EN4.{21-26,28-29} | Nose Airway and Rhinitis Disorders — Graded Quiz

Correct. The antrochoanal polyp (Killian's polyp) is a unilateral, single polyp originating from the maxillary antrum and extending posteriorly through the choana into the nasopharynx. It is more common in children and young adults. Its unilateral nature distinguishes it from the bilateral ethmoidal polyps of allergic rhinitis.

Antrochoanal (Killian's) polyp = unilateral, single, from maxillary antrum → posterior choana → nasopharynx; common in children/young adults. Ethmoidal polyps = bilateral, multiple, allergic, in adults.

Ethmoidal polyps are bilateral and multiple — arising from the ethmoid sinuses in allergic adults. A nasal dermoid is a developmental midline cystic lesion. The key distinguishing feature is unilaterality + maxillary antrum origin = antrochoanal (Killian's) polyp.

Correct. Little's area (Kiesselbach's plexus) on the anterior nasal septum is the commonest site of epistaxis. It is an anastomotic watershed of four arterial systems. Anterior epistaxis from this site is easily visible and controlled with direct pressure, silver nitrate cautery, or anterior packing.

Little's area = Kiesselbach's plexus = anterior nasal septum (~1 cm from columella); commonest site of epistaxis, especially in children. Woodruff's plexus = posterior lateral wall = site of posterior epistaxis in elderly hypertensives.

Woodruff's plexus (posterior lateral nasal wall) is the site of posterior epistaxis in elderly hypertensives — blood flows down the throat. The posterior septum near the sphenopalatine foramen is part of the posterior circulation. The superior turbinate is rarely a source of clinically significant epistaxis.

Correct. Septoplasty is the current gold-standard surgery for symptomatic DNS. It conserves the cartilage L-strut, preserves mucoperiosteum and mucoperichondrium, and has a lower rate of complications (saddle nose, perforation) compared with the older submucous resection technique.

Septoplasty (cartilage-conserving) is now the standard surgery for DNS, replacing the older SMR (which removed excess cartilage risking saddle-nose). Rhinoplasty = cosmetic external nasal reshaping. FESS = sinonasal disease.

SMR removes excess cartilage and is associated with saddle nose deformity and septal perforation — it has been largely replaced by septoplasty. Rhinoplasty addresses external nasal contour (cosmetic). FESS is for sinusitis and polyps, not septal deviation.

Correct. When adenoid hypertrophy causes obstructive nasal symptoms AND otitis media with effusion (OME/glue ear), the combined procedure — adenoidectomy plus bilateral myringotomy and grommet insertion — addresses both the causative obstruction and the established middle ear effusion. This is the standard evidence-based approach for this combined presentation.

Adenoid hypertrophy → Eustachian tube dysfunction → OME (glue ear) → conductive hearing loss. Standard management: adenoidectomy (removes the cause) + bilateral myringotomy with grommet insertion (treats the effusion). Adenoidectomy alone may not restore hearing promptly if effusion is established.

Adenoidectomy alone treats the cause but may leave the established effusion in place. Grommets alone do not address the underlying nasopharyngeal obstruction from the adenoids. Tonsillectomy is not indicated unless tonsil hypertrophy also contributes to obstruction.

Correct. Nasal smear showing eosinophilia (>20% eosinophils) supports allergic rhinitis. Combined with a positive skin prick test or elevated specific IgE, eosinophilia on nasal cytology confirms the diagnosis. In vasomotor rhinitis, the nasal smear is typically normal — this is one of the key distinguishing investigations.

Nasal smear eosinophilia is a key supporting finding in allergic rhinitis (and NARES). Vasomotor rhinitis: normal smear (no eosinophilia). Neutrophil predominance suggests acute infective rhinitis. NARES = eosinophilia on smear but negative SPT/IgE (non-allergic).

Neutrophil predominance on nasal smear suggests acute infective rhinitis (viral/bacterial). Mast cells alone are not the defining smear finding for allergic rhinitis. Vasomotor rhinitis is indeed a clinical diagnosis but nasal smear eosinophilia is the specific cytological marker that supports allergic rhinitis.

Correct. Polysomnography (PSG) is the gold-standard investigation for OSA. It measures the apnea-hypopnea index (AHI), oxygen desaturation events, sleep architecture, arousals, and respiratory effort, classifying severity and guiding treatment (mild → positional/weight loss; moderate-severe → CPAP or surgery).

Polysomnography = gold-standard for OSA: measures AHI (apnea-hypopnea index), SpO2, EEG, respiratory effort. AHI: mild 5-14/h, moderate 15-29/h, severe ≥30/h. Müller's manoeuvre: for surgical site localisation. Imaging: for anatomy, not diagnosis/severity.

