Hemostatic drugs

Mannucci P M1998 Hemostatic drugs. New England Journal of Medicine 339 245-253 Mannucci P M, Tuddenham E G D 2001 The... 

Microfibrillar collagen hemostat Microfibrillar collagen hemostat is synthesized from cow collagen. It is used for surgical intervention as an adjuvant drug for bleeding when other procedures are ineffective and impractical. A synonym of this drug is avitene. 

Hypersensitivity to the drug presence of hematopoietic disorders such as neutropenia and thrombocytopenia or a history of TTP presence of a hemostatic disorder or active pathological bleeding severe liver impairment. 

WARNING Renal impair is the major tox foUow administration instructions Uses CMV retinitis w/ HIV Action Selective inhibition of viral DNA synth Dose Rx 5 mg/kg IV over 1 h once/wk for 2 wk w/ probenecid Maint 5 mg/kg IV once/2 wk w/ probenecid (2 g PO 3 h prior to cidofovir, then 1 g PO at 2 h 8 h after cidofovir) X in renal impair Caution [C, -] Contra Probenecid or sulfa allergy Disp Inj SE Renal tox, chills, fever, HA, NA /D, thrombocytopenia, neutropenia Interactions t Nephrotox W/ aminoglycosides, amphot icin B, foscar-net, IV pentamidine, NSAIDs, vancomycin t effects W/zidovudine EMS Monitor ECG for hypocalcemia (t QT int val) and hypokalemia (flattened T waves) OD May cause renal failure hydration may be effective in reducing drug levels/effects Cilostazol (Pletal) TAntiplatelet, Arterial Vasodilator/ Phosphodiesterase Inhibitor] Uses Reduce Sxs of intermittent claudication Action Phosphodiesterase in inhibitor t s cAMP in pits blood vessels, vasodilation inhibit pit aggregation Dose 100 mg PO bid, 1/2 h before or 2 h after breakfast dinner Caution [C, +/-] Contra CHE, hemostatic disorders. 

Regulation of the fibrinolytic system is useful in therapeutics. Increased fibrinolysis is effective therapy for thrombotic disease. Tissue plasminogen activator, urokinase, and streptokinase all activate the fibrinolytic system (Figure 34-3). Conversely, decreased fibrinolysis protects clots from lysis and reduces the bleeding of hemostatic failure. Aminocaproic acid is a clinically useful inhibitor of fibrinolysis. Heparin and the oral anticoagulant drugs do not affect the fibrinolytic mechanism. 

To understand the evolution of therapy of the acute coronary syndrome (ACS), which includes unstable angina, acute myocardial infarction, and interventional therapy— percutaneous coronary intervention (PCI), it is most useful to trace the historical events that provided a rationale for the use of anticoagulant and antiplatelet drugs, The focus of this chapter is upon the explosion in knowledge of the physiology of the hemostatic mechanism and will trace the rational development of therapy based upon the pathophysiology of the ACS over the past 40 years. 

Pharmacologic inhibitors of thrombin. Thrombin is a key enzyme in the hemostatic system in that it leads to the formation of fibrin strands and is a potent stimulus for platelet activation. Thrombin inhibitors, factor Xa inhibitors, and antiplatelet drugs act at different points in the hemostatic system to regulate the amount of thrombin that is generated. 

A diagnostic parameter for specific defects of the hemostatic system and for the influence of drugs affecting hemostasis is the length of time that it takes for bleeding to stop from a standard incision, the so-called bleeding time. 

Primary intracerebral hemorrhage is more common than subarachnoid hemorrhage, and its incidence increases with age (see Fig. 1.1). It is more frequent in Southeast Asian, Japanese and Chinese populations than in whites. The most common causes are intracranial small vessel disease, which is associated with hypertension, cerebral amyloid angiopathy and intracranial vascular malformations (Sutherland and Auer 2006). Rarer causes include saccular aneurysms, hemostatic defects, particularly those induced by anticoagulation or therapeutic thrombolysis, antiplatelet drugs, infective endocarditis, cerebral vasculitis and recreational drug use (Neiman et al. 2000 O Connor et al. 2005). 

---