EN4.{27,31-34} | Sinonasal Inflammation and Tumours — Practice Quiz

Correct. Bilateral pale grape-like masses from the middle meatus in an adult female with anosmia and watery rhinorrhoea are classic ethmoidal nasal polyps. They arise from chronic eosinophilic mucosal inflammation in the ethmoid sinuses, often associated with allergy, aspirin sensitivity (Samter's triad), or CRS.

Ethmoidal polyps are bilateral, multiple, arise from the middle meatus and ethmoid sinuses, and are associated with allergy/eosinophilic inflammation in adults. Antrochoanal polyp (Killian's) is unilateral, single, arises from the maxillary antrum — common in children/young adults. Never swap laterality.

Antrochoanal polyp (A) is a single, unilateral mass originating from the maxillary antrum — not bilateral. Inverted papilloma (C) is typically unilateral, not pale, and is a benign tumour with malignant potential requiring histology. JNA (D) affects adolescent males and presents with unilateral obstruction and recurrent epistaxis — not bilateral anosmia in an adult woman.

Correct. Contrast-enhanced CT is the first-line investigation for suspected JNA. It demonstrates the characteristic vascular nasopharyngeal mass, defines its extent (pterygopalatine fossa, infratemporal fossa, intracranial), and shows the pathognomonic Holman-Miller sign (anterior bowing of the posterior wall of the maxillary sinus). Biopsy is absolutely contraindicated due to catastrophic haemorrhage risk.

JNA — NEVER BIOPSY (catastrophic haemorrhage risk from the highly vascular tumour). Contrast CT reveals a vascular nasopharyngeal mass with characteristic anterior bowing of the posterior wall of the maxillary antrum (antral sign / Holman-Miller sign) and establishes the extent. Angiography confirms vascularity before embolisation.

Biopsy (A) is absolutely contraindicated in JNA — this is the most important rule in ENT. The highly vascular tumour can bleed catastrophically when incised. MRI brain with gadolinium (C) has a role in assessing intracranial extension but contrast CT of the nose and PNS comes first. FNAC (D) is never indicated for a vascular nasopharyngeal mass in an adolescent male — the diagnosis is clinical plus imaging.

Correct. The EPOS criterion distinguishing ABRS from viral URTI is persistence of symptoms beyond 10 days without improvement OR a biphasic course (improvement then worsening, the 'double-sickening' sign). Both fever and purulent rhinorrhoea can occur in viral URTI and are therefore insufficient to diagnose ABRS alone.

ABRS vs viral URTI: symptoms >10 days without improvement, OR worsening after initial improvement ('double-sickening' sign), are the EPOS criteria distinguishing bacterial sinusitis from viral. Most viral URTIs resolve within 10 days. Fever and purulent discharge alone are not sufficient to distinguish bacterial from viral — both can occur in viral URTI.

Fever with purulent rhinorrhoea (A) can occur in viral URTI and is not specific for ABRS. Nasal polyps (C) are associated with chronic rhinosinusitis/eosinophilic disease — not acute bacterial sinusitis. Throat pain and lymphadenopathy (D) are non-specific features of URTI, not a distinguishing criterion for ABRS.

Correct. The red flag triad — middle-aged male, unilateral symptoms >3 months, bone erosion on CT — mandates exclusion of sinonasal malignancy first. The most common sinonasal malignancy is squamous cell carcinoma of the maxillary sinus. Farmers with wood dust/agricultural chemical exposure have increased risk. Histopathology (biopsy) is required for definitive diagnosis.

Unilateral nasal symptoms in a middle-aged male + bone erosion on CT = malignancy until proven otherwise. Sinonasal SCC and adenocarcinoma are associated with wood/leather dust and nickel exposure. Antrochoanal polyps do not erode bone. Inverted papilloma can cause bone remodelling but has far less aggressive erosion than malignancy.

Antrochoanal polyp (A) does not erode bone and typically occurs in younger patients — polyps are soft, translucent, non-invasive. Inverted papilloma (B) can remodel bone but does not typically cause frank erosion in this aggressive pattern; however, it has malignant potential and would also require biopsy. Rhinoscleroma (D) causes submucosal sclerotic tissue — not bone erosion with a destructive mass.

Correct. Granulomatosis with polyangiitis (formerly Wegener's) classically presents with necrotising granulomatous inflammation of the upper respiratory tract (saddle-nose deformity, epistaxis, crusting) + lower respiratory tract + kidneys. ANCA (usually c-ANCA/anti-PR3, but p-ANCA occurs) is positive. Saddle-nose deformity from cartilage/bone destruction is a hallmark ENT feature.

GPA (Wegener's) = necrotising granulomata + systemic vasculitis (lungs, kidneys) + c-ANCA (anti-PR3) typically, but p-ANCA may occur. Saddle-nose deformity due to cartilage/bone destruction is a classic ENT feature. Nasal TB shows caseous granulomata with Langhans giant cells + AFB. Sarcoidosis = non-caseating granulomata. Rhinoscleroma (Klebsiella) = Mikulicz cells + Russell bodies.

Nasal TB (A) shows caseous granulomata with Langhans giant cells and AFB; ANCA is not positive. Sarcoidosis (C) shows non-caseating granulomata without vessel destruction; ANCA is typically negative. Rhinoscleroma (B) is caused by Klebsiella rhinoscleromatis and shows characteristic Mikulicz cells and Russell bodies on histology — not necrotising granulomata.

