AMC MCQ Haematology Questions: 10 Free Practice MCQs

Ten AMC MCQ-style haematology questions with the answer and the reasoning behind it. They come from the AU.med bank, which has 12 haematology questions and many more across every topic.

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1. 1 / 10

   A 54-year-old male is recovering from orthopedic surgery and has been receiving prophylactic enoxaparin. On postoperative day 7, his platelet count drops from 220 to 95 x 10^9/L, and he is diagnosed with Heparin-Induced Thrombocytopenia (HIT).

   Which of the following describes the key pathophysiological mediator of this condition?

   • A. Direct cytotoxic destruction of platelets by heparin molecules
   • B. Sequestration of platelets in the spleen due to drug-induced hypersplenism
   • C. Inhibition of thrombopoietin synthesis in the liver by low molecular weight heparin
   • D. Autoantibodies directed against platelet factor 4 (PF4)-heparin complexes
   Show answer

   Answer: D. Autoantibodies directed against platelet factor 4 (PF4)-heparin complexes

   Why: Heparin-induced thrombocytopenia is a life-threatening immunologic reaction caused by IgG antibodies targeting complexes of heparin and platelet factor 4 (PF4). This antibody-antigen complex activates platelets, leading to thrombosis and consumption.

   • A. HIT is an immune-mediated disorder, not a direct chemical or toxic effect of heparin on platelets.
   • B. Splenic sequestration does not play a role in HIT; platelet consumption is due to immune activation and thrombus formation.
   • C. HIT is not caused by impaired platelet production; rather, it is due to accelerated platelet activation and clearance.

   Sources: AMH; THANZ Guidelines

2. 2 / 10

   A 68-year-old man with a history of rheumatoid arthritis presents with fatigue. His blood tests show: Hb 102 g/L (normal 130-170), MCV 82 fL (normal 80-100). His iron studies are: Serum Iron 6 umol/L (low), Transferrin 1.8 g/L (low-normal), Transferrin Saturation 12% (low), Ferritin 210 ug/L (normal 30-300).

   Which of the following is the most likely diagnosis?

   • A. Pure iron deficiency anaemia from occult bleeding
   • B. Beta thalassaemia minor (trait)
   • C. Sideroblastic anemia
   • D. Anemia of chronic disease (anemia of inflammation)
   Show answer

   Answer: D. Anemia of chronic disease (anemia of inflammation)

   Why: Anemia of chronic disease (anemia of inflammation) is driven by inflammatory cytokines (e.g. IL-6), which increase the production of hepcidin. Hepcidin degrades ferroportin, trapping iron inside macrophages and hepatocytes, leading to low circulating iron but normal or high stored iron (ferritin). It is commonly seen in chronic inflammatory conditions like rheumatoid arthritis.

   • A. In pure iron deficiency, the serum ferritin would be low (< 30 ug/L), whereas here it is normal/elevated due to chronic inflammation.
   • B. Thalassemia minor is characterized by microcytic anemia (MCV typically < 70) and normal iron studies, which is not the case here.
   • C. Sideroblastic anemia typically features elevated ferritin and transferrin saturation, with ring sideroblasts on bone marrow aspirate.

   Sources: AMH; RACGP Anemia Investigation Guidelines

3. 3 / 10

   A 30-year-old non-pregnant female presents with a first unprovoked proximal deep vein thrombosis (DVT) confirmed on compression ultrasonography. Renal and hepatic functions are normal.

   What is the first-line oral anticoagulant?

   • A. Warfarin with an INR target of 2 to 3
   • B. Aspirin 100 mg daily
   • C. Rivaroxaban or Apixaban (DOAKs)
   • D. Enoxaparin (Clexane) long term
   Show answer

   Answer: C. Rivaroxaban or Apixaban (DOAKs)

   Why: Direct Oral Anticoagulants (DOACs) such as Rivaroxaban or Apixaban are first-line agents for VTE treatment over Warfarin due to predictable pharmacokinetics, lack of routine INR monitoring, and lower risk of intracranial bleeding. Treatment duration is typically 3-6 months for a first VTE.

