Practice 40 MCQs on MCQ: Respiratory System Pathology with OmpathStudy. Built for Kenyan medical and health students to revise key concepts and prepare for e...
Q1. Adenocarcinoma has become the most common primary lung tumour. Which population is most characteristically affected?
Answer: Women, non-smokers, and individuals under 45 years
Explanation: Adenocarcinoma is now the most common lung cancer overall, particularly in women, non-smokers, and those under 45 — a demographic shift from squamous cell carcinoma.
Q2. A 62-year-old male smoker presents with a central hilar mass and haemoptysis. Biopsy shows keratin pearls and intercellular bridges. Which paraneoplastic syndrome is most expected?
Answer: Hypercalcaemia from PTH-related peptide secretion
Explanation: Squamous cell carcinoma secretes PTH-related peptide causing humoral hypercalcaemia — the most characteristic paraneoplastic syndrome of squamous cell carcinoma.
Q3. The overall 5-year survival for all stages of lung cancer combined is approximately:
Answer: 16%, largely unchanged over the past 35 years
Explanation: The overall 5-year survival for all stages combined remains approximately 16%, reflecting the fact that most patients present with advanced metastatic disease.
Q4. A non-smoking 40-year-old Asian woman is diagnosed with lung adenocarcinoma. Molecular testing reveals an EGFR mutation. KRAS testing is unnecessary because:
Answer: KRAS and EGFR mutations are mutually exclusive as KRAS lies downstream of EGFR
Explanation: EGFR and KRAS mutations are mutually exclusive because KRAS lies downstream of EGFR — activating either produces overlapping oncogenic effects, making co-mutation redundant.
Q5. A lung biopsy shows tumour cells growing in a monolayer along alveolar septa without stromal invasion, desmoplasia, or architectural destruction. The lesion measures 2.8 cm. What is the diagnosis?
Answer: Adenocarcinoma in situ — lepidic growth under 3 cm without invasion
Explanation: AIS is defined by lepidic growth ≤3 cm along pre-existing alveolar septa with absolutely no stromal invasion, desmoplasia, or alveolar architectural destruction.
Q6. A patient with SCLC develops proximal limb weakness that paradoxically improves with repeated movement. Electromyography shows facilitation with repetitive stimulation. This paraneoplastic syndrome is:
Answer: Polymyositis from immune complex deposition within skeletal muscle
Explanation: Lambert-Eaton myasthenic syndrome is most associated with SCLC. Unlike true myasthenia gravis, strength paradoxically improves with repetitive stimulation due to calcium accumulation.
Q7. The "field effect" in lung carcinogenesis means:
Answer: Widespread mutagenesis of respiratory mucosa with 3p deletions even in benign epithelium
Explanation: The field effect describes large areas of respiratory mucosa being mutagenised by carcinogens — loss of chromosome 3p is found even in benign bronchial epithelium of smokers without cancer.
Q8. A 58-year-old male with a right apical lung mass develops right-sided ptosis, miosis, anhidrosis, enophthalmos, and severe pain radiating down the ulnar aspect of the right arm. CT shows rib destruction. The complete diagnosis is:
Answer: Pancoast tumour causing Pancoast syndrome including Horner syndrome
Explanation: An apical lung tumour invading the brachial and cervical sympathetic plexus causes Pancoast syndrome — Horner syndrome plus ulnar nerve pain and rib destruction are collectively termed Pancoast syndrome.
Q9. Which molecular profile is most characteristic of small cell lung carcinoma?
Answer: RB mutation 90%, TP53 mutation 90%, rare KRAS mutation, absent EGFR mutation
Explanation: SCLC is characterised by RB mutations (~90%), TP53 mutations ( 90%), rare KRAS mutations, and absent EGFR mutations — a profile distinctly different from NSCLC subtypes.
Q10. A patient with ALK-rearranged adenocarcinoma responds brilliantly to crizotinib but relapses after 9 months with a new mutation at the ALK drug-binding domain. This mechanism of resistance is:
Answer: Alteration of the drug target itself through a secondary resistance mutation
Explanation: The most common mechanism of kinase inhibitor resistance involves secondary mutations within the target kinase domain that directly prevent drug binding to the altered target.
