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Pathology medical question bank

Practise every pathology topic with explained SBAs.

Recall Engine has 1,500+ pathology questions across 70+ topics in 10+ body systems. Every question explains each option.

questions
1,500+
topics
70+
topic notes
70+
clinical skills guides
1
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Pathology by body system

Pathology has 70+ topics in 10+ body systems. Each section shows how many questions it has and every topic it covers.

Cardiovascular

100+ questions across 4 topics. It also has 4 topic notes.

  • Atherosclerosis: pathogenesis and lipids
  • Cardiomyopathy and myocarditis
  • Hypertension: vascular and organ damage
  • Myocardial ischaemia and infarction

Respiratory

100+ questions across 5 topics. It also has 5 topic notes.

  • Asthma: airway inflammation and remodelling
  • Pathology of pneumonia and asthma
  • Pneumonia, lung abscess, and aspergillosis
  • Pulmonary fibrosis
  • Respiratory failure: types and causes

Gastrointestinal and liver

350+ questions across 10+ topics. It also has 10+ topic notes.

  • Barrett oesophagus, Hirschsprung disease, and coeliac disease
  • Colorectal adenocarcinoma and hereditary syndromes
  • Colorectal polyps and dysplasia
  • Fatty liver, liver failure, and tumours
  • Gallstones, cholecystitis, and gallbladder carcinoma
  • Gastric adenocarcinoma and MALT lymphoma
  • Gastritis and peptic ulcer disease
  • Gastrointestinal tumours: types and precursors
  • Gross pathology: gallbladder, liver, bowel, and bone
  • Hepatitis: viral, autoimmune, and drug-induced
  • Liver structure and injury
  • Malabsorption: causes and tests
  • Oesophagitis, Barrett oesophagus, and oesophageal carcinoma
  • Pancreas pathology
  • Pathology of gastrointestinal infections
  • Ulcerative colitis and Crohn disease

Kidney and urinary

100+ questions across 8 topics. It also has 8 topic notes and 1 clinical skills guide.

  • Acute tubular necrosis
  • Glomerular injury mechanisms
  • Glomerular syndromes
  • Prostate cancer (pathology)
  • Pyelonephritis and urinary obstruction
  • Renal vascular disease
  • Urinary tract infection: pathology
  • Urine microscopy

Endocrine and metabolic

70+ questions across 1 topic. It also has 1 topic note.

  • Thyroid nodules, thyroiditis, and cancer

Reproductive and breast

200+ questions across 9 topics. It also has 9 topic notes.

  • Benign breast lesions: types and cancer risk
  • Breast carcinoma: type, grade, and receptors
  • Cancer pathology: breast cancer
  • Cervical neoplasia: HPV, precancer, and invasion
  • Cervical, vaginal, and vulval tumours: cytology and stage
  • Endometrial hyperplasia, polyps, and endometritis
  • Gynaecological cancer: frozen section and inherited syndromes
  • Ovarian tumours and cysts: types and markers
  • Uterine corpus tumours: type, grade, and stage

Nervous system

100+ questions across 9 topics. It also has 9 topic notes.

  • Cerebral oedema
  • CNS infections
  • CSF obstruction, herniation, and intracranial haemorrhage
  • Demyelinating plaques: activity and repair
  • Glial responses and neural repair
  • Multiple sclerosis
  • Neurodegeneration: protein aggregates and repeat expansions
  • Neurodegeneration: regional loss and clinical patterns
  • Space-occupying lesions and brain tumours

Head, neck, and special senses

20+ questions across 1 topic. It also has 1 topic note.

  • Eye disease: lens, retina, and optic nerve damage

Musculoskeletal

150+ questions across 6 topics. It also has 6 topic notes.

  • Bone and soft-tissue tumours
  • Bone tumours
  • Osteomyelitis, septic arthritis, and gas gangrene
  • Red hot joint and osteomyelitis
  • Soft-tissue tumours
  • Spinal disc degeneration, herniation, and spondylolisthesis

Skin

20+ questions across 1 topic. It also has 1 topic note.

  • Dermatopathology: terms and blistering

Blood and cancer

100+ questions across 4 topics. It also has 4 topic notes.

  • Anaemia: causes and classification
  • Blood cells: identification and count changes
  • Haemoglobinopathies
  • Metastatic disease

Infection and immunity

30+ questions across 1 topic. It also has 1 topic note.

