Antiplatelet therapy.
Much new information has been gleaned about the morphology, biochemistry and function of platelets. The pathophysiology of atherosclerosis and thromboembolic disorders appears to be related to abnormal platelet function. Endothelial damage, thromboxane A2, Thrombin, adenosine diphospate and epinephrine may each promote platelet aggregation, whereas prostacyclin impairs aggregation. Aspirin, sulfinpyrazone and dipyridamole have been used as antiplatelet agents, and specific indications are being developed to guide their selection.
D000925:Anticoagulants / Q000627:therapeutic use; D001161:Arteriosclerosis / Q000188:drug therapy / Q000503:physiopathology; D001241:Aspirin / Q000494:pharmacology / Q000627:therapeutic use*; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology; D003327:Coronary Disease / Q000188:drug therapy / Q000503:physiopathology; D004176:Dipyridamole / Q000494:pharmacology / Q000627:therapeutic use*; D011464:Epoprostenol / Q000009:adverse effects; D005260:Female; D006350:Heart Valve Prosthesis; D006801:Humans; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects*; D013442:Sulfinpyrazone / Q000494:pharmacology / Q000627:therapeutic use*; D013924:Thrombophlebitis / Q000188:drug therapy / Q000503:physiopathology
D000925:Anticoagulants; D004176:Dipyridamole; D011464:Epoprostenol; D001241:Aspirin; D013442:Sulfinpyrazone