Furuncle Otosclerosis Choanal atresia Nasal polyps Adenoiditis Tonsillitis Peritonsilar abcess Acute otitis media Sinusitis Rhinitis Ositis externa Cholesteotoma Pharyngeal lymphoid ring detail information and after that make osce case

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🫁 ENT Conditions — Comprehensive Notes + OSCE Cases

PART 1: DETAILED CONDITION NOTES

1. FURUNCLE (Ear Canal Furunculosis)

Definition: A localized staphylococcal infection of a hair follicle in the outer third (cartilaginous part) of the external auditory canal, forming an abscess.

Etiology: Staphylococcus aureus (most common). Only the outer third of the EAC has hair follicles and sebaceous glands — therefore furuncles are confined to this area.

Pathophysiology: Trauma (e.g., cotton bud use, scratching) → breach of skin → S. aureus invasion → folliculitis → abscess formation → intense otalgia (due to tight adherent skin over cartilage)

Clinical Features:

Severe, throbbing otalgia — worsened by jaw movement, chewing, tragus pressure
Tragal tenderness (pathognomonic)
Conductive hearing loss if canal is occluded
Low-grade fever, regional lymphadenopathy (pre-auricular/post-auricular)
Tympanic membrane is normal (differentiates from AOM)

Diagnosis: Clinical. If fluctuant, pus visible in canal.

Treatment:

Mild: Topical antibiotic ear drops (e.g., neomycin/polymyxin B) + topical steroid; analgesia
Fluctuant abscess: Incision & drainage under local anaesthesia
Systemic: Oral flucloxacillin or co-amoxiclav if cellulitis extends; MRSA: trimethoprim-sulfamethoxazole
Warm compresses for pain relief
Avoid EAC manipulation

Complications: Spread to pinna (perichondritis), pre-auricular lymphadenitis, rarely necrotizing (malignant) otitis externa in diabetics.

2. OTOSCLEROSIS

Definition: A disease of the bony labyrinth (otic capsule) characterized by abnormal remodeling of enchondral bone, leading to fixation of the stapes footplate → conductive hearing loss.

Epidemiology:

Most common cause of conductive hearing loss (CHL) in adults with no history of trauma or infection
Incidence 1% at age 40–49 → 19% at age 80–89 (Paget overlap)
More common in women than men; bilateral in ~70%
Autosomal dominant with incomplete penetrance (~25–40%)

Pathophysiology: Foci of spongy, vascular bone replace normal compact enchondral bone → stapes footplate fixation → impaired sound transmission. Can extend to cochlea (cochlear otosclerosis) → sensorineural component.

Clinical Features:

Progressive bilateral CHL (or mixed hearing loss)
Tinnitus (low-frequency)
Paracusis Willisii — paradoxical improvement of hearing in noisy environments (pathognomonic; due to others raising their voices)
Normal tympanic membrane
Flamingo pink/Schwartze sign — reddish blush through tympanic membrane (active foci of vascular otospongiosis — rare finding)

Investigations:

Audiometry: CHL with Carhart notch (mechanical notch at 2000 Hz on bone conduction)
Tympanometry: Type As (shallow, reduced compliance) — stiff fixated stapes
CT temporal bone: radiolucent "halo" around cochlea (cochlear otosclerosis — "double ring sign")

Treatment:

Hearing aid (amplification)
Stapedectomy (gold standard) — removal of stapes + prosthesis; >95% success rate
Sodium fluoride — may retard progression (reduces osteoclast activity); bisphosphonates may stabilize SNHL component
Observation

Complications of Surgery: Worsened hearing, tympanic membrane perforation, taste changes (chorda tympani), disequilibrium (rare perilymph fistula).

— Textbook of Family Medicine 9e; Cummings Otolaryngology Head and Neck Surgery

3. CHOANAL ATRESIA

Definition: Congenital absence of communication between the posterior nasal cavity and the nasopharynx due to persistence of the bucconasal membrane (failure to rupture at 7–8 weeks of gestation).

Epidemiology: 1 in 5,000–8,000 live births. Unilateral in ~2/3 cases (right side more common). 50% have associated anomalies.

Types:

Pure bony: 29%
Mixed bony-membranous: 71% (most common)
Pure membranous: essentially none

Associated Syndromes (CHARGE):

Coloboma
Heart defects
Atretic choana
Retardation of growth/development
Genitourinary disorders
Ear abnormalities Also: Crouzon syndrome, cleft palate, craniosynostosis, polydactyly

Anatomy of obstruction:

Narrow nasal cavity
Lateral bony obstruction by pterygoid plates
Medial obstruction — thickening of vomer
Membranous obstruction

Clinical Features:

Bilateral (neonatal emergency): Cyclic respiratory distress → cyanosis relieved by crying; obligate nasal breathing neonates → "CYCLICAL CYANOSIS" is classic
Unilateral (presents later): Unilateral persistent rhinorrhoea, nasal obstruction, thick secretions filling the occluded cavity

Diagnosis:

Failure to pass 6-F catheter through nose into nasopharynx (>32 mm)
Nasal endoscopy — direct visualization
CT scan — confirms diagnosis, characterizes bony vs. membranous, thickness
Choanal stenosis: patent but <6 mm across

Treatment:

Bilateral: Emergency airway (oropharyngeal airway/intubation) → surgical repair (transnasal endoscopic approach preferred)
Unilateral: Elective surgical repair (transnasal choanoplasty)

— Cummings Otolaryngology Head and Neck Surgery

4. NASAL POLYPS

Definition: Smooth, glistening, grape-like masses of edematous inflamed nasal/sinus mucosa that protrude into the nasal cavity.

