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118 Cards in this Set
- Front
- Back
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Mechanism of axn of nitrates
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act as source of NO which increase cGMP leading to vasodilation
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physiological effects of nitrates
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preload is lowered relatively more than afterload due to preferential affect on vein more than arterioles. Primary mechanism is decrease myocardial work from peripheral vasodilation
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Adverse effects of nitrates
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Do not take with PDE-5 inhibitors which decrease breakdown of cGMP - can lead to profound hypotension
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nitrate that does not undergo significant first-pass metabolism
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anything taken sublingually:
sublingual nitroglycerin sublingual isosorbide-5-mononitrate |
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prevents the effects of catecholamines on the heart, decrease myocardial oxygen demand by decreasing contractility, afterload, and preload
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B blockers
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adverse effects of B blockers
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worsening heart failure, worsening asthma, slowing cardiac conduction, fatigue, sexual dysfunction
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B blocker that is extensively metabolized in the liver
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Metoprolol
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most effective agents in treating symptoms of CAD
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B blockers
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List drugs that bind to L-type calcium channel and reduce calcium influx
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Amlodipine
Nifedipine Nicardipine Verapamil Diltiazem |
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physiologic affects of Ca Channel blockers
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decrease contractility
decrease conduction through SA/AV nodes vasodilation |
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Which Ca channel blocker won't cause worsening of HF
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amlodipine
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drugs that reduce chest pain in patients with stable, unstable, and variant angina but no benefit following an MI
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Ca channel blockers
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Ca channel blockers that are potent vasodilators but little effect on contractility, SA/AV node conduction
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amlodipine
nifedipine nicardipine |
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Ca channel blocker that actually increases mortality when given post MI
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nicardipine
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Ca channel blockers with less potent vasodilation and more suppression of contractility, SA/AV node conduction
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Verapamil
Diltiazem |
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Metabolism of Ca channel blockers
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significant first-pass hepatic metabolism. Drug dosage in liver failure should be reduced
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mechanism of axn for aspirin
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inhibits cyclooxygenase which prevents formation of thromboxane A2
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mechanism of axn for clopidogrel
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inhibits P2Y12 receptors which inhibit ADP mediated platelet activation
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mechanism of axn for ticlopidine
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inhibits P2Y12 receptros which inhibit ADP mediated platelet activation
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mechanism of axn for tirofiban
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inhibits GP IIb/IIIa receptors on surface of platelets
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mechanism of axn for abciximab
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inhibits the GP IIb/IIIa receptors on the surface of platelets
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Drugs that prevent platelet activation and aggregation that can lead to thrombus formation
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aspirin
clopidogrel ticlopidine tirofiban abciximab dipyridamole cilostazol pentoxifylline |
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adverse effects of aspirin
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gastric mucosa irritation
hypersensitivty reaction |
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can cause severe neutropenia and very rarely associated with thrombotic thrombocytopenic purpura
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Ticlopidine
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Can cause thrombocytopenia
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Abciximab
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competitive inhibitor of GP IIb/IIIa receptor
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Tirofiban
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antibody that is a noncompetitive inhibitor of GP IIb/IIIa receptor with a longer half-life
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Abciximab
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How long does the axn of inhibiting cyclooxygenase and P2Y12 receptor lasts
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entire life of the platelet, 7-10 days
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patients taking these medications should be checked for occult bleeding
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anti-platelet drugs
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prolong the platelet-inhibiting action of intracelluar cAMP by inhibiting phosphodiestase
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pentoxifylline
dipyridamole cilostazol |
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phosphodiesterase inhibitor contraindicated in patients with CHF
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cilostazol
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used in the treatment of intermittent claudication
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cilostazol
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associated with very rare cases of causing thrombic thrombocytopenia purpura
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ticlodipine
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used in treatment anemia of chronic renal failure
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erythropoietin
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adverse effects include thromboembolic effects associated with higher hgb level (>12g/dL)
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erythropoietin
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virtually all patients on supplemented erythropoietin will need which other supplement
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Iron