Müller's manoeuvre during nasendoscopy maps the level of airway collapse for surgical planning but does not confirm the diagnosis or measure AHI. Lateral neck X-ray and CT assess anatomy and soft tissue but cannot detect nocturnal apnoeas. PSG is the diagnostic gold standard.

Correct. Woodruff's plexus is located on the posterior lateral nasal wall at the level of the inferior meatus. It is supplied by branches of the sphenopalatine artery and ascending pharyngeal artery. Posterior epistaxis arising here presents as blood flowing down the throat (because the bleeding point is posterior to the choana), is more common in elderly hypertensives, and requires posterior nasal packing for control.

Woodruff's plexus = posterior lateral nasal wall (inferior meatus); sphenopalatine + ascending pharyngeal artery territory. Source of posterior epistaxis in elderly hypertensives. Presents as blood flowing down the throat; no visible anterior source. Management: posterior nasal packing (Foley catheter balloon) ± sphenopalatine artery ligation/endoscopic cautery.

Kiesselbach's plexus (Little's area) is the anterior septal vascular zone — source of anterior epistaxis in children and young adults, visible on anterior rhinoscopy. The olfactory cleft and ethmoidal artery territory can bleed but are not the primary sites of posterior epistaxis in hypertensive patients.

Correct. Biopsy of a suspected juvenile nasopharyngeal angiofibroma is absolutely contraindicated. The tumour is extraordinarily vascular and biopsy — even with sedation or in a controlled setting — can precipitate uncontrollable haemorrhage. Diagnosis relies entirely on clinical features (adolescent male + recurrent epistaxis + unilateral mass) and imaging (CT showing Holman-Miller sign). Management is preoperative angiography and embolisation followed by surgical excision.

JNA = juvenile nasopharyngeal angiofibroma. DO NOT BIOPSY — the tumour is extremely vascular; biopsy causes catastrophic, potentially fatal haemorrhage. Diagnosis is clinical + imaging (CT Holman-Miller sign + MRI). Management: preoperative embolisation → surgical excision. This is the single most tested and important management fact for JNA.

General anaesthesia is required for surgery and is not contraindicated per se. Intranasal corticosteroids are inappropriate but not the key contraindication. MRI and CT are both used — CT is typically done first (bony margins + Holman-Miller sign); MRI adds soft tissue characterisation. The cardinal rule is: DO NOT BIOPSY.

Correct. Turbinate hypertrophy with non-shrinking mucosa is a feature of HYPERTROPHIC rhinitis — the exact opposite of atrophic rhinitis. In ozaena (atrophic rhinitis), the turbinates are atrophied and the nasal cavity is abnormally wide. Despite spacious passages, patients experience paradoxical nasal obstruction because the atrophied mucociliary apparatus cannot sense airflow. The foul green crusts result from secondary colonisation (Klebsiella ozaenae).

Atrophic rhinitis (ozaena): wide nasal cavities + atrophied turbinates + paradoxical obstruction (atrophied cilia cannot sense airflow) + foul green crusts + parosmia. Turbinate hypertrophy (firm, non-shrinking) = hypertrophic rhinitis — the OPPOSITE of atrophic rhinitis.

Paradoxical obstruction despite wide cavities, green-grey foul-smelling crusts (foetor), and mucosal and turbinate atrophy are all genuine features of atrophic rhinitis. The 'EXCEPT' feature is turbinate hypertrophy with non-shrinking mucosa — that belongs to hypertrophic rhinitis.

Correct. Per ARIA (Allergic Rhinitis and its Impact on Asthma) guidelines, intranasal corticosteroids (INCS) are the most effective first-line treatment for moderate-to-severe persistent allergic rhinitis. They reduce all four nasal symptoms — sneezing, pruritus, rhinorrhoea and congestion — and are superior to oral antihistamines for nasal congestion in particular.

ARIA guidelines: INCS = most effective first-line therapy for moderate-to-severe/persistent allergic rhinitis (all symptoms including congestion). Oral antihistamines: good for sneezing/pruritus/rhinorrhoea but inferior for congestion. SCIT (immunotherapy) = disease-modifying but not first-line monotherapy. Montelukast: adjunct, inferior to INCS.

Oral second-generation antihistamines are effective for sneezing, pruritus, and rhinorrhoea but are less effective than INCS for nasal obstruction. Montelukast (LTRA) is an adjunct — inferior to INCS as monotherapy. Allergen immunotherapy is disease-modifying (reduces allergen sensitisation) but is indicated for patients who fail or cannot tolerate pharmacotherapy, not as initial treatment.