Pathology (Robbins): Edematous mucosa with loose stroma, hyperplastic/cystic mucus glands, infiltrates of neutrophils, eosinophils, and plasma cells. Surface intact unless superinfected.

Associations:

Chronic eosinophilic rhinosinusitis (most common)
Aspirin-exacerbated respiratory disease (Samter's triad): Asthma + nasal polyps + NSAID intolerance
Cystic fibrosis (up to 50% of CF patients)
Allergic fungal sinusitis
Note: Only 0.5% of atopic patients develop nasal polyps — most polyp patients are NOT atopic

Clinical Features:

Bilateral nasal obstruction (unilateral → suspect neoplasm)
Anosmia / hyposmia
Rhinorrhoea (clear, mucoid)
Post-nasal drip
Mouth breathing, snoring
"Nasal crease" in children with allergic facies

Diagnosis:

Anterior rhinoscopy/nasal endoscopy — pale, glistening, insensate masses
CT sinuses — extent and associated sinusitis
Biopsy if unilateral / atypical

Treatment:

Topical intranasal corticosteroids (first-line) — reduce polyp size
Short course oral steroids (for acute shrinkage)
Antibiotics if superinfected
Functional endoscopic sinus surgery (FESS) — for persistent/recurrent polyps or if obstructing
Anti-IL-4/IL-13 biologics: dupilumab (for refractory eosinophilic CRS with polyps)

— Robbins Pathologic Basis of Disease; Goldman-Cecil Medicine

5. ADENOIDITIS

Definition: Inflammation/infection of the pharyngeal tonsil (adenoid) — the lymphoid tissue on the posterior wall of the nasopharynx forming part of Waldeyer's ring.

Embryology: Adenoids develop at 16 weeks gestation as subepithelial infiltration of lymphocytes.

Epidemiology: Most prevalent in children aged 2–8 years; involute at puberty.

Etiology: Viral (rhinovirus, adenovirus, EBV), bacterial (S. pneumoniae, H. influenzae, S. aureus, S. pyogenes). Biofilm formation is common.

Pathophysiology: Hypertrophied adenoids act as a bacterial reservoir (biofilm). They can obstruct the Eustachian tube orifice → recurrent otitis media and obstruct the posterior nasal choanae → nasal obstruction.

Clinical Features:

Nasal obstruction → mouth breathing, snoring, sleep-disordered breathing
Persistent mucopurulent rhinorrhoea / post-nasal drip
Adenoid facies: Open mouth, elongated face, dull expression, high-arched palate
Hyponasal voice ("nasal" quality speech)
Recurrent otitis media with effusion (glue ear)
Recurrent sinusitis
Fever in acute adenoiditis

Diagnosis: Lateral soft tissue X-ray neck (adenoid:nasopharynx ratio >0.8 = significant), flexible nasendoscopy.

Treatment:

Medical: Antibiotics (amoxicillin/co-amoxiclav), topical nasal saline, intranasal steroids
Surgical: Adenoidectomy — indications: obstructive symptoms, recurrent AOM (especially with grommet placement), recurrent rhinosinusitis, suspected malignancy
Adenoidectomy removes the biofilm reservoir → reduces recurrent AOM and sinusitis

6. TONSILLITIS

Definition: Inflammation of the palatine tonsils, usually infectious.

Anatomy: Palatine tonsils sit in the tonsillar fossa between the palatoglossal arch (anterior) and palatopharyngeal arch (posterior) on the lateral wall of the oropharynx. Blood supply: tonsillar branch of facial artery (main); also ascending pharyngeal, lingual, greater palatine, ascending palatine arteries.

Etiology:

Viral (most common): rhinovirus, adenovirus, EBV (infectious mononucleosis), RSV
Bacterial: Group A β-haemolytic streptococcus (GABHS / S. pyogenes) — most important; also H. influenzae, S. pneumoniae, S. aureus

Clinical Features:

Sore throat, odynophagia, dysphagia
Fever, malaise, halitosis
Trismus in severe cases
Enlarged, erythematous tonsils, with or without exudate
Follicular tonsillitis: Exudate from tonsillar crypts (yellow-white spots)
Tender cervical lymphadenopathy (jugulodigastric nodes)
EBV: Centor + splenomegaly + atypical lymphocytosis + negative rapid strep test

Scoring (Centor/McIsaac): Exudate, tender anterior cervical lymph nodes, fever >38°C, absence of cough (1 point each; +1 if <15 years old, −1 if >44 years old). Score ≥4 → high probability strep.

Investigations: Throat swab culture, rapid strep antigen test, monospot/EBV serology if mono suspected

Complications:

Immediate: Peritonsillar abscess, airway obstruction, dehydration
Delayed (strep): Rheumatic fever (molecular mimicry → carditis), post-streptococcal glomerulonephritis

Treatment:

Viral: supportive (analgesia, fluids)
Bacterial (GABHS): Penicillin V × 10 days (first-line); amoxicillin (avoid in EBV — rash); erythromycin if penicillin-allergic
Do NOT give amoxicillin if mononucleosis suspected (maculopapular rash in 90%)

Indications for Tonsillectomy (Paradise criteria):

≥7 episodes/year in 1 year
≥5 episodes/year × 2 years
≥3 episodes/year × 3 years
2 weeks work/school missed per year
Hypertrophy causing sleep apnoea
Peritonsillar abscess
Suspicion of malignancy
Diphtheria carrier

— K.J. Lee's Essential Otolaryngology; Gray's Anatomy for Students

7. PERITONSILLAR ABSCESS (Quinsy)

Definition: Collection of pus deep to the tonsillar capsule, between the tonsil and the superior constrictor muscle. Most common deep space infection of the head and neck.

