MLT GlobeHematology: Hemostasis & coagulation – page 6
125 Hematology MCQs on Hemostasis & coagulation with answers and explanations.
Activated protein C needs which cofactor to inactivate factors Va and VIIIa?
Protein S is the cofactor of activated protein C. Thrombomodulin helps thrombin activate protein C in the first place but is not the APC cofactor.
Plasma fibrinogen often rises in infection and inflammation because fibrinogen is:
Fibrinogen is an acute-phase protein made by the liver, so it rises with inflammation. This also helps explain the raised ESR in inflammation.
A young woman with recurrent miscarriages and a prolonged APTT that does not correct on mixing has had a DVT. Which condition is most likely?
Lupus anticoagulant prolongs APTT in vitro but causes thrombosis and pregnancy loss in vivo. Hemophilia and von Willebrand disease cause bleeding, and mixing studies correct.
A patient has prolonged PT, normal APTT, normal platelets and normal fibrinogen; PT corrects on mixing with normal plasma. Which disorder is most likely?
Only factor VII sits solely in the extrinsic pathway, so its deficiency prolongs PT alone. DIC and fibrinogen defects affect both tests.
Which condition does NOT prolong the PFA-100 closure time?
The PFA-100 reflects platelet and von Willebrand function under high shear, and is affected by low platelet count and hematocrit. Factor VIII deficiency does not prolong it.
Thrombin amplifies coagulation by activating several factors. Which is NOT one of its direct targets?
Thrombin activates factors V, VIII, XI and XIII as well as platelets. Factor VII is activated mainly by tissue factor–bound factor VIIa, Xa and IXa.
A patient's hematocrit is 65%. Using the CLSI formula, how much 3.2% citrate is needed for 4.5 mL of whole blood?
C (mL) = 1.85 × 10^-3 × (100 − Hct) × blood volume = 0.00185 × 35 × 4.5 ≈ 0.29 mL. Using the standard 0.5 mL would over-anticoagulate the smaller plasma volume and falsely prolong clotting times.
A patient's prolonged aPTT shortens markedly when plasma is pre-incubated with the silica activator for 10 minutes instead of 3. Which deficiency is most likely?
In prekallikrein deficiency, factor XII slowly auto-activates with longer contact time, correcting the aPTT. Deficiencies of XI, IX or VIII do not correct this way.
A sample drawn from a central line shows a very prolonged thrombin time but a normal reptilase time. The most likely cause is:
Reptilase is not inhibited by heparin, so a normal reptilase with long TT indicates heparin. Low or abnormal fibrinogen prolongs both tests.
An elderly woman with sudden large bruises has a prolonged aPTT that corrects in an immediate 1:1 mix but becomes prolonged again after 2 hours at 37 °C. This suggests:
Factor VIII autoantibodies are time- and temperature-dependent, so prolongation appears after incubation. Lupus anticoagulant usually acts immediately and causes thrombosis, not bruising.
A patient with mild bleeding has mild thrombocytopenia, low VWF:Rco/VWF:Ag ratio and increased platelet aggregation with low-dose ristocetin. The most likely vWD type is:
Type 2B VWF binds platelet GPIb too strongly, giving enhanced low-dose RIPA and clearance of platelets. Type 2A shows reduced aggregation with ristocetin.
Before emergency surgery, a patient on dabigatran has a normal thrombin time. This most likely means:
The TT is very sensitive to direct thrombin inhibitors; a normal TT effectively excludes significant dabigatran. Even low levels markedly prolong it, so it cannot quantify therapeutic levels.
Both liver failure and DIC can give low platelets, long PT and low fibrinogen. Which result favors DIC?
Factor VIII is made largely outside hepatocytes and is often normal or high in liver disease, but it is consumed in DIC. Factor VII falls in both.
Tissue factor pathway inhibitor (TFPI) mainly acts by:
TFPI first binds factor Xa and then the TF–VIIa complex, switching off the initiation phase. Activated protein C with protein S degrades Va and VIIIa.
A hemophilia A patient on emicizumab prophylaxis has a very short aPTT. Why is a one-stage aPTT-based factor VIII assay unreliable?
Emicizumab is a bispecific antibody that bridges factors IXa and X, acting like VIIIa and strongly shortening the aPTT. Chromogenic assays using bovine reagents are used to measure the patient's own factor VIII.
In a one-stage factor VIII assay, patient plasma dilutions give results that rise with each further dilution (nonparallel). The most likely cause is:
Inhibitors are diluted out at higher dilutions, so apparent factor activity increases; results should be parallel to the calibration curve. ISI applies to PT/INR only.
An uncentrifuged citrated sample is refrigerated overnight before PT testing. The PT is unexpectedly short. The likely reason is:
Storage at 2–8 °C can activate factor VII and damage labile factors, so whole blood for PT should be kept at room temperature. Factor VIII loss would affect the aPTT, not shorten the PT.
A patient on rivaroxaban is tested for lupus anticoagulant. A positive dRVVT result should be interpreted with caution because:
The dRVVT activates factor X directly, so anti-Xa DOACs prolong it and can mimic lupus anticoagulant. Testing is best done when the drug is absent or removed.
The free (active) form of protein S is reduced in inflammation mainly because more protein S is bound to:
About 60% of protein S is bound to C4b-binding protein, an acute-phase protein; only free protein S acts as the cofactor for activated protein C. Free protein S antigen is the preferred assay.
In a modified APC-resistance test, patient plasma is first diluted in factor V–deficient plasma. The purpose is to:
Dilution in factor V–deficient plasma corrects other factor deficiencies, making the result depend mainly on the patient's factor V, so it detects factor V Leiden with high specificity. Genotyping confirms it.