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analogous to GM-CSF
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sargramostim
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analogous to G-CSF
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filgrastim
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stimulates neutrophil production and also enhances phagocytic and cytotoxic functions of neutrophils
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filgrastim
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recombinant human IL-11
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oprelvekin
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mechanism of axn of oprelvekin
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recombinant form of human IL-11 which enhances megakaryocyte production to increase peripheral platelet counts
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common adverse effects of oprelvekin
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fatigue
headache dizziness fluid retention with edema |
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at what platelet count should oprelvekin be discontinued
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over 100,000
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selectively stimulates megakaryocytopoiesis to increase platelet production
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thrombopoietin
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two different drugs for iron deficiency
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ferrous sulfate
sodium ferric gluconate |
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acute and chronic effects of iron overaload
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acute - necrotizing gastroenteritis, abdominal pain, bloody diarrhea, shock
chronic - hemochromatosis with damage to heart, liver, pancreas with organ damage |
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when is sodium ferric gluconate indicated over ferrous sulfate
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In iron deficiency states where oral iron is ineffective such as iron malabsorption or patients intolerant to oral iron (GI problems)
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patient presents with megaloblastic anemia and neurologic deficits. what is the drug of choice
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Cyanocobalamin
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patient presents with megaloblastic anemia and no CNS deficits. what is the drug of choice
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folic acid
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folate deficiency seen in pregnant females can lead to what
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neural tube defects in the fetus
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upregulates antithrombin III which inactivates factors II and X
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heparin
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two drugs that primarily inactivate factor X rather than thrombin (factor II)
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Enoxaparin
Fondaparinux |
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massive decrease in platelets and thrombotic complications due to antibodies against which drug
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heparin
IgG antibodies form against PF4-heparin complex - HIT |
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what is used to monitor and adjust heparin dosage
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Partial thromboplastin time (PTT)
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what two drugs that are anticoagulants are contraindicated in patients with renal failure
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enoxaparin
fondaparinux |
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low molecular weight heparin
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enoxaparin
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synthetic pentasaccharide that is a factor X inhibitor
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fondaparinux
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direct thrombin inhibitors
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Lepirudin
Dabigatran |
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used to treat HIT
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Lepirudin
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indicated for treatment of thromboembolism formation in patients with nonvalvular atrial fibrillation
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Dabigatran
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recombinant form of protein C
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Drotrecogin alpha
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antagonist of vitamin K
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warfarin
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adverse effects of warfarin
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bleeding
birth defects in patients with HIT is associated with limb gangrene and multicentric skin necrosis |
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what is used to monitor and adjust warfarin dosages
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prothrombin time (PT) usually expressed as INR
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why does it take 3-5 days for warfarin to take full antithrombotic effect
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because warfarin does not alter the efficacy of coagulation proteins already synthesized
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forms stable one-to-one complex with plasminogen which is then enzymatically active
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streptokinase
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found in bacteria and used for fibrinolysis
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streptokinase
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replicates protease found in endothelial cells that activate plaminogen to plasmin
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recombinant forms of t-PA
alteplase reteplase |
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list the fibrinolytics
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streptokinase
urokinase alteplase reteplase |
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competes for lysine binding sites and blocks interaction of plasmin with fibrin
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aminocaproic acid
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potent inhibitor of fibronilysis
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aminocaproic acid
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used to reduce bleeding after prostate surgery or tooth extraction in hemophiliacs
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aminocaproic acid
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Adverse effects include excessive thrombosis, myopathy, or muscle necrosis
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aminocaproic acid
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used to reverse the anticoagulent effect of excess warfarin
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Vitamin K
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neutralizes heparin
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protamine sulfate (salmon sperm, yum!)
