This is a Third MBBS Part-2 ENT examination paper (Total: 50 marks) with Short Notes (30 marks) + MCQs (20 marks). I'll provide complete answers for all questions according to their weightage.
THIRD MBBS PART-2 ENT EXAMINATION
Total Marks: 50
Q1. WRITE SHORT NOTES (ANY 2) — 10 Marks
(Each question = 5 marks: ~2 marks per sub-part A, B, C)
Q1.1 — 55-year-old hypertensive male, profuse right-sided epistaxis, BP 190/110, on aspirin
A. Probable Diagnosis and Causes (2 marks)
Diagnosis: Posterior Epistaxis (likely from Woodruff's plexus / sphenopalatine artery territory)
Causes in this patient (Etiological framework):
Local causes:
- Idiopathic (most common overall)
- Nasal trauma / digital trauma
- Septal spur
Systemic causes (relevant here):
- Hypertension - BP 190/110 causes sustained high-pressure bleeding that does not stop with simple pinching (key in this case)
- Aspirin use - inhibits COX-1, impairs platelet aggregation (thromboxane A2 reduction), prolongs bleeding
- Arteriosclerosis (likely in a 55-year-old hypertensive)
- Coagulopathy secondary to antiplatelet therapy
B. Blood Supply of Nasal Septum with Labelled Diagram (2 marks)
Blood supply of nasal septum (Little's area / Kiesselbach's plexus anteriorly):
Arteries supplying the nasal septum:
| Artery | Origin | Area supplied |
|---|
| Anterior ethmoidal artery | Ophthalmic artery (ICA) | Antero-superior septum |
| Posterior ethmoidal artery | Ophthalmic artery (ICA) | Postero-superior septum |
| Sphenopalatine artery | Maxillary artery (ECA) | Posterior septum (main supply) |
| Greater palatine artery | Maxillary artery (ECA) | Inferior septum |
| Superior labial artery | Facial artery (ECA) | Antero-inferior septum |
Kiesselbach's plexus (Little's area): Anastomosis of all 5 arteries on the antero-inferior septum - commonest site of anterior epistaxis.
Woodruff's plexus: Posterior nasal wall, branches of sphenopalatine and ascending pharyngeal arteries - site of posterior epistaxis (as in this case).
DIAGRAM (Lateral nasal wall - septal surface):
Anterior ethmoidal a. ──┐
Posterior ethmoidal a. ─┤
├── KIESSELBACH'S PLEXUS
Sphenopalatine a. ──────┤ (Little's area - antero-inferior septum)
Greater palatine a. ────┤
Superior labial a. ─────┘
C. Stepwise Management (2 marks)
Step 1 - First Aid / Resuscitation:
- Sit patient upright, head slightly forward
- Pinch soft part of nose (Trotter's method) for 10-15 min
- IV access, blood investigations: CBC, PT/INR, BT/CT
- Control BP - IV labetalol / oral antihypertensives (critical in this patient)
- Stop aspirin / antiplatelet agents
Step 2 - Anterior Rhinoscopy / Identify bleeding point:
- Nasal suction, good illumination
- If anterior bleeding point seen: Chemical cautery (silver nitrate) or electrical cautery
Step 3 - Anterior Nasal Packing:
- BIPP (Bismuth Iodoform Paraffin Paste) ribbon gauze
- Remains for 24-48 hours
- Antibiotic cover to prevent sinusitis/toxic shock
Step 4 - Posterior Nasal Packing (if above fails):
- Brighton balloon / Foley catheter (12-14 Fr)
- Epistat balloon catheter
- Hospitalize, monitor vitals
Step 5 - Surgical / Interventional:
- Endoscopic sphenopalatine artery ligation (gold standard for posterior epistaxis)
- Anterior ethmoidal artery ligation (for anterior/superior bleeds)
- Angiographic embolization (if surgical candidate is poor)
Step 6 - Treat underlying cause:
- Antihypertensive therapy (long-term)
- Haematology referral for coagulation workup
- Consider switching from aspirin if clinically feasible
