of temporal bone gives more
information
Comments
A perforation becomes permanent when its edges are covered by squamous epithelium and it does not heal
spontaneously.
A small attic perforation may be missed due to presence of a small amount of crusted discharge.
A polyp is a smooth mass of oedematous and inflamed mucosa which protrudes through perforation and is present
in the external auditory canal.
Bacteriology
Pseudomonus aeruginosa, Proteus, Esch. coli and Staph.
Bacteroides fragilis and anerobic Streptococci.
Acute otitis media (Acute suppuratives otitis media)
More common in children and follows viral infection of upper respiratory tract but soon the pyogenic organisms
invade the middle ear.
Routes of Infection may be via Eustachian tube, external ear or blood borne.
The disease runs through the following stages:
1. Stage of tubal occlusion
2. Stage of pre-suppuration
3. Stage of suppuration
4. Stage of resolution or complication
Cholesteatoma
Normally, middle ear cleft is lined by different types of epithelium in different regions: ciliated columnar in the
anterior and inferior part, cuboidal in the middle part and pavement-like flat cells in the attic. There is no
keratinising squamous epithelium in middle ear. It is the presence of keratinising squamous epithelium in the
middle ear or mastoid that constitutes a cholesteatoma. In other words, cholesteatoma is a "skin in the wrong
place".
77
Types of Cholesteatoma
1. Congenital cholesteatoma. It arises from the embryonic epidermal cell and rests in the middle ear cleft of temporal
bone. Congenital cholesteatoma occurs at three important sites: middle ear, petrous apex and the
cerebellopontine angle, and produces symptomatology depending on its location.
2. Primary acquired cholesteatoma. It is called primary as there is no history of previous otitis media or a pre -existing
perforation. Theories on its genesis are:
a) Invagination of pars flaccida b )
Basal cell hyperplasia c) Squamous
metaplasia
3. Secondary acquired cholesteatoma In these cases, there is already a pre-existing perforation in pars tensa. This is
often associated with posterosuperior marginal perforation or sometimes large central perforation. Theories on its
genesis include:
(a) Migration of squamous epithelium (b)
Metaplasia
Features Indicating Complications in CSOM
1. Pain- uncommon in uncomplicated CSOM. Its presence may indicate extradural, perisinus or brain abscess.
Sometimes, it is due to otitis externa associated with a discharging ear.
2. Vertigo. It indicates erosion of lateral semicircular canal which may progress to labyrinthitis or meningitis. Fistula
test should be performed in all cases.
3. Persistent headache. It is suggestive of an intracranial complication.
4. Facial weakness indicates erosion of facial canal.
5. Refusing to take feeds, listlessness and excessive sleepiness in a child (extradural abscess).
6. Fever, nausea and vomiting (intracranial infection.).
7. Irritability and neck rigidity (meningitis).
8. Diplopia (Gradenigo's syndrome).
10. Abscess around the ear (mastoiditis).
Miscellaneous causes of ear discharge
Miscellaneous
Serosanguinous
Haemorrhagic
CSF Otorrhoea e.g. Tuberculosis,
e.g. trauma, tumour,
e.g. Trauma, tumour Wegeners
foreign body
granulomatosis
CSF otorrhea- Most cases of CSF otorrhea have a traumatic aetiology, following a head injury or surgery to the skull base. In
rare cases, the cause may be non traumatic such as neoplasm, congenital defects or even atticoantral type of CSOM.
Bleeding ears- Trauma to ear canal, foreign body or neoplasms can cause bleeding from ears besides in some case of
infective ears. Commonly, injury from a blow to the head, slapping, blast injuries, or sudden pressure changes (such as in
airplanes) may resulting in a perforated tympanic membrane and bleeding
Serosanguinous
Tuberculosis: typically in tuberculosis there are multiple perforations of the TM which may coalesce into a single large
perforation. There is painless ear discharge often foul smelling due to underlying bone destruction. Severe hearing loss is
out of proportion to symptoms, mostly conductive, but may have sensori neural component due to involvement of labrynth.
Facial paralysis is a common complication and may come unexpectedly.
Wegeners granulomatosis is a necrotizing, granulomatous small vessel vasculitis that occurs in all ages and often involves
upper airways, lower respiratory tract and kidneys.
78
Hearing Loss
Hearing
Loss
Sensorineura
Conductive
l Mixed
(CdHL)
(SNHL)
Cochlear Retrocochlear
External ear Middle ear (Vlll nerve & its
(Inner ear )
central connections)
Hearing loss can be an isolated symptom or associated with other aural presentations. Patients may or may not be aware
that their hearing is decreased. They may state that their ear feels muffled, blocked, or plugged, or complain of pressure or
the sensation of water in the ear. The general approach is to decide if the hearing loss is due to a problem in the outer,
middle, or inner ear. A thorough history and physical examination are essential to reach the correct diagnosis.
Hearing loss due to external ear or middle ear causes are called conductive hearing loss whereas in sensorineural hearing
loss, etiology lies in cochlea, Vlll nerve and its central connections.
Cinical Clues
While assessing the auditory function it is important to find out:
(a) Type of hearing loss
(b) Degree of hearing loss
(c) Site of lesion
(d) Cause of hearing loss
Ask for
1. Age - Otitis media with effusion, Acute suppurative otitis media (ASOM) are common in young children
- Elderly may suffer from age related hearing loss (ARHL or Presbyacusis)
2. Onset
Gradual - in case of Chronic suppurative otitis media(CSOM), otitis media with effusion(OME)etc.
Acute - in case of trauma, tumors, vascular, infective (e.g. Mumps, measles, Herpes zoster, Tuberculosis etc.),
meningoencephalitis
3. Severity of hearing loss- can hear loud sounds or cant hear at all
4. Associated symptoms
a. Discharge-persistent-CSOM
Acute - ASOM
b. Pain - AOM, Complicated CSOM, Infections like Herpes zoster, trauma, tumours etc
c. Severe headache, nausea, vomiting, loss of consciousness, double vision- may signify complication of
CSOM
d. Ringing/Dizziness- suggestive of having sensorineural component.
5. Congenital anomalies- cleft palate, microtia, atresia, preauricular skin tags etc
6. Trauma- Head injuries, ear operations, noise trauma, barotrauma, spontaneous rupture of cochlear membrane.
7. Noise exposure- occupation (hours per week exposed to noise, loudness), sudden loud noise exposure(acoustic
trauma)
8. H/O Infections- Mumps, herpes zoster, meningitis, encephalitis, syphilis, otitis media.
9. Drugs- use of any oral or topical ototoxic ear drops.
10. Medical illness (Diabetes mellitus, hypertension)
11. Autoimmune disease- Cogans syndrome, Wegeners granulomatosis
12. Family history of hearing loss e.g. Alports syndrome
79
Look for
1) Examination of the ear

a) External ear
Any obstruction in the ear canal, e.g. wax, foreign body, furuncle, acute inflammatory swelling, benign or malignant
tumor, malformation of pinna ( e.g. microtia, anotia), atresia of canal.
b) Middle ear
i. Perforation of tympanic membrane(traumatic or infective)
ii. Discharge- colour, character, amount, frequency
iii. Fluid in middle ear , e.g. acute otitis media, serous otitis media or hemotympanum
iv. Mass in middle ear, e. g. wax, foreign body, tumors
v. Disruption of ossicles, e.g. trauma to ossicular chain, chronic suppurative otitis media, cholesteatoma
vi. Fixation of ossicles, e.g. otosclerosis, tympanosclerosis, adhesive otitis media
vii. Eustachian tube blockage, e .g, retracted tympanic membrane , serous otitis media
c) Others- Facial nerve status, nystagmus, cerebellovestibular examinations
2) Hearing assessment
a. Finger friction test
b. Watch test
c. Speech tests
d. Tuning fork tests
i. Rinne test
ii. Weber test
iii. Absolute bone conduction test
d) Examination of central nervous system

