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138 Cards in this Set
- Front
- Back
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impaired hemostasis
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excessive bleeding
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stimulated hemostasis
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produce thrombi which occlude BVs and produe ischemia (arteries) or edema/inflammation (veins); can also dislodge and become emboli
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plasmin
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protease involved in fibrinolysis, breaks down clots an dlimits extent of thrombus formation
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3 proaggregation molecules
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ADP, 5HT, thromboxane
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4 anti-thrombic molecules
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prostacyclin, NO, antithrombin, protein C
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antithrombin
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protease that inactivates coagulation factors like fibrin as they escape from the injury site
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heparin mechanism
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catalyzes the activity of antithrombin which prevents fibrin formation; also block 10a
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enoxaparin
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LMW heparin; inhibit Factor 10a specifically (primary function) and also increase antithrombin 3 activation
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dalteparin
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LMW heparin; inhibit Factor 10a specifically(primary function) and also increase antithrombin 3 activation
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use of heparin
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to prevent DVTs and subsequent pulmonary embolism
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major side effect of heparin and 1 minor
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bleeding is major and thrombocytopenia is minor; requires extensive monitoring
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contraindications for heparin treatment (5)
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hemophilia, thrombocytopenia, severe HTN, liver disease, renal disease
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warfarin mechanism
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blocks the synthesis of vit K-dependent clotting factors (7,9,10,2)
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clinical use of warfarin
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anticoagulant used for DVT prevention
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contraindications for warfarin use (2)
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pregnancy: can cross the placenta and cause hemorrhage and bone formation birth defects; also hepatic disease can increase the likelihood of excessive bleeding
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warfarin drug interactions (2)
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drugs that increase bleeding (aspirin, warfarin); cephalosporins (kill gut bacteria that make Vit K)
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hirudin (mechanism, use, contraindication, side effect)
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irreversibe thrombin (2a)inhibitor (does not rely on antithrombin); can be used to treat thrombosis resulting from heparin-induced thrombocytopenia; should not be used in renally impaired patients because it cannot be cleared; may cause thrombocytopenia
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lepirudin (mechanism, use, contraindication, side effect)
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irreversibe thrombin (2a) inhibitor (does not rely on antithrombin); can be used to treat thrombosis resulting from heparin-induced thrombocytopenia; should not be used in renally impaired patients because it cannot be cleared; may cause thrombocytopenia
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bivalirudin (mechanism, use, contraindication, side effect)
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reversibe thrombin (2a) inhibitor (does not rely on antithrombin); can be used to treat thrombosis resulting from heparin-induced thrombocytopenia; should not be used in renally impaired patients because it cannot be cleared; may cause thrombocytopenia
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fibrinolytic mechanism
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lyse thrombi by increasing conversion of plasminogen to plasmin which helps to berak down thrombi
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streptokinase and urokinase
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are fibrinolytics but are not used as often because they are not specific for fibrin and have more complications than tPA
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t-PA mechanism
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fibrinolytic that preferentially activates fibrin-bound plasminogen, thereby confining the fibrinolysis to the thrombus which helps decrease systemic effects
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t-PA clinical uses
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works well in acute MI, DVT, acute stroke, peripheral vascular disease
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t-PA combo treatment
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can combine t-PA with b-blockers or ACE-I's to more effectively decrease mortality
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fibrinolytic side effect
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excessive bleeding
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aspirin mechanism
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irreversible COX 1 and 2 inhibitor thereby preventing thromboxane (platelet aggregator) generation
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aspirin clinical use
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reduces CV mortalit by reducing incidence of first time MI in at risk patients; also good as prophylaxis for arterial thrombi (use in transient ischemia, strokes, unstable angine)
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aspirin toxicity
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GI bleeding, ulcer is contraindicated
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clopidogrel
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reduces platelet aggregation by antagonizing ADP receptors on platelets, used in patients who are at risk for developing thrombi who cannot tolerate aspirin or as a superior combo with aspirin