Etiology: Usually follows acute tonsillitis. Mixed flora: S. pyogenes, anaerobes (Fusobacterium, Bacteroides), S. aureus.

Pathophysiology: Infection spreads from tonsillar crypts → Weber glands (mucous glands in supratonsillar space) → peritonsillar space abscess

Clinical Features (classic triad):

Severe odynophagia (usually unilateral)
Trismus (spasm of medial pterygoid muscle)
"Hot potato" voice (muffled, plummy speech)

Additional:

Uvula deviated away from affected side; tonsil pushed towards midline
Soft palate bulging/swelling on affected side
Drooling, severe dysphagia
Fever, malaise, foetor oris
Ipsilateral neck pain/stiffness

Diagnosis: Clinical. Intraoral ultrasound or CT if diagnosis uncertain or if deep space extension suspected.

Complications (if untreated):

Dehydration / airway obstruction
Parapharyngeal abscess (rupture through superior constrictor)
Retropharyngeal abscess
Mediastinitis (descending necrotizing)
Venous: thrombophlebitis, bacteraemia, endocarditis
Arterial: pseudoaneurysm, haemorrhage
Brain abscess
Aspiration pneumonia
Lemierre's syndrome (Fusobacterium necrophorum → septic thrombophlebitis of internal jugular vein)

Treatment:

Surgical drainage — needle aspiration (first-line), incision & drainage, or immediate tonsillectomy (quinsy tonsillectomy)
IV/oral antibiotics — co-amoxiclav or penicillin + metronidazole (to cover anaerobes)
IV fluids + analgesia
Interval tonsillectomy after 6 weeks

— K.J. Lee's Essential Otolaryngology

8. ACUTE OTITIS MEDIA (AOM)

Definition: Acute onset of signs and symptoms of middle ear inflammation with effusion.

Epidemiology:

Most common reason for pediatrician visit and antibiotic prescription in children
Peak incidence: 6–12 months of age
23–46% of children have ≥1 episode by age 1 year; 60% by age 3 years

Risk Factors:

Environmental: daycare, tobacco smoke, pacifier use, siblings, supine bottle feeding, lack of breastfeeding
Anatomic: cleft palate, Eustachian tube dysfunction, craniofacial anomalies (Treacher Collins, Down syndrome)
Genetic predisposition; low SES; prematurity

Pathophysiology: URTI → Eustachian tube mucosal oedema/obstruction (shorter, more horizontal in children) → negative middle ear pressure → reflux of nasopharyngeal bacteria → middle ear infection + effusion

Eustachian tube in children: shorter, more horizontal → poorer drainage

Microbiology:

Streptococcus pneumoniae (23.6%) — most severe
Non-typeable Haemophilus influenzae (29.1%) — most common
Moraxella catarrhalis (2.8%)
Streptococcus pyogenes (3.7%)
Viral: rhinovirus, RSV, influenza

Clinical Features:

Otalgia, ear tugging (infants)
Fever (>38°C)
Hearing loss, irritability
Otoscopy: Bulging, erythematous, opacified tympanic membrane; loss of light reflex; reduced mobility on pneumatic otoscopy
Perforation → purulent otorrhoea + pain relief

Diagnosis: Clinical (otoscopy ± pneumatic otoscopy)

Management:

Pain control: Ibuprofen (10 mg/kg q6h), paracetamol (15 mg/kg q4h); oxycodone for severe otalgia

Antibiotics — Observation option (withhold antibiotics initially):

Appropriate for: children 6–23 months with unilateral AOM + mild symptoms (ear pain <48h, temp <39°C); OR children ≥24 months with unilateral or bilateral AOM + mild symptoms
Follow-up in 48–72 hours; initiate antibiotics if no improvement

Antibiotics required immediately:

Age <6 months, severe symptoms, bilateral AOM <24 months, AOM with perforation, recurrent AOM, myringotomy tubes, immunodeficiency, craniofacial anomalies

First-line antibiotic: High-dose amoxicillin 45 mg/kg/dose PO BD × 5–10 days Second-line (allergy, treatment failure): Amoxicillin-clavulanate, cefdinir, ceftriaxone IM

Complications:

Acute mastoiditis (most common suppurative complication)
Tympanic membrane perforation
Chronic suppurative otitis media
Meningitis, intracranial abscess (rare)
Cholesteatoma (long-term)

— Tintinalli's Emergency Medicine; K.J. Lee's Essential Otolaryngology

9. SINUSITIS (Rhinosinusitis)

Definition: Inflammation of the paranasal sinus mucosa. "Rhinosinusitis" is preferred as rhinitis almost always co-exists.