To rule out central causes e.g. tumors arising in cerebellum, cerebellopontine angle, internal auditory meatus etc.
Cerebellar signs: Look for intention tremor, Ataxic gait, Finger-nose co-ordination, Heel-shin co-ordination,
Nystagmus and slurring of speech
Investigations
Pure tone audiogram
o for the type of hearing loss- conductive, SNHL or mixed
o in SNHL, which frequencies are involved (frequency specific loss seen in noise induced hearing loss, ototoxicity,
meniere's disease)
Tympanogram- helpful in Conductive hearing Loss
o A-Normal.
o As-Reduced compliance at ambient pressure (otosclerosis).
o Ad-Increased compliance at ambient pressure (ossicular discontinuity).
o B-Flat or dome-shaped (fluid in middle ear).
o C-Negative pressure in middle ear e.g. eustachian tube obstruction or early stage of otitis media with effusion.
Acoustic reflexes
Involuntary middle ear muscle reflexes to sounds, usually elicited by moderately loud tones or noises, are recorded
Auditory brainstem response(ABR)
Using clicks or tones, this test can estimate hearing threshold sensitivity and determine the integrity of the auditory
pathway from the cochlea to the level of the brainstem. Test can be done in unconscious patients and neonates as well.
Electrocochleography
Measurement of electrical potentials of the eighth cranial nerve in response to acoustic stimuli applied by an electrode
on promontory.
Otoacoustic emissions(OAE)
OAE are low-level sounds produced by the sensory hair cells of the cochlea (primarily the outer hair cells of the inner
ear) as part of the normal hearing process.
Radiology-They depend on the etiology suspected, e.g.
X-rays of temporal bone for evidence of bone destruction e.g. in cholesteatoma, congenital atresia of ears etc.
MRI /CT scan in suspected cases of glomus tumor, middle ear malignancies, acoustic neuroma or intracranial tumors.
80
Comments
*Hearing loss can be of three types:
a. Conductive hearing loss
It is caused by any disease process interfering with the conduction of sound from the external ear to the
stapediovestibular joint. Thus the cause may lie in the external ear (obstructions e.g. was, osteomas, stenosis,atresia),
tympanic membrane (perforation), middle ear (fluid,), ossicles (fixation or disruption) or the eustachian tube (obstruction).
b. Sensorineural (SN) hearing loss
It results from lesions of the cochlea (sensory type e.g. Menieres disease, ototoxicity) or VIIIth nerve and its central
connections (neural type e.g. acoustic neuroma, encephalitis). The term retrocochlear is used when hearing loss is due
to lesions of VIIIth nerve, and central deafness, when it is due to lesions of central auditory connections.
c. Mixed hearing loss
In this type, elements of both conductive and sensorineural deafness are present in the same ear. There is air-bone gap
indicating conductive element, and impairment of bone conduction indicating sensorineural loss. Mixed loss is seen in some
cases of otosclerosis, and chronic suppurative otitis media (CSOM).
Hearing loss can also be described as congenital or acquired
*Degree of Hearing loss (American Speech-language Hearing Association-ASHA Classification)
Degree of hearing loss Hearing loss range (dB HL)
Normal Up to 15
Slight 16 to 25
Mild 26 to 40
Moderate 41 to 55
Moderately severe 56 to 70
Severe 71 to 90
Profound >90
*Well established term chronic suppurative otitis media(CSOM) is nowadays more often called simply chronic otitis
media(COM) as chronic otitis media may not always necessarily be the result of gathering of pus.
81
Hearing loss in children
Hearing Loss
in children
Congenital/prenatal Acquired
Perinatal Postnatal
Children with profound (>90 dB loss) or total deafness fail to develop speech however, these children have no defect in their
speech producing apparatus. They have never heard speech and hence do not develop it. In lesser degrees of hearing loss,
speech develops but is defective. The period from birth to 5 years of life is critical for the development of speech and
language, therefore, there is need for early identification and assessment of hearing loss and early rehabilitation in
infants and children.
Clinical clues
A child should be suspected of having hearing loss if he/she fails to respond to loud noise or fails to develop
speech at 1-2 years of age .
Hearing loss in a child may develop from causes before birth (prenatal), during birth (perinatal) or after
birth (postnatal).
Ask for
A. Congenital/Prenatal Causes
a. Family history of hearing impairment (Genetic conditions)
b. History of fever, rash or viral infection in pregnancy (Infections which affect the developing foetus are
toxoplasmosis, rubella, cytomegaloviruses, herpes type 1 and 2 and syphilis Infections
c. Use of drug during pregnanacy (eg. streptomycin, gentamicin , amikacin, quinine or chloroquine, when given
to the pregnant mother, cross the placental barrier and damage the cochlea)
d. Radiation to mother in the first trimester
e. Medical illness- history of diabetes, hypothyroidism
f. History of alcohol intake or drug abuse in mother.
B. Perinatal Causes
a. History suggestive of birth asphyxia (e.g. prolonged labour, cord round the neck or prolapsed cord)
b. Prematurity and low birth weight
c. Birth injuries e .g. forceps delivery
d. Neonatal jaundice
e. Neonatal meningitis
f. Sepsis
g. Time spent in neonatal lCU.
h. Ototoxic drugs e.g. aminoglycoside, erythromycin.
C. Postnatal Causes
a. History of similar problem in other family members
b. Viral infections (measles, mumps, varicella, influenza),
c. Complications of meningitis and encephalitis.
d. Secretory otitis media.
e. Ototoxic drugs.
f. Trauma, e .g. fractures of temporal bone, middle ear surgery or perilymph leak.
g. Noise-induced deafness
h. Vaccination history (e.g. MMR which protects against mumps)
82
Look for
a. General condition of the child (e.g. height, weight, nutrition status)
b. Developmental assessment e.g. cerebellar palsy
c. External examination of the ear (external abnormalities of the ear may be associated with inner ear problems e.g.
microtia, sternosis of external auditory canal)
d. Features of child related to any syndromes which are associated with hearing loss (e.g. microcephaly, cleft
lip/palate, hypoplasia of maxilla, retrognathism)
e. Otoscopy
f. Examination under microscope(EUM)
g. Response to loud noise
h. Ability to speak or not
Investigations
a. Impedence audiometry
b. Speech audiometry
c. Acoustic reflex
d. Audiotory brainstem response
e. Electrocochleography
f. Otoacoustic emissions
g. Laboratory test as indicated
h. CT Scan/MRI as indicated
i. VDRL (for syphilis), TORCH (Toxoplasma, Rubella, Cytomegalovirus, Herpes) screening
Comments
1. Hearing loss (deafness) in relation to speech development can be categorized as:
a. Post lingual- where onset of deafness has occurred after completion of speech development
b. Perilingual- where onset of deafness has occurred while speech development was occurring
c. Prelingual where onset of deafness has occurred prior to any development of speech
83
Nasal Obstruction / Discharge
Nasal obstruction
Secretion(+) Secretion(-)
Mucopurulent Hemorrhagic Clear Deviated Nasal

Septum(DNS)
Foreign body in Benign tumors

children e.g. angiofibroma, CSF leak
Concha Bullosa
Inverted papilloma
(Pneumatised middle
Acute/chronic turbinate)
Rhinosinusitis Tumours
Coryza
e.g. Adenocarcinoma,
Polyps Squamous cell carcinoma (common cold)
(Antrochoanal/
Ethmoidal) Rhinosporidiosis Turbinate hypertrophy
Allergic rhinitis
Allergic Fungal
Rhinosinusitis Bleeding polyps
Septal hematoma
Vasomotor rhinitis
Choanal atresia
Granulomatous diseases
Mucocoele /
Mucopyocoele Idiopathic( epistaxis)
The stuffy nose (also known as nasal blockage or nasal congestion) is the sensation of having difficulty breathing through
the nose. It may be unilateral or bilateral, transient or permanent, usually caused by anatomic variations, tumours or
changes in the function of the nasal mucosa, which narrow the nasal cavity and increase resistance to the air flow.
Therefore, there exist conditions such as atrophic rhinitis or viscosity changes of mucus, which elicit the same sensation
despite the wide patency of the nasal cavities. Most of the time, nasal discharge is associated with nasal obstruction.
84
Nasal
obstruction
Secretions Secretions
present absent
Mucopurulent Haemorrhagic Clear
Clinical clues
Ask for:
Presence of discharge and its character
Character of discharge Associated conditions

Watery (clear)
CSF Rhinorrhoea, Coryza (common cold)
Mucoid (clear) Allergic, Infective (viral) and Vasomotor rhinosinusitis. Mucinous in case
of allergic fungal sinusitis
Mucopurulent Infective (bacterial) rhinosinusitis(Acute/Chronic), Foreign body
Serosanguinous Rhinosporidiosis,Granulomatous diseases,Tuberculosis
Hemorrhagic (Epistaxis) Trauma, Neoplasia, Bleeding diathesis, Idiopathic