Q11. A 30-year-old non-smoking male develops spontaneous left pneumothorax. CT reveals a subpleural bulla. Which emphysema subtype is responsible?
Answer: Distal acinar (paraseptal) emphysema producing subpleural bullae in young adults
Explanation: Distal acinar emphysema affects the subpleural distal acinus in young adults without smoking history, producing subpleural bullae that rupture causing spontaneous pneumothorax.
Q12. At the time of lung cancer diagnosis, what proportion already have distant metastases?
Answer: More than 50%, with an additional 25% having regional lymph node disease
Explanation: More than 50% of lung cancer patients already have distant metastases at diagnosis, with an additional 25% having regional lymph node involvement — only a minority have truly localised disease.
Q13. The Azzopardi effect in SCLC refers specifically to:
Answer: Basophilic encrustation of vascular walls by DNA from necrotic tumour cells
Explanation: The Azzopardi effect is the basophilic encrustation of vascular walls by DNA released from necrotic SCLC cells — a specific and diagnostically recognisable morphologic hallmark.
Q14. Heavy smokers with asbestos exposure face approximately what level of increased lung carcinoma risk?
Answer: Approximately 55-fold increased risk from synergistic interaction of both carcinogens
Explanation: Asbestos alone increases lung carcinoma risk 5-fold in non-smokers; combined with heavy smoking the risk rises synergistically to approximately 55-fold due to carcinogen adsorption onto fibres.
Q15. A patient with mesothelioma is also a 25 pack-year smoker with asbestos exposure. Which statement correctly describes the relationship between smoking and mesothelioma risk?
Answer: Smoking does not increase mesothelioma risk despite greatly amplifying lung carcinoma risk
Explanation: Cigarette smoking does NOT increase mesothelioma risk — mesothelioma is driven solely by asbestos. However, smoking + asbestos dramatically increases lung carcinoma risk (~55-fold).
Q16. What is the correct precursor sequence leading to invasive squamous cell carcinoma of the lung?
Answer: Basal cell hyperplasia → squamous metaplasia → dysplasia → carcinoma in situ → invasion
Explanation: The squamous cell carcinoma precursor sequence is basal cell hyperplasia → squamous metaplasia → squamous dysplasia → carcinoma in situ → invasive squamous cell carcinoma.
Q17. Typical carcinoid tumours fundamentally differ from SCLC in which way?
Answer: Typical carcinoids are low-grade with greater than 85% 5-year survival versus SCLC median 1 year
Explanation: Both are neuroendocrine tumours but typical carcinoids are low-grade with 85% 5-year survival, while SCLC is extremely aggressive with a median survival of approximately 1 year even with treatment.
Q18. An atypical carcinoid differs from a typical carcinoid by which features?
Answer: Higher mitotic rate, focal necrosis, greater metastatic potential, and TP53 mutations in 20–40%
Explanation: Atypical carcinoids show higher mitotic rates, focal necrosis, increased metastatic potential, and TP53 mutations in 20–40% of cases — features absent in typical carcinoids.
Q19. A patient with a central lung mass develops Cushing syndrome with high urinary cortisol that fails high-dose dexamethasone suppression. Which tumour is most responsible?
Answer: Small cell carcinoma producing ectopic ACTH causing Cushing syndrome
Explanation: SCLC produces ectopic ACTH causing Cushing syndrome that characteristically fails high-dose dexamethasone suppression — distinguishing it from pituitary-driven Cushing disease.
Q20. Malignant mesothelioma most commonly arises from which location and with what asbestos exposure history?
Answer: Parietal or visceral pleura with asbestos history in 80–90% of cases
Explanation: Malignant mesothelioma arises from the parietal or visceral pleura (also peritoneum/pericardium rarely), with 80–90% of cases having a history of asbestos exposure.