  • HIV: opportunistic and skin infections

General principles

300+ questions across 10+ topics. It also has 10+ topic notes.

  • Acute inflammation: vascular and cellular events
  • An introduction to pathological sciences
  • Cell injury: adaptation and degeneration
  • Connective tissue and epithelial disorders
  • Delayed and abnormal healing
  • Hallmarks of cancer
  • Hyperaemia, congestion, and oedema
  • Hyperplasia, metaplasia, dysplasia, and neoplasia
  • Inflammation: patterns and outcomes
  • Metaplasia, dysplasia, and neoplasia
  • Thrombosis, embolism, and infarction
  • Tissue repair: regeneration and healing
  • Tumour spread: invasion and metastasis

Pathology sample questions

These 5 are published pathology questions shown exactly as students see them. Open an answer to see why it is right and why every other option is wrong.

Question 1 · Pathology, Preclinical

A woman with acute pancreatitis develops hypotension and shock, followed by acute suppression of renal function. Which renal lesion is most likely?

  1. A. Tubulointerstitial nephritis
  2. B. Benign nephrosclerosis
  3. C. Nephrotoxic acute tubular necrosis
  4. D. Haemolytic uraemic syndrome
  5. E. Ischaemic acute tubular necrosis
Show the answer and explanation

Answer: E. Ischaemic acute tubular necrosis

Marked trauma, septicaemia, and acute pancreatitis reduce the blood supply to peripheral organs and induce hypotension and shock, as well as ischaemic ATN. Acute suppression of renal function is the clinical side of ATN.

Why the other options are wrong

  • A. Tubulointerstitial nephritis: Tubulointerstitial nephritis is caused by infections, drugs (commonly antibiotics and NSAIDs), and immunological disease.
  • B. Benign nephrosclerosis: Nephrosclerosis is sclerosis of small renal arteries and arterioles strongly associated with hypertension.
  • C. Nephrotoxic acute tubular necrosis: Poisons, drugs, and organic solvents cause nephrotoxic ATN.
  • D. Haemolytic uraemic syndrome: Complement regulatory protein abnormalities or exogenous toxins lead to endothelial cell injury in haemolytic uraemic syndrome.

Key point: Marked trauma, septicaemia, and acute pancreatitis cause hypotension, shock, and ischaemic ATN.

References

Question 2 · Pathology, Preclinical

A pancreatic tumour carries a RAS mutation that abolishes its GTPase activity. Which kinase does the mutant RAS keep directly activated?

  1. A. MEK
  2. B. Akt
  3. C. MAPK
  4. D. Raf
  5. E. Abl tyrosine kinase
Show the answer and explanation

Answer: D. Raf

RAS mutations cause loss of the GTPase activity needed to switch active RAS-GTP off to inactive RAS-GDP, so RAS stays GTP-bound and active. RAS-GTP activates Raf, a serine/threonine kinase. MEK is phosphorylated only afterwards by activated Raf.

Why the other options are wrong

  • A. MEK: Activated Raf phosphorylates MEK, one step after RAS-GTP activates Raf.
  • B. Akt: PI3K activation recruits Akt to the membrane, where it is phosphorylated.
  • C. MAPK: Activated MAPKs enter the nucleus to phosphorylate and activate transcription factors.
  • E. Abl tyrosine kinase: Abl tyrosine kinase is activated through the bcr-abl fusion protein in CML.

Key point: RAS mutations remove the GTPase switch-off, so RAS-GTP keeps activating Raf.

References

Question 3 · Pathology, Preclinical

A cervical screening sample contains highly atypical squamous cells. The patient asks whether these detached cells prove that a lesion has crossed its basement membrane. Which investigation provides tissue architecture needed to assess that question?

  1. A. High-risk HPV DNA testing
  2. B. Colposcopy without tissue sampling
  3. C. Ultrasound measurement of cervical length
  4. D. Histological examination of an appropriately obtained cervical biopsy
  5. E. Repeat cervical cytology
Show the answer and explanation

Answer: D. Histological examination of an appropriately obtained cervical biopsy

Detached cytological cells can identify significant atypia, but they do not preserve the spatial relationship between epithelium, basement membrane and stroma. Appropriately sampled biopsy tissue provides that architecture. HPV testing and colposcopy contribute to risk assessment and locating lesions, but neither substitutes for histology when assessing invasion.

Why the other options are wrong

  • A. High-risk HPV DNA testing: HPV testing detects infection with high-risk viral types; it does not show whether malignant cells have crossed the basement membrane.
  • B. Colposcopy without tissue sampling: Colposcopy can localise suspicious areas but visual inspection alone cannot establish the microscopic depth of invasion.
  • C. Ultrasound measurement of cervical length: Cervical length on ultrasound does not provide the microscopic epithelial-stromal relationship required for this histological question.
  • E. Repeat cervical cytology: Repeating cytology may reassess cellular abnormalities but still does not preserve the epithelial-stromal architecture needed to demonstrate invasion.

Key point: Cytology evaluates individual cells; assessment of epithelial architecture and stromal invasion requires appropriately sampled tissue.

References

Question 4 · Pathology, Preclinical

A renal arteriole from a patient with longstanding hypertension has homogeneous pink wall material and luminal narrowing, without concentric cellular layers or destructive wall necrosis. Which process best explains the wall material?

  1. A. Diabetic mesangial matrix expansion
  2. B. Platelet-fibrin aggregation within capillaries
  3. C. Chronic plasma-component leakage and matrix accumulation
  4. D. Concentric smooth-muscle and wall proliferation
  5. E. Acute tubular epithelial necrosis
Show the answer and explanation

Answer: C. Chronic plasma-component leakage and matrix accumulation

Chronic endothelial injury, plasma leakage and extracellular matrix accumulation contribute to hyaline thickening.

Why the other options are wrong

  • A. Diabetic mesangial matrix expansion: Diabetic mesangial matrix expansion would instead require nodular matrix expansion within glomeruli, which is not the defining change described.
  • B. Platelet-fibrin aggregation within capillaries: Platelet-fibrin aggregation within capillaries would instead require luminal thrombi rather than homogeneous wall accumulation, which is not the defining change described.
  • D. Concentric smooth-muscle and wall proliferation: Concentric smooth-muscle and wall proliferation would instead require concentric onion-skin vascular layers, which is not the defining change described.
  • E. Acute tubular epithelial necrosis: Acute tubular epithelial necrosis would instead require ragged necrotic tubular epithelium after hypotension, which is not the defining change described.

Key point: Use homogeneous arteriolar wall thickening to recognise chronic plasma-component leakage and matrix accumulation.

References

Question 5 · Pathology, Preclinical

A laboratory translates the expanded HTT coding sequence and finds an unusually long repeated amino-acid tract. Which protein change is expected?

  1. A. APP gene dosage on chromosome 21
  2. B. Disrupted microtubule support from abnormal tau
  3. C. Intraneuronal tau neurofibrillary tangles
  4. D. Polyglutamine expansion in huntingtin
  5. E. Repeat-length-associated earlier onset
Show the answer and explanation

Answer: D. Polyglutamine expansion in huntingtin

CAG encodes glutamine, linking the DNA expansion to a polyglutamine tract. A coding CAG expansion lengthens a polyglutamine tract in huntingtin. The observations should be interpreted at this specific mechanistic level; the alternative processes require their own distinguishing findings.

Why the other options are wrong

  • A. APP gene dosage on chromosome 21: The APP gene lies on chromosome 21, linking chromosome dosage to amyloid biology. This does not explain the decisive finding here: cAG encodes glutamine, linking the DNA expansion to a polyglutamine tract.
  • B. Disrupted microtubule support from abnormal tau: Tau normally contributes to microtubule function; abnormal tau can disrupt neuronal transport and accumulate in tangles. This does not explain the decisive finding here: cAG encodes glutamine, linking the DNA expansion to a polyglutamine tract.
  • C. Intraneuronal tau neurofibrillary tangles: Neurofibrillary tangles contain abnormally aggregated tau within neurons. This does not explain the decisive finding here: cAG encodes glutamine, linking the DNA expansion to a polyglutamine tract.
  • E. Repeat-length-associated earlier onset: Larger pathogenic HTT repeat expansions generally correlate with earlier onset, without making age perfectly predictable. This does not explain the decisive finding here: cAG encodes glutamine, linking the DNA expansion to a polyglutamine tract.

Key point: A coding CAG expansion lengthens a polyglutamine tract in huntingtin.

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