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ticlopidine
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reduces platelet aggregation by antagonizing ADP receptors on platelets, used in patients who are at risk for developing thrombi who cannot tolerate aspirin
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abciximab
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Ab against 2b/3a complex on platelets, prevents fibrinogen cross linking; used in acute coronary syndromes; major side effect is bleeding
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eptifibatide
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is structurally similar to fibrinogen and occupies its receptor on platelets but inhibits cross linking between platelets; used in acute coronary syndromes; major side effect is bleeding
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tirofiban
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antagonizes the 2b/3a receptor on platelets, prevents fibrinogen cross linking; used in acute coronary syndromes; major side effect is bleeding
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mechanism of nitrates
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at theurapuetic doses, nitrates are venodilators which cause venous pooling which means less blood returns to the heart which decreases end diastolic volume (preload) which decreases the work of the heart (and decreases wall stress) which has the ultimate achievement of lowering O2 consumption of the heart; veins are much more sensitive than arteries to nitrates; may be used in CHF to decrease preload and thus improve pulmonary edema; also in angina
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clinical uses of nitrates
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angina pectoris; also in varient angina
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cellular mechanism of nitrates
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are converted to NO which activates cGMP which relaxes SM by decreasing cytosolic Ca++
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common relatively mild side effects of nitrates
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throbbing headache and flushing due to dilation of meningeal and facial vessels; is dose dependant so pts learn to use lowest dose possible
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serious side effects of nitrates
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postural hypotension and tachycardia (reflex response to lowered BP)
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contraindication to nitrates
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Viagra; together they can cause a life threatening hypotension via severely elevated cGMP
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nitroglycerin (admin, onset of action and duration of action)
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readily absorbed from the sublingual mucosa, gut or skin; fast onset of action but short duration of action; used to treat acute anginal attacks
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isorbide dinitrate (admin, onset of action and duration of action)
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readily absorbed from the sublingual mucosa, gut or skin; has longer onset of action but also longer duration; used in prophylaxis regimen
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2 mechanisms for nitrate tolerance
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1. deplete cystein which is required to produce NO 2. generate peroxtnirate which inhibits conversion of GTP to cGMP
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b-blocker mechanism in angina
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blocks norepi binding in the heart which causes lowered HR, lowered contractility (- inotropy) and slower conduction velocity; this all contributes to decreasing the O2 demand of the heart
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inotropy
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relates to contractility
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b-2 receptors
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activation causes bronchorelaxation and vasodilation; blockage does the opposite
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propranolol
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non-selective b-blocker
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atenolol
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cardioselective b-blocker (b1>b2)
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acebutolol
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cardioselective b-blocker and has partial agonist activity
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pindolol
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non-selective partial agonist b-blocker
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side effects of b-blockers
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lipophilic b-blockers can cross into CNS and cause depression and nightmares (ex: propanolol); must also be careful in patients with asthma or bradycardia; also mask the warning signs of hypoglycemia in diabetics; can decrease HDL and increase TGs
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mechanism for Ca+ blockers
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inhibit the functions in the heart and arterioles that rely on an inward Ca++ current; can decrease firing of SA node, slow conduction of impulse through the AV node, decrease contractility of the atria and ventricles and cause vasodilation in arterioles (decr afterload)
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verapamil (mech, used for, side effect)
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Ca++ channel blocker usefule in angina; has a potent depressant action on the heart (decreases AV node conduction, HR and contractility) but less arteriolar dilation; side effect is that it can cause severe bradycardia
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nifedipine
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Ca++ channel blocker; potent arteriolar dilator but very little cardiac depressant activity; causes a decrease in BP but this causes a reflex tachycardia, so useful in HTN but not really angina
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variant angina (what it is and which drugs to treat with)
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vasospastic angina where coronary blood flow is reduced by a spasm which occurs at rest; is helped by NG or Ca channel blockers but not b-blockers
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contraindications for b-blockers (5)
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severe bradycardia, AV conduction defects, bronchial asthma, diabetes, severe mental depression