Age
Nasal masses in children are commonly due to lesions like dermoid, glioma, meningocoele, encephalocoele,
rhabdomyosarcoma etc. Bilateral choanal atresia presents as soon as delivery of the baby though unilateral may
present late. Adenoid enlargement is another important cause of nasal obstruction in younger childrens. Some
diseases can have bimodal age of presentation e.g. nasopharyngeal carcinoma. Juvenile angiofibroma affects
mostly the teenagers. Sinonasal polyposis is common in middle aged population.In vasomoror rhinitis, age of onset
nd
is normally after 2 decade of life.
Sex
Juvenile angiofibroma is found exclusively in male, only few cases in females have been reported in literature.
Rhinosporidiosis is more common in males. Inverted papilloma and vasomotor rhinitis are more common in
females.
Address
Rhinosporidiosis in more common in people indwelling in Terai region. Nasopharyngeal carcinoma is more
common in certain Chinese population/Mongloid races. People from the area with radiation fall out are more
prone to malignancy.
Occupation
Wood workers/ nickel industries workers are prone to sinonasal malignancies.
Onset and progression
Infective pathologies have generally acute presentation whereas malignancies have progressive course over
months. Sinonasal polyposis also have progressive course. Congenital/developmental pathologies presents at early
ages
Frequency
Allergic rhinitis/Chronic rhinosinusitis(CRS) presents with intermittent nasal obstruction whereas any mass in the
nasal cavity will have persistent nasal obstruction. Sometimes physiological nasal cycle may be perceived by patient
with alternate nasal obstruction as problematic.
Snoring/mouth breathing
Adenoid hypertrophy, nasopharyngeal carcinoma, other nasal, nasopharyngeal masses, obesity.
85
Laterality
DNS, AC Polyp, choncha bullosa, Inferior turbinate hypertrophy, fungal sinusitis, tumors, foreign bodies etc can
commonly cause unilateral nasal obstruction. Ethmoidal polyps, CRS, granulomatous diseases, septal hematoma etc
may cause bilateral nasal obstruction
Associated sneezing/irritation
In case of allergic rhinitis, fungal sinusitis, vasomotor rhinitis (less severe than allergic rhinitis)
Itching
Common in allergic and vasomotor rhinitis
Local pain
In case of nasal vestibulitis,there may is severe pain in the vestibular and surrounding area.
Alteration/loss of smell
In allergic rhinitis, CRS, ethmoidal polyps, atrophic rhinitis etc.
Headache/facial pain/post nasal drip
In case CRS, tumors
Hearing loss/aural fullness
Commonly in case of adenoid hypertrophy, nasopharyngeal carcinoma, CRS etc.
Nasal intonation/regurgitation
In case of nasopharyngeal mass/tumors, cleft palate etc.
Trismus, diplopia, diminished vision, loosening of teeth, proptosis
May occur when tumor progresses, invades nearby structures
History of trauma/head injury
In case of CSF leak, epistaxis.
Past history, drugs & allergy history and surgical history
Synechiae develops in the patient who has undergone nasal surgery. Sinonasal polyposis has very high recurrence
rate and in the revision cases the anatomy may be distorted.
Family history
Asthma, allergy runs in the family. Nasopharyngeal carcinoma is common amongst Mongloid races, southern
Chinese and retained high incidence in later generations of southern Chinese emigrants who settled in areas of low
incidence.
Personal history
Cocaine abuse is associated with nasal septal perforation. Sniffing cocaine causes a perforated septum by
continuous use of the drug, tissues in the nose are deprived of blood and die.
Nose picking habit is often associated with recurrent nasal vestibulitis i.e.inflammation of the tissue around the
entrance to the nose- the nasal vestibule. Minor infections at the opening of the nose may result in folliculitis and
sometimes crusts around the nostrils. More serious infections result in boils, or furuncles. Cellulits, or spreading of
the infection in the tissue layer under the skin, occasionally may involve veins draining from the brain. A life-
threatening condition called cavernous sinus thrombosis can develop if the bacteria spread to the brain through
these veins.
Look for:
Examination of external nose and sinuses
Are there deformities of the nasal framework? e.g. Deviated or twisted nose, hump, depressed bridge (saddle
nose), bifid or pointed tip, destruction of nose
Does the nasal valve collapse at forced inspiration? e.g. old age, polychondritis, nasal masses, adenoid hypertrophy
etc.
Nasal patency test: cotton wool test, cold spatula test
Is there any swelling over nose, cheeks, lips, sinuses, eye lids, vision, proptosis, diplopia?
Palpate the nose to find raised temperature, fixity of skin, tenderness, fluctuation or crepitation, integrity of orbital
rim.
Examination of nasal vestibule

Projecting the nasal tip upwards
Is the skin of the nasal vestibule swollen? e.g. furuncle, abscess, crusts, hemangioma, Rhinosporidiosis etc.
Are there deformities of the nasal framework?
Is the caudal septum deviated?
Is there narrowing of the nasal valve?
86
Anterior Rhinoscopy
In some cases examination vasoconstriction may also be required.
Are there deformities, hematomas or perforation of the nasal septum?
Is there turbinate hypertrophy (CRS, allergic rhinitis, concha bullosa)/atrophy (atrophic rhinitis)?
Is the mucosa/turbinates red (infection/vasomotor rhinitis) or pale/bluish (allergic rhinitis)?
Are there polyps, single (Antrochoanal polyp) or multiple (Sinonasal polyposis)?
Is there purulent secretion, crusting?
Is a tumour visible?
If any swelling seen, probe test has to be performed. In probe test, look for pain, attachment, extent, mobility and
bleeding. Septum and turbinates are painful whereas polyps and tumour are painless. Vascular lesion
(angiofibroma, hemangioma), rhinosporidiosis and tumours may bleed on touch.
Posterior Rhinoscopy
Is there hypertrophy of posterior ends of turbinate?
Is there discharge present in middle meatus (maxillary, frontal and anterior ethmoid sinuses) or above middle
turbinate (sphenoid and posterior ethmoid sinuses)?
Is there choanal atresia, choanal polyp, adenoid hypertrophy or other swelling in nasopharynx?
Oral cavity and oropharynx examination

Is there swelling or ulceration in the hard palate, gums, upper gingivobuccal sulcus, retromolar trigone area or soft
palate?
Is there loosening of maxillary teeth?
Is there mass hanging in the oropharynx (AC polyp, retropharyngeal abscess)?
Neck examination
Are there enlarged lymph nodes?
Aural examination
Are there features suggestive of fluid in the middle ear?
Endoscopy of the nose/nasopharynx

In some cases vasoconstriction may be required.
Are there posterior septal spurs?
Are the turbinates swollen?
Does the middle meatus have purulent discharge?
Are there bleeding or pulsating polyps?
Are there synechiae?
Is choanal atresia evident?
Is there adenoid hypertrophy?
Are there polyps?
Is a tumour visible?
Additional diagnostic procedures:

X-ray PNS
CT scan (tumours, CSF rhinorrhoea, complications of sinusitis)
MRI (tumours, CSF rhinorrhoea, complications of sinusitis)
Eosinophil in nasal discharge
Biopsy (always after CT scan)
Handkerchief test: stiffening of the handkerchief occurs with rhinitis due to presence of mucus but not in CSF
rhinorrhoea
Protein and sugar content of secretions (if suspect CSF)
-2 transferrin in nasal secretion for suspected CSF rhinorrhoea (usually not available in Nepal)
Rhinometry-measurement of nasal patency, obstruction
Nasomucociliary clearance (dye or reactive particles e.g. methylene blue, saccharine)
87
Comment:
In case of children presenting with unilateral nasal discharge, foreign body has to be ruled out.
Bilateral choanal atresia is fatal if not diagnosed soon after birth. Unilateral choanal atresia may present later in childhood.
Deviated nasal septum (DNS) is a common cause of nasal obstruction. Though up to 80-90% population have DNS, only few
are symptomatic. It may cause unilateral or bilateral nasal obstruction. DNS can be classified as simple, obstructed and
impacted on the basis of severity of symptoms. Nasal cycle, rhythmic cyclical congestion and decongestion of alternate nasal
mucosa, may sometimes be perceived by patients. Paradoxical nasal obstruction in patient with DNS is due to compensatory
turbinate hypertrophy in contralateral side. Pneumatisation of middle turbinate, concha bullosa may also cause nasal
obstruction.
Septal hematoma following trivial trauma sometimes unnoticed in children may present with bilateral nasal obstruction.
Septal hematoma may get infected and develop abscess.
Simple deviated nasal septum, concha bullosa(pneumatised and enlarged middle turbinates), turbinate hypertrophy,
unifected septal hematoma may cause obstruction without nasal discharge.
Epistaxis is commonly idiopathic and may or may not be associated with nasal obstruction. It can be unilateral or bilateral.
The most common site for epistaxis is Littles area. In old age, posterior epistaxis is common and is more severe.
Systemic review There is a high chance of patient developing asthma with sinonasal polyposis, that too when the patient
has aspirin intolerance. Tuberculosis, leprosy and syphilis are systemic diseases which may present with nasal
manifestations and if not evaluated properly, diagnosis may be missed. Sarcoidosis is a multisystem disease primarily
affecting the lower respiratory tract but which may involve the upper respiratory tract. Wegener's Granulomatosis is
characterized by granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small- to
medium-sized vessels (e.g. capillaries, venules, arterioles and arteries) with necrotizing glomerulonephritis.
There are several causes of rhinosinusitis.
Intermittent (Seasonal)
Allergic
Persistent (Perennial)
Acute (< 12 weeks)
Chronic (>12 weeks) Nonspecific: Strep. pneumoniae, H. influenzae

Infectious
Specific: Tuberculosis, Leprosy, Rhinoscleroma,
Syphilis, Fungal
Nonallergic non- Occupational, Hormonal, Drug incuded, Irritants, Food, Emotional,

infectious/Vasomotor Hormonal, Gastro-oesophageal reflux, Idiopathic
Acute rhinosinusitis is most often caused by viruses and may get secondarily infected by bacteria.
Multiple pale polypoidal painless mass generally bilateral on anterior rhinoscopy is seen in sinonasal polyposis. Unilateral
polyposis is seen in allergic fungal sinusitis. Single polypoidal mass going posteriorly towards nasopharynx is seen in
antrochoanal polyp.
Vasomotor Rhinitis: Vasomotor rhinitis refers to a condition in which the nose is stuffy or runny for reasons other than
allergies or infections. In many cases, the cause of vasomotor rhinitis is not known, but triggers include emotions, odors,
poor air quality, spicy foods, and medication side effects. The symptoms of vasomotor rhinitis can occur very frequently or
sporadically. Symptoms include drainage of the nose (rhinorrhea), congestion, and irritation. The pathology of vasomotor
rhinitis appears to involve neurogenic inflammation . Vasomotor rhinitis appears to be significantly more common in women
than men, leading some researchers to believe that hormones play a role. In general, age of onset occurs after 20 years of
age, in contrast to allergic rhinitis which can be developed at any age.
88
Samters triad: Nasal polyposis, bronchial asthma, aspirin sensitivity
Rhinosporidiosis caused by aquatic protozoan is common in people indwelling Terai region who have access to fresh water
ponds and presents with leafy polypoidal pedunculated pinkish mass with strawberry appearance arising commonly from
floor of nose or septum on anterior rhinoscopy which bleeds on touch.
Atrophic rhinitis is defined as a chronic nasal disease characterised by progressive atrophy of the nasal mucosa
along with the underlying bones of turbinates. There is also associated presence of viscid secretion which rapidly
dries up forming foul smelling crusts. This fetid odor is also known as ozaena. The nasal cavity is also abnormally
patent. The patient is fortunately unaware of the stench emitting from the nose as this disorder is associated with
merciful anosmia.
Juvenile angiofibroma is found exclusively in male generally of adolescent age group and may present with epistaxis.
Sinonasal malignancy commonly presents with unilateral progressive nasal obstruction with blood tinged nasal discharge. In
late stages tumour may involve the surrounding structures e.g. cheek swelling, proptosis, loosening of teeth, difficulty in
opening mouth and neck nodes.
Trotters triad: seen in nasopharyngeal carcinoma
1. Conductive hearing loss