   • A. Incorrect. Warfarin requires initial heparin bridging and frequent blood INR monitoring, making it second-line to DOACs.
   • B. Incorrect. Aspirin is insufficient for acute treatment of proximal DVT and is not recommended as primary anticoagulation.
   • D. Incorrect. Low Molecular Weight Heparin (Clexane) is preferred in pregnancy or active cancer, but oral DOACs are preferred in standard VTE.

   Sources: THANZ Guidelines

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5. 4 / 10

   A 68-year-old strict vegan presents with progressive paresthesia in his feet and general fatigue. A full blood count shows: Hb 95 g/L (normal 130-170), MCV 112 fL (normal 80-100). Blood film reveals hypersegmented neutrophils.

   What is the most likely nutritional deficiency causing these findings?

   • A. Iron deficiency with mixed red cell indices
   • B. Folate deficiency from a restricted diet
   • C. Vitamin B12 (Cobalamin) deficiency
   • D. Vitamin C deficiency
   Show answer

   Answer: C. Vitamin B12 (Cobalamin) deficiency

   Why: Vitamin B12 is found exclusively in animal-derived foods, putting vegans at high risk of deficiency. Megaloblastic anemia (macrocytosis, hypersegmented neutrophils) and neuropsychiatric symptoms (due to demyelination of the dorsal and lateral columns of the spinal cord) are classic presentations of Vitamin B12 deficiency.

   • A. Iron deficiency typically causes microcytic hypochromic anemia (MCV < 80), not macrocytic anemia.
   • B. Folate deficiency causes macrocytic anemia, but is less likely to present with progressive neurologic symptoms (e.g. subacute combined degeneration) typical of B12 deficiency.
   • D. Vitamin C deficiency causes scurvy (bleeding gums, perifollicular hemorrhage) and does not present with macrocytic megaloblastic anemia.

   Sources: Australian Medicines Handbook (AMH); RACGP Nutritional Assessment Guidelines

6. 5 / 10

   A 24-year-old G2P1 woman at 10 weeks gestation presents to the emergency department with light vaginal bleeding and mild lower abdominal cramping. Ultrasound confirms an intrauterine pregnancy consistent with dates. Blood group testing reveals she is A-negative with a negative antibody screen.

   What is the most appropriate management regarding Rh D immunoglobulin (Anti-D) administration?

   • A. Defer Anti-D administration until the routine dose at 28 weeks gestation
   • B. Give 250 IU of Anti-D immunoglobulin within 72 hours of the onset of bleeding
   • C. Check the partner's blood type before administering Anti-D
   • D. Give a full 625 IU dose of Anti-D immunoglobulin immediately
   Show answer

   Answer: B. Give 250 IU of Anti-D immunoglobulin within 72 hours of the onset of bleeding

   Why: Under Australian guidelines, Rhesus-D-negative women with a sensitising event (such as threatened miscarriage, miscarriage, ectopic pregnancy, or trauma) in the first trimester (up to 12 weeks gestation) should receive 250 IU of Anti-D immunoglobulin within 72 hours of the event. After 12 weeks, the standard dose is 625 IU.

   • A. Sensitising events in the first trimester require immediate Anti-D administration to prevent maternal isoimmunisation.
   • C. While useful if known, administration of Anti-D should not be delayed to wait for paternal blood testing in an emergency setting.
   • D. A 625 IU dose is standard for second and third-trimester sensitising events; 250 IU is sufficient in the first trimester (up to 12 weeks).

   Sources: National Blood Authority Australia: Guidelines on the use of antenatal RhD Immunoglobulin

7. 6 / 10

   A 70-year-old man is diagnosed with multiple myeloma. He presents with lethargy and is found to have a serum creatinine of 220 umol/L. Urinalysis shows trace protein on dipstick, but a formal 24-hour urine collection confirms significant proteinuria.