Q1.2 — 9-year-old boy, AOM not responding, painful swelling behind ear, pinna displaced forward and downward
A. Most Likely Diagnosis (1 mark)
Acute Mastoiditis with Subperiosteal Abscess
Classic features present:
- Incomplete treatment of AOM
- Post-auricular painful swelling with redness
- Pinna displaced forward and downward/outward (pathognomonic - due to subperiosteal abscess pushing the auricle)
- Fever, ear pain, purulent discharge
B. Etiopathogenesis and Clinical Features (2 marks)
Etiopathogenesis:
- Acute otitis media → infection spreads to mastoid air cells (mastoiditis always accompanies AOM) → inadequate treatment → coalescence of air cells (coalescent mastoiditis) → cortex eroded → pus collects under periosteum → Subperiosteal abscess
Organisms: Streptococcus pneumoniae, Streptococcus pyogenes, Staphylococcus aureus, Pseudomonas (in treated cases)
Clinical Features:
Symptoms:
- High fever, toxicity
- Severe otalgia (earache)
- Purulent otorrhoea
- Decreased hearing
- Post-auricular pain and swelling
Signs:
- Post-auricular swelling: red, tender, fluctuant
- Pinna pushed forward, downward, and outward (key sign)
- Post-auricular crease (sulcus) obliterated
- Sagging of postero-superior meatal wall
- Perforated TM with pulsatile discharge
Complications if untreated:
- Bezold's abscess (via mastoid tip into neck)
- Meningitis, brain abscess
- Lateral sinus thrombosis
- Facial nerve palsy
- Labyrinthitis
C. Investigation and Management (2 marks)
Investigations:
- HRCT Temporal bone - investigation of choice; shows coalescent mastoiditis, bone erosion, abscess
- Pure tone audiogram
- CBC, CRP, ESR
- Blood culture
- Ear swab for culture and sensitivity
- X-ray mastoid (Schuller's view) - shows haziness of air cells (less used now)
Management:
Medical:
- Hospitalization, IV antibiotics: IV Amoxicillin-clavulanate or Cefotaxime + Metronidazole
- IV fluids, antipyretics, analgesics
- Myringotomy + grommet (ear tube) for drainage
Surgical:
- Cortical mastoidectomy (Schwartze operation) - definitive treatment
- Post-auricular incision
- Exenteration of all diseased mastoid air cells
- Drainage of subperiosteal abscess
- If intracranial complications: modified radical mastoidectomy
Q1.3 — 17-year-old male, progressive unilateral nasal obstruction, blood-stained discharge, cheek fullness, mass on endoscopy
A. Most Likely Diagnosis (1 mark)
Juvenile Nasopharyngeal Angiofibroma (JNA)
Key indicators:
- Young male (almost exclusively in adolescent males)
- Progressive unilateral nasal obstruction
- Recurrent blood-stained / epistaxis
- Mass in posterior nasal cavity on endoscopy
- Cheek fullness (extension into pterygopalatine fossa)
- Treated multiple times for "sinusitis" with no improvement
B. Clinical Features and Investigations (2 marks)
Clinical Features:
Symptoms:
- Progressive unilateral (later bilateral) nasal obstruction
- Recurrent severe epistaxis (hallmark)
- Nasal discharge (blood-stained)
- Headache, cheek fullness (pterygopalatine fossa extension)
- Proptosis (orbital extension)
- Diplopia, visual changes (advanced)
- Conductive hearing loss (Eustachian tube blockage)
- Nasal twang in voice
Signs:
- Greyish-white/pink, smooth, firm, non-tender mass on endoscopy
- Arises from posterior nasal wall near sphenopalatine foramen
- DO NOT BIOPSY (risk of severe haemorrhage - highly vascular tumour)
- Holman-Miller sign on lateral X-ray: anterior bowing of posterior wall of maxillary sinus
Investigations:
- MRI with contrast - investigation of choice; shows "salt and pepper" appearance (due to flow voids + contrast enhancement); shows extent