2. Ipsilateral immobility of soft palate
3. Neuralgic pain in the distribution of Mandibular division of trigemminal nerve
Mikulicz cells and Russell bodies are characteristically seen in histology in Rhinoscleroma.
89
Abnormal Anxiety
PANIC AND ANXIETY
(Rule out non-psychiatric
disease/drugs)
Intermittent acute Other Psychiatric

Persistent and symptoms Disorders
Excessive anxiety and [Schizophrenia,
worry Panic Disorder
Obsessive- depression,
Generalized Anxiety Trauma/ stress Compulsive Disorder
Disorder related neuropsychiatric
Phobias conditions (dementia)],,
substance use
Anxiety disorders are pervasive in all age groups and all clinical settings, ranging from normal reactions in healthy individuals
to severe and crippling conditions. Anxiety (a signal of impending danger from an unknown or poorly defined threat) should
be differentiated from fear, a response to an identifiable threat. By obtaining an accurate history, it is possible for the
physician to identify pathological anxiety that is associated with psychiatric or other medical causes.
CLINICAL CLUES
Ask about
o Acute / chronic pain, diarrhoea, vomiting (to rule out systemic illness)
o Cardio-respiratory diseases, endocrine and metabolic disordersin orderto identify anxiety caused by medical
conditions.
o History of drug or substance usage, prescribed as well as non-prescribed which can give rise to anxiety features
during intoxication or withdrawal state (alcohol /benzodiazepines/ cannabis/ nicotine/ caffeine and other drugs).
Be aware that patients will often deny or minimize substance abuse. A wide variety of medication and dietary
supplements can also be anxiogenic(eg:bronchodilator, caffeine, nicotine)
o Differentiate between discrete, intermittent attacks of anxiety (panic attacks,phobias, acute stress responses) and
pervasive anxiety about almost anything (Generalized Anxiety Disorder).
o Identify patients with anxiety associated with another psychiatric disorder:
Anxietyis a common symptom in mood disorders and many other disorders.
Obsessive-compulsive disorder is a specific type ofanxiety disorder that is dealt with in this presentation.
Look for external signs of anxiety
o Hyperhydrosis
o Hypertension
o Palpitations/ Tachycardia
o Tremulousness/ Restlessness
o Dizziness
o Hypereflexia
o Upset stomach/Abdominal tenderness
Look for presence of other pathologic/medical conditions, including features of alcohol / benzodiazepine withdrawal.
INVESTIGATION
Urine (or serum) toxicology when substance abuse is suspected.
Other laboratory tests if indicated by history or physical exam indicates (Eg.- ECG, CXR, hemogram, complete blood
count,serum electrolytes, blood sugar,metabolic profile, cardiac enzymes, thyroid function test).
Mental status examination.
DIAGNOSES TO RULE OUT
Severe anxiety associated with acute/emergent medical condition (Myocardial infarct, asthma attack).
Delirium (acute brain failure) manifests as a confusional state in a medicallycompromised patient and is often
associated with anxiety.
COMMENTS
Anxiety disorders are often undiagnosed in the primary care setting, despite the fact that they are quite common.
Studies around the world have established that about 20% of patients in primary care had at least one anxiety disorder.
Anxiety disorders are often mislabeled as cardiac / neurological illness and huge resource and time is wasted.
90
Persistent and Excessive

Anxiety and Worry
Generalized Anxiety Disorder (GAD)
CLINICAL CLUES
Ask about the nature of the anxiety
o Exist most days for at least several weeks at a time, and usually for several months
o Free floating anxiety : Apprehension, feeling on edge , difficulty in concentration
Ask about specific associated symptoms (autonomic overactivity and motor tension)) that are required for a formal
diagnosis ofGAD:
o Sweating , tachycardia or tachypnoea, light headedness, dizziness
o Restlessness
o Epigastric discomfort
o Muscle tension/ Tension headache
o trembling
o Sleep disturbance
Look for
o Signs of significant distress or impairment in social, occupational or other important areas of daily
living(like sleep, appetite, interpersonal relationship)
o Expressions of anxiety on the physical /mental status exam.
INVESTIGATION
Only to rule out other medical condition(ECG. TFT,cardiac enzymes, CXR etc)
Careful follow-up visits will help confirm the diagnosis and further rule out co-existing medical conditions or other
psychiatric disorders.
DIAGNOSES TO CONSIDER
A significant number of GAD patients will later develop a mood disorder.
Intermittent
Acute
Symptoms
Panic
Stress related Phobias
Disorders
Post- Agoraphobia
With Without Acute Stress Traumatic Adjustment without a Specific Social
Agoraphobia Agoraphobia Disorder Stress Disorder history of Phobia Phobia
Disorder panicdisorder
91
Panic Disorder
Panic
Disorders
With Without
Agoraphobia Agoraphobia
panic attack is a sudden extreme anxiety with a sense of impending doom, like( I am about to- die,-collapse,-
have heart attack,- be crazy, etc)ususally in response to threatening stimulus
when people have frequent unexpected apanic attacks they start to worry about further attacks all the time.
this is called anticipatory anxiety.
frequent paroxysmal panic attacks along with anticipatory anxiety for a period of more than 1 month
constitute panic disorder
CLINICAL CLUES
Ask about the nature of the onset of the attacks. This group of anxiety disorders is characterized by
o Spontaneous and intermittent episodes
o A discrete, sudden period of intense discomfort accompanied by physical symptoms as well as a cognitive
component.
o The physical component often leads patients to emergency care settings.
o Fears of a heart attack/ unconsciousness/ choking to death in progress are common.
o The cognitive symptoms are intense and can be crippling.
Panic patients, because they are having recurrent episodes, typically have concerns about having additional attacks,
known as anticipatory anxiety
Ask about the presence (or absence) of agoraphobia (the fear of being alone in public places.)
o Especially frightening are areas where the patient envisions lack of access to help should a panic episode
occur.
OTHER DIAGNOSES TO CONSIDER

Psychiatric co-morbidity.
Panic disorder patientscommonly have depressive disorders.
o Panic attacks are common, and panic disorder less common.
o Panic disorder has a high co-morbidity with other anxiety disorders, such as social phobia, OCD and GAD.
o Panic attacks that occur during sleep are seen in obstructive sleep apnea.
COMMENTS
There are many differential diagnoses for organic causes of panic attacks (Cardiovascular, metabolic, pulmonary,
neurological and others).
excludealcohol or drug related conditions.
92
Stress
Related
Acute Stress Adjustment

PTSD
Reaction Disorder
Clinical clues
Ask for:
Timing of appearance of symptoms since the stressor.
Duration of the symptoms
Comments
Timing is the critical determinant in differentiating these disorders. Acute stress disorders begin within one month
of a traumatic event and last at least 2 days. Unlike PTSD, acute stress disorder remits in no more than 4 weeks.
Adjustment disorder arise within a month in the period of adaptation to a significant life changes and does not
usually exceed six months.
PTSD
CLINICAL CLUES
Ask about
o How has the patient responded to the extreme traumatic stressor (these are stressors that are exceptionally
threatening or catastrophic, of such magnitude that virtually anyone would be affected by them).
o The event or events that are associated with actual or threatened death or serious injury, or threat to the
physical integrity of self or others.
o Whether patients suffer intense fear, helplessness or horror.
o Patients respond with symptomatic experiencing or re-experiencing of the traumatic event, avoiding stimuli
associated with the trauma and suffersymptoms of arousal.
o Whether there is a characteristic recurring, intrusive recollections (flashbacks) of the overwhelming event.
+
o Duration of PTSD (acute: less then 3 months; chronic: 3 months)
Look for
o Physiological reactivity on exposure to cues that represents the traumatic episode.
o Repetitive distressing dreams of the event or actions/emotions that indicate a painful re-experiencing of the
event.
o Efforts to avoid the trauma recurringoften associated with symptoms of numbing of general responsiveness.
o Symptoms of hyper-arousal: sleep disorders, irritability , hyper-vigilance, concentration problems and startle
reactions.
o Signs of dysfunction/impairment in important areas of functioning.
o Mental status findings of severe anxiety, dissociative phenomena and feelings of guilt, anger or aggressiveness.
o Cognitive dysfunction (memory problems, attention deficit) may be present.
INVESTIGATION
Toxicology is often indicated (there is a high incidence of psychiatric co-morbidityin PTSD, including substance
abuse disorders).
Psychometric tests to assess cognition/ personality factors can be very useful extensions of the mental status exam.
COMMENTS
Forensic issues are common in PTSD owing to criminal aspect of catastrophic trauma like rape, torture,
victimization during terrorism/ war and others.
There are no formal epidemiological survey of PTSD in Nepal but worldwide data varies from 5-75 % of those
exposed to such trauma
93
PHOBIAS
Agoraphobia Social Phobias

