MPMSU ENT 2022 question paper with answers

1. NON-NEOPLASTIC / INFLAMMATORY LESIONS

A. Nasal Polyps

Ethmoidal (Allergic/Inflammatory) Polyps
Usually bilateral, pale, edematous. Associated with allergy, asthma, aspirin sensitivity (Samter’s triad). Arise from ethmoidal labyrinth. Present with nasal obstruction, anosmia, postnasal drip.

Antrochoanal Polyp
Arises from maxillary sinus → through ostium → nose → choana. Unilateral, occurs in children and young adults. Presents with unilateral obstruction, nasal discharge, snoring.

B. Fungal Masses

Allergic Fungal Rhinosinusitis (AFRS)
Nasal polyposis with thick “allergic mucin.” Common in atopic young adults.

Fungal Ball / Mycetoma
Usually in maxillary sinus. Caused commonly by Aspergillus. Appears as hyperdense mass on CT.

Invasive Fungal Disease
Seen in diabetics/immunocompromised; rapidly progressive with tissue necrosis.

C. Granulomatous Diseases

Wegener’s granulomatosis (GPA): crusting, friable tissue, saddle-nose deformity.
Sarcoidosis: strawberry-like mucosa.
Rhinoscleroma (Klebsiella rhinoscleromatis): woody induration, midline granuloma.
Rhinosporidiosis: reddish, polypoid mass that bleeds easily.

D. Mucoceles

Usually frontal/ethmoid sinus. Slowly expanding; may erode bone and extend into nose or orbit.

2. BENIGN TUMORS OF THE NASAL CAVITY

A. Inverted Papilloma

Locally aggressive; arises from lateral nasal wall. Unilateral. Risk of malignant transformation (~10%). CT shows bony remodeling; MRI shows “convoluted cerebriform pattern.”

B. Vascular Tumors

Juvenile Nasopharyngeal Angiofibroma (JNA)
Occurs in adolescent males. Recurrent epistaxis + nasal obstruction. Highly vascular; arises from sphenopalatine region. Biopsy contraindicated.

Hemangioma
Capillary or cavernous; causes epistaxis.

C. Osseous & Cartilaginous Tumors

Osteoma (usually frontal sinus), chondroma, osteochondroma.

D. Neural Tumors

Schwannoma, neurofibroma.

E. Miscellaneous Benign Tumors

Fibroma, lipoma, angioleiomyoma.

3. MALIGNANT TUMORS OF NASAL CAVITY / PARANASAL SINUSES

A. Squamous Cell Carcinoma (SCC)

Most common sinonasal malignancy. Arises from lateral nasal wall or maxillary sinus. Presents with unilateral obstruction, epistaxis, facial pain, cheek swelling, orbital symptoms.

B. Adenocarcinoma

Common in woodworkers and leather workers. Often arises in ethmoidal sinus.

C. Adenoid Cystic Carcinoma

Perineural spread; slow-growing but aggressive.

D. Olfactory Neuroblastoma (Esthesioneuroblastoma)

Arises from olfactory neuroepithelium in cribriform plate. Presents with anosmia + mass ± epistaxis.

E. Lymphoma

Often NK/T-cell type; destructive midline lesions.

F. Rhabdomyosarcoma

Seen in children; rapidly growing.

G. Melanoma

May be pigmented or amelanotic.

H. Sinonasal Undifferentiated Carcinoma (SNUC)

Highly aggressive; fast growth; poor prognosis.

4. CONGENITAL LESIONS

A. Dermoid and Epidermoid Cysts

Midline masses; may have sinus tract.

B. Nasal Glioma

Firm, non-compressible, non-pulsatile; glial tissue without intracranial communication.

C. Encephalocele / Meningoencephalocele

Mass increases with crying (Furstenberg sign). Pulsatile, compressible. **Biopsy contraindicated.**

D. Choanal Atresia

Bilateral causes cyclic cyanosis relieved by crying; unilateral presents later.

5. SYSTEMIC / MISCELLANEOUS CONDITIONS

A. Hematologic Disorders

Leukemic infiltrates, plasmacytoma.

B. Autoimmune / Vasculitic

Midline granuloma (GPA).

C. Metastatic Lesions

Kidney, lung, thyroid (rare).

APPROACH TO A NASAL MASS

History

Duration, progression, unilateral/bilateral symptoms. Epistaxis, obstruction, anosmia. Occupational exposures (wood/leather dust). Allergy, asthma, aspirin sensitivity. Immunocompromised states.