- CT scan - shows bone erosion, Holman-Miller sign
- Angiography (DSA) - defines feeding vessels (mainly internal maxillary artery / sphenopalatine artery); also used for pre-operative embolization
- Biopsy is CONTRAINDICATED in clinic
- Sessons/Andrews staging on imaging
C. Management (2 marks)
Staging (Andrews/Sessons system used):
- Stage I: Limited to nasopharynx
- Stage II: Extension to paranasal sinuses / pterygopalatine fossa
- Stage III: Orbital / infratemporal fossa extension
- Stage IV: Intracranial extension
Treatment:
Pre-operative embolization:
- Done 24-48 hours before surgery
- Reduces intraoperative blood loss significantly
Surgical (definitive treatment):
- Endoscopic resection - preferred for Stage I and II (modern approach)
- Lateral rhinotomy / midfacial degloving - for Stage II-III
- Infratemporal fossa approach - for Stage III-IV
- Le Fort I osteotomy for large tumors
Adjuvant:
- Hormonal therapy (testosterone antagonists - flutamide): used in inoperable/recurrent cases
- Radiotherapy: for intracranial extension or recurrent inoperable disease (Stage IV)
Prognosis:
- May spontaneously regress after puberty
- Recurrence rate: 20-25% (due to residual tumour at skull base)
Q2. WRITE SHORT NOTES (ANY 4) — 20 Marks
(Each = 5 marks)
1. Atrophic Rhinitis (5 marks)
Definition: A chronic nasal condition characterized by progressive atrophy of the nasal mucosa, turbinates, and bony nasal walls, with presence of crusts and foul smell (ozaena).
Types:
- Primary (Ozaena): Unknown etiology; more common in females, young adults, developing countries
- Secondary: Post-surgical (turbinate resection), post-infective, granulomatous diseases (syphilis, leprosy, sarcoidosis), irradiation
Etiology / Pathogenesis:
- Klebsiella ozaenae (primary causative organism in primary type)
- Nutritional deficiency (iron, Vitamin A, D)
- Endocrine factors (puberty, menstruation)
- Autonomic imbalance
- Hereditary / racial factors
Pathology: Columnar ciliated epithelium → stratified squamous metaplasia; endarteritis/periarteritis of vessels → mucosal atrophy; turbinate resorption
Clinical Features:
- Nasal obstruction (paradoxical - despite wide nasal cavity, patient feels blocked due to absent air turbulence)
- Anosmia / Hyposmia
- Foul smell (ozaena) - patient unaware due to anosmia; friends/family notice
- Greenish-black dry crusts lining nasal cavity
- Epistaxis on crust removal
- Wide nasal cavity ("empty nose syndrome")
- Atrophic turbinates
Investigations:
- Nasal endoscopy: wide nasal cavity, atrophic turbinates, crusts
- CT PNS: shows widened nasal cavity, thinned turbinates
- Culture: Klebsiella ozaenae
- CBC, serum iron, Vitamin A levels
Management:
Medical:
- Nasal irrigation with alkaline douche (sodium bicarbonate + sodium chloride + sodium biborate in warm water) - removes crusts
- 25% glucose in glycerine nasal drops - inhibits proteolytic organisms
- Oestrogen nasal drops / sprays
- Systemic antibiotics: Rifampicin, Ciprofloxacin (anti-Klebsiella)
- Iron supplementation, Vitamin A
Surgical:
- Young's operation: Closure of both nostrils by mucosal flaps for 6 months → reduces airflow → allows mucosal regeneration; nostrils re-opened later
- Submucosal injection of Teflon/paraffin to narrow nasal cavity
- Turbinate implants (cartilage, bone, fat)
2. Ototoxic Drugs - Enlist and Describe One (5 marks)
Definition: Drugs that cause damage to the cochlea (auditory toxicity) and/or vestibular system.