   Which of the following describes the primary mechanism of renal impairment in multiple myeloma?

   • A. Deposition of amyloid fibrils in the glomerular capillaries, causing nephrotic-range proteinuria
   • B. Direct infiltration of myeloma plasma cells into the renal parenchyma, causing interstitial nephritis
   • C. Precipitation of monoclonal free light chains (Bence Jones proteins) in the distal tubules, causing cast nephropathy
   • D. Hyperuricemia leading to acute uric acid nephropathy
   Show answer

   Answer: C. Precipitation of monoclonal free light chains (Bence Jones proteins) in the distal tubules, causing cast nephropathy

   Why: The most common cause of renal failure in multiple myeloma is myeloma cast nephropathy (light chain cast nephropathy). Monoclonal free light chains (Bence Jones proteins) are filtered by the glomerulus and exceed the reabsorptive capacity of the proximal tubule. In the distal tubule, they bind to Tamm-Horsfall mucoprotein, forming casts that plug the lumen and trigger inflammatory and fibrotic reactions.

   • A. While AL amyloidosis can occur in myeloma, the primary and most common cause of acute/subacute renal failure is cast nephropathy.
   • B. Plasma cell infiltration of the kidneys is extremely rare and is not the mechanism of renal failure in myeloma.
   • D. Uric acid nephropathy is seen during tumor lysis syndrome, not as the primary driver of myeloma renal impairment.

   Sources: Medical Journal of Australia (MJA) Myeloma Guidelines; International Myeloma Working Group (IMWG) Criteria

8. 7 / 10

   A 48-year-old man presents to his GP complaining of chronic fatigue, joint pain in his hands, and mild abdominal discomfort. Routine blood tests reveal: ferritin 1200 ug/L (normal < 300) and transferrin saturation 68% (normal < 45%).

   Which of the following is the most appropriate next step to confirm the diagnosis of Hereditary Hemochromatosis?

   • A. Refer for a liver biopsy to stain for iron deposition
   • B. Start therapeutic venesection immediately
   • C. Schedule a CT scan of the abdomen to measure liver attenuation
   • D. Perform genetic testing for HFE gene mutations (C282Y and H63D)
   Show answer

   Answer: D. Perform genetic testing for HFE gene mutations (C282Y and H63D)

   Why: Hereditary Hemochromatosis is primarily caused by homozygosity for the C282Y mutation in the HFE gene. In patients presenting with elevated ferritin (>300 ug/L) and transferrin saturation (>45%), the diagnosis is confirmed by genetic testing for HFE mutations, avoiding the need for liver biopsy in most cases.

   • A. Liver biopsy is invasive and is now reserved for staging fibrosis, not for primary diagnostic confirmation.
   • B. Venesection is the treatment, but diagnosis should be confirmed via genetic testing first.
   • C. CT scan is not diagnostic for hemochromatosis and cannot replace genetic or tissue confirmation.

   Sources: Haemochromatosis Australia Guidelines; RACGP Red Book

9. 8 / 10

   A 56-year-old asymptomatic man is found to have a hemoglobin of 115 g/L (normal 130-170) and a ferritin of 12 ug/L (normal 30-300) during a routine health assessment.

   What is the most appropriate next diagnostic step?

   • A. Initiate oral iron supplements and repeat the ferritin level in 3 months
   • B. Recommend a faecal occult blood test (FOBT) to determine if GI bleeding is present
   • C. Refer the patient for both a gastroscopy and a colonoscopy
   • D. Perform genetic testing for coeliac disease
   Show answer

   Answer: C. Refer the patient for both a gastroscopy and a colonoscopy

   Why: Iron deficiency anemia in adult men and postmenopausal women is commonly caused by chronic occult gastrointestinal bleeding. Common etiologies include gastrointestinal malignancies (e.g. colorectal cancer), peptic ulcer disease, or angiodysplasia. Bidirectional endoscopy (gastroscopy and colonoscopy) is the gold standard investigation to locate the site of bleeding.

