MOA: Corrects bleeding associated with vitamin K deficiency

SE: Neonates- hemolytic anemia and kernicterus; anaphylaxis

MOA: Inhibits coagulation by activating Antithrombin III, which inhibits serine proteases (II, IX, X, XI, XII, XIII)

     --Heparin targets the intrinsic pathway, so its actions are measured by aPTT

Clinical use: Initiate tx for venous thrombosis and PE; initial management of unstable angina or MI; coronary angioplasty, stent placement, and cardiopulmonary bypass

     --Anticoagulant of choice in pregnancy (give SQ for long-term therapy)

SE: hemorrhage (treat with discontinuation and protamine sulfate); heparin-induced thrombocytopenia (treat with discontinuation and lepirudin, argatroban, or danaparoid); osteoporosis, hepatic function change, hyperkalemia, allergic reactions

MOA: Increase action of antithrombin III on factor Xa only

Clinical use: Tx DVT, PE, and angina (Enoxaparin: after knee replacement; Dalteparin: high-risk patients during abdominal surgey)

SE: less than standard heparin

MOA: Mediates inhibition of factor Xa by antithrombin III

Clinical use: thromboprophylaxis, pulmonary embolism, DVT

MOA: Vitamin K antagonist; competes with vitamin K for binding to vitamin K reductase (inhibit factors II, VII, IX, and X)

Kinetics: good oral absorption; bound to albumin; metabolized by CYP2C9 and 1A2

Clinical use: Prevention progression or recurrence of DVT or PE following initial heparin; prevent embolism in acute MI, prosthetic heart valve, or chronic a-fib

     --Monitor with PT test (to check INR)

Interactions: vitamin K rich diet; aspirin, clofibrate; CYP2C9 activators (barbituates, carbamazepine, rifampin); CYP2C9 inhibitors (amiodarone, azole antifungals, disulfram)

SE: major = hemorrhage; skin necrosis, birth defects, purple toes syndrome, venous limb gangrene, alopecia, urticaria, dermatitis, fever, nausea, diarrhea, abdominal cramps, anorexia

MOA: Oral anticoagulant

MOA: Oral anticoagulant

MOA: Oral anticoagulant

MOA: Oral anticoagulant

MOA: Oral anticoagulant (long acting)

MOA: Oral anticoagulant (direct thrombin inhibitor)

MOA: Recombinant hirudin; irreversible binding to fibrin-binding and catalytic sites of thrombin (direct thrombin inhibitor)

Clinical use: tx heparin-induced thrombocytopenia (HIT)

SE: anaphylaxis

MOA: Direct thrombin inhibitor

Clinical use: alternative to heparin for coronary angioplasty

MOA: Direct thrombin inhibitor (binds catalytic site only)

Clinical use: alternative to lepirudin for treatment/prophylaxis of HIT

MOA: Mixture of non-heparin glycosaminoglycans; promotes inhibition of factor Xa by antithrombin

Clinical use: prophylaxis of DVT, possibly tx of HIT (but similar to heparin, so this might not work)

MOA: recombinant activated protein C; inhibits Va and VIIIa; anti-inflammatory

Clinical use: severe sepsis

SE: bleeding

MOA: Blocks production of TXA₂ by inhibition of COX-1

Clinical use: Antiplatelet; prevent thromboses that lead to MI, stroke, and peripheral vascular thrombosis

SE: Bleeding, heartburn, stomach upset, allergic reaction

MOA: Increases cellular concentration of cAMP by inhibiting phosphodiesterase and blocking adenosine reuptake (leaving more adenosine to stimulate adenylyl cyclase, thus promoting cAMP formation)

Clinical use: Vasodilator and antiplatelet; use with warfarin to decrease thrombosis after valve replacement

MOA: Permanently inhibits P2Y12 receptor, preventing ADP binding (ADP binding causes decrease in AC, thus decrease in cAMP and increase in platelet aggregation)

Clinical use: secondary prevention of stroke (1st line = aspirin)

SE: GI reactions (most common), neutropenia, thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS)

MOA: Inhibits P2Y12 receptor (see ticlopidine)

Clinical use: secondary prevention of stroke

SE: less than ticlopidine; especially less TTP-HUS and leukopenia; therefore does not require blood count monitoring

MOA: Fab fragment of antibody against α_IIbβ3 receptor (receptor for fibrinogen and von Willebrand factor)

