ANTITHROMBICSII

**Anti-coagulants and Fibrinolytic Drugs** are used to alter the physiological processes of blood coagulation and clot (thrombus) breakdown. The [|coagulation process]consists of a cascading series of proteolytic reactions which ultimately transforms soluble fibrin into insoluble fibrin, the protein which reinforces platelet plugs converting them into a clot. Anticoagulants inhibit the coagulation process -- the earlier in the cascade an anticoagulant works, the more effectivtive it is in preventing clot formation. Anticoagulants are also used to prevent the extension of clots (i.e. prevent them from getting bigger). However, they cannot dissolve clots. This is accomplished by thrombolytic (fibrinolytic) drugs -- the so called "clot busters". These drugs activate an enzyme (plasmin) which breaks down fibrin and thus breaking apart the clot. However, thrombolytic drugs cannot inhibit clot formation. [|View a flash presentation of the coagulation process] Physiologically, to maintain blood fluidity and to confine blood clots to the smallest possible area, naturally occurring anticoagulants and thrombolytic agents circulate in the blood. The naturally occurring anticoagulant is **antithrombin III** which inhibits fibrin formation and the naturally-occurring thrombolytic agent is **tissue plasminogen activator** which dissolves fibrin. Both anticoagulant and fibrinolytic therapy are used in treat thrombi and emboli (in this case emboli refer to masses of undissolved clots that break off a thrombus). For example, treatment of an MI caused by coronary artery thrombosis can involve thrombolytic drugs to dissolve the thrombus, followed by heparin in the hospital to prevent the reformation (re-occlusion) of a new clot, and oral anticoagulant like warfarin on an out patient basis to prevent clot reformation. **TYPE of DRUG** enhances the anti- coagulant effects of antithrombin III (NOTE: not effective orally) NOTE: not used in those with hemophilia, ulcers of the GI tract, nor recent head injury inhibit the synthesis of clotting factor which require Vit. K for their production in the liver NOTE: effects are not immediate NOTE: drugs of choice for long-term anti- coagulant therapy dissolve clots by stimulating the con- version of an inactive enzyme (plasminoogen) into an active enzyme (plasmin) which breaks down fibrin. NOTE: these drugs break down emboli AND protective clots, bleeding compications (hematomas), allergic reactions (to strepto- kinase) inhibits plalet activation (i.e. platelets can't aggregate) by inhibiting the enyzme (cyclo- oxygenase) which makes thromboxane A2 (the chemical which causes platelets to aggregate)
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 * MECHANISM of ACTION**
 * USES**
 * SIDE-EFFECTS**
 * parenteral anti- coagulant** (e.g. heparin)
 * SIDE-EFFECTS**
 * parenteral anti- coagulant** (e.g. heparin)
 * parenteral anti- coagulant** (e.g. heparin)
 * parenteral anti- coagulant** (e.g. heparin)
 * 1) preventing venous and pulmonary emboli
 * 2) preventing re- occulsion after thrombo- lysis
 * 3) preventing clot formation during hemodialyis ||
 * 4) hemorrhage
 * 5) allergic reactions
 * 6) thrombocytopenia
 * 1) thrombocytopenia
 * oral anticoagulants** e.g. warfarin (COMADIN)
 * oral anticoagulants** e.g. warfarin (COMADIN)
 * 1) prevent venous thromboemboli
 * 2) treat deep venous thrombosis
 * 3) prevent clot following heart valve replacement.
 * 1) prevent clot following heart valve replacement.
 * 1) hemorrhage (Vit. K is the antidote)
 * 2) fetal hemorrhagis disorder (drugs cross the placenta)
 * 3) 3. skin necrosis (death of skin cells --mechanism?) || ||
 * thrombolytics** (fibrino- lytics) or "clot busters" e.g. tissue plasminogen activator (tPA), strepto- kinase (STREPTASE)
 * thrombolytics** (fibrino- lytics) or "clot busters" e.g. tissue plasminogen activator (tPA), strepto- kinase (STREPTASE)
 * 1) ntra-arterially for coronary thrombosis (best if used withihn 2-4 h after MI)
 * 2) i.v. for pulmonary emboli too small for surgical removal
 * 3) certain types of strokes ||
 * 1) certain types of strokes ||
 * antiplatelet drugs** e.g aspirin
 * antiplatelet drugs** e.g aspirin
 * 1) prevent TIAs (transient ischemic attacks) and MIs in those with a history
 * 2) prevention of TIA.MIs in those without a history
 * 3) improve blood flow in post-op bypass ||
 * 4) prolonged bleeding times
 * 5) gastric bleeding || ||
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