without a history of Specific Phobias (Social Anxiety
panic disorder Disorder)
CLINICAL CLUES
Ask about how symptoms occur, relative to:
o Situations where symptoms are expressed
o The circumstance surrounding the event.
o Specific objects that precipitate the anxiety (heights, needles, animals, blood).
Look for patterns of anticipatory anxiety.
o Agoraphobic patients fear being trapped in situations or places without a way to escape easily. These
patients are also very fearful of being in these situations without a source of help.
o Social phobia is extreme anxiety associated with a social setting or a performance situation.
o Look for the level of dysfunction
o Social phobia is often mistaken for shyness or loneliness.
COMMENTS
Some phobias cause little distress (city dwellers not exposed to an animal they fear), but others can be crippling (acrophobia
in a person may not be able to climb up a multi-storey building).
Obsessive-Compulsive
Disorder
Obsessive compulsive disorder (OCD) is primarily diagnosed by history and mental status examination.
CLINICAL CLUES
Ask about
o Anxiety-provoking Ideas,Impulses& Images ( 3 Is :obsessions) and
o Urges (compulsions), generated in an attempt to lessen theanxiety.
Ask about the quality of obsessional thoughts:
o Are they recurrent, intrusive and persistent?
o Do they cause marked distress?
o Are they inappropriately intense, given the real life situation?
Look for evidence of a pre-existing obsessive-compulsive personality disorder (OCP). Most patients with OCD do
not have OCP. People with premorbid obsessional traits do not usually demonstrate the crippling anxiety
seen in OCD patients.
94
Rule out a psychotic disorder.

o Patients with OCD recognize that their obsessional activity is a product of their own minds.
o Patients with a psychosis with delusions of thought insertion feel these ideas, impulses or images are
being inserted from external source.
o Determine the extent of compulsions. Most patients with OCD have compulsions (behaviors intended to
reduce obsessional anxiety), but are often reluctant to discuss them. OCD patients often fear being
ridiculed or embarrassed if their compulsions are exposed.
o Ask about a history of repetitive, often ritualistic behavior such as hand washing, checking, or counting.
o Other compulsions include mental activity such as praying, or repeating specific words or numbers.
o Ask about clinical evidence of marked distress and significant impact on the patients daily performance at
home, the work place and in relationships. OCD symptoms are time consuming, and at some point
patients become aware of the excessive and unreasonable nature of their behavior.
Look for external signs of the disorder
o red, chapped hands
o severe fingernail biting
o gum lesions from excessive cleaning.
COMMENTS:
Both obsessions and compulsion are usually present in the same patient. However some have predominance of
either one.
In children and in long standing cases the absurdity of their behavior (insight) may be absent.
Obsessions and compulsion may be part of mood disorder.
Many people have only obsessive traits(punctuality, meticulous planning, etc) that doesnt create problem but
actually constructive. Those who have problematic traits may have obsessive compulsive personality disorder
Other Psychiatric Disorders

[Schizophrenia,
depression,
neuropsychiatric conditions (dementia)]
CLINICAL CLUES
Ask the patient and collaborate historians(friends, family and others) about
o Co-existing psychiatric problems, such as bizarre behavior, intense mood swings or confusion. A primary
anxiety disorder is excluded when the major psychopathology is expressed by one of these disorders.
Look for signs and symptoms with a biopsychosocial approach (In ruling out non-anxiety disorder):
o Biological (lab, physical examination, for example, to exclude cardiac origin or delirium),
o Psychological (other psychiatric disorders) or
o Social (is the patient in a jail, seeking drugs or malingering).
REFERENCE
Oxford Shorter Textbook of Psychiatry
th
Kaplan &Saddocks Synopsis of Psychiatry, 10 Edition
95
Abnormal Mood
Mood disorder, particularly depression is pervasive in all age group and clinical setting. According to WHO, depression is
currently the second most common health problem of human race and is projected to be the number one by 2020.
Unfortunately the condition is often not recognized and even when recognized not properly treated.
By obtaining an accurate history, simple clinical interview, it is possible for the physician to identify pathological sadnessthat
is associated with psychiatric or other medical causes.
CLINICAL CLUES
Ask about
o Acute/chronic pain, pulmonary diseases (for eg PTB, COAD), anaemia, neurological , metabolic disorders
and terminal illnesses in order to identify sadness caused by medical conditions(DM, Stroke, Rheumatic
heart disease)
o Presence of any overwhelming life stressor to which person is reacting.
o History of drug or substance usage. {Be aware that patients will often deny or minimize substance abuse
(alcohol and other drugs/ steroids) that will cause mood symptoms or withdrawal symptoms.}
o Pervasive sadness, (anhedonia) in which patient losses of interest in all previously pleasurable activities.
o Undue guilt, pessimism, low self esteem, decreased confidence/ indecisiveness, worthlessness,
helplessness, hopelessness, repeated death wishes, suicidal ideas/plan/ attempts
o Unexplained aches and pain
o Alteration in biological rhythm: sleep, appetite, libido
o Loss of functioning ( decreased concentration, memory, poor scholastic/ occupational / social functioning )
o Previous mood episodes (depression and mania/hypomania)
o Duration of the above mentioned signs/symptoms
Look for external signs of
o Self neglect (poor grooming, personal hygiene, weight loss/ self injury)
o Psychomotor retardation (Easy fatiquibility, slow reaction,low flow of speech etc.)
Look for presence of other pathologic/medical conditions.
INVESTIGATION
Urine (or serum) toxicology when substance abuse is suspected.

Other laboratory tests if indicated by history or physical exam indicates (serum electrolytes, metabolic profile, CBC,
blood sugar, thyroid panel, cardiac enzymes).
Mental status examination.
DIAGNOSES TO CONSIDER
Common physical illness leading to anemia, weightloss, fatigue

Many metabolic / endocrine disorder presents with mood symptoms, thyroid/ corticosteroid
anomalies(hyperthyroidism, cushing syndrome)
Common Substance ( alcohol, cannabis, opioids) dependence syndrome, can have moodsymptoms during acute
intoxication or withdrawal states.
Other psychotic illness which has mood symptoms together.
In cases of old age population, dementia (progressive deterioration of executive functions of brain). Confabulation
(typical memory deficits in which patient tend to fill in the gaps with wrong information of which patient lacks
insight. In depression ( also known as pseudodementia) patient often answer with I do not know/remember
96
COMMENTS
History should be obtained from patient and well as person living with patient. Many times depression can impair
communication ability severely. Even when able, people tend to deny psychological sign symptoms due to attached
social stigma.
Not all the features are mandatory to diagnose depression. Persistence sadness and anhedonia/ easy fatiguibility
present for 2 weeks and more points towards the presence of the disorder.The number of associated features, not
necessarily suicidality, decides the grading of severity. Presence of any psychotic feature automatically makes it
severe. The subtyping is significant in terms of management.
Depression can occur,independent of any psychosocial stressors. .In case of reactions to stress (adjustment disorder),
all the sign symptoms is assumed to disappear once the stress is removed. Grief due to bereavement is considered
normal reaction.
In depressive features resulting from physical illnesses, the patient rarely has the cognitive triad (worthlessness,
helplessness and hopelessness).
Often mood ,anxiety features, substance use problems co-exist together. Similarly, severe depression can have
psychotic features. The diagnosis based on which sign/symptom is predominant longitudinally.
Patients with previous attempts or active plan of self harm/suicide should ideally be admitted in psychiatry ward, or
cared with high level of vigilance.
Bipolar mood disorder (BPAD, alternating between depression and mania/hypomania is less common (1: 15)
compared to recurrent depressive disorder (RDD). But the identification is essential for management purpose
REFERENCES
1. International Classification of Diseases (ICD-10). WHO 1992
2. Shorter Oxford Textbook of Psychiatry. Ed 5th
ANNEX
Mania: this is just opposite of depression. The features must be present at least for 7 days or lesser if admission is required.
Hypomania is lesser degree of mania
1. Elevated/ irritable mood, keeping out of individuals circumstances

2. Over-activity
3. over talkativeness (pressure of speech: difficulty to intervene)
4. decreased need for sleep
5. disinhibitions
6. distractibility
7. inflated self esteem, boastfulness, over-optimistic, grandiosity
Dysthymia : this is a chronic low mood state with numerous periods of depressive symptoms but never meeting the
criteria for depression,more often than not during the last 2 years.
Adjustment disorder with depressed mood :numerous periods of depressive symptoms not fulfilling the criteria of
depression less often than not for past 2 years in response to a major stressor.
Cyclothymia: this is also a chronic mood disorder with numerous frequent periods of hypomanic or depressive
symptoms for last 2 years but not fulfilling the criteria of hypomania or mania or depression.
Psychotic symptoms: hallucination , delusion and disorganized behaviour .
Bipolar affective disorder: recurrent switching of hypomanic, manic or depressive episode with periods of symptom free
interval .
97
Depressed Mood
Rule out mood disorder due to

the physiologic effects of General
Medical condition or substances
(medication, drugs and toxins)
Depressive features 2weeks of Depressed mood or Loss of

in the past Greater Interest Plus Associated Symptoms**
than 2 weeks Ago Not better accounted for by
Bereavement
Numerous Periods with Numerous Periods with

