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16 Cards in this Set

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Mechanism of

Heparin
(and Enoxaparin)
Catalyzes the activation of antithrombin 3, decreases thrombin and Xa. Short half-life.


Newer low-molecular weight heparins (enoxaparin) act more on Xa, have better bioavailability and 204 times longer half-life. Can be administered subcutaneously and without laboratory monitoring. Not easily reversible.
Clinical use of

Heparin
Immediate anticoagulation for:
-pulmonary embolism
-stroke
-angina
-MI
-DVT.
-used during pregnancy b/c it does not cross the placenta. Follow PTT
5 things
Toxicity of

Heparin

(and treatment of toxicity)
-Bleeding
-Thrombocytopenia
-Drug-drug interactions

For rapid reversal of heparinization, use PROTAMINE SULFATE (
Mechanism of:

Warfarin (Coumadin)
Interfers with normal synthesis and gamma carboxylation of vitamin K-dependent clotting factors 2, 7, 9, 10, and proteins C & S. Affects EXtrinsic pathway and increases PT.

Long half-life.
The EX-PaTriot went to WAR(farin)
Clinical use of:

Warfarin (Coumadin)
Chronic anticoagulation
Not used in pregnant women because it crosses the placenta, unlike Heparin.
Follow PT values.
Toxicity of:

Warfarin (Coumadin)
-Bleeding
-Teratogenic
-Drug-drug interactions
there are 3
4 examples of:

Thrombolytics
-Streptokinase
-urokinase
-tPA (alteplase)
-APSAC (anistreplase)
Mechanism of:

Thrombolytics
Directly or indirectly aid conversion of plasminogen to plasmin, the major fibrinolytic enzyme, which cleaves thrombin and fibrin clots.
Clinical use: (2)

Thrombolytics
Early MI
early ischemia stroke
Toxicity of:

Thrombolytics

(and treatment for it)
Bleeding.
Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diathesis, or severe hypertension.

Treat toxicity with AMINOCAPROIC ACID, an inhibitor of fibrinolysis
Mechanism of:

Asprin (ASA)
Acetylates and irreversibly inhbits cyclooxygenase (both COX-1 and COX-2) to prevent conversion of arachidonic acid to prostaglindins.
Increased bleeding time.
No effect on PT or PTT
Clinical use: (4)

Asprin (ASA)
-antipyretic
-analgesic
-anti-inflammatory
-antiplatelet drug
Toxicity of: (5)

Asprin (ASA)
-Gastric ulceration
-bleeding
-hyperventilation
-Reye's syndrome
-Tinnitus (CN 8)
Mechanism of:

Clopidogrel, Ticlopidine
Inhibits platelet aggregation by irreversibly blocking ADP receptors.
Inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa expression
Clinical use: (3)

Clopidogrel, Ticlopidine
-Acute coronary syndrome
-coronary stenting
-decreased incidence or recurrence of thrombotic stroke
Toxicity of: (1)

Clopidogrel, Ticlopidine
Ticlopidine -> Neutropenia