Classification:

Acute: <4 weeks; Subacute: 4–12 weeks; Chronic: >12 weeks; Recurrent acute: ≥4 episodes/year

Etiology:

Acute viral (most common) — rhinovirus, influenza, parainfluenza
Acute bacterial (ABRS): Develops in ~2% of viral URTIs. Pathogens: S. pneumoniae, non-typeable H. influenzae, M. catarrhalis
Chronic rhinosinusitis (CRS): S. aureus, Pseudomonas aeruginosa, anaerobes; loss of mucosal bacterial diversity
Fungal: Mucormycosis (diabetic/immunocompromised) — invasive, life-threatening; Allergic fungal sinusitis
Odontogenic: Maxillary sinusitis from periapical dental infection (extension through bony sinus floor)

Pathophysiology: Mucosal oedema (from rhinitis/URTI) → obstruction of ostiomeatal complex → impaired mucociliary clearance → stasis → bacterial overgrowth. Maxillary and frontal sinuses most commonly involved.

Clinical Features:

Nasal congestion, purulent nasal discharge
Facial pain/pressure/fullness (over affected sinus)
- Maxillary: cheek pain, dental pain
- Frontal: forehead pain (worse bending forward)
- Ethmoid: periorbital/nasal bridge pain
- Sphenoid: vertex/occipital pain (rare, dangerous)
Hyposmia
Post-nasal drip, cough
Fever, malaise
ABRS hallmarks: symptoms >10 days without improvement; severe symptoms (fever >39°C + purulent discharge); "double-sickening" pattern (initial improvement then worsening)

Diagnosis:

Clinical. CT sinuses (not routine for acute; use for chronic, recurrent, or complications)
Nasal endoscopy ± sinus culture (for chronic)

Treatment:

Viral/mild acute: Saline irrigation, topical decongestants (<3–5 days), analgesics; No antibiotics for most viral
ABRS (moderate–severe or >10 days): Amoxicillin-clavulanate (first-line); amoxicillin (low-risk); doxycycline or respiratory fluoroquinolone if penicillin allergy
Topical intranasal corticosteroids (adjunct, especially for CRS)
CRS: INCS, saline irrigation, antibiotics for acute exacerbations; FESS for refractory cases

Complications (rare but serious):

Orbital: periorbital cellulitis → orbital abscess → cavernous sinus thrombosis
Intracranial: meningitis, subdural empyema, epidural abscess, brain abscess, septic dural sinus thrombophlebitis
Osteomyelitis (Pott's puffy tumour — frontal sinus)
Mucocele

— Robbins Pathologic Basis of Disease; Goldman-Cecil Medicine

10. RHINITIS

Definition: Inflammation of the nasal mucosa characterised by nasal congestion, rhinorrhoea, sneezing, and/or nasal itching.

Classification:

Type	Mechanism	Key Features
Allergic (seasonal)	IgE-mediated	Pollens; seasonal
Allergic (perennial)	IgE-mediated	Dust mites, animal dander, moulds
Non-allergic (vasomotor)	Autonomic dysregulation	Irritants, temperature change; no IgE
Infectious	Viral/bacterial	URTI; common cold
Occupational	Allergen/irritant at work	Latex, flour, animal proteins
Drug-induced	Rhinitis medicamentosa	Decongestant overuse; β-blockers; cocaine
Hormonal	Pregnancy, hypothyroid	Progesterone-mediated vasodilatation

Pathophysiology (Allergic):

Early phase (minutes): Allergen → IgE cross-linking on mast cells/basophils → degranulation → histamine, leukotrienes, prostaglandins → sneezing, itching, watery rhinorrhoea, congestion
Late phase (4–8 hours): Chemoattractants → eosinophil, CD4+ lymphocyte, basophil infiltration → persistent congestion
Priming effect: Cumulative allergen exposure increases sensitivity; non-specific irritant hyperreactivity

Comorbidities: 80% of allergic asthma patients also have allergic rhinitis; rhinitis is a risk factor for asthma.

Clinical Features:

Sneezing, watery rhinorrhoea, nasal pruritis
Nasal congestion (dominant in late phase)
Conjunctival injection, tearing (allergic rhinoconjunctivitis)
Allergic salute (wiping nose upward) → nasal crease
Pale, boggy, bluish nasal mucosa
"Allergic shiners" (infraorbital dark circles — venous congestion)

Diagnosis: Clinical. Skin prick test / serum specific IgE (RAST) for allergen identification. Nasal smear (eosinophilia in allergic).

Treatment:

Allergen avoidance
Topical intranasal corticosteroids — most effective for congestion (first-line)
Oral/intranasal antihistamines — best for sneezing, rhinorrhoea, itching
Decongestants (oxymetazoline <3–5 days; avoid rhinitis medicamentosa)
Leukotriene receptor antagonists (montelukast) — useful if asthma coexists
Ipratropium nasal spray — for rhinorrhoea-predominant
Allergen immunotherapy (subcutaneous or sublingual) — desensitisation; only disease-modifying treatment

— Goldman-Cecil Medicine; Tietz Textbook of Laboratory Medicine

11. OTITIS EXTERNA (OE)

Definition: Inflammation/infection of the skin of the external auditory canal (EAC). Sometimes called "swimmer's ear."

Etiology:

Acute diffuse OE (most common): Pseudomonas aeruginosa (most common bacterial), Staphylococcus aureus, occasionally fungi (Candida, Aspergillus — otomycosis)
Furunculosis: S. aureus confined to outer cartilaginous EAC
Malignant (necrotising) OE: P. aeruginosa in diabetics/immunocompromised → osteomyelitis of skull base (life-threatening)

Predisposing Factors: Swimming/water exposure, humidity, trauma (cotton buds), eczema, psoriasis, hearing aid use, narrow EAC, diabetes.