Hypomanic/Depressive Symptoms Depressive Symptoms for Less
for over 2 yrs than 2yrs
Psychotic symptoms No Psychotic
present symptoms present
No prior manic or Prior Manic or

Depressed less often Than Depressed more often Hypomanic
Than not During Last 2 hypomanic No prior
DYSTHY
not During Last 2 years episode Episode Prior Manic or
CYCLOTHYMIC
MIA DS years Manic or
DEPRESSIV
Hypomanic
E Hypomanic
BIPOLAR
Episode
DISORDER Episode
DISORDER
Psychotic Psychotic WITH
Symptoms Symptoms PSYCHOTIC
In response to a Present at Not present SYMPTOM
Major Stressor BIPOLAR
other than
ADJUSTMENT Ds Not Meeting Criteria for a Time other DISORDE
UNSPECIFIED
Specific Mood Disorder SCHIZOAFFFECTIV
than during during
WITH DEPRESSED R **Assoicated
DEPRESSIVE Ds EEpisodes
DISORDER Episode
MOOD Symptoms
DEPRESIVE TYPE
Sleep
Interest
Guilt
Energy
Concentration
Appetite
Psychomotor
Suicide
Abnormal Mood Schema

98
ABNORMAL THOUGHT
Psychotic disorder
Psychosis (delusions and/or hallucinations and /or disorganization of behavior)

Rule out Psychotic Disorder due to Substance Use or a General medical condition
Prominent mood syndrome (Depression, Mania) Mood syndrome absent (or brief relative to
present for significant portion of illness duration of psychotic symptoms)
Psychotic psychotic Psychotic

symptoms symptoms not symtpoms
present limited to limited to non-
exclusively Psychotic bizarre delusions
delusions
during major symptoms also only
mood present outside
syndrome of mood Duration of
Duration
episodes illness < 1 Delusions
-MOOD illness >
month developed in
DISORDER SCHIZOAFFECTI 1month
-ACUTE & Non - the context
WITH VE DISORDER -
TRANSIENT bizarre ofclose
PSYCHOTIC SCHIZOPHRE delusions relationship
FEATURES PSYCHOTIC
NIA in one with another
DISORDER
individual person who has
- already
DELUSION established
AL similar delusion
DISORDER SHARED
PSYCHOTIC
DISORDER
When a person is no longer in contact with the reality, not able to differentiate between real and unreal world, the
condition is known as psychosis. Person with psychosis usually present with abnormal thought, -perception, -,
behavior.
False (incorrectly inferred) belief , held firmly despite proofs against contrary, and not keeping up with the
individuals socio-cultural and educational background are known as delusion.
Perception by sense organ, in absence of external stimulus is known as hallucination. For the person, the
experience is as genuine as the real one and he cannot differentiate it from the real ones. Hallucination usually
results in abnormal thinking.
Apparently goalless actions are termed disorganized behavior. Maintaining odd postures, (e.g. keeping ones hand
raised for hours, disrobing in public, playing with own excreta), usually in response to delusions and hallucinations,
are some examples.
Ask for
Total duration, onset ( whether abrupt, insidious), course ( episodic/ continuous),any precipitating / relieving
factors for the above psychotic symptoms
In case of abnormal thinking ask for the individual socio-cultural belief system.
Muttering/ talking / smiling/ crying/ gesturing to self. If hallucination in a modality is suspected, ask for such
experiences in all the other modalities. Also ask whether the experience is in internal / external space,
control, clarity, duration. Also ask for individuals reaction to such experiences.
Symptoms of delirium (disorientation with time , place and person)
Altered level of consciousness : seizure attacks, head injury, CVA etc
Substance use, prescribed or non-prescribed medication particularly in elderly.
Any acute/chronic medical illness
Previous mental illness, family history, treatment
Fever
Children- with high fever
Elderly- acuteconfusional state with some psychotic symptoms
Beware of Infection (sometimes without fever) eg urinary tract infection, chest infection.
99
Look for
Hallucinatory behavior: muttering / smiling/ gesturing to self
In case of suspected delusions, degree of conviction, acting on, look for content that are culturally
inappropriate and completely impossible (bizarre)
Indicators of substance use: multiple IV injection marks, inflammation, abscess/ scars, Signs of
intoxication, withdrawal etc
Catatonic behavior, such as mutism, posturing, waxy flexibility, excitement,etc
Impact of psychotic symptoms, decreased socio-occupational functioning, poor self care etc.
Threat for self or others
Investigations
Complete blood count, blood sugar, serum electrolyte, serum calcium,Liver Function Test, Thyroid
Function Test, oxygen saturations to r/o medical conditions
EEG to r/o seizure disorder
CT/MRI head to r/o head injury, Intracranial space occupying lesion, Cerebrovascular accident,
degenerative illness etc
Urine test for screening drugs/ substance of abuse
Substance use disorder: acute intoxication, withdrawal state, substance induced psychotic disorder
Head injury, seizure disorder, all physical condition that can lead to altered consciousness/ delirium
Personality disorder, particularly borderline personality which can have flitting psychotic signs/symptoms
for a brief period of time.
Comments
Psychotic symptoms may be due to physical illnesses or substance use disorder. Auditory Hallucination,
particularly third person, or running commentary arepathognomic to schizophrenia. Hallucinations in
other modalities , altered consciousness, impaired intellectual capacity usually indicate more towards
organicity.
Substance e induced Psychotic symptoms usually disappear spontaneously after 4weeks of complete
abstinence
Apparent threat to self or the society warrants inpatient treatment
Psychiatric diagnosis is primarily based on careful history taking and clinical examination (mental state)
.the investigations are basically to rule out physical illnesses and sometimes for monitoring the side
effects of the psychotropic medications.
100
Psychotic disorder with prominent mood syndrome
Psychotic disorder

Prominent mood syndrome (Depression, Mania)

present for significant portion of illness
Psychotic symptoms present exclusively Psychotic symptoms also present outside

during major mood syndrome of mood episodes
-MOOD DISORDER WITH PSYCHOTIC FEATURES SCHIZOAFFECTIVE DISORDER
Clinical Clues
Ask for
Persistent abnormal mood: persistent sadness for more than 2 weeks; or elevated or irritable mood for 1
week.
Ask for associated symptoms of depression:
o Anhedonia, easy fatigability, pessimism, guilt, worthlessness, helplessness, hopelessness, death-
wishes, suicidal plans, attempts, disturbance of bio-rhythms
Associated symptoms of mania:
o Increased energy and activity, talkativeness, over familiarity,sociability, boastfulness, grandiose/
foolish plans whose risk the person does not realize,
Presence and absence of psychotic symptoms during mood syndrome
Previous episodes of mania/ depression
Look for
Abnormal mood, associated signs of depression/ mania
Investigations:
As mentioned previously to r/o physical illness/ substance use disorder
Psychometric tests (Eg. Rorschachs test, Thematic apperception test , etc) when history and mental state
examination cannot decide
101
Psychotic disorder without mood syndrome
Psychotic disorder