Examination

Anterior & posterior rhinoscopy; endoscopic evaluation. Assess color, surface, bleeding tendency, attachment.

Imaging

CT PNS for bony details. MRI for soft tissue, intracranial/orbital extension.

Biopsy

Indicated except in: • JNA • Encephalocele • Highly vascular masses • Suspected intracranial communication

Management

Based on diagnosis: • Medical therapy for inflammatory causes • Endoscopic excision for benign tumors • Multimodal therapy for malignancies

TUBOTYMPANIC CSOM

AETIOLOGY

The disease starts in childhood and is therefore common in that age group.

1. It is the sequela of acute otitis media usually following exanthematous fever and leaving behind a large central perforation.

2. Ascending infections via the eustachian tube. Infection from tonsils, adenoids and infected sinuses may be responsible for persistent or recurring otorrhoea. Ascending infection occurs more easily in the presence of infection.

3. Persistent mucoid otorrhoea is sometimes the result of allergy to ingestants such as milk, eggs, fish, etc.

PATHOLOGY

The tubotympanic disease remains localized to the mucosa, mostly in the anteroinferior part of the middle ear cleft. Healing and destruction occur simultaneously, depending on organism virulence and patient resistance, so acute exacerbations are common.

The pathological changes are:

1. Perforation of Pars Tensa. A central perforation of varying size and position.

2. Middle Ear Mucosa. Normal in quiescent stage; oedematous and velvety when active.

3. Polyp. Smooth, oedematous mass protruding through perforation; pale in color compared to atticoantral disease polyps.

4. Ossicular Chain. Usually intact and mobile but may show necrosis, commonly of the long process of incus.

5. Tympanosclerosis. Hyalinization and calcification of subepithelial connective tissue. Appears as white chalky deposits on promontory, ossicles, tendons, windows. May cause conductive deafness.

6. Fibrosis and Adhesions. Result of healing, may impair ossicular mobility or block eustachian tube.

BACTERIOLOGY

Pus cultures in CSOM commonly show multiple organisms.

Aerobes: Pseudomonas aeruginosa, Proteus, Escherichia coli, Staphylococcus aureus.

Anaerobes: Bacteroides fragilis, anaerobic Streptococci.

CLINICAL FEATURES

1. Ear Discharge. Nonoffensive, mucoid or mucopurulent, constant or intermittent. Usually appears during URTI or after water entry into ear.

2. Hearing Loss. Conductive type; usually < 50 dB. Sometimes hearing is paradoxically better during discharge due to “round window shielding effect.” Long-standing cases may develop mixed loss due to toxin absorption by cochlea.

3. Perforation. Always central—may be anterior, posterior or inferior to malleus; may range from small to subtotal.

4. Middle Ear Mucosa. Seen when perforation is large; pale pink normally; red, swollen and oedematous when inflamed. Polyp may be seen.

ASSESSMENT

1. Examination Under Microscope. Essential to look for granulations, ingrowth of squamous epithelium, ossicular status, tympanosclerosis, adhesions. Hidden discharge may be detected. Rarely cholesteatoma may coexist.

2. Audiogram. Assesses type and degree of loss—usually conductive but may show a sensorineural component.

3. Culture and Sensitivity. Helps choose appropriate antibiotic ear drops.

4. Mastoid X-rays / CT Temporal Bone. Mastoid usually sclerotic or may show clouded cells; no bone destruction (features of atticoantral disease).

TREATMENT

The aim is to control infection, eliminate discharge, and later restore hearing.

1. Aural Toilet

Remove discharge and debris by dry mopping, suction under microscope, or irrigation with saline (not forceful syringing). Ear must be dried afterward.

2. Ear Drops

Antibiotic drops containing neomycin, polymyxin, chloromycetin or gentamicin, usually combined with steroids. Patient lies with ear up; drops instilled and tragus pressed intermittently for entry into middle ear.

1.5% acetic acid useful for pseudomonas.

Care: risk of maceration, local allergy, fungal growth, resistance, and possible ototoxicity.

3. Systemic Antibiotics

Useful in acute exacerbations. Otherwise limited role.

4. Precautions

Keep water out of the ear (bathing, swimming). Avoid hard nose blowing.

5. Treatment of Contributory Causes

Treat infections of tonsils, adenoids, sinuses and nasal allergy.

6. Surgical Treatment

Remove aural polyp or granulations before starting topical treatment. **Never avulse** a polyp—it may arise from stapes, facial nerve, or horizontal canal.

