MLT GlobeHematology: Hemostasis & coagulation – page 5
125 Hematology MCQs on Hemostasis & coagulation with answers and explanations.
The main circulating inhibitor that rapidly neutralizes free plasmin is:
Alpha-2-antiplasmin quickly binds free plasmin, limiting fibrinolysis to the clot surface. Its inherited deficiency causes a bleeding tendency. Antithrombin mainly inhibits thrombin and Xa.
A man with hemophilia A and a non-carrier wife has children. Which statement about inheritance is correct?
Hemophilia A is X-linked recessive. An affected father passes his X to every daughter (obligate carriers) and his Y to every son, so sons are unaffected.
A patient has prolonged PT and aPTT. Factor V is 95%, and factors II, VII, IX and X are low. The most likely cause is:
Factor V is not vitamin K–dependent, so it stays normal in vitamin K deficiency or warfarin use. In liver disease factor V is also low because the liver makes it.
The ISTH overt DIC score uses which combination of tests?
The ISTH score gives points for platelet count, D-dimer/FDP, PT prolongation and fibrinogen; a score of 5 or more is compatible with overt DIC. The aPTT is not part of the score.
A citrate tube drawn after an EDTA tube gives prolonged PT and aPTT in a patient with previously normal results. The most likely reason is:
EDTA carryover binds calcium, which added calcium cannot fully correct, giving falsely prolonged clotting times. The citrate tube should be drawn before EDTA, heparin and serum tubes with additives.
According to CLSI guidance, uncentrifuged or centrifuged citrated whole blood for PT/INR, kept capped at room temperature, should be tested within:
PT samples are stable for up to 24 hours at room temperature. Samples for aPTT (non-heparinized) should be tested within 4 hours because factor VIII is labile.
In a patient with a normal fibrinogen antigen but low Clauss (functional) fibrinogen and prolonged thrombin time, the most likely diagnosis is:
A functional-to-antigen discrepancy indicates an abnormal fibrinogen molecule. In hypofibrinogenemia both activity and antigen are proportionally low; factor XIII deficiency does not prolong clotting times.
A heparin-contaminated sample needs aPTT testing. Which agent can be added to neutralize heparin in vitro?
Heparinase enzymatically breaks down heparin (polybrene and protamine also neutralize it) so the underlying clotting time can be seen. Tranexamic acid is an antifibrinolytic.
Low-molecular-weight heparin causes little prolongation of the aPTT because it:
Most LMWH chains are too short to bridge antithrombin to thrombin, so anti-Xa activity dominates. Anti-Xa assays are used when monitoring is needed.
A patient with HIT is treated with intravenous argatroban. Which test is commonly used to adjust the dose?
Argatroban, a direct thrombin inhibitor, is usually monitored by aPTT (target about 1.5–3 times baseline). It also raises the INR, which matters when switching to warfarin.
According to ISTH guidance, lupus anticoagulant testing should use:
Two tests based on different principles (dRVVT and an LA-sensitive aPTT) are recommended, each with screen, mix and confirm steps. Anticardiolipin ELISA detects antibodies but not LA activity.
A patient has a positive lupus anticoagulant test after a DVT. To support antiphospholipid syndrome, the test should be repeated after at least:
Laboratory criteria require persistent positivity on two occasions at least 12 weeks apart, because transient antibodies occur with infections or drugs.
The recommended first-line screening test for inherited antithrombin deficiency is:
A heparin-cofactor activity assay detects both type I (low amount) and type II (abnormal function) deficiency. Antigen alone misses type II deficiency.
A term newborn develops purpura fulminans within hours of birth with undetectable protein C activity. The likely cause is:
Severe (homozygous or compound heterozygous) protein C deficiency causes neonatal purpura fulminans with skin necrosis and DIC. NAIT and vitamin K deficiency cause bleeding, not thrombosis.
A woman suspected of vWD is tested during late pregnancy and has normal VWF levels. Why should results be interpreted cautiously?
VWF is an acute-phase reactant that rises with pregnancy, estrogen, exercise and inflammation, which can hide mild type 1 vWD. Testing may need to be repeated in a baseline state.
Desmopressin (DDAVP) is used in mild hemophilia A and type 1 vWD because it:
DDAVP releases stored VWF from Weibel-Palade bodies, raising VWF and factor VIII 2–5 fold. Tranexamic acid, not DDAVP, inhibits fibrinolysis.
Most chromogenic coagulation assays measure the release of para-nitroaniline (pNA), read at a wavelength of:
Enzymes such as thrombin or Xa cleave a synthetic peptide–pNA substrate, releasing yellow pNA read at 405 nm. 340 nm is used for NADH-based chemistry reactions.
A PT reagent with an ISI of 1.0 compared with one of 2.0 is:
A lower ISI means the thromboplastin behaves close to the WHO reference and is more responsive to factor deficiency, giving more precise INRs. Reagents with ISI near 1.0 are preferred.
The thrombin time mainly tests:
In the thrombin time, thrombin is added to plasma, so only the fibrinogen-to-fibrin step is tested. It is prolonged by low or abnormal fibrinogen and by thrombin inhibitors such as heparin.
Which set of results is typical of acute disseminated intravascular coagulation (DIC)?
In acute DIC, widespread clotting uses up platelets and factors (low platelets, prolonged PT/aPTT, low fibrinogen), while fibrinolysis raises D-dimer.