Classification of Ototoxic Drugs:
| Class | Examples |
|---|
| Aminoglycoside antibiotics | Gentamicin, Streptomycin, Amikacin, Tobramycin, Neomycin |
| Loop diuretics | Furosemide, Ethacrynic acid |
| Salicylates | Aspirin (high dose) |
| Antimalarials | Quinine, Chloroquine |
| Antineoplastics | Cisplatin, Carboplatin |
| Others | Vancomycin, Erythromycin (high dose) |
Memory: "PLACE" - Platinum compounds, Loop diuretics, Aminoglycosides, Cisplatin, Erythromycin
Detailed Description: Aminoglycoside Ototoxicity (Gentamicin)
Mechanism:
- Aminoglycosides enter the cochlear outer hair cells (OHCs) via mechano-electrical transducer channels
- Generate reactive oxygen species (ROS) / free radicals → oxidative stress
- Damage the stria vascularis and outer hair cells of the basal turn (high-frequency region first)
- Gentamicin is primarily vestibulotoxic (vestibular hair cells preferentially)
- Streptomycin, Amikacin are primarily cochleotoxic
- Neomycin is most cochleotoxic (used topically only)
Risk Factors:
- Pre-existing renal impairment (reduced excretion → accumulation)
- High doses, prolonged use
- Concomitant loop diuretics (synergistic toxicity)
- Genetic susceptibility: mitochondrial mutation 1555A>G (12S rRNA gene)
- Age extremes (neonates, elderly)
- Prior noise exposure
Clinical Features:
- High-frequency SNHL (4000-8000 Hz first) → progressive
- Tinnitus (often the first symptom)
- Vertigo, imbalance, oscillopsia (gentamicin vestibulotoxicity)
- Dandy's syndrome (bilateral vestibular failure): oscillopsia + ataxia + SNHL
Monitoring:
- Baseline and serial pure tone audiometry (PTA) - monitoring 8-12 kHz (ultra-high frequencies)
- Serum drug levels (trough/peak monitoring)
- Renal function tests
Prevention:
- Use lowest effective dose, shortest duration
- Once-daily dosing (less nephrotoxic and ototoxic than multiple daily doses)
- Avoid concurrent loop diuretics
- N-acetylcysteine / antioxidants (investigational)
- Genetic screening (1555A>G mutation) before aminoglycoside use
Treatment:
- Discontinue drug immediately on any sign of ototoxicity
- Cochlear implantation for severe bilateral SNHL
- Vestibular rehabilitation for gentamicin vestibulotoxicity
- Hearing aids
3. Pure Tone Audiogram (5 marks)
Definition: A pure tone audiogram (PTA) is a subjective, behavioural hearing test that measures the threshold of hearing at different frequencies (250-8000 Hz) for both air conduction and bone conduction.
Equipment: Audiometer (generates pure tones at calibrated intensities)
Symbols used:
| Right ear | Left ear |
|---|
| Air conduction | O (red) | X (blue) |
| Bone conduction (unmasked) | < | > |
| Bone conduction (masked) | [ | ] |
| No response | ↓ | ↓ |
Normal values: Hearing threshold 0-25 dB HL at all frequencies (adults)
Degree of hearing loss:
| dB HL | Degree |
|---|
| 26-40 | Mild |
| 41-55 | Moderate |
| 56-70 | Moderately severe |
| 71-90 | Severe |
| >90 | Profound |
Types of Audiogram Patterns:
1. Conductive Hearing Loss:
- Air conduction thresholds elevated (>25 dB)
- Bone conduction thresholds normal (0-25 dB)
- Air-Bone Gap (ABG) ≥15 dB present
- Causes: Wax, CSOM, otosclerosis, OME
2. Sensorineural Hearing Loss:
- Both air and bone conduction elevated equally
- No air-bone gap
- Causes: Noise-induced, presbyacusis, Meniere's, ototoxicity
3. Mixed Hearing Loss:
- Both AC and BC elevated
- Air-bone gap present (BC better than AC)
- Causes: CSOM with labyrinthitis, otosclerosis with cochlear involvement
Specific Patterns:
- Noise-induced HL: Characteristic notch at 4000 Hz (4kHz dip)
- Meniere's disease: Low-frequency SNHL (rising audiogram) early; flat later
- Otosclerosis: Carhart's notch at 2000 Hz on bone conduction
- Presbyacusis: High-frequency SNHL, bilateral, symmetrical (downsloping curve)
Pure Tone Average (PTA):
PTA = (500 + 1000 + 2000 Hz thresholds) ÷ 3
(Speech frequencies used for hearing aid candidacy, medicolegal purposes)
4. Rhinosporidiosis (5 marks)
Definition: A chronic granulomatous infection of the mucous membranes (predominantly nasal), caused by Rhinosporidium seeberi.
