MLT GlobeHematology: Platelets – page 4
90 Hematology MCQs on Platelets with answers and explanations.
Which substances are stored in platelet alpha granules?
Alpha granules contain adhesive and growth proteins such as fibrinogen, VWF, platelet factor 4 and PDGF. ADP, serotonin and calcium are in dense granules.
A patient given a GP IIb/IIIa inhibitor such as eptifibatide during coronary stenting would show which aggregation pattern?
Blocking GP IIb/IIIa prevents fibrinogen bridging, giving a Glanzmann-like pattern; ristocetin agglutination via GP Ib–VWF is preserved. Aspirin affects mainly the arachidonic acid response.
Flow cytometry of platelets from a bleeding patient shows absent CD41 and CD61. The diagnosis is:
CD41 and CD61 are GP IIb and GP IIIa, which are missing in Glanzmann thrombasthenia. Bernard-Soulier syndrome lacks CD42a/CD42b (GP IX/GP Ib).
In a manual platelet count, blood is diluted 1:100. A total of 180 platelets is counted in the two central large squares (1 mm² each, depth 0.1 mm). The platelet count is:
Count = cells ÷ volume counted × dilution = 180 ÷ (2 × 1 × 0.1 µL) × 100 = 90 000/µL = 90 × 10^9/L.
A patient's blood contains many microcytic red cells (MCV 55 fL). On an impedance analyzer, the platelet count may be:
Very small red cells fall into the platelet size window and are counted as platelets. An optical/fluorescent platelet count or smear estimate helps confirm the true count.
A pregnant woman at 34 weeks with hypertension has schistocytes, high LDH, raised ALT and platelets of 60 × 10^9/L. The most likely diagnosis is:
HELLP means Hemolysis, Elevated Liver enzymes and Low Platelets, a severe form of preeclampsia. Gestational thrombocytopenia is mild with no hemolysis or liver damage.
A multiparous woman develops severe thrombocytopenia and purpura 8 days after a red cell transfusion. Which antibody is most often responsible?
Post-transfusion purpura usually occurs in HPA-1a–negative women previously sensitized by pregnancy; the antibody destroys transfused and the patient's own platelets. Anti-PF4/heparin causes HIT.
A patient has repeated poor 1-hour platelet increments after fresh ABO-compatible platelets, with no fever, sepsis or splenomegaly. The most common immune cause is antibodies to:
Immune platelet refractoriness is most often caused by HLA class I antibodies from earlier transfusion or pregnancy. HLA-matched or crossmatched platelets are used. HPA antibodies are less common.
In a patient with suspected HIT, the '4Ts' score is used to:
The 4Ts (thrombocytopenia, timing, thrombosis, other causes) estimate clinical probability. A low score has a high negative predictive value, and lab testing is directed at intermediate/high scores.
A patient with chronic kidney failure has bleeding after a minor procedure. Platelet count, PT and aPTT are normal. The most likely cause is:
Uremic toxins impair platelet adhesion and aggregation despite a normal count; dialysis, DDAVP and correcting anemia help. Hemophilia and vitamin K deficiency prolong clotting tests.
Ibuprofen affects platelet function differently from aspirin because ibuprofen:
NSAIDs such as ibuprofen are reversible COX inhibitors, so their effect ends once the drug is cleared. Aspirin acetylates COX-1 irreversibly for the platelet's life.
An adult has had immune thrombocytopenia for 14 months. By international terms, this is:
ITP is newly diagnosed up to 3 months, persistent from 3 to 12 months and chronic after 12 months. 'Secondary' refers to an underlying cause, not duration.
A newborn has thrombocytopenia with bilateral absent radii but normal thumbs. The most likely diagnosis is:
Thrombocytopenia–absent radius syndrome keeps the thumbs, while Fanconi anemia typically affects the thumbs as well as the radii. Wiskott-Aldrich shows small platelets and eczema.
In the platelet response to ristocetin, platelets clump by:
Ristocetin makes VWF bind GP Ib, causing passive agglutination that also occurs with fixed platelets. That is why it stays normal in Glanzmann thrombasthenia and on aspirin.
In a patient with massive splenomegaly, the platelet count is low mainly because of:
Normally about one-third of platelets are held in the spleen. An enlarged spleen holds a much larger share, lowering the circulating count (hypersplenism).
Clot retraction depends mainly on:
Platelets contract through their actin-myosin system and pull on fibrin through GP IIb/IIIa. Clot retraction is poor in thrombocytopenia and Glanzmann thrombasthenia.
Ristocetin-induced platelet aggregation is absent, but becomes normal when normal plasma is added. This pattern points to:
Ristocetin aggregation needs plasma von Willebrand factor and platelet GP Ib. Correction by normal plasma shows the missing part is plasma VWF. In Bernard-Soulier syndrome the defect is in the platelet and is not corrected.
Which platelet glycoprotein binds directly to collagen?
GPIa/IIa (with GPVI) mediates collagen adhesion. GPIb-V-IX binds von Willebrand factor, and GPIIb/IIIa binds fibrinogen for aggregation.
Giant platelets, thrombocytopenia and absent aggregation with ristocetin (not corrected by normal plasma) indicate:
Bernard-Soulier syndrome is a deficiency of the GP Ib-IX-V receptor for von Willebrand factor. Unlike von Willebrand disease, adding normal plasma does not fix ristocetin aggregation, because the defect is in the platelets.
Platelets that fail to aggregate with ADP, collagen and epinephrine but respond normally to ristocetin suggest:
GP IIb/IIIa binds fibrinogen to link platelets together, and every agonist except ristocetin needs it. Ristocetin agglutination depends on GP Ib and von Willebrand factor, which are normal.