EN4.{37-39,45} | Throat Pharynx and Oesophagus — Practice Quiz

Correct. The classic triad — progressive dysphagia (solids first, then semi-solids), significant weight loss, and an irregular circumferential endoscopic lesion — strongly indicates oesophageal carcinoma. Squamous cell carcinoma typically involves the middle third; adenocarcinoma typically involves the lower third on a background of Barrett's oesophagus.

Progressive solid→semi-solid dysphagia, significant weight loss, and an irregular endoscopic lesion at mid-oesophagus are hallmarks of oesophageal carcinoma. Achalasia causes dysphagia to both solids and liquids from the outset (motility disorder). Zenker's produces regurgitation of undigested food. Plummer-Vinson (iron-deficiency, post-cricoid web) affects upper oesophagus in middle-aged women but presents with an iron-deficiency phenotype and thin webs, not a friable mass.

Achalasia presents with dysphagia to both solids and liquids simultaneously (motility disorder), not a progressive solid-then-liquid pattern. Zenker's diverticulum presents with regurgitation of undigested food, halitosis, and gurgling sounds, with the pouch visible on barium swallow. Plummer-Vinson syndrome (sideropenic dysphagia) occurs in iron-deficient middle-aged women and involves a post-cricoid web, not a mid-oesophageal mass.

Correct. Solid-only dysphagia indicates the lumen is narrowed (mechanical obstruction) — the patient can still swallow liquids because they are able to pass around or through a partial obstruction. Dysphagia to both solids and liquids from the beginning indicates a neuromuscular/motility disorder (e.g., achalasia) where the oesophageal muscle cannot generate propulsive peristalsis.

Solid-only dysphagia = mechanical obstruction (narrowed lumen — stricture, carcinoma, web). Dysphagia to both solids AND liquids from onset = motility disorder (achalasia, diffuse oesophageal spasm). This distinction guides the next investigation: rigid lumen → endoscopy/barium; motility → manometry.

Severity is not reliably inferred from the solid vs liquid distinction. The oropharyngeal vs oesophageal level is better distinguished by whether the patient has difficulty initiating the swallow (oropharyngeal) or senses obstruction after swallowing (oesophageal). Both benign and malignant lesions can cause mechanical solid-food dysphagia.

Correct. Quinsy (peritonsillar abscess) is characterised by: unilateral swelling of the peritonsillar space (left here), uvular deviation contralateral to the side of abscess, trismus (restricted mouth opening from pterygoid spasm), severe odynophagia, hot-potato voice, and drooling. Management: drainage (needle aspiration or incision) ± tonsillectomy after the acute episode.

Peritonsillar abscess (quinsy) is diagnosed by the triad: unilateral bulging of the anterior pillar/soft palate, uvular deviation to the opposite side, and trismus (restricted mouth opening due to pterygoid muscle spasm). It is a complication of acute tonsillitis — pus collects in the peritonsillar space. EBV (mononucleosis) causes grossly enlarged tonsils with exudate but typically has posterior cervical lymphadenopathy, hepatosplenomegaly, and no uvular deviation.

Acute follicular tonsillitis does not cause uvular deviation or trismus — it is bilateral erythema with exudate without peritonsillar space involvement. Ludwig's angina is a bilateral, rapidly spreading cellulitis of the floor of the mouth (submandibular space) — not a unilateral peritonsillar process. EBV (infectious mononucleosis) causes bilateral tonsillar enlargement, grey-white membrane, cervical lymphadenopathy, and hepatosplenomegaly — uvular deviation and trismus are not features.

Correct. The tonsillar branch of the facial artery enters at the lower pole of the tonsil and is the main vessel at risk during tonsillectomy. Paratonsillar veins are also vulnerable, especially during dissection of the lower pole. This explains why primary haemorrhage (within 24 hours) is most commonly from the lower pole. The internal carotid artery, though close, is protected by the superior pharyngeal constrictor and lateral pharyngeal wall.

The tonsil is supplied by the tonsillar branch of the facial artery (main supply), the ascending pharyngeal artery, dorsal lingual arteries, and branches of the greater palatine artery. The tonsillar branch of the facial artery and paratonsillar veins near the lower pole are at greatest risk during dissection — injury causes primary haemorrhage. The internal carotid artery lies ~2.5 cm posterolateral to the tonsil.

The superior thyroid artery is a branch of the external carotid supplying the thyroid — it is not in the operative field. The ascending pharyngeal artery supplies the tonsil but is not the primary vessel at greatest surgical risk. The lingual artery supplies the tongue — not the tonsil.

Correct. Day 8 haemorrhage = secondary haemorrhage, caused by infection and sloughing of the fibrinous eschar covering the tonsil bed. It is NOT a 'minor' event — it can be life-threatening. Management requires urgent hospital admission, IV access, resuscitation, broad-spectrum antibiotics (to treat underlying infection), and return to theatre for haemostasis if conservative measures fail. Sending this patient home would be dangerous.

Post-tonsillectomy haemorrhage classification: Primary = within 24 hours of surgery (immediate surgical bleed); Reactionary = 24 hours to a few days (from a clot detaching); Secondary = Day 5–10 (due to sloughing of infected eschar — the 'white scab'). Secondary haemorrhage is the most dangerous because parents and patients underestimate it ('just the scab coming off'). Management: hospital admission, IV access, resuscitation, antibiotics; return to theatre if bleeding does not arrest.

Primary haemorrhage occurs within 24 hours of surgery — not on day 8. Reactionary haemorrhage occurs in the first few days as clots detach. Discharging with oral tranexamic acid alone is inadequate and potentially dangerous — secondary haemorrhage requires hospital admission and IV management.