Pathophysiology: Water → loss of protective cerumen + alkalinisation of EAC → disruption of skin barrier → bacterial/fungal invasion

Clinical Features:

Acute diffuse OE (swimmer's ear):
- Otalgia (worsened by tragus pressure and pinna traction — differentiates from AOM)
- Pruritus
- Otorrhoea (scanty initially, then purulent)
- EAC oedematous, erythematous, debris-filled
- Tragal tenderness + pain on pulling pinna
- Conductive hearing loss (if canal swollen shut)
- TM appears normal (when visible)
Malignant OE: Severe pain, granulation tissue at bony-cartilaginous junction, cranial nerve palsies (VII most common → facial palsy; then IX, X, XI, XII as it spreads)

Diagnosis: Clinical. Culture swab for refractory/recurrent cases. CT/MRI for malignant OE to assess bone destruction.

Treatment:

Aural toilet (microsuction — critical first step)
Topical antibiotic/steroid drops (first-line): ciprofloxacin + dexamethasone; acetic acid drops (mild); gentamicin + hydrocortisone
Analgesia (NSAIDs, opioids for severe)
Keep ear dry (cotton wool with petroleum jelly during showers)
Pope wick/ear wick if canal too swollen for drops to penetrate
Malignant OE: IV anti-pseudomonal antibiotics (ciprofloxacin PO × 6–8 weeks; piperacillin-tazobactam/ceftazidime IV for severe); management of diabetes; surgical debridement if needed; long-term follow-up

12. CHOLESTEATOMA

Definition: An abnormal, destructive accumulation of keratinising squamous epithelium in the middle ear and/or mastoid, behaving like a locally invasive "cyst."

Types:

Congenital: Keratinous cyst behind intact TM; no prior perforation/surgery; typically anteromedial to the malleus in the middle ear (white pearly cyst, intact TM)
Acquired (primary): Retraction pocket of pars flaccida (Shrapnell's membrane) → Eustachian tube dysfunction → negative ME pressure → retraction → accumulation of keratin; no perforation initially
Acquired (secondary): Squamous epithelium migrates through a marginal or attic TM perforation into middle ear

Pathophysiology: Keratinising squamous epithelium accumulates in layers ("onion skin") + enzymatic activity (collagenases, proteases) → erosion of ossicles, mastoid, tegmen, lateral semicircular canal, facial nerve canal, sigmoid sinus

Clinical Features:

Foul-smelling, painless otorrhoea (classic)
Progressive conductive (± sensorineural) hearing loss
Facial nerve palsy (if erodes facial canal)
Labyrinthine fistula → vertigo, SNHL
Attic or posterosuperior perforation ± visible white pearly mass or keratin flakes in Prussak's space
Pars flaccida retraction pocket (primary acquired)

Investigations:

Otoscopy/microscopy (gold standard for diagnosis)
CT temporal bone (best for assessing extent, ossicular erosion, tegmen, sigmoid sinus involvement)
MRI (diffusion-weighted MRI) — excellent for detecting residual/recurrent cholesteatoma without revision surgery

Complications (due to bone erosion):

Ossicular chain erosion → CHL (long process of incus most commonly eroded)
Labyrinthine fistula (lateral SCC most common)
Facial nerve paralysis
Meningitis, intracranial abscess
Sigmoid sinus thrombosis
Tegmen dehiscence → cerebrospinal fluid leak

Treatment: Surgical — mastoidectomy ± tympanoplasty

Canal wall up (CWU): Preserves EAC posterior wall; requires second-look surgery
Canal wall down (CWD): Creates open mastoid cavity (radical/modified radical mastoidectomy); better visualisation, lower recurrence, requires lifelong cavity care

13. PHARYNGEAL LYMPHOID RING (Waldeyer's Ring)

Definition: A circular arrangement of lymphoid tissue surrounding the oropharyngeal inlet, forming the first line of immunological defence at the entry of the aerodigestive tract.

Embryology (K.J. Lee):

Palatine tonsil → 8 weeks, from 2nd pharyngeal pouch
Lingual tonsil → 6.5 weeks, from 2nd/3rd arch ventrally
Pharyngeal tonsil (adenoids) → 16 weeks, subepithelial lymphocyte infiltration

Components (clockwise from superior):

Component	Location	Epithelium
Pharyngeal tonsil (adenoids)	Posterior nasopharynx roof	Ciliated pseudostratified columnar
Tubal tonsils (Gerlach tonsils)	Around Eustachian tube orifice	Ciliated columnar
Palatine tonsils	Tonsillar fossa (oropharynx lateral walls)	Stratified squamous (non-keratinised)
Lingual tonsil	Posterior tongue base	Stratified squamous
Smaller lymphoid aggregates	Posterior pharyngeal wall, soft palate	—

Blood Supply (Palatine Tonsil):

Main: Tonsillar branch of facial artery
Others: Ascending pharyngeal, lingual, greater palatine, ascending palatine arteries
Venous drainage: Tonsillar venae comitantes → pharyngeal venous plexus
External palatine (paratonsillar) vein lies between tonsil and superior constrictor — vulnerable during tonsillectomy

Functions:

Mucosal immune surveillance: first lymphoid contact for inhaled/ingested antigens
IgA production (secretory IgA)
T and B lymphocyte activation
Part of MALT (mucosa-associated lymphoid tissue)
Adenoids: particularly important for Eustachian tube protection (Gerlach tonsil guards ET orifice)

Clinical Importance:

Waldeyer's ring lymphoma: Most common site for extranodal NHL in head and neck; tonsil most common single site; Burkitt's lymphoma involves Waldeyer's ring in children
Adenoids: biofilm reservoir → recurrent AOM, sinusitis
Palatine tonsils: recurrent tonsillitis, peritonsillar abscess
Unilateral tonsillar enlargement → always investigate for lymphoma/malignancy
Post-adenotonsillectomy: temporary reduction in local IgA; replaced systemically

PART 2: OSCE CASES

🏥 OSCE CASE 1 — Acute Otitis Media

Station: History + Management

Opening: "A mother brings her 18-month-old son to the emergency department at 2 AM. He has been crying inconsolably for 4 hours and pulling at his right ear. He had a runny nose 5 days ago."