Correct. JNA has a rich blood supply primarily from the internal maxillary artery (branch of external carotid artery). Pre-operative embolisation of the feeding vessels 24–48 hours before surgery significantly reduces intraoperative haemorrhage, which is the major risk during resection. Without embolisation, blood loss can be catastrophic.

Pre-operative embolisation in JNA (typically of the internal maxillary artery branches, 24–48 hours before surgery) reduces blood loss during what is otherwise a very haemorrhagic resection. The tumour is fed by the internal maxillary artery (from external carotid). Embolisation does NOT significantly reduce tumour size, does NOT prevent spread, and biopsy remains contraindicated.

Embolisation reduces intraoperative blood loss — it does not significantly shrink the tumour (A). Intracranial spread (C) is a concern in advanced tumours, but embolisation does not prevent spread — wide surgical resection does. Biopsy (D) remains absolutely contraindicated even after embolisation — the diagnosis is made clinically and radiologically.

Correct. Samter's triad (also called Aspirin-Exacerbated Respiratory Disease, AERD) is the combination of (1) nasal polyps, (2) asthma, and (3) aspirin/NSAID hypersensitivity causing bronchospasm. It is due to COX-1 inhibition causing a leukotriene surge. Leukotriene receptor antagonists (montelukast) are particularly effective as adjuncts.

Samter's triad = nasal polyps + asthma + aspirin/NSAID sensitivity (now called AERD — Aspirin-Exacerbated Respiratory Disease). Mechanism: cyclooxygenase-1 inhibition diverts arachidonic acid to the lipoxygenase pathway, generating excess cysteinyl leukotrienes. Management includes intranasal steroids, leukotriene antagonists, aspirin desensitisation.

Kartagener's syndrome (A) = bronchiectasis + situs inversus + sinusitis (due to primary ciliary dyskinesia). Young's syndrome (C) = obstructive azoospermia + bronchiectasis + sinusitis. Churg-Strauss (D) = eosinophilic granulomatosis with polyangiitis — asthma + eosinophilia + vasculitis; nasal polyps may occur but aspirin sensitivity is not the defining feature.

Correct. The Chandler Stage III orbital complication is a subperiosteal abscess — a collection of pus between the periorbita (periosteum lining the orbit) and the bony orbital wall, most commonly from ethmoid sinusitis. Clinical features: proptosis, restricted eye movements, chemosis, fever. CT shows a lenticular collection medial to the orbital fat. Urgent surgical drainage (endoscopic or external) plus IV antibiotics are required.

Chandler classification of orbital complications: I = preseptal cellulitis (oedema anterior to orbital septum, no proptosis); II = orbital cellulitis (diffuse infection in orbital fat, mild proptosis); III = subperiosteal abscess (collection between periorbita and bony orbit — CT finding described, proptosis + restricted EOM); IV = orbital abscess (pus within orbital fat, severe); V = cavernous sinus thrombosis. Stage III needs urgent surgical drainage.

Preseptal cellulitis (A) has inflammatory oedema anterior to the orbital septum with lid swelling but no proptosis and no restricted eye movements. Orbital cellulitis (B) causes diffuse infection in orbital fat with mild proptosis but without a discrete fluid collection on CT. Orbital abscess (D) is Stage IV — pus within the orbital fat itself (not between periorbita and bone wall), causing more severe proptosis and ophthalmoplegia.

Correct. Nasopharyngeal carcinoma classically presents with painless unilateral upper deep cervical lymphadenopathy as the first or presenting complaint in 50–70% of patients. The primary tumour in the fossa of Rosenmüller may be small and clinically silent. NPC must be excluded in any adult with unexplained unilateral cervical lymphadenopathy using nasopharyngoscopy and biopsy (of nasopharynx — NOT lymph node FNAC alone).

NPC typically presents in adults (peak 40–60 years, EBV-associated) with unilateral cervical lymphadenopathy — often as the FIRST presenting symptom (in 50–70% of cases) — because the primary tumour is small but lymph drainage is rich. The associated features are Eustachian obstruction (unilateral SOM → conductive HL), nasal obstruction, and cranial nerve palsies. An adult with unexplained unilateral upper cervical lymphadenopathy must have NPC excluded.

Bilateral conductive hearing loss (A) occurs in NPC due to bilateral Eustachian tube obstruction and bilateral SOM, but it also occurs in adenoid hypertrophy — it does not distinguish the two. Nasal obstruction and rhinorrhoea (C) occur in both conditions. Nosebleeds without nasal mass (D) can occur in NPC but are non-specific; unilateral cervical lymphadenopathy is far more specific.

Correct. The ostiomeatal complex (OMC) is the key surgical target in FESS. It is the functional drainage pathway for the anterior ethmoid, frontal and maxillary sinuses. Obstruction of the OMC (by polyps, mucosal oedema, or deviated septum) drives CRS. FESS opens and enlarges the OMC to restore ventilation and mucociliary clearance.

The ostiomeatal complex (OMC) — the functional unit comprising the maxillary sinus ostium, infundibulum, uncinate process, ethmoid bulla, and middle meatus — is the anatomical bottleneck obstructed in CRS/nasal polyps. FESS restores ventilation and drainage by opening the OMC. The goal is to restore mucociliary clearance by correcting anatomical obstruction at this key junction.

The superior turbinate (A) may occasionally be partially resected for sphenoethmoid cell access but is not the primary target in FESS for CRS. The sphenopalatine ganglion (C) can be targeted for neurogenic rhinitis but is not the key target for CRS/polyp surgery. The cribriform plate (D) is a critical structure to AVOID in FESS — damage causes CSF leak.