Mood syndrome absent (or brief relative to duration

of psychotic symptoms)
psychotic symptoms not limited

to delusions
Duration of illness < 1 months Duration illness > 1month

-ACUTE & TRANSIENT PSYCHOTIC DISORDER -SCHIZOPHRENIA
Clinical Clues:
Ask for
Total duration of psychotic symptoms present (less or more than a month)
Prodromal phase: loss of interest in work, social activities, and personal appearance and hygiene, together
with generalized anxiety and mild degrees of depression and preoccupation, preceded the onset of psychotic
symptoms by weeks or even months
Hearing of owns thought being spoken aloud ( Thought echo), someones thought forcefully intruding the
mind(thought insertion/alienation), thought being forcefully taken away by external force ( withdrawal), ones
thought being known to others without one expressing it by any means ( thought broadcasting/ diffusion)
Breaks in interpolation in the train of thought ( thought block), incoherent or irrelevant speech (in response to
questions asked, even after properly understanding), neologism( creation of completely new word or word
with personalized meaning)
Delusions of control, influence, passivity, delusional perception
Negative symptoms such as marked apathy, paucity of speech, blunting or incongruity of emotional responses,
social withdrawal
Look for
Thought echo, thought insertion/ withdrawal, broadcasting
Breaks in interpolation in the train of thought ( thought block), incoherent or irrelevant speech, neologism(
complete new word or word with personalized meaning)
Delusions of control, influence, passivity, delusional perception
Negative symptoms such as marked apathy, paucity of speech, blunting or incongruity of emotional responses,
social withdrawal.
Investigations
As mentioned previously to r/o physical illness/ substance use disorder
Psychometric tests ( foreg. Rorschachs test, Thematic apperception test , etc) when history and mental state
examination cannot decide
Comment
Acute and transient psychotic disorder usually onset abruptly, i.e. the full blown clinical picture appears within
24 hours and disappear within a month, with / without treatment
Onset of Schizophrenia is difficult to establish exactly and usually preceded by subtle changes in mood and
behavior and habits, known as prodrome.
102
SUBSTANCE USE DISORDERS
SUBSTANCE
USE
DISORDERS
Substance-
Substance
Substance Induced
Harmful Use/
Dependence Psychiatric
Abuse
Disorders
During During
Alcohol others Intoxication Withdrawal
The word substance actually mean psycho-active substance and is preferred to the word drug, because drug
implies a manufactured chemical, meant to cure, prevent or diagnose disease.Many psycho-active substances
occur naturally (like opium) or are not meant for human consumption (like glue and gasoline). The word narcotics
mean illegal substances.Depending on mechanism of action, substances can also be classified as CNS stimulants
or depressants
The life time prevalence of substance use disorders (SUDs) is very high, although exact epidemiological data of
Nepal is unavailable, one can imply that the problem is not less, rather more than the worldwide prevalence of
around 20%. It is one of top 10 causes of global health burden and prime cause of youth mortality by road traffic
accidents.Co morbid psychiatric disorders like mood disorder, anxiety disorders antisocial personality disorder, are
common. In Nepal, alcohol is the number one problematic substance of abuse.
Substance dependence is a collection of features like tolerance, withdrawal, craving,loss of control over amount,
time of use; significant amount of time spent obtaining substance and neglect of other important activities over a
12-month period.
Substance abuse/ harmful use signifies failure to fulfill major role obligations, hazardous activities duringsubstance
use, substance-related legal problems, or continued use despite social problems during a 12-month period that
does not include tolerance, withdrawal or compulsive use.
Substance Intoxication is a reversible syndrome caused by recent exposure to a substance and often concurrently
diagnosed, with substance abuse or dependence. This category does not apply to nicotine.
Substance withdrawalis a behavioral, physiological, and cognitive state by the cessation of, or reduction in, heavy
and prolonged substance use. Craving is a part of the withdrawal syndrome. Withdrawal can also by triggered by
concomitant use of antagonists
Terms like addict, addictionis better avoided due to its ambiguity and derogatory connotation.
103
Clinical clues
Ask about
(history may be unreliable; often patient deny/ minimize the use. Sometimes he/she may not be in a
position to communicate properly due to ongoing medicalcondition or legal situations. Any effort to
establish therapeutic alliance and rapport is always worthwhile. Respect privacy and ensure
confidentiality). If possible, obtain collateral information from family, friends, neighbors, primary care
physicians, social workers, police etc.
o Duration, onset, access to substances, dosage and frequency of use of substances, reasons for
switching substances,
o Current pattern of use in previous month, minimum and maximum daily dosage, the average
daily expense, the last dosages.
o Relevant physical, psychological, social, legal, financial complications
o Symptoms of tolerance
o Features of withdraw leg. Tremor, nausea , vomiting, craving
o Reason for seeking medical treatment, motivation to quit, abstinence attempts
o Pattern of substance use like sharing needles, exchanging sex for substance, individual risk taking
strategies, etc.
o Previous use of naltrexone, disulfiram, methoadone, buprenorphine.
o Complete medical history for comorbidities like liver problems, heart problems, etc.
o Occupational dysfunctions (acts of violence self and towards others), with and without
substance use
Look for
o Possession of non-prescribed pills, bottles
o Watch for co-existing psychiatric disorders
o Neglect in self care, personal hygiene and nutritional status
o Injury marks, Needle tracks/scars, cigarette burns, nicotine stains abscess, fasciitis etc
o Heart murmur especially tricuspid regurgitation due to its association with IV drug use
o Tell-tale signs of intoxication / withdrawal of individual substances
Tachycardia/bradycradia, hypertension/hypotension, dyspnoea, Miosis/ mydriasis, eye
congestion, skin flushing, hyperthermia/hypothermia (core temperature)
Altered mental status: cns stimulation/ depression; delirium ,disorganized behavior/ psychotic
experiences.
Investigation
ECG
Breathalyzer or blood alcohol concentration (if available)
Urine toxicology screening (if available)
EEG if indicated(if LOC/seizure attacks)
Head CT scan or MRI, if needed to rule out traumatic injury or stroke
Complete blood count (CBC) ( to reveal macrocytosis and anemia)
Complete metabolic profile ,including serum electrolytes, blood sugar
Serum calcium, magnesium, vitamin B12 and thiamine level
Thyroid stimulating hormone (TSH), creatine kinase (CK)
Hepatitis(HBsAg,HCV), HIV status in case of IV drug users
LFT with INR to assess degree of liver damage in alcoholics
Mental status exam
Diagnoses to consider
Substance intoxication/ Potentially lethal poisoning
Substance withdrawal
Delirium secondary to medical condition
Dementia
Comments
IV access should be obtained and airway should be assessed. Intubation should be considered if the
patients ability to protect airway and avoid aspiration is questionable. Advanced cardiac life support
measures are provided as required
If lethal intoxication is suspected, respective antidote is to be administered
If patient is agitated, excited, prone to injury to self or others physical or chemical restraint should be
considered
104
SUBSTANCE USE
DISORDERS
Harmful Subs. induced

Dependence Use/Abuse Disorder
Alcohol Other
substances
After the initial management, SUDs should be categorized as substance dependence, or substance abuse / harmful
use.
Clinical clues
Ask about
o CAGE questionnaire for screening of alcohol dependence
Have you ever felt the need to Cut down on your drinking?
Have you ever felt Annoyed by criticism of your drinking?
Have you ever felt Guilty about drinking?
Have you ever had to take a morning Eye opener?
o If definite yes in any one question , evaluate all the features of dependence
o Familyhistory of alcohol dependence or other substance dependence
o Social / occupational /Financial problems
o Legalproblems like traffic tickets for driving under influence; charges of theft, quarrel, public nuisance
o Medical complications : gastritis, hemetemesis, malena, peripheral neuropathy, bleeding tendencies,
decreased libido, seizure attacks, ataxia
o Psychiatric complications: memory lapses, abnormal sensations, hallucinations, delusions. disorientation
Look for
o Signs of chronic malnutrition like anemia, wasting, edema, etc.
o Signs withdrawal
o Signs of liver disease like ascites, spider telengiectasia, palmar erythema, gynecomastia, jugular venous
dilatation, edema, etc.
o Psychosis, memory problem or dementia, confabulation
o Signs of encephalopathy like confusion/ disorientation, agitation
o Nystagmus, ataxia
o Seizures, tremors, weakness
o Skin hyperpigmentation (pellagra)
o Mental status examination
Investigation
Repeat ECG
EEG, if needed
Liver function tests (LFTs) (include aspartate aminotransferase and gamma glutamyltransferase)
USG abdomen
Hepatitis B, Hepatitis C and HIV testing, if not done already.
Comments
If withdrawal symptoms present , watch for possibility of withdrawal seizures
Keep in mind the possibility of polysubstance abuse
Alcohol dependence
Other substance dependence like cocaine, heroin, cannabis, amphetamine, benzodiazepine, LSD, PCP,
nicotine
Stroke
Seizure disorder
Chronic hypoglycemia
Dyselectrolytemia
105
SUBSTANCE
DEPENDENCE
Other
Alcohol
Substances
Wernickes Korsakoffs
encephalopathy psychosis
If the diagnosis is alcohol dependence, Wernicke's encephalopathy and Korsakoffs psychosis should be ruled out.
Clinical clues
Ask about
o Alcohol intake, how long, how much, what is the maximum amount of alcohol drink, etc.
o Use of other substances
o Withdrawal symptoms
o Previous detoxifications and rehabilitations including previous h/o seizures during withdrawal
Look for
o Ophthalmoplegia and nystagmus
o Gait for ataxia
o Confusion
o Recent memory deficits
Investigation
random blood level(RBS), serum electrolytes(Na,Ca, k)
Thiamine level
Vitamin B12 level
Magnesium level
Folic acid level
CT/MRI brain, if needed to rule out organic brain injury
Comments
Wernicke-Korsakoff syndrome is the classical name for alcohol induced persisting amnestic disorder.
Wernickes encephalopathy is a triad of reversible acute symptoms namely ataxia, confusion,
ophthalmoplegia.
Korsakoffs syndrome is a chronic mainly irreversible condition. Diagnostic features include recent
memory deficit, and anterograde amnesia in an alert and responsive patient. 80% cases are irreversible.
The neuropathological lesions are symmetrical and paraventricular, involoving the mammillary bodies, the
thalamus, hypothalamus, midbrain, pons, medulla, fornix and cerebellum.
In early stages Wernickes encephalopathy responds to large doses of parenteral thiamine 100mg PO 2-3
times daily for 1-2 weeks. Thiamine should be continued 100mg PO daily for 3-12 months
Keep in mind the possibility of polysubstance abuse
Watch for co-existing psychiatric disorders
Alcohol dependence
Stroke
Acute psychosis
Traumatic brain injury/subdural haematoma
106
SUBSTANCE
ABUSE
Other
Alcohol
Substances
Depressants Stimulants Miscellaneous
Nicotine and caffeine remain the most common substances abused worldwide. Marijuana is also commonly
abused substances in Nepal due to easy availability and low cost. Opiates is also common among youth, its smoke
is chased or liquid preparations injected. Cocaine ,amphetamines, LSD are not very common but are slowly gaining
popular among the affluent societies. Non prescribed / prescribed benzodiazepines are abused in the oral tablet
form or injection. Use of inhalants is common in early teenagers and street children.
Clinical clues
Ask about
o Drug intake, how long, how much, what is the maximum amount of used, in how much time,
etc.
o Procurement methods without specific details to rule out risk taking behaviors like sharing
needles and exchanging sex for drugs
o Previous withdrawal/intoxication symptoms and how the response to treatment
o Previous detoxifications and rehabilitations
Look for
o Injury marks, scars, stains burns etc
o Monitor vital signs for signs of tachycardia/bradycardia, hypotesion/hypertension
o Sweating
o Pupil size-
-mydriasis s/o cocaine ,other stimulant
-miosis s/o opiates
o Spymptoms of stimulant drug use eg insomnia, aggression, hyperalert