Correct. The Paradise criteria for tonsillectomy are: ≥7 documented episodes in the preceding 12 months, OR ≥5 per year over 2 consecutive years, OR ≥3 per year over 3 consecutive years. Each episode must meet at least one clinical criterion: temperature >38.3°C, cervical lymphadenopathy, tonsillar exudate, or positive GABHS throat culture. One peritonsillar abscess (quinsy) is an additional absolute indication.

Paradise criteria (Dhingra): ≥7 episodes/year × 1 year; OR ≥5 episodes/year × 2 consecutive years; OR ≥3 episodes/year × 3 consecutive years — each episode must be physician-documented and meet clinical criteria (fever >38.3°C, cervical adenopathy, tonsillar exudate, or positive GABHS culture). A single peritonsillar abscess is an absolute indication for interval tonsillectomy.

Three infections over 3 years (i.e., 1/year) does not meet Paradise criteria — this is an inadequate frequency. Four per year for 2 years does not meet the criteria (requires 5 per year for 2 years). Peritonsillar abscess is an absolute indication, but the question asks specifically about the Paradise criteria for recurrent tonsillitis — the stated answer incorporates the correct Paradise thresholds.

Correct. Amoxicillin (and ampicillin) administration during EBV infectious mononucleosis causes a florid maculopapular rash in up to 80–90% of patients. This is an immune-mediated drug reaction specific to active EBV infection — not a true penicillin allergy — but it can be alarming and cause the patient to be incorrectly labelled 'penicillin allergic' for life. EBV mononucleosis is managed supportively. Steroids may be used for airway compromise or severe thrombocytopenia.

EBV infectious mononucleosis is the most important differential for tonsillitis in young adults. The clinical trap: prescribing amoxicillin (or ampicillin) to an EBV-positive patient triggers a widespread non-allergic maculopapular rash in up to 80–90% of cases — this is not a true penicillin allergy but an immune-complex-mediated reaction specific to EBV infection. The correct management for EBV tonsillitis is supportive (analgesics, hydration, rest) — not antibiotics.

Amoxicillin does not cause nephrotoxicity in this context. Haemolytic anaemia can occur in EBV infection itself (cold agglutinin haemolysis) but is not specifically induced by amoxicillin. The concern is a drug-EBV immune interaction causing a maculopapular rash — not antibiotic resistance selection.

Correct. Squamous cell carcinoma of the oesophagus classically involves the upper and middle thirds (25 cm = mid-oesophagus) and is strongly associated with alcohol and tobacco use — both act as direct chemical carcinogens on the non-keratinised squamous epithelium. GORD/Barrett's oesophagus leads to metaplasia and adenocarcinoma of the lower oesophageal third — a different entity.

Oesophageal SCC: middle and upper thirds; risk factors = alcohol, tobacco, hot beverages, nutritional deficiency, Plummer-Vinson syndrome, achalasia (chronic stasis). Oesophageal adenocarcinoma: lower third; risk factors = chronic GORD, Barrett's oesophagus, obesity. Alcohol + tobacco in a middle-aged male = SCC of the mid-oesophagus.

GORD and Barrett's oesophagus are the risk factors for ADENOCARCINOMA of the lower oesophagus — not squamous cell carcinoma. Plummer-Vinson syndrome causes SCC at the post-cricoid region (upper oesophagus) in iron-deficient women. Achalasia is a risk factor for SCC through chronic food stasis but is less common than alcohol/tobacco and typically involves the mid-lower oesophagus.

Correct. Zenker's diverticulum presents with regurgitation of undigested food (no bile — it is above the stomach), halitosis from food decomposing in the pouch, characteristic gurgling sounds (Boyce's sign) in the neck, and positional worsening. Barium swallow is the diagnostic investigation of choice. Treatment: endoscopic stapling (Dohlman's procedure) or open surgical repair.

Zenker's diverticulum (pharyngeal pouch) is a pulsion diverticulum arising through Killian's dehiscence (between the thyropharyngeus and cricopharyngeus parts of the inferior constrictor). Hallmark features: regurgitation of undigested, non-bile-stained food (sometimes hours after eating), halitosis, a gurgling neck swelling (Boyce's sign), and nocturnal aspiration. Barium swallow confirms.

Achalasia presents with dysphagia to both solids and liquids (motility failure) but without regurgitation of undigested food or neck gurgling — the dilated oesophagus may regurgitate semi-digested food. Oesophageal carcinoma causes progressive dysphagia with weight loss but not halitosis or neck gurgling. GORD causes heartburn, acid regurgitation, and waterbrash — not undigested food regurgitation.

Correct. Obstructive sleep apnoea (OSA) from tonsillar/adenoidal hypertrophy is one of the most compelling indications for tonsillectomy in children — the neurocognitive consequences (poor concentration, behavioural issues, academic under-performance) and cardiovascular effects (pulmonary hypertension in severe cases) make this urgent. OSA confirmed on overnight oximetry + tonsillar hypertrophy is a sufficient independent indication, even if the recurrence frequency alone might not meet Paradise criteria.

Absolute indications for tonsillectomy beyond Paradise criteria include: obstructive sleep apnoea (OSA) — the most compelling because of adverse neurocognitive and cardiovascular consequences in children. OSA confirmed by overnight oximetry + tonsillar hypertrophy = surgical urgency. Other absolute indications: peritonsillar abscess, suspected malignancy (asymmetric tonsil), diphtheria carrier. Relative indications: halitosis, tonsil stones. GABHS positivity alone is not a surgical indication.

A positive GABHS swab indicates the infection organism but is not by itself a surgical indication. Grade 2 tonsils (reaching the anterior pillar but not the midline) are not enlarged enough to indicate surgery on size alone. Halitosis alone is a relative indication at best — not the strongest argument for surgery in a child.