MLT GlobeHematology: Platelets – page 3
90 Hematology MCQs on Platelets with answers and explanations.
Thrombopoietin, the main regulator of megakaryocyte production, is produced mostly by the:
TPO is produced constantly by hepatocytes; its free level falls as it is bound by platelets and megakaryocytes. The kidney is the main source of erythropoietin.
A patient has EDTA-dependent platelet clumping. A recollected sodium citrate sample gives a platelet count of 90 × 10^9/L. The reported count should be:
The citrate tube dilutes blood 9:10, so the count is multiplied by 1.1: 90 × 1.1 = 99 × 10^9/L. Reporting 90 underestimates the count.
An EDTA smear shows platelets arranged in rings around neutrophils, and the analyzer count is low. This phenomenon is:
Platelet satellitism is an in-vitro EDTA-dependent antibody effect causing platelets to adhere to neutrophils, producing false thrombocytopenia. A citrate sample usually corrects it.
A patient with an MYH9 disorder has many giant platelets. On an impedance counter the platelet count is most likely to be:
Impedance counters exclude particles above the platelet size window, so giant platelets are missed or counted as RBCs. Optical, fluorescent or CD61-based counts and smear review are better.
A burn patient has many red cell fragments. The impedance platelet count may be:
Small RBC fragments (schistocytes) and very microcytic cells fall into the platelet size range and are counted as platelets. A smear check or optical method is advised.
A high immature platelet fraction (IPF) in a patient with thrombocytopenia most suggests:
IPF reflects young, RNA-rich platelets; it rises when the marrow responds to destruction such as ITP. It stays low when production fails.
A 35-year-old has confusion, fever, platelets 18 × 10^9/L and many schistocytes. Which laboratory result confirms the most likely diagnosis?
Severe ADAMTS13 deficiency (<10%) confirms TTP, usually from an autoantibody. Unprocessed large VWF multimers then form platelet thrombi.
Schistocytes and thrombocytopenia are present. Which result favors TTP over DIC?
In TTP the coagulation cascade is not consumed, so PT, aPTT and fibrinogen are usually normal. In DIC they are prolonged or low.
A patient on unfractionated heparin has a platelet fall from 260 to 110 × 10^9/L on day 7 and a new DVT. While HIT testing is pending, the right approach is:
HIT is prothrombotic; all heparin (including LMWH, which cross-reacts) must stop and a non-heparin anticoagulant such as argatroban started. Platelet transfusion is avoided.
The antibodies causing heparin-induced thrombocytopenia are directed against:
HIT antibodies (mainly IgG) bind PF4–heparin complexes, then activate platelets via FcγRIIa. GPIIb/IIIa is the usual target in ITP.
Aggregation studies show absent response to arachidonic acid, reduced secondary wave with epinephrine and ADP, and normal ristocetin. The most likely cause is:
Aspirin blocks COX-1, preventing thromboxane A2 formation from arachidonic acid. Glanzmann thrombasthenia would abolish ADP, epinephrine and collagen responses completely.
A patient on clopidogrel is most likely to show reduced platelet aggregation with:
Clopidogrel irreversibly blocks the P2Y12 ADP receptor. Arachidonic acid response is mainly affected by aspirin.
Large platelets that look pale grey and nearly agranular on Wright stain, with mild thrombocytopenia and marrow fibrosis, suggest:
Gray platelet syndrome (NBEAL2) lacks alpha granules, giving grey platelets; released growth factors cause fibrosis. Wiskott-Aldrich platelets are small.
Platelet dense (delta) granules store:
Dense granules contain ADP, ATP, serotonin, calcium and pyrophosphate. Fibrinogen, VWF and PF4 are alpha-granule proteins.
Why does a single aspirin dose affect platelet function for about a week?
Aspirin acetylates COX-1 irreversibly; anucleate platelets cannot synthesize new enzyme, so the effect lasts their lifespan (7–10 days). The drug itself is cleared within hours.
A woman with heavy menstrual bleeding has platelets of 620 × 10^9/L, microcytic anemia and low ferritin. The thrombocytosis is most likely:
Iron deficiency is a common cause of reactive thrombocytosis, which resolves with iron therapy. ET should be considered only after reactive causes are excluded.
A boy has eczema, recurrent infections and thrombocytopenia with abnormally small platelets. The most likely diagnosis is:
Wiskott-Aldrich syndrome is X-linked, with microthrombocytes (low MPV), eczema and immunodeficiency. Bernard-Soulier and May-Hegglin show giant platelets.
A patient develops sudden severe thrombocytopenia a week after starting quinine; counts recover after stopping it. The mechanism is:
Quinine causes drug-dependent antibodies that bind platelet GPs (often GPIb or GPIIb/IIIa) only when the drug is present. Recovery occurs after the drug is cleared.
Which handling practice is correct for platelet aggregation samples?
Platelet function samples are citrated, kept at room temperature and tested within 4 hours. Cold, pneumatic tube transport and EDTA activate or impair platelets.
About what fraction of the total platelet mass is normally pooled in the spleen?
About one-third of platelets are held in the spleen. In massive splenomegaly more are pooled, causing thrombocytopenia, while splenectomy raises the platelet count.