MCQ: Respiratory System Pathology – 40 MCQs | Kenya MBChB

40 Year 3: Respiratory System Pathology exam questions on MCQ: Respiratory System Pathology for medical students. Includes MCQs, answers, explanations and writt

This MCQ set contains 40 questions on MCQ: Respiratory System Pathology in the Year 3: Respiratory System Pathology unit. Each question includes the correct answer and a detailed explanation for active recall and exam preparation.

Q1: Adenocarcinoma has become the most common primary lung tumour. Which population is most characteristically affected?

  1. A. Women, non-smokers, and individuals under 45 years
  2. B. Elderly males with occupational asbestos exposure history
  3. C. Middle-aged males with greater than 40 pack-year smoking history
  4. D. Immunocompromised patients with recurrent pulmonary infections

Correct answer: A – Women, non-smokers, and individuals under 45 years

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?

  1. A. SIADH causing hyponatraemia and concentrated urine output
  2. B. Hypercalcaemia from PTH-related peptide secretion
  3. C. Cushing syndrome from ectopic ACTH production by tumour
  4. D. Lambert-Eaton syndrome from calcium channel antibody production

Correct answer: B – Hypercalcaemia from PTH-related peptide secretion

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:

  1. A. 35%, reflecting improved early detection programmes
  2. B. 25%, with most patients dying within three years
  3. C. 45%, applicable only to localised disease at diagnosis
  4. D. 16%, largely unchanged over the past 35 years

Correct answer: D – 16%, largely unchanged over the past 35 years

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:

  1. A. KRAS mutations never occur in adenocarcinoma of non-smoking women
  2. B. KRAS mutations only predict response to chemotherapy not targeted therapy
  3. C. KRAS and EGFR mutations are mutually exclusive as KRAS lies downstream of EGFR
  4. D. KRAS testing is replaced entirely by ALK rearrangement testing in Asian patients

Correct answer: C – KRAS and EGFR mutations are mutually exclusive as KRAS lies downstream of EGFR

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?

  1. A. Adenocarcinoma in situ — lepidic growth under 3 cm without invasion
  2. B. Minimally invasive adenocarcinoma — invasive component present but under 5 mm
  3. C. Atypical adenomatous hyperplasia — well-demarcated focus under 5 mm
  4. D. Invasive mucinous adenocarcinoma — pneumonia-like multifocal consolidation

Correct answer: A – Adenocarcinoma in situ — lepidic growth under 3 cm without invasion

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:

  1. A. Polymyositis from immune complex deposition within skeletal muscle
  2. B. Peripheral neuropathy from anti-neuronal IgG antibody production
  3. C. Hypertrophic pulmonary osteoarthropathy causing periosteal new bone formation
  4. D. Lambert-Eaton myasthenic syndrome from voltage-gated calcium channel antibodies

Correct answer: D – Lambert-Eaton myasthenic syndrome from voltage-gated calcium channel antibodies

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:

  1. A. Bilateral synchronous primary lung tumours developing simultaneously
  2. B. Reactive bronchial hyperplasia triggered by repeated pulmonary infections
  3. C. Haematogenous tumour cell dissemination throughout the pulmonary vasculature
  4. D. Widespread mutagenesis of respiratory mucosa with 3p deletions even in benign epithelium

Correct answer: D – Widespread mutagenesis of respiratory mucosa with 3p deletions even in benign epithelium

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:

  1. A. Superior vena cava syndrome from mediastinal lymph node compression
  2. B. Paraneoplastic autonomic neuropathy from small cell carcinoma
  3. C. Horner syndrome alone from direct sympathetic chain involvement
  4. D. Pancoast tumour causing Pancoast syndrome including Horner syndrome

Correct answer: D – Pancoast tumour causing Pancoast syndrome including Horner syndrome

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?

