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Causes, clinical features, and management of low platelet counts and other platelet function disorders.
Mastering this deck will enhance your ability to diagnose and manage thrombocytopenia and platelet function disorders effectively, improving patient outcomes through accurate interpretation of clinical and laboratory findings and appropriate treatment strategies.
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| # | Front | Back | Hint |
|---|---|---|---|
| 1 | What is thrombocytopenia? | Thrombocytopenia is a condition characterized by a platelet count below 150,000/μL, leading to increased bleeding risk due to impaired clot formation. | Think 'thrombo' (clot) and 'penia' (deficiency) |
| 2 | List common causes of thrombocytopenia. | Common causes include decreased platelet production (e.g., aplastic anemia, leukemia), increased destruction (e.g., immune thrombocytopenic purpura, drugs), sequestration (e.g., splenomegaly), and dilutional effects (massive transfusions). | Remember 'DID'—Destruction, Production, Sequestration, Dilution |
| 3 | What is immune thrombocytopenic purpura (ITP)? | ITP is an autoimmune disorder where antibodies target platelet surface glycoproteins, leading to increased platelet destruction and often presenting with petechiae, purpura, and mucosal bleeding. | Think 'immune attack on platelets' |
| 4 | How is ITP diagnosed? | Primarily a diagnosis of exclusion, based on isolated thrombocytopenia with normal bone marrow findings and absence of other causes; antiplatelet antibody tests are supportive but not definitive. | Exclude other causes first |
| 5 | What are common management options for ITP in adults? | First-line treatments include corticosteroids, IV immunoglobulin (IVIG), and platelet transfusions in severe cases; splenectomy is considered if refractory. | Think steroids first |
| 6 | Define thrombotic thrombocytopenic purpura (TTP). | TTP is a life-threatening disorder caused by deficiency of ADAMTS13 enzyme, leading to large von Willebrand factor multimers, platelet aggregation, microthrombi, and consumption thrombocytopenia. | Remember 'TTP' as 'Thrombotic' and 'Platelet' consumption |
| 7 | What are the characteristic clinical features of TTP? | Features include microangiopathic hemolytic anemia, thrombocytopenia, neurological symptoms, renal impairment, and fever—collectively remembered as the pentad. | Think 'FAT RN'—Fever, Anemia, Thrombocytopenia, Renal, Neuro |
| 8 | How is TTP treated? | Emergently with plasma exchange therapy to remove autoantibodies and replenish ADAMTS13; corticosteroids are also used, and rituximab may be considered in refractory cases. | Plasma exchange is key |
| 9 | What distinguishes platelet function disorders from thrombocytopenia? | Platelet function disorders involve qualitative defects where platelet count is normal but their ability to aggregate or adhere is impaired, leading to bleeding. | Think 'function' not 'number' |
| 10 | Name two inherited platelet function disorders. | Bernard-Soulier syndrome and Glanzmann thrombasthenia. | Remember B-S for 'Big' platelets and G for 'G' defect |
| 11 | Describe Bernard-Soulier syndrome. | An inherited disorder caused by deficiency or dysfunction of glycoprotein Ib-IX-V complex, leading to large platelets, defective adhesion, and bleeding tendency. | GPIb complex defect |
| 12 | Describe Glanzmann thrombasthenia. | An inherited disorder caused by deficiency or dysfunction of glycoprotein IIb/IIIa, impairing platelet aggregation despite normal platelet count. | GPIIb/IIIa defect |
| 13 | What is the primary management for inherited platelet function disorders? | Treatment mainly supportive—platelet transfusions during bleeding episodes; gene therapy is experimental. Avoid medications that impair platelet function, like NSAIDs. | Supportive care focus |
| 14 | What laboratory test assesses platelet function? | Platelet aggregometry, which evaluates platelet response to various agonists like ADP, collagen, epinephrine, and ristocetin. | Think 'aggregation' test |
| 15 | What is the significance of a low platelet count in splenomegaly? | Splenomegaly can cause sequestration of platelets, leading to thrombocytopenia; splenic pooling reduces circulating platelet levels. | Splenic 'trap' for platelets |
| 16 | How does medication-induced thrombocytopenia occur? | Certain drugs (e.g., heparin, quinine, sulfonamides) trigger immune-mediated destruction or bone marrow suppression, leading to low platelet counts. | Think 'drug triggers' |
| 17 | What is heparin-induced thrombocytopenia (HIT)? | An immune-mediated adverse reaction to heparin characterized by antibody formation against platelet factor 4-heparin complexes, causing paradoxical thrombosis despite low platelet counts. | HIT: low platelets, high risk of clots |
| 18 | How is HIT diagnosed? | Clinically with the 4 Ts score (Thrombocytopenia, Timing, Thrombosis, oTher causes) and confirmed with immunoassays like PF4-heparin ELISA. | 4 Ts helps guide suspicion |
| 19 | What management strategies are used for HIT? | Discontinue heparin immediately and initiate alternative anticoagulation with non-heparin agents like argatroban or bivalirudin; warfarin should be avoided initially. | Stop heparin, start direct thrombin inhibitors |
| 20 | What is the role of platelet transfusions in thrombocytopenia? | Generally reserved for severe bleeding, platelet transfusions can temporarily increase platelet counts but are avoided in immune-mediated destruction unless bleeding is life-threatening. | Use cautiously |
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