MLT GlobeHematology: Hemostasis & coagulation – page 4
125 Hematology MCQs on Hemostasis & coagulation with answers and explanations.
In a dilute Russell viper venom time (dRVVT) test, which pattern supports lupus anticoagulant?
LA antibodies are phospholipid-dependent; excess phospholipid in the confirm reagent overcomes them, shortening the time. ISTH advises pairing dRVVT with an LA-sensitive aPTT.
A woman of Ashkenazi Jewish descent bleeds after dental extraction. aPTT is prolonged, PT normal, and it corrects on mixing. The most likely deficiency is:
Factor XI deficiency (hemophilia C) is autosomal, affects both sexes and is common in Ashkenazi Jews. Factor VIII and IX deficiencies are X-linked and rare in women.
A child has severe mucosal bleeding and hemarthroses, undetectable VWF antigen and factor VIII activity of 3%. This is:
Type 3 vWD has virtually absent VWF, so factor VIII loses its carrier and falls very low. Type 2N has low factor VIII but normal VWF antigen.
When interpreting borderline-low VWF antigen, which factor normally gives lower VWF levels?
People with blood group O have about 25–30% lower VWF levels. Pregnancy, stress, exercise and inflammation raise VWF and can mask mild vWD.
For monitoring unfractionated heparin by anti-Xa activity, the commonly used therapeutic range is:
The widely used therapeutic range for UFH is 0.3–0.7 anti-Xa IU/mL. Higher ranges apply to peak LMWH levels, not UFH.
A pregnant woman on twice-daily subcutaneous LMWH needs monitoring. The best test and timing is:
LMWH has little effect on the aPTT; anti-Xa is measured at peak, about 4 hours after subcutaneous dosing. INR is used for warfarin.
A patient needs very high heparin doses but the aPTT barely changes. Antithrombin activity is 40%. The best explanation is:
Heparin works by accelerating antithrombin; low antithrombin reduces its effect. Lupus anticoagulant would prolong the baseline aPTT rather than blunt heparin response.
Plasma levels of rivaroxaban or apixaban are best measured by:
Direct Xa inhibitors are quantified with drug-specific calibrated anti-Xa assays. The thrombin time is unaffected by Xa inhibitors.
A negative D-dimer result in an outpatient with low clinical probability of DVT is useful because:
D-dimer is sensitive but not specific; a negative result with low pretest probability safely excludes VTE. Positive results occur in many conditions.
The prothrombin G20210A variant increases thrombosis risk mainly by:
This 3' untranslated region variant increases prothrombin mRNA stability and plasma prothrombin level. It does not change the structure of thrombin.
A patient on warfarin for a recent DVT has low protein C and protein S activity. What is the best interpretation?
Warfarin lowers vitamin K–dependent proteins C and S, and acute thrombosis can also consume them. Testing should be repeated off warfarin (usually at least 2 weeks).
The main physiologic inhibitor of tissue plasminogen activator is:
PAI-1 inhibits tPA and urokinase. Alpha-2-antiplasmin inhibits plasmin itself, not the activator.
According to the cell-based model of coagulation, the initiation phase begins when:
Initiation occurs on tissue factor–bearing cells, where TF–VIIa activates factors IX and X and makes a small amount of thrombin. Factor XII is not needed for in vivo hemostasis.
When thrombin binds thrombomodulin on endothelial cells, it mainly activates:
Thrombomodulin switches thrombin from procoagulant to anticoagulant action, activating protein C (and TAFI). Bound thrombin no longer clots fibrinogen efficiently.
A PT sample is strongly icteric and lipemic, and the photo-optical analyzer gives an error. The best next step is:
High bilirubin and lipids interfere with light-based clot detection; mechanical (viscosity-based) systems are not affected. Diluting would change factor levels.
A 3-day-old breast-fed baby who did not receive vitamin K at birth has GI bleeding. PT and aPTT are prolonged; platelets and fibrinogen are normal. The most likely cause is:
Newborns have low vitamin K stores and breast milk contains little vitamin K, so factors II, VII, IX and X fall. DIC would also lower platelets and fibrinogen.
Warfarin lowers active vitamin K–dependent factors by inhibiting which enzyme?
Warfarin blocks VKORC1, preventing recycling of vitamin K to its active reduced form. Variants in VKORC1 and CYP2C9 explain much of the variation in warfarin dose requirements.
The intrinsic tenase complex that activates factor X on phospholipid surfaces is made of:
Factor IXa with its cofactor VIIIa activates factor X very efficiently; this is why deficiency of VIII or IX causes hemophilia. Xa with Va forms the prothrombinase complex.
When thrombin acts on fibrinogen, the first products released are:
Thrombin cleaves fibrinopeptides A and B from the alpha and beta chains, forming fibrin monomers that polymerize. Fragments D and E and D-dimers are plasmin degradation products.
D-dimer is more specific for active clot formation and breakdown than total FDPs because it:
D-dimer contains two D domains joined by factor XIIIa cross-links, which exist only in stabilized fibrin. Other FDPs can come from fibrinogen breakdown without clot formation.