Causative Organism:
- Rhinosporidium seeberi
- Currently classified as a Mesomycetozoa (between fungi and animals; not a true fungus)
- Forms large sporangia (up to 300-350 μm) filled with endospores
- Cannot be cultured in vitro
Epidemiology:
- Endemic in South Asia: India (Tamil Nadu), Sri Lanka most commonly
- Rural populations, bathing in ponds/stagnant water
- More common in males; all age groups
- Transmission: inoculation through nasal mucosa while bathing in contaminated water
Pathology:
- Organism enters through microabrasion of nasal mucosa
- Forms large sporangia in subepithelial tissue
- Polypoidal granulomatous masses with sporangia at various stages
- Strawberry-like surface due to white dots (sporangia visible through mucosa)
Clinical Features:
Nasal (most common - 70%):
- Unilateral nasal obstruction (progressive)
- Epistaxis (recurrent)
- Pink/red polypoidal mass hanging from nasal cavity (sometimes visible at nostril)
- Soft, friable, pedunculated, strawberry-like surface (white dots = sporangia)
- Nasal discharge
Other sites (less common):
- Conjunctiva/lacrimal sac (second most common)
- Oropharynx, larynx, urethra, penis, vagina, skin
Diagnosis:
- Clinical appearance (strawberry polyp) is characteristic
- Histopathology - definitive diagnosis:
- Large sporangia (200-350 μm) at various maturation stages
- Mature sporangia contain thousands of endospores
- Surrounding granulomatous reaction
- Nasal endoscopy: friable, pedunculated polyp
- CT/MRI: extent of disease
Treatment:
Surgical (definitive):
- Wide local excision with electrocautery of base - treatment of choice
- Diathermy of the base essential to destroy endospores and prevent recurrence
- Endoscopic removal preferred currently
- Recurrence rate: 10-15%
Medical (adjuvant):
- Dapsone (50-100 mg/day) - inhibits sporangia maturation; used as adjuvant to prevent recurrence
- No proven curative medical therapy alone
Complications:
- Recurrence (if base not adequately cauterized)
- Disseminated rhinosporidiosis (rare, immunocompromised)
5. Bell's Palsy (5 marks)
Definition: Bell's palsy is an acute, unilateral, idiopathic, lower motor neuron (LMN) facial nerve palsy of sudden onset, caused by inflammation and edema of the facial nerve within the stylomastoid foramen/fallopian canal.