History (gather from examiner/role-player):

Right ear pain/tugging, irritability
Fever: 38.7°C
Rhinorrhoea for 5 days (viral URTI)
No otorrhoea
No vomiting/rash/neck stiffness
Vaccinated (including pneumococcal)
No recent antibiotics; attends daycare; breastfed ×6 months; no siblings

Examination findings:

Right TM: bulging, opaque, intensely erythematous, loss of light reflex; reduced mobility on pneumatic otoscopy
Left TM: normal
Temp 38.7°C, HR 145

Questions the examiner may ask:

Q: What is the diagnosis? Acute otitis media, right ear (unilateral).

Q: Does this child require antibiotics immediately? This child is 18 months with unilateral AOM and mild–moderate symptoms (fever <39°C, ear pain <48h). Per AAP guidelines, observation is appropriate. A wait-and-see antibiotic prescription may be given. If bilateral or if severe: immediate antibiotics.

Q: What would you prescribe if antibiotics are needed? High-dose amoxicillin 45 mg/kg/dose PO BD × 5–10 days (achieves MIC for resistant S. pneumoniae)

Q: What are the complications of untreated AOM? Acute mastoiditis (most common suppurative complication), tympanic membrane perforation, intracranial spread (meningitis, brain abscess), cholesteatoma (long-term recurrent disease)

Q: When would you refer to ENT? Recurrent AOM (≥3 in 6 months or ≥4 in 12 months), AOM with effusion >3 months (glue ear), failed antibiotic treatment, complications, craniofacial anomalies

🏥 OSCE CASE 2 — Peritonsillar Abscess (Quinsy)

Station: History, Examination, Management

Opening: "A 22-year-old student presents to A&E with worsening sore throat for 5 days. He cannot open his mouth fully and his speech sounds like 'he has a hot potato in his mouth'."

History:

5 days sore throat — initially bilateral, now predominantly left-sided and severe
Dysphagia — cannot swallow solids or liquids (drooling)
Trismus — difficulty opening mouth
Muffled ("hot potato") voice
Fever 39.2°C, malaise
Similar episode last year treated with antibiotics
No stridor (important negative)
No neck swelling/stiffness

Examination findings:

Unwell, drooling
Restricted mouth opening (trismus)
Left tonsil displaced medially, uvula deviated to the RIGHT (away from abscess)
Left soft palate bulging, erythematous
Left peritonsillar fullness/fluctuance
Tender left jugulodigastric lymphadenopathy
No stridor, no tracheal deviation

Questions the examiner may ask:

Q: What is the diagnosis? Left peritonsillar abscess (quinsy) — pus between the tonsil capsule and the superior constrictor muscle.

Q: How do you differentiate peritonsillar abscess from peritonsillar cellulitis? Cellulitis: no fluctuance, no trismus or less marked; no uvular deviation. Abscess: fluctuance, trismus, uvula deviated away from affected side, hot potato voice. Intraoral ultrasound or CT can confirm.

Q: What is the immediate management?

Surgical drainage — needle aspiration (1st line; aspiration at point of maximum bulge in supratonsillar space; medial to anterior tonsillar pillar); I&D if aspiration fails
IV antibiotics — benzylpenicillin + metronidazole (anaerobic cover), or co-amoxiclav
IV fluids + analgesia (IV paracetamol, NSAID, consider IV opioid)
Hospital admission

Q: What are the complications if untreated? Airway obstruction, parapharyngeal abscess, retropharyngeal abscess, descending mediastinitis, Lemierre's syndrome, septicaemia, brain abscess

Q: What is Lemierre's syndrome? Septic thrombophlebitis of the internal jugular vein caused by Fusobacterium necrophorum following pharyngeal infection → septic emboli to lungs.

Q: When is tonsillectomy indicated? Interval tonsillectomy after 4–6 weeks; or quinsy tonsillectomy at time of admission (hot tonsillectomy) for recurrent episodes.

🏥 OSCE CASE 3 — Otosclerosis

Station: History + Audiogram Interpretation + Management

Opening: "A 34-year-old woman presents to ENT outpatients with a 3-year history of progressive hearing loss in both ears. Her mother had the same problem and had an operation on her ears."