Q21. At autopsy a lung is ensheathed by thick yellow-white firm tumour obliterating the pleural space. Microscopy shows cuboidal cells with papillary buds lining tubular and microcystic spaces. This pattern is most likely confused with:
Answer: Pulmonary adenocarcinoma due to similar glandular architecture
Explanation: The epithelial pattern of malignant mesothelioma — the most common pattern — is most frequently confused with pulmonary adenocarcinoma due to strikingly similar glandular morphology.
Q22. After asbestos exposure ceases, what happens to the lifetime risk of mesothelioma?
Answer: Lifetime risk does not diminish because asbestos fibres remain permanently in body tissues
Explanation: Unlike smoking where risk decreases after cessation, inhaled asbestos fibres persist permanently in body tissues, meaning the lifetime risk of mesothelioma never diminishes after any exposure.
Q23. Which gene is most commonly mutated in both sporadic and familial malignant mesothelioma?
Answer: BAP1 — tumour suppressor involved in DNA repair affected in familial cases
Explanation: BAP1 is the most commonly mutated gene in sporadic mesothelioma and is also affected by germline mutations in familial mesothelioma — asbestos generates reactive oxygen species causing DNA damage.
Q24. A pleural effusion with protein 30 g/L and neutrophilic infiltrate develops following right lower lobe pneumonia. This is best classified as:
Answer: Exudate from microbial invasion — suppurative pleuritis progressing toward empyema
Explanation: An exudate (protein 30 g/L with inflammatory cells) from pneumonia represents suppurative pleuritis from direct microbial extension — one of the four principal causes of pleural exudate formation.
Q25. A young male develops sudden dyspnoea, absent right breath sounds, tracheal deviation to the left, and rapidly falling blood pressure. The immediately life-threatening mechanism is:
Answer: Tension pneumothorax — ball-valve air leak causing mediastinal shift and circulatory collapse
Explanation: Tension pneumothorax occurs when a ball-valve leak allows air into but not out of the pleural space — the resulting mediastinal shift compresses the pulmonary circulation and can cause rapid death.
Q26. Chylothorax is described as always clinically significant. The most important reason is:
Answer: It implies major lymph duct obstruction, most commonly by intrathoracic malignancy
Explanation: Chylothorax (milky lymphatic fluid with lipid microglobules) is always significant because it implies obstruction of major lymph ducts, most commonly by an intrathoracic malignancy such as lymphoma.
Q27. In approximately what percentage of common cold cases can no causative agent be identified?
Answer: About 40%, possibly from undiscovered respiratory viral agents
Explanation: In approximately 40% of common cold cases, no causative agent can be identified despite thorough investigation — possibly involving as-yet undiscovered respiratory viruses.
Q28. A 4-year-old presents with sudden fever, drooling, refusal to swallow, and a muffled voice while sitting leaning forward with her neck extended. The most critical immediate management is:
Answer: Immediate airway maintenance and ENT consultation for acute epiglottitis
Explanation: Acute bacterial epiglottitis (H. influenzae) can cause fatal airway obstruction — maintaining a patent airway is the absolute immediate priority before any other investigation or intervention.
Q29. Streptococcal tonsillitis must be identified and treated early to prevent:
Answer: Peritonsillar abscess, acute rheumatic fever, and poststreptococcal glomerulonephritis
Explanation: Untreated group A streptococcal tonsillitis risks peritonsillar abscess (quinsy), acute rheumatic fever, and poststreptococcal glomerulonephritis — all potentially serious non-suppurative complications.
Q30. Diphtheritic laryngitis produces its classic dirty-grey pseudomembrane through which mechanism?
Answer: Corynebacterium diphtheriae exotoxin causing mucosal necrosis and fibrinopurulent exudate
Explanation: C. diphtheriae elaborates a powerful exotoxin causing necrosis of the mucosal epithelium with a dense fibrinopurulent exudate forming the characteristic dirty-grey pseudomembrane.
Q31. A 3-year-old develops a barking cough, inspiratory stridor, and low-grade fever following a mild cold. Which statement is correct?
