Page 23 of 25

PA20.1-2 | Hemostasis & Bleeding Disorders — Graded Quiz

Graded 12 questions · Untimed · 2 attempts

Click any question card to reveal the correct answer.

Q1 PA20.1 1 pt

A 52-year-old woman with advanced cirrhosis presents with haematemesis. Investigations: PT 26 s (INR 2.2), aPTT 58 s, platelets 55,000/µL, fibrinogen 1.4 g/L. You give her 4 units of fresh frozen plasma. Her PT corrects to 18 s but the aPTT remains prolonged at 48 s. After the FFP, her ionised calcium falls to 0.72 mmol/L. Which consequence of the FFP transfusion best explains the persistent aPTT prolongation?

A FFP contains insufficient factor VIII to correct the intrinsic pathway
B Citrate in FFP chelates ionised calcium, impairing calcium-dependent coagulation steps in the intrinsic pathway
C Dilutional thrombocytopenia worsened by the FFP volume load
D Liver disease–associated factor V deficiency is uncorrectable with FFP

Click to reveal answer

Q2 PA20.2 1 pt

A 3-year-old girl presents with petechiae on her lower limbs after a viral upper respiratory tract infection 2 weeks ago. Platelet count is 11,000/µL. Blood film shows small, sparse platelets and no other abnormalities. PT and aPTT are normal. Her parents are not consanguineous and her CBC prior to the illness was normal. Bone marrow biopsy shows markedly increased megakaryocytes with normal morphology. Which of the following laboratory findings would MOST definitively confirm the immune mechanism of her thrombocytopenia?

A Elevated serum thrombopoietin level confirming peripheral platelet destruction
B Platelet-associated IgG antibodies directed against GPIIb/IIIa or GPIb/IX on platelet surface
C Correction of platelet count after 3 weeks of intravenous immunoglobulin (IVIG) therapy
D Normal ADAMTS13 activity ruling out TTP as the cause of thrombocytopenia

Click to reveal answer

Q3 PA20.1 1 pt

A 7-year-old boy with known severe haemophilia A (factor VIII 1% of normal) falls from a bicycle and develops a large haematoma in his right thigh. His mother gives him recombinant factor VIII concentrate at home. Six months later he returns with an unexpectedly poor haemostatic response to factor VIII therapy. Mixing study shows the aPTT does not correct with normal plasma (remains prolonged at 70 s after 1:1 mix). Which investigation will MOST directly characterise the cause of his treatment failure?

A Factor VIII gene mutation analysis to identify a new pathogenic variant
B Bethesda inhibitor assay to quantify neutralising antibodies against factor VIII
C Platelet aggregation studies to exclude an acquired qualitative platelet defect
D Von Willebrand factor multimer analysis to detect acquired vWD

Click to reveal answer

Q4 PA20.1 1 pt

During an elective hernia repair, a 58-year-old man's pre-operative work-up reveals: PT 24 s (INR 2.0), aPTT 55 s, platelets 230,000/µL, fibrinogen 2.8 g/L. He takes no anticoagulants and has no liver disease. He is not jaundiced. Urine is dark yellow. He reports no recent dietary change but has been on a broad-spectrum antibiotic (cefoperazone) for 3 weeks for a chest infection. His serum bilirubin is normal, and his liver enzymes are mildly elevated. Which mechanism MOST directly explains his coagulopathy?

A Cefoperazone directly inhibits vitamin K epoxide reductase (VKORC1), mimicking warfarin effect
B Antibiotic-induced eradication of gut flora reduces vitamin K2 (menaquinone) availability for hepatic γ-carboxylation of clotting factors
C Cephalosporin-mediated immune thrombocytopenia causing platelet consumption and secondary coagulopathy
D Antibiotic-associated liver injury causing impaired hepatic synthesis of clotting factors

Click to reveal answer

Q5 PA20.2 1 pt

A 38-year-old woman delivers her baby at 38 weeks and develops severe postpartum haemorrhage. She receives multiple blood products. Three days later she develops widespread purpura, haemoptysis, haematuria, and worsening renal function. Investigations: platelets 22,000/µL, PT 30 s, aPTT 72 s, fibrinogen 0.6 g/L, D-dimer >20 µg/mL, blood film shows schistocytes. Which finding would MOST reliably distinguish her coagulopathy from that of thrombotic thrombocytopenic purpura (TTP)?

A Schistocytes on blood film — more prominent in TTP than in DIC
B Profoundly low fibrinogen (0.6 g/L) and elevated D-dimer — both typically normal or mildly elevated in TTP
C Thrombocytopenia severity — TTP causes more severe thrombocytopenia than DIC
D Renal involvement — present in DIC but not in TTP

Click to reveal answer

Q6 PA20.2 1 pt

A 16-year-old girl has had recurrent mucosal bleeding since childhood. She now presents with menorrhagia lasting 12 days. Platelet count is 195,000/µL. PT and aPTT are both normal. Platelet aggregation studies show normal aggregation with ristocetin but absent aggregation with ADP, arachidonic acid, and collagen. Electron microscopy of platelets shows absence of dense granules. Which disorder MOST likely explains her platelet function defect?

A Glanzmann thrombasthenia — absence of GPIIb/IIIa preventing fibrinogen bridging between platelets
B Storage pool disease (delta storage pool deficiency) — absent dense granules causing impaired ADP/serotonin release and secondary aggregation failure
C Bernard-Soulier syndrome — absence of GPIb/IX preventing platelet adhesion to vWF
D Platelet-type vWD — gain-of-function GPIb mutation causing platelet hyperactivation and consumption

Click to reveal answer

Q7 PA20.1 1 pt

An 8-year-old boy with severe factor IX deficiency (Christmas disease, factor IX <1%) develops recurrent haemarthroses in his right knee. Plain X-ray shows periarticular osteoporosis and joint-space narrowing. Histologically, the synovium shows haemosiderin deposits, synovial hypertrophy, and pannus formation. Which sequence of events best explains the pathogenesis of haemophilic arthropathy?