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this phosphodiesterase inhibitor is contraindicated in patients with Heart Failure
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cilostazol
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General role of Group 1 antiarrhythmics
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Sodium channel blockers
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List group 1A antiarrhythmics
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procainamide
quinidine disopyramide |
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mechanism of action and physiologic effects for group 1A antiarryhthmics
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blocks sodium channels and some potassium channels, results in prolonged action potential in atria, purkinje, and ventricles (prolonged QRS) and refractory period due to potassium effect (prolonged QT interval)
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associated with increased arrhythmias and lupus-like syndrome
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procainamide
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associated with cinchonism (tinnitus, headache, GI disturbances) and TTP
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quinidine
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associated with antimuscarinic effects and heart failure
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disopyramide
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group 1A antiarrhythmic especially associated with torsades de pointes
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quinidine
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when to use group 1A antiarrhythmics
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post-MI atrial and ventricular arrhythmias
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List Group 1B antiarrythmics
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Lidocaine
Mexiletine Phenytoin |
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Mechanism of action and physiologic effects of Group 1B antiarrhythmics
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highly selective sodium blockers to ischemic purkinje or ventricular tissue
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drugs associated with CNS excitation (convulsions) that is give to patient for ventricular arrhythmia post-MI
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Lidocaine
Mexiletine |
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class of drugs used for digoxin-induced arrhythmias
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Group 1B
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anticonvulsant used for digoxin-induced arrhythmias
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phenytoin
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list group 1C antiarrhythmics
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flecainide
propafenone |
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powerful sodium channel blockers that increase QRS duration, but no effect on QT interval
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Group 1C antiarrythmics
Flecainide Propafenone |
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Group 1 antiarrythmics that don't prolong QRS
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Group 1B
lidocaine mexiletine |
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what exacerbates the cardiac toxicity of group 1 drugs
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hyperkalemia
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mechanism of action and physiologic effects of group 2 antiarrythmics
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B blockers result in reduction of both sodium and calcium currents, AV node is particularly sensitive and PR interval is prolonged
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adverse effects of propanolol
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bronchospasm (watch out for asthma), cardiac depression, AV block, hypotension
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differentiate uses of propanolol and esmolol
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propanolol- prophylaxis treatment of sudden death ventricular fib post-MI, and thyrotoxicosis arrhythmias
esmolol - exclusive in acute arrhythmias, perioperitive or thryotoxicosis (IV only) |
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List Group 3 antiarrythmics
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Amiodarone
Dronedarone Sotalol Ibutilide Dofetilide |
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these drugs block sodium, calcium, potassium, and B receptors
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Amiodarone
Dronedarone |
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drugs associated with prolonged PR, QRS, and QR intervals
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amiodarone
dronedarone |
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associated with microcrystals in cornea and skin, thyroid dysfunction, tremor, pulmonary fibrosis
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amiodarone
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similar to amiodarone but only approved for atrial fibrillation
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dronedarone
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general mechanism of group 3 antiarrhythmics
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Potassium channel blockers
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blocks both potassium and B receptors
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Sotalol
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physiologic effects of sotalol
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potassium effect prolongs action potential (increases QT) and B blocker effect slows pacemaker activity prolonging PR interval
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adverse effects of sotalol
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torsades de pointes
excessive B blockage - sinus bradycardia, bronchoconstriction |
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selective potassium channel blockers
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Ibutilide
Dofetilide |
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physiologic effects of potassium channel blockers
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prolongs action potentials - increases QT interval
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differentiate Ibutilide and Dofetilide
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Ibutilide - IV only used for acute atrial fibrillation
Dofetilide - oral only used for prophylaxis treatment of atrial fibrillation |
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what is seen on EKG with calcium channel blockers
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slows AV conduction - prolonged PR interval
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drugs used for treatment of AV nodal reentry (nodal tachycardia)
what is the drug of choice |
verapamil
adenosin - drug of choice |
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adverse effects of adenosine
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flushing
bronchospasm chest pain headache |
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used for treatment for digitalis or torsades de pointes arrhythmias, thought to increase Na/K ATPase
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Magnesium
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physiologic effects of blocking:
sodium potassium calcium beta receptors |
sodium - slow conduction velocity prolonging QRS in atria, purkinje, and ventricles
potassium - slow the AP causing prolonged QT interval Calcium/Beta - decreases AV conduction causing prolonged PR interval |
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drug that slows or blocks AV node conduction
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Adenosine
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most effective therapy for procainamide toxicity - markedly prolonged QRS
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sodium lactate, increases sodium current by increasing the ionic gradient
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increases diatolic (phase 4) potassium influx in AV node
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Adenosine
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drug that increases Na/K ATPase activity and reduces intracellular [Na]
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magnesium ion
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drug that reduces abnormal automaticity in ventricles
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lidocaine
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