Clinical use: Combined with percutaneous angioplasty for coronary thrombosis

SE: bleeding, thrombocytopenia

MOA: Analog of C-terminal of fibrinogen; binds α_IIbβ3 receptor and prevents platelet aggregation

Clinical use: acute coronary syndrome; angioplasty

SE: bleeding, thrombocytopenia, hypotension

MOA: Analog of C-terminal of fibrinogen; binds α_IIbβ3 receptor and prevents platelet aggregation

Clinical use: MI and unstable angina; use with heparin for acute coronary syndrome

SE: Bleeding, coronary artery dissection, bradycardia, dizziness, headache

MOA: NOT a kinase; promotes formation of plasmin

Clinical uses: acute coronary arterial thrombosis, acute PE, DVT, acute venous thrombosis, acute arterial thromboembolism and thrombosis, occlusion of arteriovenous cannulae

SE: anaphylaxis

MOA: Directly converts plasminogen to plasmin

Clinical use: acute coronary arterial thrombosis, acute PE, fix IV catheters

SE: decreased anaphylaxis compared to streptokinase or anistreplase

MOA: Indirectly promotes formation of plasmin

Clinical use: acute coronary arterial thrombosis

SE: anaphylaxis

MOA: Recombinant tPA; directly converts plasminogen to plasmin

Clinical uses: acute coronary arterial thrombosis, acute PE, acute ischemic stroke

SE: Stroke/cerebral hemorrhage

MOA: Modified tPA

Clinical use: Acute MI

SE: anaphylaxis

MOA: Competes with fibrin for binding to plasminogen and plasmin

Clinical use: reduce bleeding (prostate surgery, hemophiliacs in tooth extraction, prevent subarachnoid hemorrhage)

SE: bradycardia, hypotension, myopathy, muscle necrosis

MOA: Bind to negatively-charged bile acids in intestine, inhibiting bile acid absorption; this increases cholesterol conversion to bile acids in the liver, decreasing hepatic cholesterol and increasing LDL receptor expression on hepatic cells; this decreases plasma levels of LDL-C

Clinical use: dose-dependent reduction of LDL-C

SE: Increase TG levels, increase endogenous cholesterol synthesis, bloating and constipation, interefere with absorption of fat-soluble vitamins; drug interactions with thiazide, digoxin, and warfarin (give 1 h before or 3 h after resin)

MOA: Increases apoA-I, which increases HDL-C; decreases diacylglycerol acetyltransferase, which decreases TG and VLDL synthesis

Clinical use: Treatment for patients with low HDL-C and high TG

SE: flushing and pruritis, dyspepsia, n/v/d, hepatotoxicity, insulin resistance, elevated uric acid

     --Should not be used in pregnancy

MOA: Competitive inhibition of HMG-CoA reductase (inhibits cholesterol biosynthesis), increase LDL receptor expression on hepatocytes

Kinetics:

Absorption: Atorvastatin, pravastatin, and rosuvastatin: OATP2 transporter; Simvastatin, lovastatin: Simple diffusion

Metabolism: Atorvastatin and rosuvastatin: 20h, others: 1-4h; metabolized by CYP3A4 and CYP2C9

Clinical use: Lowers LDL by a lot, moderate lowering of TGs and moderate increase in HDL; weaken cap of plaques; antiinflammatory; reduce platelet aggregation

Side effects: Hepatotoxicity (monitor ALT); myopathy and rhabdomyolysis (monitor serum creatine phosphokinase)

     --do not use in pregnancy

MOA: Bind PPARα, which turns on gene expression to stimulate LPL expression (which causes breakdown of TGs), increase HDL-C levels (via apoA-I and apoA-II), and decrease LDL (by increase of CETP and SREBP-1 transcription factors for hepatic LDL receptor)

Kinetics: Take with food, protein bound (interact with warfarin), excreted in urine

Clinical use: Hypertriglyceridemia (>1000 mg/dL)

SE: lithogenicity (clofibrate), myopathy (gemfibrozil + statin), GI effects, rash, urticaria, hair loss, myalgias, fatigue, headache, impotence, anemia

Contraindications: renal failure, hepatic dysfunction, children, pregnant

MOA: Inhibit cholesterol uptake from intestine by inhibiting NPC1L1 transporter

Clinical use: Lowers LDL, no effect on TG's, useful as monotherapy if statin-intolerant or as dual therapy with a statin

SE: allergy (rare), don't use if pregnant