A Repeated intra-articular bleeding → iron-mediated chondrocyte apoptosis and synovial fibroblast proliferation → cartilage destruction and fibrous ankylosis
B Factor IX deficiency → complement activation within joints → neutrophil-mediated cartilage proteolysis
C Haemarthrosis → IgG autoantibody formation against cartilage collagen → erosive autoimmune arthritis
D Recurrent haemarthrosis → vascular microthrombi in synovial vessels → avascular necrosis of articular cartilage

Click to reveal answer

Q8 PA20.2 1 pt

A 32-year-old man with chronic kidney disease stage 5 (on haemodialysis) presents with severe epistaxis and oozing from his arteriovenous fistula site. Platelet count is 210,000/µL. PT and aPTT are normal. PFA-100 closure time with collagen/ADP cartridge is markedly prolonged. Which mechanism MOST directly explains his bleeding tendency?

A Uraemic toxins impair platelet GPIb–vWF adhesion by directly modifying GPIb on platelet surface
B Retained uraemic toxins (guanidinosuccinic acid, phenolic acids) interfere with platelet activation and thromboxane A2 synthesis
C Heparin used in dialysis circuits inhibits thrombin-mediated platelet activation
D Dialysis membrane–induced thrombocytopenia from complement-mediated platelet destruction

Click to reveal answer

Q9 PA20.2 1 pt

A 28-year-old woman with obstetric antiphospholipid syndrome (APS) is found to have a markedly prolonged aPTT (82 s) on a routine pre-natal screen. Her PT is normal. Platelet count is 140,000/µL. She has no personal history of bleeding. The 1:1 mixing study with normal plasma does NOT correct the aPTT (remains 78 s). Which clinical implication best reflects the paradox in this patient?

A The prolonged aPTT indicates a factor deficiency requiring factor replacement before delivery
B The lupus anticoagulant causes in vitro aPTT prolongation but is associated with thrombosis (not bleeding) in vivo
C The non-correcting mixing study confirms haemophilia B (factor IX inhibitor) requiring bypassing therapy
D The isolated aPTT prolongation with normal PT indicates a severe factor VIII or IX deficiency causing high bleeding risk in childbirth

Click to reveal answer

Q10 PA20.2 1 pt

A 55-year-old man with metastatic prostate cancer is admitted with bleeding from multiple sites (venepuncture, gums, haematuria). Investigations: platelets 28,000/µL, PT 32 s, aPTT 68 s, fibrinogen 0.7 g/L, D-dimer 18 µg/mL (markedly elevated), schistocytes on film. His oncologist considers initiating heparin therapy to break the DIC cycle. Which statement MOST accurately describes the rationale for heparin in this clinical context?

A Heparin inhibits thrombin directly, stopping fibrinogen consumption and platelet activation, thereby conserving haemostatic factors
B Heparin augments antithrombin to neutralise thrombin and Xa, interrupting the DIC cycle and halting further consumption of clotting factors; it is considered in chronic/compensated DIC driven by ongoing thrombin generation (e.g. mucin-secreting cancers)
C Heparin directly inhibits tissue factor release from tumour cells, addressing the root cause of DIC in cancer
D Heparin corrects the prolonged aPTT by competing with antiphospholipid antibodies for phospholipid binding sites

Click to reveal answer

Q11 PA20.1 1 pt

A 55-year-old man with decompensated liver cirrhosis has: PT 24 s (INR 2.0), aPTT 52 s, platelets 65,000/µL, fibrinogen 1.6 g/L. You administer parenteral vitamin K 10 mg IV. After 24 hours: PT 16 s (INR 1.3), aPTT 40 s. Which factor was MOST responsible for the initial PT prolongation and why did it respond fastest to vitamin K?

A Factor II (prothrombin) — the most abundant vitamin K–dependent factor; large hepatic reserve depletes last
B Factor VII — has the shortest plasma half-life (~3–6 hours) among vitamin K–dependent factors; its level falls first and recovers first after vitamin K supplementation
C Factor V — a non-vitamin K–dependent factor whose hepatic synthesis falls in liver disease, primarily prolonging PT
D Von Willebrand factor — its depletion in liver disease reduces factor VIII stability, secondarily prolonging PT

Click to reveal answer

Q12 PA20.2 1 pt

A 45-year-old woman undergoes surgery for a ruptured ectopic pregnancy and receives 14 units of PRBC over 4 hours. Her body temperature falls to 34.8°C. Post-operatively: PT 26 s, aPTT 60 s, platelets 38,000/µL, ionised calcium 0.68 mmol/L, fibrinogen 0.9 g/L. D-dimer is 2.8 µg/mL (mildly elevated). Which combination BEST explains the coagulopathy and should guide immediate correction?

A Massive transfusion DIC triggered by ischaemia–reperfusion injury; treat with heparin infusion
B Dilutional coagulopathy + hypothermia-induced enzyme dysfunction + hypocalcaemia (citrate load) — the 'lethal triad'; treat with FFP, cryoprecipitate, platelet concentrate, calcium, and active rewarming
C Liver injury–associated coagulopathy from intraoperative hepatic ischaemia; treat with vitamin K IV
D Acquired haemophilia A from dilutional factor VIII loss; treat with recombinant factor VIIa alone

Click to reveal answer