History:

Bilateral progressive hearing loss (worse in right ear)
Tinnitus (low-pitched)
Paradoxically hears better in noisy environments (paracusis Willisii)
Family history — mother had stapedectomy
Worsened after pregnancy
No ear infections, no trauma, no ear discharge
No vertigo, no facial weakness
No noise exposure

Examination:

External ear: normal
TM: intact, normal colour (no Schwartze sign today)
No exudate, no retraction
Rinne's test: Negative bilaterally (BC > AC — CHL)
Weber's test: Lateralises to worse ear (right) — confirms CHL

Investigations to request:

Audiogram: Conductive hearing loss with Carhart notch at 2000 Hz on bone conduction
Tympanometry: Type As (reduced compliance/stiffness pattern — stapes fixation)
CT temporal bone (if surgical planning): radiolucent halo around cochlea

Questions:

Q: What is the diagnosis? Bilateral otosclerosis — autosomal dominant hereditary stapedial fixation

Q: What does the Carhart notch represent? A mechanical artefact at 2000 Hz on bone conduction audiometry. It is NOT true SNHL — it is caused by the mechanical resonance of the ossicular chain being disrupted. It resolves after successful stapedectomy.

Q: What are the management options?

Observation (mild loss)
Hearing aid (especially bilateral; non-invasive)
Stapedectomy (gold standard for CHL component): stapes removed, replaced with prosthesis; >95% success
Sodium fluoride (may slow progression; still controversial)
Bisphosphonates (may stabilise SNHL component)

Q: What are complications of stapedectomy? Worsened hearing, TM perforation, perilymph fistula, disequilibrium (vertigo), altered taste (chorda tympani damage), tinnitus, sensorineural hearing loss (rare, 1–2%)

🏥 OSCE CASE 4 — Cholesteatoma

Station: History, Examination, Investigations

Opening: "A 45-year-old man is referred to ENT with a 2-year history of right ear discharge and hearing loss. His GP has treated him multiple times with antibiotic drops with no lasting improvement."

History:

Persistent foul-smelling, painless right ear discharge ×2 years
Unilateral right-sided hearing loss (progressive)
Multiple failed courses of topical antibiotics
No prior ear surgery
History of recurrent right ear infections as a child
No vertigo, no facial weakness (important red flag to screen)
No headache, no neck stiffness

Examination:

Attic/posterosuperior retraction pocket with keratinous debris (cholesteatoma matrix)
Pearly white mass visible in pars flaccida
EAC: moist, debris
Conductive hearing loss on tuning fork tests

Questions:

Q: What is your diagnosis? Acquired primary cholesteatoma (pars flaccida/attic type)

Q: What investigations would you request?

CT temporal bone — assess extent, ossicular erosion, tegmen, sigmoid sinus, facial canal involvement
Diffusion-weighted MRI — identifies residual/recurrent cholesteatoma (high specificity, avoids second-look surgery)
Audiometry (PTA + tympanometry)

Q: Why is this condition dangerous? Cholesteatoma erodes bone via enzymatic activity → can destroy ossicles (CHL), erode into the labyrinth (SNHL, vertigo), facial nerve canal (facial palsy), tegmen (CSF leak, meningitis), or sigmoid sinus (thrombosis) → life-threatening intracranial complications

Q: What is the treatment? Surgery (mastoidectomy):

Canal wall up (CWU) mastoidectomy — preserves EAC anatomy; requires planned second-look operation at 12–18 months
Canal wall down (CWD) / modified radical mastoidectomy — creates open cavity; lower recurrence rate; requires lifelong ear cavity care

🏥 OSCE CASE 5 — Choanal Atresia

Station: Neonatal Emergency

Opening: "A midwife calls you urgently to the newborn nursery. A term neonate, born 2 hours ago, is noted to have episodes of turning blue that improve when the baby cries."

History (from midwife/notes):

Term, normal vaginal delivery
Cyclical cyanosis — blue at rest, pink when crying
Increasing respiratory effort between cry episodes
No feeding yet attempted
Antenatal: polyhydramnios noted (impaired fetal swallowing?)
No family history

Examination:

Neonate cyanotic at rest, chest retractions, nasal flaring, no audible nasal airflow
Cyanosis resolves immediately with crying
Attempt to pass 6-F suction catheter through each nostril → fails bilaterally (does not reach nasopharynx at 32 mm)

Questions:

Q: What is the diagnosis? Bilateral choanal atresia (neonatal emergency — neonates are obligate nasal breathers)

Q: Why does crying relieve cyanosis? Crying opens the mouth → bypasses the nasal obstruction → restores oxygenation via the oral airway

Q: What is the immediate management?

Oral airway (McGovern nipple/oropharyngeal airway) — maintains airway immediately
Intubation if unable to maintain airway
NG tube for feeding
Urgent CT scan to characterise the atresia (bony vs. mixed, unilateral vs. bilateral, thickness)
Assess for associated anomalies — CHARGE syndrome (ECG, echo, ophthalmology, renal USS)
Surgical repair — transnasal endoscopic choanoplasty (definitive)

Q: What does CHARGE stand for? Coloboma, Heart defects, Atretic choana, Retardation of growth/development, Genitourinary abnormalities, Ear anomalies

🏥 OSCE CASE 6 — Sinusitis with Complications

Station: History + Emergency Management

Opening: "A 28-year-old man presents to A&E with 10 days of right facial pain and blocked nose that initially improved then worsened over the last 2 days. He now has a swollen right eye and fever 39°C."

History:

URTI 12 days ago → initial nasal congestion, then right-sided facial pain/pressure
Initial improvement day 5–6 → then sudden worsening (double-sickening pattern)
Right periorbital swelling, redness
Proptosis / pain on eye movement (red flags)
Fever 39°C, severe headache
No change in vision yet (important to ask)
No neck stiffness (meningism)

Examination:

Right periorbital oedema + erythema
Right eye proptosis (exophthalmos)
Restricted right eye movements (ophthalmoplegia)
Visual acuity — check formally (preserved = pre-septal/orbital cellulitis; reduced = cavernous sinus/orbital abscess)
Tenderness over right maxillary and frontal sinuses

Questions:

Q: What is the complication? Orbital complication of acute sinusitis — likely orbital cellulitis or subperiosteal abscess (Chandler classification stage II–III)

Q: What are Chandler's stages?

