MLT GlobeHematology: Hemostasis & coagulation – page 3
125 Hematology MCQs on Hemostasis & coagulation with answers and explanations.
A hemophilia patient is classed as severe. What is his factor activity level?
Severe hemophilia is below 1%, moderate 1–5% and mild 5–40%. Severe cases have spontaneous joint and muscle bleeds.
A child has palpable purpura on the buttocks and legs, abdominal pain and hematuria. What platelet count is expected?
Henoch–Schönlein purpura (IgA vasculitis) is a vascular purpura with a normal platelet count. Small platelets suggest Wiskott–Aldrich syndrome, prolonged clotting times DIC, and teardrop cells myelofibrosis.
Thrombin-generated fibrin polymerizes, but the clot becomes stable and insoluble only after cross-linking by:
Thrombin activates factor XIII, which in the presence of calcium forms covalent bonds between fibrin monomers, making the clot insoluble. Factor Xa acts earlier, generating thrombin.
Which condition characteristically prolongs the bleeding time or PFA closure time?
Bleeding time tests primary hemostasis (platelets and von Willebrand factor). Hemophilias and vitamin K deficiency affect coagulation factors, prolonging APTT or PT but not bleeding time.
Which coagulation factor belongs to the common pathway rather than the intrinsic pathway?
Factors XII, XI, IX and VIII form the intrinsic pathway; factor X, V, II and fibrinogen form the common pathway where intrinsic and extrinsic routes meet.
Activated protein C inactivates which coagulation factors?
APC, with protein S as cofactor, cleaves the activated cofactors Va and VIIIa. Factor V Leiden resists this cleavage.
A patient's APTT is prolonged while the PT is normal. The defect most likely involves:
APTT assesses intrinsic and common pathways; isolated prolongation suggests factors XII, XI, IX or VIII. Factor VII deficiency prolongs PT alone.
A prolonged aPTT does NOT correct when the patient's plasma is mixed 1:1 with normal plasma. This suggests:
Normal plasma supplies at least 50% of every factor, enough to correct a deficiency. If the time stays prolonged, something in the patient's plasma is blocking clotting: an inhibitor.
A woman with heavy periods and easy bruising has a prolonged PFA-100 closure time and low ristocetin cofactor activity. The most likely diagnosis is:
von Willebrand factor links platelets to damaged vessel walls and carries factor VIII. Its deficiency causes mucosal bleeding, poor platelet adhesion and low ristocetin cofactor activity; aPTT may be mildly prolonged.
Only a light-blue citrate tube is ordered and a winged (butterfly) set is used. What should the phlebotomist do first?
Air in the winged-set tubing would underfill the citrate tube, so a discard tube (plain or citrate) is drawn first. EDTA before citrate risks additive carryover.
For routine coagulation testing, centrifugation should produce platelet-poor plasma with a platelet count below:
CLSI requires platelet-poor plasma <10 × 10^9/L. Residual platelets release phospholipid and PF4, which can shorten clotting times and neutralize heparin.
A capped, citrated sample from a patient not on heparin is kept at room temperature. Per CLSI, the aPTT should be tested within:
CLSI allows 4 hours for aPTT (1 hour if the patient is on unfractionated heparin). PT samples are stable for up to 24 hours.
A patient's PT is 26 s, the geometric mean normal PT is 13 s and the thromboplastin ISI is 1.2. The INR is about:
INR = (PT/MNPT)^ISI = (26/13)^1.2 = 2^1.2 ≈ 2.3. Forgetting the ISI exponent gives 2.0.
Why does the PT rise within the first 1–2 days of starting warfarin, before full anticoagulation?
Factor VII's half-life is about 6 hours, so it falls first and prolongs the PT. Full antithrombotic effect needs prothrombin (half-life ~60 h) to fall.
A woman develops painful skin necrosis 3 days after starting warfarin without heparin cover. Which underlying deficiency is most likely?
Protein C falls quickly on warfarin, creating a temporary hypercoagulable state; hereditary protein C deficiency increases the risk of skin necrosis. Factor XII deficiency does not cause this.
A pre-operative patient with no bleeding history has aPTT 90 s, normal PT, correction on 1:1 mixing, and very low factor XII. What does this mean for surgery?
Factor XII deficiency greatly prolongs the aPTT but does not cause bleeding in vivo. Treatment is not required for surgery.
A newborn has delayed bleeding from the umbilical stump. PT, aPTT, fibrinogen and platelets are normal. Which test should be done next?
Factor XIII cross-links fibrin after clotting, so its deficiency does not affect PT or aPTT. The clot dissolves in 5 M urea; a quantitative factor XIII assay is preferred.
PT and aPTT are both prolonged, thrombin time is normal and both correct with 1:1 normal plasma. Which deficiency best fits?
A common pathway factor (X, V or II) prolongs both PT and aPTT but not the TT. Low fibrinogen would prolong the TT as well.
In the Clauss fibrinogen method, diluted plasma is clotted with excess thrombin. The clotting time is:
With high thrombin, the clotting time depends on fibrinogen: the lower the fibrinogen, the longer the time. Results are read from a calibration curve.
In the Bethesda assay, one Bethesda unit is the amount of inhibitor that:
One BU destroys half of the factor VIII activity of an equal volume of normal plasma after 2 hours' incubation at 37 °C. Titers guide treatment choices.