Answer: Parainfluenza virus is the most common cause; occasionally airway narrowing causes respiratory failure
Explanation: Parainfluenza virus causes most cases of croup. It is generally self-limited with barking cough and stridor, but occasional cases develop dangerous subglottic oedema causing respiratory failure.
Q32. Nasopharyngeal carcinoma contains EBV genome in virtually all cases worldwide. How does EBV drive carcinoma development?
Answer: EBV integrates into squamous epithelial DNA causing immediate malignant transformation
Explanation: EBV first replicates in nasopharyngeal epithelium then infects nearby tonsillar B lymphocytes — this sequence leads to transformation of epithelial cells in genetically susceptible individuals.
Q33. The undifferentiated variant of nasopharyngeal carcinoma is characterised by:
Answer: Large epithelial cells with syncytial growth, prominent eosinophilic nucleoli, and dense T cell infiltrate
Explanation: The undifferentiated variant — most common and most EBV-linked — shows large cells with syncytial growth, prominent eosinophilic nucleoli, and dense T cell infiltration responding to viral antigens.
Q34. Laryngeal papillomas in children (RRP) differ from those in adults because:
Answer: Children acquire HPV 6/11 vertically during delivery developing multiple recurrent lesions
Explanation: Children acquire HPV 6/11 via vertical transmission during delivery developing recurrent respiratory papillomatosis — multiple lesions that recur after excision, unlike the typically single adult lesions.
Q35. A 55-year-old male smoker has a pearly-grey plaque on the right true vocal cord confirmed as SCC confined to the glottis. What prognosis does this location confer?
Answer: Favourable prognosis as approximately 90% of glottic tumours are confined to the larynx at diagnosis
Explanation: Glottic tumours cause early symptoms (hoarseness), have sparse lymphatics limiting spread, and approximately 90% are larynx-confined at diagnosis — conferring the best prognosis among laryngeal locations.
Q36. Which laryngeal tumour location carries the worst prognosis due to rich lymphatics causing early cervical nodal metastases?
Answer: Supraglottic tumours — rich lymphatics cause nodal metastases in approximately one-third
Explanation: Supraglottic tumours have rich lymphatic spaces causing approximately one-third to metastasise to cervical lymph nodes at diagnosis — worse nodal involvement than glottic but subglottic tumours present latest.
Q37. A 2 cm incidental coin lesion on chest X-ray in a 50-year-old shows mature cartilage, fat, and fibrous tissue on biopsy. Cytogenetics reveals clonal chromosomal abnormalities. The correct statement is:
Answer: This is a pulmonary hamartoma — technically a benign neoplasm despite the developmental-sounding name
Explanation: Clonal cytogenetic abnormalities confirm this is a true benign neoplasm. Despite being called a hamartoma, it is not a developmental anomaly — the name is technically a misnomer.
Q38. The neuroendocrine spectrum of lung tumours ordered from lowest to highest malignant potential is:
Answer: Typical carcinoid → atypical carcinoid → large cell neuroendocrine carcinoma → SCLC
Explanation: The correct spectrum of increasing aggressiveness is: typical carcinoid → atypical carcinoid → large cell neuroendocrine carcinoma → SCLC.
Q39. A patient with lung cancer has adrenal glands nearly obliterated by metastases on CT but shows no clinical signs of adrenal insufficiency. This is explained by:
Answer: Residual islands of cortical cells being sufficient to maintain adequate adrenal function
Explanation: Even when adrenal glands are nearly obliterated by metastatic tumour, residual islands of cortical cells persist and produce sufficient cortisol to prevent clinical Addison disease.
Q40. A non-smoking woman with lung adenocarcinoma responds dramatically to gefitinib but relapses after 11 months. Rebiopsy shows a T790M secondary EGFR mutation. This represents:
Answer: Alteration of the drug target itself through a secondary resistance mutation preventing drug binding
Explanation: T790M is a secondary EGFR mutation altering the drug-binding domain, directly preventing gefitinib from binding — the most common mechanism of acquired resistance to first-generation EGFR inhibitors.