  1. A. EGFR mutation 20%, KRAS mutation 30%, ALK rearrangement 5%, RB mutation 20%
  2. B. RB mutation 90%, TP53 mutation 90%, rare KRAS mutation, absent EGFR mutation
  3. C. p16/CDKN2A mutation 50%, KRAS mutation 30%, TP53 mutation 50%, RB mutation 20%
  4. D. ALK rearrangement 15%, HER2 mutation 8%, MET amplification 10%, absent RB mutation

Correct answer: B – RB mutation 90%, TP53 mutation 90%, rare KRAS mutation, absent EGFR mutation

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:

  1. A. Circumventing pathway dependence through alternative downstream pathway activation
  2. B. Epigenetic silencing of ALK preventing drug access to the mutated receptor
  3. C. Field cancerisation producing an independent second primary lung tumour
  4. D. Alteration of the drug target itself through a secondary resistance mutation

Correct answer: D – Alteration of the drug target itself through a secondary resistance mutation

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?

  1. A. Centriacinar emphysema destroying respiratory bronchioles from cigarette smoking
  2. B. Panacinar emphysema from α1-antitrypsin deficiency affecting the entire acinus
  3. C. Distal acinar (paraseptal) emphysema producing subpleural bullae in young adults
  4. D. Irregular emphysema from healed pulmonary inflammation adjacent to scar tissue

Correct answer: C – Distal acinar (paraseptal) emphysema producing subpleural bullae in young adults

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?

  1. A. Less than 25%, as most cancers are caught on routine surveillance
  2. B. More than 50%, with an additional 25% having regional lymph node disease
  3. C. Approximately 35%, mostly adrenal and liver deposits at presentation
  4. D. About 15%, with the remainder having only localised pulmonary disease

Correct answer: B – More than 50%, with an additional 25% having regional lymph node disease

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:

  1. A. Nuclear moulding from close apposition of tumour cells with scant cytoplasm
  2. B. Crush artefact when fragile SCLC cells are compressed in small biopsy specimens
  3. C. Salt-and-pepper chromatin pattern reflecting neuroendocrine differentiation
  4. D. Basophilic encrustation of vascular walls by DNA from necrotic tumour cells

Correct answer: D – Basophilic encrustation of vascular walls by DNA from necrotic tumour cells

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?

  1. A. 5-fold increased risk — the same as asbestos alone in non-smokers
  2. B. 15-fold increased risk — a modest additive effect of both carcinogens
  3. C. 30-fold increased risk — primarily driven by cigarette smoking alone
  4. D. Approximately 55-fold increased risk from synergistic interaction of both carcinogens

Correct answer: D – Approximately 55-fold increased risk from synergistic interaction of both carcinogens

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?

  1. A. Smoking doubles mesothelioma risk through synergistic carcinogenesis with asbestos fibres
  2. B. Smoking reduces mesothelioma risk by competing with asbestos at mesothelial binding sites
  3. C. Smoking combined with asbestos increases mesothelioma risk only if exposure began before age 30
  4. D. Smoking does not increase mesothelioma risk despite greatly amplifying lung carcinoma risk

Correct answer: D – Smoking does not increase mesothelioma risk despite greatly amplifying lung carcinoma risk

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?

  1. A. Goblet cell hyperplasia → mucinous metaplasia → AIS → invasive carcinoma
  2. B. Atypical adenomatous hyperplasia → AIS → minimally invasive → invasive carcinoma
  3. C. Basal cell hyperplasia → squamous metaplasia → dysplasia → carcinoma in situ → invasion
  4. D. Reserve cell hyperplasia → mucinous metaplasia → moderate dysplasia → invasive carcinoma

Correct answer: C – Basal cell hyperplasia → squamous metaplasia → dysplasia → carcinoma in situ → invasion

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?

