Anticoagulant And Thrombolytic Drugs

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Erythrocytes

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Red blood cells which carry oxygen to tissues.
The lack of or malformation of RBC is called anemia.

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Leukocytes

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White blood cells involved in immune response, leukopenia/leukocytosis.

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Platelets

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Thrombocytes involved in blood clotting.
The lack of is called thrombocytopenia

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Blood Plasma

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Liquid part of blood before clotting, serum after clotting.

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Hemostasis:

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The physiological processes that prevent blood loss. Vasoconstriction, platelet plug formation and clot formation (coagulation)

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Platelet Plug Formation

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The inner surface of blood vessels is lined by endothelial cells under which is a layer of collagen. Normally, endothelial cells release prostacyclin, which stimulates the production of cAMP, inhibiting platelet aggregation.

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Platelet Activation

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When injury to blood vessels occur, the collagen layer is exposed to circulating blood components, and the damaged endothelial cells release platelet-attracting substances, including kallikrein.
Platelets adhere to the exposed subendothelial surfface, where they release the chemical signals Adenosine Diphosphate (ADP) and Thromboxane A2, which activate platelet aggregation.
ADP acts on other nearby platelets, causing activation. The thromboxane A2 is also a powerful stimulator of platelet aggregation.
Platelets also release serotonin (5HT), a potent vasoconstrictor and phospholipids that are cofactors for clot formation.

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Adenosine Diphosphate (ADP) and Thromboxane A2

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Activate platelet aggregation, which is the clumping of blood platelets leading to a thrombus

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Fibrin Clott Formation:

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Factor XII binds to exposed collagen at the site of vessel injury. This initiates a series of events leading to fibrin clot formation through the intrinsic or extrinsic pathways.

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Clot Dissolution (Thrombolysis)

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Plasminogen is converted to plasmin. Plasmin breads down fibrin clots to fibrin degredation products.

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Thrombosis

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A clot that adheres to the side of a blood vessel

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Embolism

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A clot that travels in the blood stream.

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Hemophilia:

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A hereditary lack of coagulation factors such as VII or IX.

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Heparin

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Parenteral Anticoagulation, IV
Almost immediate action. Combines with Antithrombin Mechanism: Factor III to break down activation factors in the clotting pathway inactivates Factor Ia (and other Factors).
Prevents clots but does not dissolve preexisting clots. Causes thrombocytopenia, Contraindicated: Low platelet counts.
Extended use can cause osteoporosis.
Overdose can cause bleeding. Monitored by a PTT test, do not give if monitoring is not available.

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Active Clotting Factors

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IIa, IXa, XIa, Xa, XIIa, XIIIa.
Slow antithrombin III
With Heprine these factors are rapid antithrombin III plus heparin

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Low Molecular Weight Heparin (LMWH)

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Indicated to prevent thrombosis in hip replacement surgery, unstable angina, or pulmonary embolism. More selective than regular heparin, which means that is can be given without constant monitoring. Very expensive though. Ex: Enoxaparin

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Protamine Sulfate:

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Parenteral anticoagulant antiagonist given routinely after cardiac surgery.
Antagonist for heparin, binds it and blocks its effect. Give lowest dose possible, since protamine has anticoagulant effects on its own.
Causes anaphylactic shock in 1% of diabetic patients taking insulin containing protmaine (NPH) or protamine-zine insulin (PZI).

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Warfarin

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Oral Anticoagulants
Mechanism: Inhibits regeneration of Vitamin K.
Metabolized in liver. Requires days to take effect. Contraindication: Pregnancy (teratogenic).
Side effects: Bleeding, skin necrosis and purple-toe syndrome (rare).
Many drug interactions are possible. Can be used with heparin. Anticoagulants have no effect on an established thrombosis. Monitored using Prothrombin Time (PT) or international normalized ratio (INR).
Increased Clotting: Anabolic/androgenic steroids. Non-steroidal Anti-inflammatory Drugs (NSAID's), Antibiotics. Decreases anticoagulant effect: increase in dose. Antidiabetic agents, estrogens, barbiturates.

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Alteplase

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Used to dissolve existing clots but don't discriminate between good and bad clots.
Properties: Activate palsminogens to plasmin. IV, IA, Short half-lives (20-35 minutes.

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Alteplase Action

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Indications: Myocardial Infarction evolving from an acute coronary artery thrombus (should be initiated within 6 hours). Acute Ischemic stroke (must be used within 3 hours, but after a CT stan to rule out hemorrhagic stroke). Also used for pulmonary embolism. In low doses used to flush IV's.
Mechanism: Binds to fibrin --> converts plasminogen to plasmin. Plasmin -->breaks down fibrin to destroy the clot. Has little activity in the absence of fibrin.
Contraindications: Active internal bleeding, cardiovascular process within 2 months. Major surgery, postpartum period, severe uncontrolled hypertension.
Adverse Effects: Hemorrhage, N/V, cerebral edema if given after 3 hours.

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Aminocaproic Acid

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Antidote for thrombolytics (specifically warfarin) given IV, often given after cardiac surgery. Also used to block breakdown of clots in systemic or urinary hyperfibrinolysis and treatment of dental bleeding in hemophelia A patients. Use is limited by the formation of clots by this drug (thromboembolism). Used only in life-threatening situations where hyperfibrolysis is documented. Other serious adverse effects: Seizures, rabdomylosis, or renal failure. Do not use with Factor IX or estrogen.

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Clopidogrel

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Anti-platelet
Indication: To prevent atherosclerotic events in patients at risk for myocardial infarction or stroke.
Mechanism: Prevents APT-induced platelet aggregation.
Drug Interactions: Use caution with aspirin and other NSAID's or anti- platelet. Must be metabolized by liver to be effective, interacts with many drugs. Contraindications: Active bleeding disorders, or existing neutropenia (decreased number of neutrophils), but not as bad as ticlopidine.
Side effects: Increases risk of bleeding and GI distress.

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Anti-hemophilic Factor VIII (AHF)

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Missing factor in Type A hemophilia. Always given IV. Purpose is to replace missing factor needed for normal blood clotting. Some patients develop antibodies against AHF.

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Hemorrheologicals: Pentoxifyline

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Indications: Peripheral vascular disease, claudication (a cramping pain due to insufficient blood to muscles during exercise). CNS, GI and cardiovascular.
Mechanism: Decreases viscosity of the blood by increasing the flexibility of red blood cells.
Side effects: Headache, N/V, dizziness, angina, tachycardia, hypotension. Taken orally, takes several weeks to see effects.