Term
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Definition
anticoagulant
-usually used in an inpatient setting
-heterogeneous mixture
MOA: binds to endothelial cell surfaces, activates antithrombin III; inhibits factor X (LMW) and thrombin (HMW)-overall greater effect on thrombin; inhibits in vivo and in vitro blood clotting
PK: admin IV, excreted by kidney (zero-order kinetics)
CI: one-stage tests of coagulation (?), deep vein thrombosis and pulmonary embolism, major abdominal or pelvic surgery, arterial embolism, MI and CAD, reduces incidence of coronary occlusion and reinfarction, DIC, large increase in coagulation (depletion of protein factors)
AE: bleeding, thrombocytopenia
Contra: hypersensitivity to heparin, pt actively bleeding, hemophilia, GI ulcerative lesions, active TB, severe hypertension, advanced renal or hepatic disease
DI: drugs that inhibit platelet aggregation, synergistic effects with oral anticoagulants
-excessive anticoagulant heparin -> discontinue, if bleeding occurs -> IV protamine sulfate |
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Term
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Definition
anticoagulant
-used in inpatient and outpatient setting
MOA: blocks gamma-carboxylation of gluatmate residues in prothrombin and factors VII, IX, X, anticoagulant proteins C and S (inhibit synthesis); blocks epoxide reductase -> inhibit hepatic synthesis of clotting factors; only inhibit in vivo clotting
PK: oral admin, 8-12 hr delayed onset of action, rapidly absorbed, >90% bound to plasma albumin, relatively long half-life, does not cross BBB, hydoxylated in liver
CI: prevention of arterial emboil from heart valve disease/valve replacement, conditions of high thromboembolic risk (prophylaxis), coronary artery bypass graft and angioplasty -> combo with antiplately drugs reduce incidence of thrombus formation and reocclusion after surgery
SE: hemorrhage, cutaneous necrosis; minor hemorrhage -> discontinue drug and give vit K, serious bleeding -> admin plasma and plasma concentrates containing K-dependent factors
Contra: chronic alcoholism -> decreases drug metabolism rate, pregnancy -> hemorrhagic disorder of fetus, serious birth defects
DI: enzyme induction (barbituates/ rifampin) -> decrease anticoagulant effect; enzyme inhibition (pyrazolones phenylbutazone and sulfinpyrazone) -> inhibit warfarin metabolism; reduced plasma protein binding (pyrazolones) -> displace albumin-bound warfarin; synergism with certain drugs; competitive antagonism (vit K); altered physiologic control loop for vit K (hereditary resistance to oral anticoagulants); aspirin, hepatic disease, hyperthyroidism -> augment warfarin PDs; heparain -> directly prolongs prothrombin time
-narrow window of safety
-pts with variant of vkorc1 (associated with body’s processing of vit K) need lower drug doses |
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Term
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Definition
heparin neutralizer
MOA: treat bleeding due to excessive anticoagulant heparin |
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Definition
fibrinolytic
-human protease enzyme synthesized by kidney, directly converts plasminogen -> plasmin
MOA: lyse already formed thrombi, catalzye formation of plasmin from precursor plasminogen |
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Term
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Definition
-unmodified recombinant human t-PA
MOA: lyse already formed thrombi, catalzye formation of plasmin from precursor plasminogen
CI: treatment of coronary artery thrombosis associated with MI |
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Term
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Definition
fibrinolytic inhibitor
MOA: competitively inhibits plasminogen activation, reverse effects of thrombolytic agents
PK: dosage and route of admin adjusted to specific situation
AE: intravascular thrombosis, hypotension
Contra: DIC or GU bleeding of uppe r tract b/c potential for excessive clotting |
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Term
| Vitamin K1 (phytonadione) |
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Definition
MOA: increases synthesis of clotting factors, confers biological activity upon prothrombin, factors VII, IX, X by participating in their post-ribosomal modification
PK: oral admin
CI: treat decreased prothrombin activity due to excess warfarin or vit K1 deficiency, admin to all newborns as prophylaxis for hemorrhagic disease of vit K deficiency |
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Term
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Definition
antiplatelet
MOA: inhibit thromboxane A2 synthesis by irreversible acetylation, inhibit plately content release and aggregation -> prolong bleeding time
CI: small doses for primary prophylaxis of myocardial mortality (prevention of 1st heart attack)
AE: increase risk of occurrence of stroke, peptic ulcer, GI bleeding |
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Term
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Definition
ADP receptor blocker/antiplatelet
-useful in pts non-tolerating aspirin
MOA: prodrug, reduce platelet aggregation by irreversibly inhibiting BINDING of ADP to its platelet receptors
PK: effectiveness depends on activation to an active metabolie by CYP2C19
-some pts are CYP2C19 poor metabolizers, if these pts with acute coronary syndrome or undergoing coronary intervention with recommended doses -> exhibit higher CV event rates
CI: prevention of vascular events in pts with TIAs, complex strokes, unstable angina; prevent thrombosis in pts undergoing placement of coronary stent
SE: nausea and diarrhea, leukopenia, hemorrhage
DI: heart attack pts that take an acid-reduction PPI (prilosec, nexium, prevacid, aciphex) in combo with this drug -> more likely to have 2nd heart attack or need revascularization procedures |
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Term
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Definition
GP IIB/IIIA receptor blocker/antiplatelet
MOA: Fab (fragment antigen binding), platelet-inhibiting drug that blocks platelet receptors for integrin and other aggregating substances
PK: admin IV
CI: adjunct in percutaneous angioplasty for coronary thromboses; in combo with aspirin and heparain -> effective in preventing restenosis, recurrent MI, death |
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