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ivabradine
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used in angina; reduces HR by blocking the cardiac pacemaker funny current (If, inward Na current activated by hyperpolarization) but has no effects on AV conduction or contractility
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total cholesterol
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HDL + LDL + TG/5; should be less than 200
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LDL levels
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should be less than 130
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HDL levels
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should be greater than 40
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TG levels
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should be less than 150
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LDL
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BAD cholesterol; transports cholesterol into the arterial wall
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HDL
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sequesters cholesterol from the arterial wall and inhibits the oxidation of lipoproteins
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chylomicrons
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largest of the lipoproteins, located in the intestine, carry dietary TG's
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mechanism of statins
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structurally similar to and inhibitors of HMG-CoA which is the rate limiting step in synthetis of cholesterol; cause a dec in LDL, some inc in HDL and some dec in TGs; this reduces the lipid content of atherosclerotic plaques and promotes plaque stability; also enhance NO production, inhitibit monocyte penetration of arterial wall, inhibit LDL oxidation and supress inflammation
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use of statins
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used in adult CAD and children with familial hypercholesterolemia
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toxicity of statins
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GI stress, muscle pain, myositis, CNS effects
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niacin mechanism
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inhibit secretion of VLDL which causes a decrease in TGs and and increas in HDL; also decr lipoprotein(a)
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clinical use of niacin
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lipid lowering drug; can be used with statins or bile acid-binding resins; has short half life so it requires frequent dosing and cannot be tolerated by 50% of people
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side effects of niacin
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occur in up to 50% of patients; include flushing, occasional heart palpatations and itching
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mechanism of bile acid-binding resins
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bind bile acids in the intestinal lumen and prevent absorption, this causes an increase in bile acid secretion, further conversion of cholesterol to bile acids, decreased cholesterol signals with ultimate effect of decreasing LDLs; only works in patients with functional LDL receptors
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side effects of bile acid-binding resins
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constipation and bloating; can be relieved by increasing dietary fiber
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colestipol
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bile acid-binding resin
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cholestyramine
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bile acid-binding resin
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gemfibrozil mechanism and clinical use
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increases lipolysis of TGs; causes small decrease in LDLs and small increase in HDL; most successful for treatment of hypertriglyceridemia in which VLDL levels are high
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gemfibrozil side effects
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rashes, GI distress, myopathy, arrhythmias, hypokalemia
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gemfibrozil contraindications
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patients with hepatic or renal failure or patients with both hyperlipidemia and atherosclerosis
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exetimibe(mechanism and contraindications (3))
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blocks absorption of cholesterol from the intestine; cant be used with bile acid-binding resins since they would bind the drug as well; not for use in children or pregnant/nursing mothers
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treatment for pulmonary edema (basic)
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decrease venous return via diuretics or venodilators
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morphine
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can be used to decrease preload in patients with pulmonary edema, tachypnea and anxiety; is a venodilator, decreases respiratory rate and has anti-anxiety action
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lasix
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diuretic, decreases preload by decreasing intravascular volume
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drugs (2) that decrease preload and afterload
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ACE inhibitors and nitroprusside; also combo of hydralazine and isosorbide together
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dopamine at low doses
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binds to D-1 receptors in renal and mesenteric BVs which causes dilation of arterioles which increases circulation and decreases afterload
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dopamine at moderate doses
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it is transported into the adrenergic terminal and releases norepi which together these act on the b-1 receptors of the heart to cause +ionotropy with minimal increase in HR
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dopamine at high doses
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causes vasoconstriction
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clinical use of dopamine