Etiology:
- Idiopathic (by definition), but likely viral (HSV-1 reactivation) - most accepted theory
- Inflammation → edema → nerve compression within the bony fallopian canal → ischemia → demyelination
- Other associations: Herpes zoster (Ramsay Hunt - NOT Bell's), pregnancy, diabetes, hypertension
Clinical Features:
LMN Facial Palsy (ALL divisions affected):
- Inability to close eye (Lagophthalmos) - most worrying feature (corneal exposure)
- Bell's phenomenon (upward rolling of eyeball on attempted eye closure)
- Flattening of nasolabial fold
- Drooping of angle of mouth
- Inability to raise eyebrow (distinguishes from UMN palsy)
- Asymmetrical smile, inability to whistle/puff cheeks
Additional features depending on site of lesion:
- Above geniculate ganglion: Loss of taste (anterior 2/3 tongue via chorda tympani) + hyperacusis (stapedius branch) + reduced lacrimation (greater petrosal nerve)
- Below stylomastoid foramen: Pure motor palsy only
Onset: Sudden (hours); may have prodrome of pain behind ear (mastoid pain)
Grading: House-Brackmann Scale (I-VI)
- Grade I: Normal
- Grade VI: Complete paralysis, no movement
Investigations:
- Clinical diagnosis primarily
- Topognostic tests (Schirmer's, stapedial reflex, taste testing) - to localize level of lesion
- EMG/Nerve conduction studies - prognosis; done after 72 hours
- CT/MRI temporal bone (to rule out other causes)
- Blood: FBS, CBC (rule out diabetes, Lyme disease)
Differential Diagnosis: Ramsay Hunt syndrome (VZV), cholesteatoma, parotid tumour, acoustic neuroma, Melkersson-Rosenthal syndrome
Management:
Medical:
- Oral prednisolone (1 mg/kg/day for 10 days, then taper) - started within 72 hours of onset; improves recovery rate
- Acyclovir/Valacyclovir (if started within 72 hours): controversial as monotherapy; used with steroids in severe cases
- Eye care: Artificial tears (day), eye lubricant ointment (night), protective spectacles, taping eye shut at night (most important to prevent exposure keratitis)
Physiotherapy:
- Facial exercises
- Electrical stimulation (controversial)
Surgical (rare):
- Facial nerve decompression (for complete paralysis with poor prognostic EMG findings, within 14 days)
- Tarsorrhaphy (for corneal exposure not controlled medically)
- Nerve grafting (late cases)
Prognosis:
- 80-85% recover completely without treatment
- Recovery begins within 3-6 months
- Poor prognostic signs: complete palsy, advancing age, hyperacusis, diabetes, no recovery by 3 weeks, denervation on EMG
MCQ ANSWERS (20 marks - 1 mark each, No Negative Marking)
| Q | Answer | Key Point |
|---|
| 1 | B | Lateral semicircular canal fistula (Tragal pressure → fistula test +ve in CSOM) |
| 2 | C | Pseudomonas aeruginosa (>95% malignant OE) |
| 3 | C | Unilateral SNHL + tinnitus (earliest in acoustic neuroma) |
| 4 | D | Foreign body nose (unilateral foul-smelling discharge in child) |
| 5 | B | Frontal sinusitis (Pott's puffy tumour) |
| 6 | D | Conductive HL (NOT a feature - Meniere's = SNHL) |
| 7 | C | Beta-2 transferrin assay (gold standard for CSF rhinorrhoea) |
| 8 | C | Otosclerosis (CHL + paracusis Willis + absent stapedial reflex + normal TM) |
| 9 | B | Sensorineural hearing loss (Rinne positive = AC>BC) |
| 10 | A | Type I hypersensitivity (IgE-mediated) |
| 11 | A | HRCT Temporal bone (cholesteatoma investigation of choice) |
| 12 | A | Sneezing (hallmark of allergic rhinitis) |
| 13 | C | V3 mandibular nerve (tensor tympani) |
| 14 | C | Nasopharynx (Eustachian tube opening) |
| 15 | C | OAE (outer hair cell function) |
| 16 | B | Otitis media with effusion (type B tympanogram) |
| 17 | B | Cribriform plate (commonest site CSF rhinorrhoea) |
| 18 | C | Labyrinthine fistula (Hennebert's sign) |
| 19 | A | Asthma + nasal polyp + aspirin sensitivity (Samter's triad) |
| 20 | D | Nasal valve (Cottle's test) |
Exam tip: For Q1, attempt the case with the most familiar topic first. For Q2, the five topics listed (atrophic rhinitis, ototoxics, PTA, rhinosporidiosis, Bell's palsy) are all high-yield standard ENT topics - attempt all 4 best ones. MCQs carry 1 mark each with no negative marking, so attempt all 20.