  1. A. Typical carcinoids lack all neuroendocrine markers present in SCLC
  2. B. Typical carcinoids are low-grade with greater than 85% 5-year survival versus SCLC median 1 year
  3. C. Typical carcinoids produce ACTH and ADH more frequently than SCLC
  4. D. Typical carcinoids arise exclusively in the peripheral lung unlike central SCLC

Correct answer: B – Typical carcinoids are low-grade with greater than 85% 5-year survival versus SCLC median 1 year

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?

  1. A. Loss of neuroendocrine marker expression and origin in peripheral lung location
  2. B. Absence of salt-and-pepper chromatin with replacement by clear vesicular nuclei
  3. C. Absence of neurosecretory granules on electron microscopy examination
  4. D. Higher mitotic rate, focal necrosis, greater metastatic potential, and TP53 mutations in 20–40%

Correct answer: D – Higher mitotic rate, focal necrosis, greater metastatic potential, and TP53 mutations in 20–40%

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?

  1. A. Squamous cell carcinoma producing ectopic PTH-related peptide
  2. B. Adenocarcinoma with bilateral adrenal metastases destroying cortical tissue
  3. C. Small cell carcinoma producing ectopic ACTH causing Cushing syndrome
  4. D. Large cell carcinoma with direct hypothalamic invasion altering cortisol feedback

Correct answer: C – Small cell carcinoma producing ectopic ACTH causing Cushing syndrome

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?

  1. A. Peripheral lung parenchyma invading pleura secondarily in 60% of cases
  2. B. Mediastinal pleura with asbestos history in approximately 50% of cases
  3. C. Parietal or visceral pleura with asbestos history in 80–90% of cases
  4. D. Diaphragmatic pleura with asbestos history in approximately 40% of cases

Correct answer: C – Parietal or visceral pleura with asbestos history in 80–90% of cases

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:

  1. A. Squamous cell carcinoma with central cavitation and keratin production
  2. B. Large cell neuroendocrine carcinoma with prominent nucleoli and necrosis
  3. C. Pulmonary adenocarcinoma due to similar glandular architecture
  4. D. Metastatic renal cell carcinoma with clear cytoplasm and prominent vascularity

Correct answer: C – Pulmonary adenocarcinoma due to similar glandular architecture

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?

  1. A. Risk decreases by 50% after 20 years similar to smoking cessation benefit
  2. B. Risk is only significant during the active occupational exposure period itself
  3. C. Risk peaks at 10–15 years post-exposure then gradually diminishes with fibre clearance
  4. D. Lifetime risk does not diminish because asbestos fibres remain permanently in body tissues

Correct answer: D – Lifetime risk does not diminish because asbestos fibres remain permanently in body tissues

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?

  1. A. TP53 — involved in cell cycle arrest and apoptosis regulation
  2. B. BAP1 — tumour suppressor involved in DNA repair affected in familial cases
  3. C. KRAS — oncogene activated by asbestos-induced reactive oxygen species
  4. D. BMPR2 — bone morphogenetic protein receptor linked to pulmonary hypertension

Correct answer: B – BAP1 — tumour suppressor involved in DNA repair affected in familial cases

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:

  1. A. Transudate from reduced oncotic pressure secondary to hypoalbuminaemia
  2. B. Hydrothorax from elevated hydrostatic pressure in congestive heart failure
  3. C. Chylothorax from lymphatic obstruction by reactive hilar lymphadenopathy
  4. D. Exudate from microbial invasion — suppurative pleuritis progressing toward empyema

Correct answer: D – Exudate from microbial invasion — suppurative pleuritis progressing toward empyema

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:

  1. A. Massive haemothorax from intercostal vessel laceration compressing the lung
  2. B. Tension pneumothorax — ball-valve air leak causing mediastinal shift and circulatory collapse
  3. C. Massive pulmonary embolism causing acute right-sided heart failure
  4. D. Spontaneous oesophageal rupture with mediastinal emphysema and pleural contamination

Correct answer: B – Tension pneumothorax — ball-valve air leak causing mediastinal shift and circulatory collapse

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.

View on OmpathStudy