Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
16 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
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
|
|