7. Reconstructive Surgery

Once ear is dry, myringoplasty with or without ossicular reconstruction can be performed to restore hearing and prevent recurrent infection.

Scattered throughout the pharynx in its subepithelial layer is the lymphoid tissue which is aggregated at places to form masses, collectively called Waldeyer’s ring. The masses are:

1. Nasopharyngeal tonsil or the adenoids
2. Palatine tonsils or simply the tonsils
3. Lingual tonsil
4. Tubal tonsils (in fossa of Rosenmüller)
5. Lateral pharyngeal bands
6. Nodules (in posterior pharyngeal wall)

Paracusis Willisii. An otosclerotic patient hears better in noisy than in quiet surroundings. This is because a normal person will raise his voice in noisy surroundings.

Nose & Smell

Loss of smell (anosmia) – sudden and often without nasal congestion; one of the most distinctive early COVID signs.

Loss or change in taste (ageusia/dysgeusia).

Nasal congestion or runny nose – can mimic a cold.

Throat

Sore throat – common with newer variants.

Dry throat / scratchiness – often early.

Cough – usually dry; may progress.

Ear

Ear fullness or pressure – from Eustachian tube inflammation.

Tinnitus – ringing in the ears (less common, but reported).

Hearing changes – rare, but possible in acute infection.

CLINICAL FEATURES

Age and sex. Disease is commonly seen in the age group of 35–60 years. Males are affected more than females. Usually, disease is unilateral but the other ear may be affected after a few years.

Cardinal symptoms of Ménière’s disease are (i) episodic vertigo, (ii) fluctuating hearing loss, (iii) tinnitus and (iv) sense of fullness or pressure in the involved ear.

1. Vertigo

It comes in attacks. The onset is sudden. Patient gets a feeling of rotation of himself or his environment. Sometimes, there is feeling of “to and fro” or “up and down” movement. Attacks come in clusters, with periods of spontaneous remission lasting for weeks, months or years.

Usually, an attack is accompanied by nausea and vomiting with ataxia and nystagmus. Severe attacks may be accompanied by other symptoms of vagal disturbances such as abdominal cramps, diarrhoea, cold sweats, pallor and bradycardia.

Usually, there is no warning symptom of an oncoming attack of vertigo but sometimes the patient may feel a sense of fullness in the ear, change in character of tinnitus or discomfort in the ear which herald an attack.

Some cases show Tullio phenomenon: loud sounds or noise produce vertigo due to the distended saccule lying against the stapes footplate. This phenomenon is also seen when there are three functioning windows in the ear.

2. Hearing Loss

It usually accompanies vertigo or may precede it. Hearing improves after the attack and may be normal during the periods of remission. This fluctuating nature is characteristic. With recurrent attacks, improvement becomes incomplete and permanent progressive deterioration occurs.

Distortion of sound. A tone may appear normal in one ear and of higher pitch in the other (diplacusis). Music appears discordant.

Intolerance to loud sounds. Patients cannot tolerate amplification due to recruitment phenomenon. They are poor candidates for hearing aids.

3. Tinnitus

It is low-pitched roaring type and aggravated during acute attacks. Sometimes hissing. It may persist during remission. Change in intensity or pitch may warn of an attack.

4. Sense of Fullness or Pressure

It fluctuates and may accompany or precede an attack of vertigo.

5. Other Features

Patients often show signs of emotional upset due to apprehension of repeated attacks. Earlier, emotional stress was considered the cause.

Vocal Nodules (Singer’s or Screamer’s Nodes)

They appear symmetrically on the free edge of the vocal cord, at the junction of anterior one-third with the posterior two-thirds, as this is the area of maximum vibration and trauma. Their size varies from pin-head to half a pea.

They result from vocal trauma when a person speaks in unnatural low tones for prolonged periods or at high intensities. Common in teachers, actors, vendors, pop singers and in assertive, talkative school children.

Pathology

Vocal abuse or misuse leads to oedema and haemorrhage in the submucosal space. This undergoes hyalinization and fibrosis. The overlying epithelium undergoes hyperplasia, forming a nodule.

Early nodules are soft, reddish and oedematous; later they become greyish or white.

Clinical Features

Patients complain of hoarseness. Vocal fatigue and neck pain on prolonged phonation are also common.

Treatment

Early cases are treated conservatively by educating the patient in proper voice use. Many nodules in children disappear completely.

Surgery is required for large nodules or long-standing nodules in adults. They are excised under an operating microscope using cold instruments or laser, avoiding trauma to the vocal ligament.