   • A. While iron supplementation is necessary, it is critical to investigate the cause of iron deficiency in a male patient first to exclude occult malignancy.
   • B. FOBT is a screening tool and is not indicated for patients who already have documented iron deficiency anemia; they require diagnostic endoscopy directly.
   • D. Coeliac disease can cause iron malabsorption, but structural GI evaluation with endoscopy/colonoscopy is the priority to exclude malignancy.

   Sources: GESA Clinical Update: Iron Deficiency Anemia; RACGP Preventive Care Guidelines (Red Book)

10. 9 / 10

    A 65-year-old man who was started on therapeutic intravenous Heparin for deep vein thrombosis 6 days ago is found to have a platelet count drop from 250 x 10^9/L to 90 x 10^9/L (a 64% reduction). He has no signs of active bleeding.

    What is the most appropriate immediate management step for suspected Heparin-Induced Thrombocytopenia (HIT)?

    • A. Continue heparin and order a platelet transfusion to correct the thrombocytopenia
    • B. Stop heparin immediately and initiate a non-heparin anticoagulant (e.g., Danaparoid or Argatroban)
    • C. Stop heparin and switch the patient to Warfarin immediately
    • D. Maintain heparin and repeat the platelet count in 24 hours to confirm the trend
    Show answer

    Answer: B. Stop heparin immediately and initiate a non-heparin anticoagulant (e.g., Danaparoid or Argatroban)

    Why: Heparin-Induced Thrombocytopenia (HIT) is an immune-mediated reaction caused by antibodies to the heparin-platelet factor 4 (PF4) complex. It typically presents with a > 50% drop in platelets 5-10 days after starting heparin. Immediate management requires stopping all heparin products (including flushes) and initiating therapeutic anticoagulation with a non-heparin alternative (such as Danaparoid, Argatroban, or Fondaparinux) because HIT is highly prothrombotic.

    • A. Continuing heparin worsens the immunologic response. Platelet transfusions are contraindicated in HIT as they can trigger thrombotic events.
    • C. Warfarin is contraindicated in acute HIT because it can cause rapid depletion of Protein C, leading to skin necrosis and venous gangrene.
    • D. Delaying action in suspected HIT is dangerous due to the extremely high risk of arterial and venous thromboembolism.

    Sources: THANZ (Thrombosis and Haemostasis Society of Australia and New Zealand) Guidelines; eTG complete, Haematology

11. 10 / 10

    A 70-year-old male presents with persistent low back pain, lethargy, serum calcium of 2.9 mmol/L, eGFR of 32 mL/min/1.73m2, normocytic anaemia, and an ESR of 105 mm/h.

    Likely diagnosis?

    • A. Multiple Myeloma
    • B. Osteoporosis
    • C. Prostate Cancer
    • D. Hypothyroidism
    Show answer

    Answer: A. Multiple Myeloma

    Why: Multiple Myeloma is a malignant plasma cell dyscrasia presenting with the CRAB pentad: HyperCalcemia, Renal insufficiency, Anaemia, and Bone lesions (osteolytic back pain). ESR is often markedly elevated (>100 mm/h) due to rouleaux formation driven by monoclonal paraprotein.

    • B. Incorrect. Osteoporosis causes fragility fractures but does not cause hypercalcaemia, renal failure, or a marked paraproteinaemic ESR elevation.
    • C. Incorrect. Metastatic prostate cancer typically produces blastic (sclerotic) bone lesions with elevated PSA rather than the CRAB profile.
    • D. Incorrect. Hypothyroidism can cause fatigue and mild anaemia, but does not account for lytic bone pain, severe hypercalcaemia, or renal failure.

    Sources: Myeloma Foundation Australia

Exam-style questions written by MedHub for practice. They are not official exam questions.