o Psychotic symptoms eg visual or auditory hallucination
o Symptoms s/o depressant drug use eg drowsiness, lethargy, constipation
o Opthalmoplegia and nystagmus
o Gait for ataxia
o Confusion
o Recent memory deficits
Investigation
CBC, metabolic profile, urine analysis, urine toxicology screen, LFTs, RFT, HIV, Hep B and Hep C,VDRL,
breathalyzer, vitamin B12 level,magnesium level,folic acid level (if not already done)
107
Comments
Bhang, ganja, charas, hashish are different forms of Cannabis or Marijuana.
Cannabis is associated with amotivational syndrome (chronic use leads to laziness and lack of
motivation), time distortion, and munchies (binge eating during intoxication).
Cannabis is not associated with physical withdrawal symptoms although psychological cravings are
reported. Overdoses are usually not life threatening.
Cocaine is a stimulant drug causing insomnia, tachycardia, mydriasis, hypertension, sweating,
hyperalertness, aggressiveness, delirium, psychosisin the form of intense paranoia, formications
(patient thinks that bugs are crawling under or over the skin).
Overdoses can be fatal due to arrhythmia, heart attack, seizure or stroke. Withdrawal, patients become
sleepy and hungry while in intoxication they have anorexia. After the initial stimulation there is possible
severe depression. Withdrawal is not dangerous, but the psychological cravings are intense.
Amphetamines are stimulants. They have similar affects as cocaine, however, its use is associated with
more classic psychotic symptoms (patients may appear to be full-blown schizophrenics).
Opioids include heroin and related agents.
Opioids cause euphoria, analgesia, drowsiness, miosis, constipation, and CNS/respiratory depression.
Opioids overdose can be fatal because of respiratory depression. Antidote of opioids overdose is
naloxone.
Heroin abuse is associated with medical comorbidities because of IV use. Common are endocarditis
(especially tricuspid valve), HIV, Hep C and Hep B, cellulitis etc.
Opioid withdrawal is not life threatening, however, patients believe that they are going to die due to the
associated symptoms of gooseflesh, diarrhea, insomnia, muscle cramping or pain.
Methadone, buprenorphine, naltrexone and levo-alpha acetyl methadol (LAAM) are used for step-wise
detoxification and maintenance protocol for opioids dependence.
Lysergic acid diethylamide (LSD/Mushrooms) cause visual hallucinations (as opposed to auditory in
schizophrenia), mydriasis, tachycardia, diaphoresis, and perception and mood disturbances. Overdose is
not life threatening and there is no withdrawal symptoms. Brief feeling of being on the drug again, even
though none was taken may occur months to years later and are termed as Flashbacks. Bad trip is the
acute panic reaction or dysphoria associated with LSD and similar to cannabis acute reaction. Treatment
requires reassurance and/or benzodiazepine/antipsychotic agents, if true psychotic symptoms are
produced.
Inhalants (gasoline, glue, varnish remover, correction fluid and paint) cause euphoria, dizziness, slurred
speech, a feeling of floating, ataxia, and/or a sense of heightened power. Inhalant use is usually seen in
younger teenagers and street children
Inhalant overdose can be fatal (respiratory depression, cardiac arrhythmias, asphyxiation) or cause
permanent sequelae (nervous system, liver, or kidney toxicity, peripheral neuropathy).
Inhalants withdrawal syndrome may occur beginning 24-48 hours after cessation of use and can last up to
5 days with symptoms including sleep disturbances, tremors, irritability, diaphoresis, nausea, and fleeting
illusions.
Benzodiazepine/barbiturates cause sedation and drowsiness as well as reduced anxiety and disinhibition.
Overdose can be fatal due to respiratory depression. Antidote is flumazenil.
Withdrawal can be fatal because ofseizures and/or cardiovascular collapse. Treatment is inpatient basis
with benzodiazepines, and gradual taper the dose over several days to weeks.
Benzodiazepines and barbiturates are dangerous when mixed with alcohol due there CNS depressant
properties.
Caffeine, a methylxanthine, is more potent than theophylline. Excess of 250mg use may cause mild
intoxication symptoms like irritability and insomnia, while 1 gram may lead to seizures, coma and death.
Alcohol abuse/intoxication or withdrawal
Specific substance abuse/intoxication or withdrawal
Acute psychosis
Anxiety disorder/Panic disorder
Cardiac ischemia/arrhythmia
Adult respiratory distress syndrome
Substance Induced Psychiatric Disorder

Substance-Induced Psychiatric Disorders
108
Substance-Induced
Psychiatric
Disorders
During During
Intoxication Withdrawal
Substance use disorder and psychiatric disorder forms a vicious circle begets the another condition.
Problematic use of sunbstances induce all sorts of pyschiatric conditions. Alcohol induced organic condition(for
eg encephalopathy), psychosis, mood and anxiety dcisoderarequitecommon.cannabisindeiuced psychosis are
also common.
Clinical cues:
Ask for
Precedence of substance or psychiatric symptoms.

Relationship of substance intake and emergence/ disappearance of psychiatric symptoms
Prolong abstenance and its effects on psychiatric symptoms
Look for
Established signs/symptoms of induced psychiatric conditions of particular substance use
Invvestigations
CBC, metabolic profile, urine analysis, urine toxicology screen, LFTs, RFT, HIV, Hep B and Hep C,VDRL,
breathalyzer, vitamin B12 level,magnesium level,folic acid level (if not already done)
Comments
The sign/ symptoms of induced psychiatric conditions usually disappear spontaneously after 4 weeks of
complete absteinance .
Reference
Sadock, BJ, Sadock, VA. Kaplan and Sadocks concise textbook of clinical psychiatry: substance-related
disorders. Lippincott and Williams & Wilkins, Philadelphia
109

Minor CP-Final (Print) - Less Anesthesia

Caricato da

Informazioni sul documento

Titolo originale

Copyright

Formati disponibili

Condividi questo documento

Condividi o incorpora il documento

Opzioni di condivisione

Hai trovato utile questo documento?

Questo contenuto è inappropriato?

Copyright:

Formati disponibili

Minor CP-Final (Print) - Less Anesthesia

Caricato da

Copyright:

Formati disponibili

PAHS MBBS CPs- Jr.

Clerkship (2nd Rotation)

Mouth Sore and Ulcers

Acute (up to Chronic (>

Acute Stomatitis : An acute inflammation of the mucous membrane of the mouth.

Acute necrotizing ulcerative gingivitis (ANUG):(Trench Mouth; Vincent's Stomatitis)

Acute mouth ulcers

Trauma Burn Drugs

Diagnoses to consider in Acute mouth ulcers:

Bacterial: acute necrotizing ulcerative gingivitis, primary chancre of syphilis

Investigation: As indicated by clinical history and examination

These are common and important

Certain conditions are said to be pre-malignant and need to be monitored if found:

Non ulcerative causes of oral soreness:

Orofacial Swelling and Pain

Swelling without Pain without

Oral tumour Trauma Tooth sensitivity

Salivary gland Facial pain /

Swelling without pain

Oral tumour Salivary gland tumour Cyst

Malignant Benign Malignant

ODONTOGENIC TUMORS OF THE JAWS

ADENOMATOID ODONTOGENIC TUMOR (AOT)

ODONTOMA: COMPOUND AND COMPLEX TYPES

MYXOMA (ODONTOGENIC MYXOMA)

NON ODONTOGENIC BENIGN TUMORS

NONODONTOGENIC BENIGN TUMORS OF THE JAWS

NON ODONTOGENIC MALIGNANT TUMORS

Salivary gland Cyst of oral

Major glands Minor

Parotid Submandibular Sublingual

Lymphangioma (cystic hygroma)

Developmental cysts Inflammatory cysts

Odontogenic cysts Follicular cyst Radicular cyst:

Non-odontogenic cysts Cyst of the nasopalatine duct

Dental Lamina Cyst (Gingival Cyst of Newborn)

Traumatic Bone Cyst

Mucus Retention Cyst

Swelling with Pain

Viral Bacterial Fungal

The main symptoms of gingivitis are:

Symptoms early on resemble gingivitis. Later, get : loose teeth in addition.

Tooth Facial pain & Temperomand

e.g. Dental Chronic

Temperomandibular joint (TMJ) disorders

Chronic idiopathic/atypical facial pain.

Hypopigmentaion Depigmentation Hyperpigmentation

Dark brown Light brown,

Oval, scaly Appear after No change after Melasma

Hyperpigmentation is usually caused by:

Hyperpigmentation in systemic disorders:

Drug induced hyperpigmentation:

Acquired Papulosqua- Tuberculoid

Hypo- Prior inflammatory Post inflammatory

Generalized Congenital Albinism

Hypopigmentation usually results from

Depigmentation: Diagnosis to consider

DISORDERS OF HAIR AND NAIL

Alopecia Increased Hair shaft

Non- Cicatricial Hypertrichosis

Scaly Non-scaly Recent Gradual

Tinea Alopecia All over

Types of hair in human: