NRE Step 1 Pathology MCQs
12 sample questions from the 281 Pathology questions in NRE-1 Prep. Choose an answer to see why it is right and why each other option is wrong.
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Sample Pathology questions
1. A 22-year-old woman is screened before marriage to her cousin. Hb 10.8 g/dL, MCV 63 fL, RBC count 5.8 × 10¹²/L, serum ferritin 85 µg/L (normal). What is the most appropriate next investigation?
Answer: Haemoglobin HPLC / electrophoresis. Microcytosis with a high red cell count and normal ferritin suggests β-thalassaemia trait. Mentzer index (MCV ÷ RBC) = 63 ÷ 5.8 ≈ 10.9 (under 13 favours thalassaemia). Hb HPLC/electrophoresis shows raised HbA₂ (>3.5%) and confirms it. This matters for premarital and cousin-marriage counselling — two carriers have a 1 in 4 chance of a child with thalassaemia major.
- Repeat ferritin after 3 months of oral iron: Ferritin is normal, so iron is unnecessary and can be harmful in thalassaemia trait.
- Serum vitamin B12 and folate: B12 and folate deficiency cause macrocytosis, not microcytosis.
- Direct Coombs test: The Coombs test is for immune haemolysis, which is not suggested here.
2. A 9-year-old boy has cola-coloured urine, periorbital puffiness and BP 140/95 mmHg, 2 weeks after a sore throat. Serum C3 is low. What would electron microscopy of a renal biopsy most likely show?
Answer: Subepithelial humps. Post-streptococcal glomerulonephritis follows pharyngitis by 1–3 weeks (skin infection by 3–6 weeks). Immune complexes deposit beneath the epithelium as "humps" and activate complement, so C3 falls and normalises within about 8 weeks. Most children recover fully with supportive care.
- Foot process effacement only: Minimal change disease — nephrotic, not nephritic.
- Split basement membrane: A split, laminated GBM is typical of Alport syndrome (hereditary nephritis with deafness), not post-streptococcal GN.
- Mesangial IgA deposits: IgA nephropathy — haematuria 1–2 days after infection, normal C3.
3. In a healthy adult, which test best reflects how actively the bone marrow is producing red cells?
Answer: Reticulocyte count. Reticulocytes are young red cells released from marrow; normally ~0.5–2%. A high count indicates increased production (haemolysis, bleeding, response to iron/B12 treatment); a low count with anaemia points to marrow failure or lack of building blocks (iron, B12, folate, EPO). Red cells live about 120 days; in adults erythropoiesis is in the axial skeleton (vertebrae, pelvis, sternum).
- Mean corpuscular volume: MCV measures red cell size, not how many new cells the marrow is making.
- Red cell distribution width: RDW measures variation in red cell size; it is not a measure of marrow output.
- Serum ferritin: Ferritin reflects iron stores, not the rate of red cell production.
4. A man with chest pain had an MI 4 days ago. Today he has new chest pain, and you suspect re-infarction. Which biomarker is most useful because it returns to normal within about 2–3 days?
Answer: CK-MB. Troponins rise 3–6 hours after MI, peak at 12–24 h and stay raised for 7–14 days, so they can’t easily detect a second event a few days later. CK-MB rises in 3–6 h and returns to normal in 48–72 h, so a new rise suggests re-infarction (serial high-sensitivity troponin dynamics are also used). LDH and AST are slow and non-specific.
- Troponin T: Stays raised for up to 2 weeks.
- Troponin I: Stays raised for 7–10 days.
- LDH: Rises late and lasts long; non-specific.
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5. A 45-year-old has enlarging hands and feet, coarse facial features, sweating, sleep apnoea and type 2 diabetes. What is the screening and confirmatory test?
Answer: IGF-1, then OGTT. Acromegaly (GH-secreting pituitary adenoma): coarse features, prognathism, macroglossia, large hands/feet, sweating, carpal tunnel, sleep apnoea, hypertension, diabetes, cardiomyopathy, colonic polyps, bitemporal hemianopia. Screening: IGF-1 (stable). Confirm: OGTT — GH fails to suppress below ~1 µg/L. MRI pituitary. Treatment: trans-sphenoidal surgery; somatostatin analogues (octreotide), pegvisomant, radiotherapy. Random GH is pulsatile and unreliable.
- Random GH: GH is released in pulses, so a single random level is unreliable.
- Dexamethasone suppression: Dexamethasone suppression is for Cushing syndrome.
- Prolactin: Prolactin does not confirm acromegaly.
6. In a lymph node, which region is mainly populated by T cells and is poorly developed in DiGeorge syndrome?
Answer: Paracortex. Lymph node architecture: cortex — follicles (B cells; germinal centres in secondary follicles), paracortex — T cells, high endothelial venules (lymphocyte entry), expands in viral infections and is underdeveloped in T-cell deficiency (DiGeorge); medulla — medullary cords (plasma cells, macrophages) and sinuses. Spleen: white pulp — periarteriolar lymphoid sheath (T cells), follicles (B cells); red pulp — filters red cells.
- Follicles of the cortex: Follicles contain B cells.
- Medullary cords: Medullary cords contain plasma cells.
- Subcapsular sinus: The subcapsular sinus contains macrophages.
7. Which HIV envelope glycoprotein binds the CD4 receptor on helper T cells?
Answer: gp120. HIV entry: gp120 binds CD4, then a co-receptor (CCR5 on macrophages/early infection; CXCR4 on T cells later); gp41 mediates membrane fusion (enfuvirtide blocks it). Maraviroc blocks CCR5; CCR5-Δ32 homozygotes are resistant. Reverse transcriptase (NRTIs, NNRTIs), integrase (dolutegravir, raltegravir), protease (darunavir) are other targets. p24 antigen appears early (4th-generation tests detect p24 + antibodies).
- gp41: gp41 mediates membrane fusion.
- p24: p24 is the capsid antigen.
- Reverse transcriptase: Reverse transcriptase is an enzyme.
8. Minutes after the renal artery is unclamped in a kidney transplant, the graft becomes mottled, cyanotic and stops making urine. What is the mechanism?
Answer: Preformed recipient antibodies. Transplant rejection: hyperacute (minutes–hours — preformed antibodies to ABO or HLA → complement activation, thrombosis; prevented by ABO matching and crossmatch); acute (days–months — cellular (T cells, tubulitis) or antibody-mediated; treat with steroids, anti-thymocyte globulin); chronic (months–years — vascular intimal fibrosis, interstitial fibrosis). GVHD: donor T cells attack recipient (bone marrow transplants) — skin, gut, liver.
- T-cell mediated rejection: T-cell rejection takes weeks to months.
- Chronic vascular rejection: Chronic rejection takes months to years.
- Graft-versus-host disease: GVHD is donor cells attacking the host, not the graft failing.
9. A child from a consanguineous family has recurrent pyogenic infections, partial albinism, peripheral neuropathy and giant granules in neutrophils on the blood film. What is the defect?
Answer: Lysosomal trafficking (LYST) defect. Chediak–Higashi: autosomal recessive LYST mutation → defective phagosome–lysosome fusion and microtubule-dependent trafficking → giant granules in neutrophils, recurrent pyogenic infections (staph, strep), oculocutaneous albinism (defective melanosome transfer), peripheral neuropathy, bleeding (platelet dense granule defect), accelerated lymphohistiocytic phase. Treatment: bone marrow transplant. Autosomal recessive disorders are more common with consanguinity, as in Pakistan.
- NADPH oxidase deficiency: NADPH oxidase deficiency (CGD) has no albinism or giant granules.
- CD18 integrin deficiency: CD18 deficiency is leucocyte adhesion deficiency.
- Bruton tyrosine kinase deficiency: BTK deficiency is X-linked agammaglobulinaemia.
10. A young man from rural Pakistan has raised JVP with a rise on inspiration, ascites out of proportion to oedema, a pericardial knock and a calcified pericardium on X-ray. What is the commonest cause in this setting?
Answer: Tuberculosis. Constrictive pericarditis: thick fibrotic/calcified pericardium restricts diastolic filling — Kussmaul sign (JVP rises on inspiration), prominent y descent, pericardial knock, hepatomegaly and ascites, pulsus paradoxus less common. Commonest cause in developing countries (including Pakistan) is tuberculosis; elsewhere post-cardiac surgery, radiation, viral/idiopathic. Treatment: antituberculous therapy (± steroids in TB effusion), pericardiectomy for established constriction.
- Viral pericarditis: Viral pericarditis rarely causes calcific constriction in this setting.
- Rheumatic fever: Rheumatic fever causes pancarditis and valve disease.
- Uraemia: Uraemia causes effusion, rarely constriction.
11. A woman with anaemia has a corrected reticulocyte count of 8%. Which cause is most likely?
Answer: Haemolysis. Reticulocytes (immature RBCs with RNA — supravital stain, normal ~0.5–2.5%) reflect marrow output. High reticulocyte count (correct for haematocrit; reticulocyte production index > 2–3) → appropriate marrow response — haemolysis or acute blood loss, or response to treatment (iron/B12, 5–10 days). Low → production failure — iron/B12/folate deficiency, aplasia, marrow infiltration, CKD, anaemia of chronic disease, parvovirus B19 crisis.
- Aplastic anaemia: Aplastic anaemia has low reticulocytes.
- Iron deficiency untreated: Untreated iron deficiency has low reticulocytes.
- Anaemia of CKD: CKD anaemia has low reticulocytes from EPO deficiency.
12. A 24-year-old has recurrent sinusitis and pneumonias since adolescence, chronic Giardia diarrhoea and early bronchiectasis. IgG and IgA are very low, with poor antibody response to vaccines; B cells are present. What is the diagnosis and treatment?
Answer: CVID — immunoglobulin replacement. Common variable immunodeficiency: commonest symptomatic primary antibody deficiency; onset usually adolescence/adulthood; low IgG with low IgA and/or IgM and poor specific antibody responses; B cells usually present but fail to differentiate into plasma cells. Features: recurrent sinopulmonary infections (encapsulated bacteria), bronchiectasis, Giardia, autoimmunity (cytopenias), granulomatous disease, lymphoma risk. Treatment: lifelong IV or subcutaneous immunoglobulin, prompt antibiotics, bronchiectasis care.
- X-linked agammaglobulinaemia — stem cell transplant: In XLA, B cells are absent.
- Selective IgA deficiency — no treatment: With IgA deficiency alone, IgG would be normal.
- Severe combined immunodeficiency — bone marrow transplant: SCID presents in infancy with absent T cells.
Topics covered
GI, Microbiology, Haematology, Chemical pathology, Immunology, Neoplasia, Haemodynamics, Cardiovascular pathology, Cardiovascular, Renal, Female, Respiratory, Musculoskeletal, Inflammation, Renal pathology, Microbiology — bacteria, Genetics, GI pathology, Endocrine, Haematology — anaemia, Haematology — malignancy, Respiratory pathology, Microbiology — parasites, Cell injury, Skin, Haematology — bleeding, Amyloidosis, Microbiology — general, Microbiology — viruses, Female genital pathology, Bone pathology, Endocrine pathology, CNS pathology, CNS, Type II hypersensitivity, Cell injury & necrosis, Healing & repair, Cellular adaptation, Hepatobiliary pathology, Immunopathology
Frequently asked questions
How many NRE Step 1 Pathology questions are in the bank?
There are 281 Pathology questions in NRE-1 Prep, each with an explanation for every option.
Are these past paper questions?
No. Every question is original, written by us and mapped to the published PMDC NRE syllabus.
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