Speech therapy and re-education in voice production are essential to prevent recurrence.

PREOESOPHAGEAL CAUSES

1. Oral Phase

Food must be masticated, lubricated with saliva, formed into a bolus, and pushed into the pharynx. Disturbances cause dysphagia.

(a) Disturbance in mastication
Trismus, mandibular fractures, tumours of jaws, temporomandibular joint disorders.

(b) Disturbance in lubrication
Xerostomia after radiotherapy, Mikulicz’s disease, Sjögren’s disease.

(c) Disturbance in tongue mobility
Paralysis of tongue, painful ulcers, tongue tumours, lingual abscess, total glossectomy.

(d) Defects of palate
Cleft palate, oronasal fistula.

(e) Lesions of buccal cavity and floor of mouth
Stomatitis, ulcerative lesions, Ludwig’s angina.

2. Pharyngeal Phase

Food must enter the pharynx and be directed into the oesophagus while unwanted passages close.

(a) Obstructive lesions
Tumours of tonsil, soft palate, pharynx, base of tongue, supraglottic larynx; hypertrophic tonsils.

(b) Inflammatory conditions
Acute tonsillitis, peritonsillar abscess, retropharyngeal/parapharyngeal abscess, acute epiglottitis, oedema of larynx.

(c) Spasmodic conditions
Tetanus, rabies.

(d) Paralytic conditions
• Soft palate paralysis (diphtheria, bulbar palsy, cerebrovascular accidents) → nasal regurgitation.
• Paralysis of larynx, vagus lesions & bilateral superior laryngeal nerve lesions → aspiration.

OESOPHAGEAL CAUSES

Lesions may involve the lumen, the wall, or structures outside the wall.

1. Lumen

Atresia, foreign body, strictures, benign or malignant tumours.

2. Wall

Acute or chronic oesophagitis; motility disorders:

(a) Hypomotility
Achalasia, scleroderma, amyotrophic lateral sclerosis.

(b) Hypermotility
Cricopharyngeal spasm, diffuse oesophageal spasm.

3. Outside the Wall

Extrinsic compression causes obstruction.

(a) Hypopharyngeal diverticulum

(b) Hiatus hernia

(c) Cervical osteophytes

(d) Thyroid lesions
Thyroid enlargement, tumours, Hashimoto thyroiditis.

(e) Mediastinal lesions
Mediastinal tumours, lymph node enlargement, aortic aneurysm, cardiac enlargement.

(f) Vascular rings
Dysphagia lusoria.

COMPLICATIONS

1. Pain
2. Vertigo
3. Persistent Headache
4. Facial Weakness
5. A listless Child Refusing to Take Feeds
6. Fever, Nausea and Vomiting
7. Irritability and Neck Rigidity
8. Diplopia
9. Ataxia
10. Abscess Round the Ear

Vertigo

It indicates erosion of lateral semicircular canal which may progress to labyrinthitis or meningitis. Fistula test should be performed in all cases.

TREATMENT

General

1. Reassurance.
2. Relief of ear pain by analgesics.
3. Care of the eye as outlined on p. 108. Eye must be protected against exposure keratitis.
4. Physiotherapy or massage of the facial muscles gives psychological support to the patient. It has not been shown to influence recovery. Active facial movements are encouraged when there is return of some movement to the facial muscles.

Medical Management

• Steroids. Their utility has not been proved beyond doubt in carefully controlled studies. Prednisolone is the drug of choice. If patient reports within 1 week, the adult dose of prednisolone is 1 mg/kg/day divided into morning and evening doses for 5 days. Patient is seen on the fifth day. If paralysis is incomplete or is recovering, dose is tapered during the next 5 days. If paralysis remains complete, the same dose is continued for another 10 days and thereafter tapered in next 5 days (total of 20 days). Contraindications to use of steroids include pregnancy, diabetes, hypertension, peptic ulcer, pulmonary tuberculosis and glaucoma. Steroids have been found useful to prevent incidence of synkinesis, crocodile tears and to shorten the recovery time of facial paralysis. Steroids can be combined with acyclovir for Herpes zoster oticus or Bell palsy.

• Other drugs. Vasodilators, vitamins, mast cell inhibitors and antihistaminics have not been found useful.

Surgical Treatment

Nerve decompression relieves pressure on the nerve fibres and thus improves the microcirculation of the nerve. Vertical and tympanic segments of nerve are decompressed. Some workers have suggested total decompression including labyrinthine segment by postaural and middle fossa approach.