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Hirudin
- -a Direct Thrombin Inhibitor (DTI)
- -prevents the fibrinogen -> fibrin conversion
- -prevents ADP and TXA2 release from platelets
- -must be percutaneous
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Unfractionated Heparin
- -a mixture of high and low molecular weight heparins
- -produces a high level of activity
- -Stimulate Antithrombin 3 (inhibiting the clotting cascade)
- -must be percutaneous
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Enoxaparin
- -low molecular weight heparin
- -less activity then unfractionated
- -Stimulate Antithrombin 3 (inhibiting the clotting cascade)
- -must be percutaneous
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Warfarin
- -prevents the activation of vitamin K
- -vitamin K is needed to form active clotting factors
- -can be given orally, a delay is seen before effect
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Alteplase
- -a recombinant version of t-PA (grown from human genes)
- -activates plasminogen -> plasmin
- -produces fibrin degradation
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Tissue Plasminogen Activator (t-PA)
- -activates plasminogen -> plasmin
- -produces fibrin degradation
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Streptokinase
- -a purified bacterial enzyme that activates plasminogen
- -activates plasminogen -> plasmin
- -produces fibrin degradation
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Aspirin
- -irreversibly inhibit COX 1 and 2
- -prevents TXA2 synthesis (and release from clotting)
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Clopidogrel
- -ADP receptor blockers
- -prevent the effects of ADP released from platelets
- -a prodrug (must pass through liver)
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Tirofiban
- -A platelet-receptor antagonist
- -GPIIa/IIIb receptor is fibrin binding site
- -must be percutaneous
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Niacin
- -inhibit VLDL synthesis in liver (more powerful)
- -stimulate VLDL->LDL by lipoprotein lipase
- -decreases LDL levels
- -increases HDL levels
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Gemfibrozil
- -inhibit VLDL synthesis in liver
- -stimulate VLDL->LDL by lipoprotein lipase
- -produces no net effect on LDL levels (only on VLDL)
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Colestipol & Cholestyramine
- -Bind to bile in GI tract
- -prevents re-absorption leading to an up-regulation of LDL receptors
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Pravastatin
- -a low efficacy statin
- -Inhibits HMG-CoA reductase (the rate-limiting step in cholesterol synthesis)
- -pushes cell to generate more LDL receptors for a cholesterol source
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Simvastatin
- -a medium efficacy statin
- -Inhibits HMG-CoA reductase (the rate-limiting step in cholesterol synthesis)
- -pushes cell to generate more LDL receptors for a cholesterol source
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Atorvastatin & Rosuvastatin
- -a high efficacy statin
- -Inhibits HMG-CoA reductase (the rate-limiting step in cholesterol synthesis)
- -pushes cell to generate more LDL receptors for a cholesterol source
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Lovastatin & Fluvastatin
- -a statin
- -Inhibits HMG-CoA reductase (the rate-limiting step in cholesterol synthesis)
- -pushes cell to generate more LDL receptors for a cholesterol source
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Ezetimibe
- -Binds to a protein on GI epithelial cells that promotes cholesterol absorption
- -reduces LDL levels
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Vytorin
- -Simvastatin and Ezetimibe
- -effects of the two medicines are additive
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Nitroglycerin, Isosorbide & di-/mono-nitrate
- -dilate veins and large arteries
- -Converted into NO gas, and then stimulate cGMP pathway in smooth muscle cells
- -K+ channel opens and smooth muscle hyperpolarizes/relaxes
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Atenolol
- -a cardioselective Beta Blocker
- -Selective for Beta1 receptor -> decreased cardiac output
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Propranolol
- -a nonselective Beta Blocker
- -Targets both Beta1 and 2 -> decreased cardiac output and vasoconstriction (lungs, liver, etc.)
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Amlodipine
- -a non-cardioactive Calcium Channel Blocker
- -targets only Ca++ channels in vascular smooth muscles
- -vasodilation by preventing depolarization
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Verapamil
- -a cardioactive Calcium Channel Blocker
- -vasodilates by preventing depolarization
- -decreases cardiac output by weakening the contractions
- -arterial dilation targets coronary arteries most strongly
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Dobutamine
- -a Beta1 agonist
- -stimulates an increase in cAMP production within heart cells, increasing force of contraction
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Milronone
- -a Phosphodiesterase 3 inhibiter (PD3)
- -PD3 breaks down cAMP, so the inhibitor increases cAMP concentrations
- -increases the force of contraction
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Atropine
- -a muscarinic receptor antagonist
- -blocks parasympathetic effects on the heart
- -increases cardiac output
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Captopril
- -an ACE inhibitor
- -by inhibiting Agiotension Converting Enzyme: relaxes arterial smooth muscle and prevents aldosterone release
- -decreases afterload and preload
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Spironolactone
- -an aldosterone antagonist
- -prevents the function of aldosterone in h2o retention
- -works well in conjunction with ACE inhibitors
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Digoxin
- -a cardiac (digitalis) glycoside
- -functions by inhibiting cardiac Na/K exchanger; producing a reduction in Ca release
- -Ca becomes sequestered in sarcoplasmic reticulum; producing an increased contractile force
- -binds commutatively at K+ site so K+ concentrations are very important
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Hydrochlorothiazide & Furosemide
- -Diuretics that decrease Na+ and H2O re-absorption
- -decrease preload
- -used to treat edema and good with ACE inhibitors
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Carvedilol
- -a Beta blocker (non-selective) with Alpha 1 antagonist effects
- -decreases cardiac output
- -constricts arteries in lungs and liver
- -dilates arteries in non-essential areas
- -theory says it would hurt, but improvement is seen (likely due to inhibition of myocardial remodeling)
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Isosorbide Dinatrate
- -a venous dilator
- -decreases preload on the heart
- -good for R. Heart issues and pulmonary edema
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Hydralazine
- -an arterial dilator
- -decreases afterload on the heart
- -good for L. Heart issues and fatigue
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