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Excessive irreversible inactivation of the cyclo-oxygenase enzyme
0%
0/37
Formation of antibodies to heparin-platelet factor-4 complex
84%
31/37
Decreased hepatic synthetic function leading to antithrombin deficiency
5%
2/37
Deposition of immune complex nuclear antigens in kidneys
3%
1/37
Inherited mutation in clotting factor V, which cannot be degraded by activated protein C
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This patient's presentation is consistent with a diagnosis of heparin induced thrombocytopenia (HIT). The pathophysiology of HIT is a type II hypersensitivity reaction, where antibodies form against and bind to heparin-platelet factor 4 complexes on the surface of platelets. Clinical features of HIT may include skin reactions (necrosis), deep venous thrombosis, pulmonary embolism, ischemic stroke, or myocardial infarction. HIT occurs more commonly with unfractionated heparin and less commonly with low molecular weight heparin. Lab values seen with HIT include a decreased platelet count (typically > 50% of baseline), normal PT/INR, and an increased bleeding time. Gauer et al. discuss the presentation and management of HIT. Declining platelet counts and clot formation or easy bruising/bleeding are expected within 5-10 days after first exposure to heparin. If HIT is suspected, heparin should be discontinued immediately, and the patient should be switched to a direct thrombin inhibitor, such as lepirudin or argatroban. Linkins et al. discuss the prevention and treatment of HIT. For patients at elevated risk of developing HIT, a platelet count should be monitored every 2-3 days from day 4 to 14 of heparin therapy. For patients receiving heparin who are not at elevated risk of developing HIT, no platelet count monitoring is necessary. Illustration A depicts the pathophysiology of HIT. Illustration B reviews the diagnosis and management of HIT. Illustration C shows the "4 T's" grading system for assessing HIT; patients with a lower 4 T's score have a very small chance that they are experiencing HIT Incorrect Answers: Answer 1: Aspirin overdose can lead to excessive irreversible inactivation of cyclo-oxygenase, causing platelet dysfunction and a propensity to bleed. Answer 3: Liver disease can decrease antithrombin production, leading to deficiency of this enzyme and a resultant pro-thrombotic state. Answer 4: Systemic lupus erythematosus is a type III hypersensitivity reaction leading to formation and deposition of immune complexes to nuclear antigens in the kidneys (lupus nephritis), skin, and joints (arthritis). Answer 5: Factor V Leiden mutation involves an aberrant clotting factor that cannot be degraded by activated protein C; this leads to hypercoagulability.
5.0
(3)
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