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used in CHF associated with severe hypotension (to increase BP via + ionotropic effects) and increase blood flow to the kidneys (in severe hypotension, the symp NS attempts to compensate by vasoconstricting the vessels which can be detrimental in the kidneys; DA can cause vasodilation here)
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hydralazine (use and side effect)(
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arteriolar dilator (works by preventing oxidation of NO); causes lupus like side effect
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isosorbide + hydralazine
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iso is a long acting nitrate, hyral is a arteriolar dilator that acts via inhibition of NO oxidation; together, hydral helps prevent tolerence that occurs if iso is used alone; together they decrease pre and afterload; used to treat CHF (may be better than ACEI in AA pts)
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ACE inhibitors (2)
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enalapril (longer) and captopril (shorter); dilate veins (decr preload) and arteries (decr afterload); inhibits formation of Ang II and inhibits degredation of bradykinin; causes decreased symp, vasodilation and decreased retention of Na and water; clinical use in CHF and HTN
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losartan
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Ang II receptor blocker; similar effects to ACE-I's (decr pre and afterload by both vein and arteriole dilation) does not have cough as a side effect so it can be an effective alternative to those who cant tolerate ACEI's
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nitroprusside
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used to treat hypertensive crisis as well as severe CHF; acts on veins and arterioles, decreases both preload and afterload; admin is IV
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side effect of nitroprusside
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during metabolism it creates cyanide which can cause toxicity like metabolic acidosis or CNS effects
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digitoxin
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highly lipid soluble cardiac glycoside (easily absorbed by GI), 1/2 life of 1 week, metabolized by the liver
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digoxin
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medium lipid soluble cardiac glycoside, 1/2 life of 1.5 days. excreted unchanged by the kidneys
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ouabain
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water soluble (poorly absorbed from GI) cardiac glycoside, excreted unchanged from the kidney, 1/2 life is 21 hours
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digitalis/cardiac glycosides
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inhibits the Na/K ATPase which causes transient increase in intracellular Na which decreases Ca extrusion by Na/Ca exchanger which allows Ca to be pumped into SR and give stronger contraction; also blunts symptathetic drive which decreases afterload; does not increase life expectancy but improves symptoms
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special situation where digitalis is esp important in treatment of CHF
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when you have CHF and atrial fibrilation
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adverse effects of digitalis
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GI symptoms (anorexia, vommitting, nausea), visual changes, arrhythmias (toxic level for these is at same concentration as GI toxicity; hypokalemia puts resting potential closer to threshold and thus predisposes a pt to this side effect)
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b-blockers in HTN mechanism
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block b receptors in heart which decreases SV and HR, in kidney it decreases renin and angII release which decreases TPR;
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b-blockers in HTN (who does they work for)
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most effective in young and caucasion patients (not elderly of AA)
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b-blockers side effects
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can alter blood glucose, increase LDL and TG, decrease HDL, cause bronchospasms in asthmatics
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diuretics in HTN (who do they work for)
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effective in AAs and elderly
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diuretics in HTN- side effects
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increase blood glucose LDLs and TGs, increase serum urate and decrease K+; can cause impotence; contraindicated in diabetes, gout, hyperlipidemia
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ACE inhibitors in HTN mech
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decrease ang II which causes vasodilation; also decreases aldosterone which decreases fluid reabsorption;
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side effects of ACE-I's
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hperkalemia (due to dec aldosterone which dec K+ excretion), cough, first dose effect
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Losartin
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ARB, effective in HTN but with no cough side effect
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Ca++ channel inhibitors- mech
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arteriolar dilator, some have cardiac depressent action
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Ca++ channel inhibitors- who do they work on
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effective in ALL patients regardless of age or race
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propanolol
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b-blocker, non-selective, no intrinsic activity
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pindolol
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b-blocker, non-selective, partial agonist
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atenolol
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cardio selective b-blocker with no intrinsic activity
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acebutolol
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cardio selective b-blocker, partial agonist
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contraindications of b-blockers (3 conditions)
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peripheral vascular disease (because you are blocking the dilating b-2 receptors in the peripheral vasculature which leaves constriction unopposed), diabetics (enhances insulin hypoglycemia and masks hyperglycemic warning signs) and asthma (cause bronchocontriction)
