MLT GlobeHematology: Platelets – page 5
90 Hematology MCQs on Platelets with answers and explanations.
A healthy term newborn has platelets of 15 × 10^9/L and petechiae. The mother's platelet count is normal and she is HPA-1a negative. The most likely diagnosis is:
Maternal alloantibodies to fetal HPA-1a cross the placenta and destroy fetal platelets. In maternal ITP the mother herself is usually thrombocytopenic.
Which test is regarded as the reference (gold standard) functional assay for heparin-induced thrombocytopenia?
The washed-platelet serotonin release assay shows platelet activation by patient antibodies and is highly specific. The ELISA is sensitive but gives many false positives.
A patient with oculocutaneous albinism and bleeding has absent secondary wave aggregation and platelets lacking dense granules on electron microscopy. The diagnosis is:
Hermansky-Pudlak syndrome is a dense-granule (δ-storage pool) disorder with albinism. Without released ADP, the secondary wave is lost.
A PFA-100 test shows a prolonged collagen/epinephrine closure time but a normal collagen/ADP closure time. This pattern most suggests:
Aspirin typically prolongs only the collagen/epinephrine cartridge. vWD, Glanzmann thrombasthenia and low platelet counts usually prolong both.
Which flow cytometry marker on the platelet surface indicates alpha-granule release (platelet activation)?
P-selectin lines the alpha-granule membrane and appears on the surface after activation and degranulation. GP Ib is present on resting platelets.
A patient receives 4 × 10^11 platelets. Body surface area is 2.0 m². Pre-count is 10 × 10^9/L and the 1-hour post-count is 30 × 10^9/L. The corrected count increment (CCI) is:
CCI = increment (per µL) × BSA ÷ platelets transfused (×10^11) = 20 000 × 2.0 ÷ 4 = 10 000. A 1-hour CCI above 7500 indicates an adequate response.
A child has hemolytic anemia with schistocytes, thrombocytopenia and acute kidney injury without diarrhea. ADAMTS13 activity is 60%. Which pathway is most likely abnormal?
Atypical (complement-mediated) HUS is caused by uncontrolled alternative complement activation, e.g., factor H mutations or antibodies. Normal ADAMTS13 excludes TTP; no diarrhea argues against STEC-HUS.
A newborn has severe thrombocytopenia with absent megakaryocytes in the marrow, normal limbs, and very high thrombopoietin. Which gene is most likely mutated?
Congenital amegakaryocytic thrombocytopenia is caused by MPL (thrombopoietin receptor) mutations and often progresses to marrow failure. ITGA2B mutations cause Glanzmann thrombasthenia.
A patient has a bleeding tendency, normal platelet aggregation and normal counts, but platelets fail to expose phosphatidylserine for coagulation. This defect is:
Scott syndrome is a defect in platelet procoagulant activity (phospholipid scrambling, ANO6/TMEM16F); aggregation tests are normal. Glanzmann and Hermansky-Pudlak show abnormal aggregation.
Which platelet receptor mainly mediates firm adhesion and activation by collagen after initial capture?
GP Ib–VWF provides initial tethering under high shear, and GP VI (with integrin α2β1) binds collagen directly and triggers activation. P2Y12 is an ADP receptor.