Pre-septal (periorbital) cellulitis
Orbital cellulitis
Subperiosteal abscess
Orbital abscess
Cavernous sinus thrombosis

Q: What investigations?

Urgent CT orbits + sinuses with contrast — to differentiate orbital cellulitis from abscess, assess sinus involvement
Blood cultures, FBC, CRP, ESR
Ophthalmology review (visual acuity, afferent pupillary defect)

Q: What is the management?

IV antibiotics — co-amoxiclav ± metronidazole; or ceftriaxone + metronidazole
Stages III–V: Urgent surgical drainage (ENT + ophthalmology joint management)
Nasal decongestants, saline irrigation
Close monitoring of visual acuity (every 1–2 hours)

🏥 OSCE CASE 7 — Allergic Rhinitis

Station: History + Management Counselling

Opening: "A 19-year-old university student presents to the GP. Every spring for the last 4 years she has a runny nose, sneezing, and red itchy eyes. It is affecting her studies, especially around exam time in May."

History:

Seasonal onset (spring/summer — tree/grass pollens)
Sneezing (especially in morning), bilateral watery rhinorrhoea, nasal itching
Red, itchy, watery eyes (allergic rhinoconjunctivitis)
Nasal obstruction (especially evening and night)
No improvement with OTC antihistamines alone
History of childhood eczema; mother has asthma
No asthma symptoms (check — "any wheeze, chest tightness, breathlessness?")

Examination:

Pale, boggy nasal mucosa bilaterally
Clear watery discharge
Bilateral conjunctival injection
Allergic salute crease over nose

Questions:

Q: What is the diagnosis? Seasonal allergic rhinitis (hay fever) — IgE-mediated hypersensitivity to seasonal aeroallergens (grass/tree pollen)

Q: What is the first-line treatment? Topical intranasal corticosteroids (e.g., fluticasone or mometasone) — most effective for nasal congestion; can take 1–2 weeks for full effect; start before season if possible

Q: How would you manage her comprehensively?

Allergen avoidance: Check pollen forecasts, keep windows closed, wear sunglasses outdoors, shower after outdoor exposure
Intranasal corticosteroids — daily (fluticasone 2 sprays each nostril OD)
Non-sedating oral antihistamine (cetirizine, loratadine, fexofenadine) — for sneezing, itching, rhinorrhoea
Antihistamine eye drops (olopatadine) for conjunctival symptoms
If inadequate: add LTRA (montelukast) especially if coexisting asthma
Short course oral steroids (prednisolone 5-day burst) for exam period if severe
Allergen immunotherapy (SLIT/SCIT) — if symptoms persist despite pharmacotherapy; only disease-modifying treatment

Q: What is the link between rhinitis and asthma? United Airway Disease / One Airway concept: 80% of allergic asthmatics have allergic rhinitis. Shared IgE-mediated eosinophilic inflammation. Treating rhinitis can reduce asthma symptoms.

Quick Reference Summary Table

#	Condition	Key Pathogen/Cause	Classic Sign	First-line Rx
1	Furuncle (EAC)	S. aureus	Tragal tenderness	Topical antibiotics ± I&D
2	Otosclerosis	Autosomal dominant bony fixation	Carhart notch; paracusis Willisii	Stapedectomy
3	Choanal Atresia	Bucconasal membrane persistence	Cyclic cyanosis (bilateral)	Oral airway → choanoplasty
4	Nasal Polyps	Chronic eosinophilic inflammation	Pale insensate bilateral masses	Topical INCS ± FESS
5	Adenoiditis	Biofilm reservoir (S. pneumoniae, H. flu)	Adenoid facies; mouth breathing	Adenoidectomy
6	Tonsillitis	Viral / GABHS	Exudative tonsils; cervical LN	Penicillin V (bacterial)
7	Peritonsillar Abscess	Mixed: GABHS + anaerobes	Uvula deviated away; trismus	Needle aspiration + amoxicillin/metronidazole
8	Acute Otitis Media	H. flu, S. pneumoniae	Bulging opaque TM	High-dose amoxicillin (45 mg/kg)
9	Sinusitis	Viral; S. pneumoniae, H. flu (bacterial)	Facial pain; double-sickening	Amoxicillin-clavulanate (ABRS)
10	Rhinitis	Allergen (IgE) / irritant	Pale boggy mucosa; sneezing	Intranasal corticosteroids
11	Otitis Externa	Pseudomonas aeruginosa	Tragal tenderness; pinna traction pain	Ciprofloxacin/dex ear drops + aural toilet
12	Cholesteatoma	Keratinising squamous epithelium	Foul smelly painless discharge; attic perforation	Mastoidectomy
13	Waldeyer's Ring	Lymphoid tissue (palatine + pharyngeal + lingual + tubal tonsils)	Unilateral enlargement → suspect lymphoma	Depends on condition

Sources: Cummings Otolaryngology Head and Neck Surgery; K.J. Lee's Essential Otolaryngology; Robbins Pathologic Basis of Disease; Goldman-Cecil Medicine; Textbook of Family Medicine 9e; Tintinalli's Emergency Medicine; Gray's Anatomy for Students.

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