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thiazide diuretics
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inhibit Na and Cl co-transport, very commonly used diureticsl decrease preload and long term can also cause some dec in TPR; slow onset of action
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hydrochlorthiazide
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thiazide diuretic
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loop diuretics
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use in HTN and possibly CHF; not more effective than thiazide diuretics but have more adverse effects; ex is lasix
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potassium sparing diuretics
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prevent K+ loss, are not effective alone at dec BP but use them with thiazide diuretics to prevent hypokalemia
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pseudotolerence
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occurs with vasodilators; BP falls initiall but the dose need incr, this is due to the compensation the body initiates after sensing dec BP (incr symp tone, incr renin secretion)
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quinidine
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moderate Na+ blocker as well as some K+ block; prolongs ADP segment as well as prolonging P and QRS, slows phase 4 depol and increases threshold potential; has some anti-cholinergic effects; has a-1 block also which causes dec TPR and dec venous return; works on both atiral and ventricular arrhythmias
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quinidine side effects
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GI problems and cinchonism (tinnitus)
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procainamide
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Na and K+ channel block; prolongs ADP, P wave and QRS; also slows phase 4 depol and incr threshold potential; works on atrial and ventr arrhythmias; less anti-cholinergic effects compared to quinidine
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adverse side effect to procainamide
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lupus like syndrome
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disopyramide
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Na and K+ channel block; prolongs ADP, P wave and QRS; also slows phase 4 depol and incr threshold potential; works on atrial and ventr arrhythmias; severe anti-cholinergic effects and - ionotrope
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lidocaine
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used to supress ventricular arryhthmias associted with MI; IV admin; only affects damaged myocardium (not normal) in which it markedly inhibits Na channels and K+ channels; only effective in ventricular arrhythmias; very safe
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tocainide
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analog to lidocaine, can be given orally
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mexilitene
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analog to lidocaine, can be given orally
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flecinide
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most potent inhibitors of Na fast channel but no K block; ventr and atrail arrhythmias; can be pro-arrythmic so only use if other drugs don't work first
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propafenone
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similar to flecinide
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bretylium
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admin is IV to treat life-threatening ventricular tachycardia or fibrillation when lidocaine or cardioconversion have failed; inhibit K+ only; displaces norepi (initial symp effects) but then it is released from the nerve terminal instead (it itself has no intrinsic effects) and therefore dec HR and BP
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amiodarone
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very effective anti-arryhtmic drug; both atrial and ventricular arrythmias; blocks Na+ and K+ as well as b-blocking and Ca+ blocking action; has a very long 1/2 life (up to 60 days) so it is difficult to regulate toxicity
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adverse effects of amiodarone
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life threatening pulmonary fibrosis, bradycardia, concentrates in all organs and can cause corneal deposits, photodermatitis, hypo or hyperthyroidism
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adenosine
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inhibits the Ca+ current inward which is needed in AV node for conduction; inhbits AV nodal re-entry arrythmias; 10 sec half life; IV admin
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treatment of UA or NSTEMI
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consists of anti-ischemic meds to restore balance between supply and demand (includes b-blockers, nitrates, Ca blockers) as well as anti-thrombotic therepy (aspirin, clopidogrel, 2a/3b antagonists, heparin, warfarin)
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treatement of STEMI
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Since vessel is completely occluded you want to reperfuse ASAP (either mechanical or with a fibrinolytic such as tPA), then also give drugs like heparin, aspirin, b-blocker, nitrate
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drug interaction of nitrates
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absolute contrindication for patients to use vigra when on nitrates because it may cause a life threatening hypotension
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treatment of angina
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NTG for acute episodes, possibly isorbide dintrate for long term prophylaxis; addition of a b-blocker can also help by blocking the reflex actions that nitrates may stimulate; Ca+ channel blocker with cardiac depressant action such as Verapamil
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side effects of ACE-Is
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cough, first dose hypotension, hyperkalemia
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use of b-blockers
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IHD, HTN, HF, tachyarrhythmias
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cilostazol
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PDE III inhibitor, has antiplatelt and vasodilation effects; use in pts with PAD which can improve quality of life; causes cardiac depression so don't give to paitents with HF
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