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62 Cards in this Set
- Front
- Back
Name the antilipemic drugs
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simvastatin, pravastatin, atorvastatin, rosuvastatin, ezetimibe, cholestyramine, colestipol, colesevelan, niacin, gemfibrozil, fenofibrate
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Statin drugs
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Simvastatin, Pravastatin, Rosuvastatin, Atorvastatin
MOA: block HMG CoA reductase which causes an increase in LDL receptors and more enzyme; also dec synthesis of ApoB100, anti-inflammatory SE: hepatic damage, (metabolized by CYP3A4), myopathy and myositis, PG category X(fatal rhabdomyolysis) |
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Ezetimibe
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blocks protein mediated transporter that absorbs cholesterol from the GIT -- leads to incr LDL receptor and HMG CoA reductase
- often added to statin therapy to lower LDL even more |
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Cholestyramine, Colestipol, Colesevelan
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bile exchange resins - bind bile acids so excreted in feces - incr LDL receptor, HMG CoA reductase
SE: GI (constipation, pain, bloating), PG C, **dec bioavailability of warfarin, propanolol, furosemide, HCTZ, pravastatin, fluvastatin, thyroxine (cholesevelan does not)** |
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Niacin
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MOA unknown, inhibits lipolysis so less FFAs means less TGs and decreased synthesis of VLDL; decr catabolism of ApoA1 which incr. HDL
- used as additive therapy to incr HDL, pts w dyslipidemia (high TG, low HDL); lower Tc SE: flushing, pruritis, incr liver enzymes, dont use if DM, sx of gout |
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Gemfibrozil and Fenofibrate
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activates lipoprotein lipase which increases hydrolysis of VLDL which leads to dec LDL
- pt w hypertriglyceridemia, dec TGs and incr HDL SE: myopathy, gallstones, avoid w hepatic/renal dz |
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Antiangina drugs
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atenolol, propanolol, nitroglycerin, isosorbide mononitrate/dinitrate, diltiazem, verapamil, amlodipine
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Atenolol and propanolol (antiangina)
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beta blockers; dec HR, contractility, DBP; incr flow to endocardium
SE: bronchoconstriction, exacerbates heart failure, sudden withdrawl precipitates MI |
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Nitroglycerin, Isosorbide dinitrate/mononitrate
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donate NO that preferentially dilates veins (large does, sublingual, dilates arteries)
- dec wall tension, preload; incr endocardial blood flow; inhibit platelet aggregation SE: headache, orthostatic hypotension |
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Diltiazem, Verapamil
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inhibit Ca channels (Ltype) of heart
- dec HR, AV conduction, contractility, depress SV and CO; dilation of epicardial and endocardial arteries (inc BF) - Prinzmetal's angina (prevent vasospasm) SE: bradycardia, SA nodal failure, AV block (esp if taking class IA antidysrhythmic), HF in pt w systolic dysfunction or taking Bblocker, hypotension, potentiates effects of digoxin, |
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Amlodipine
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blocks ca channels (DHP) in arteries
- dec DBP, relieve angina w/o dec CO; decr O2 demand and increase O2 delivery SE: hypotension, paradoxical angina, grapefruit juice increases drug concentration |
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Aspirin
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converted to salicyclate and reversibly inhibits COX -> no TXA2 -> inhibit platelet aggregation and SM contraction --- large dose, acetylsalicylic acid irreversibly inhibts COX -> inhibits PGI2 & PGE2
SE: increases bleeding time |
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Abciximab, Tirofiban, Eptifibatide
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blocks IIb/IIIa receptors so fibrin cant bind and there is no platelet aggregation
- T & E cleared by the kidney |
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Ticlopidine and Clopidogrel
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inhibit P2Y(12) receptor -> ADP cant bind -> cAMP remains high and Ca low -> no aggregation
- DOC for pt who cant take aspirin SE: neutropenia, thrombocytopenia, agranulocytosis |
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Heparin
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Antiplatelet - keeps torn endothelium negative, repels platelets
Anticoagulation - enhances ANTIII binding and inactivating factors 2,9,10,11,12 - given IV, cleared by RES; DOC in PG Resistance: pulm embolism increases heparin clearance; ANTIII deficiency (genetic & acquired); acute phase proteins bind and inactivate heparin |
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Dalteparin and Enoxaparin
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LMW heparins, aid ANTIII inactivation of factor Xa
ADVTGs: not altered by plasma proteins, greater F and T1/2, cleared by kidnery, can be self administered, less thrombocytopenia, can be selfadministered sc |
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Contraindications and adverse effects of heparin and LMW heparin
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Contraindication: spinal anesthesia, LP, bleeding
SE: bleeding, HIT, osteoporosis, elevated K due to inhibited aldosterone synthesis |
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Danaproid and Fondaparinux
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indirect inhibitors of factor Xa (requires ANTIII)
- used in pt with HIT |
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Lepirudin and Argatroban
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direct inhibitor of IIa (thrombin); incr aPTT (A can incr PT in overdoase)
- A reversibly inhibits, L irreversibly inhibits |
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Warfarin
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inhibits reduction of vitK-> factors 2,7,9,10 cant be carboxylated and are inactive
- DVT, thromboembolism in pt w Afib, prosthetic valves, mitral valve dz, unstable angina - transition from inpatient heparin use to outpatient warfarin SE: bleeding, teratogenesis, cutaneous necrosis - cleared by liver - incr PT (INR) - antidote = phytonadione |
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factors that cause warfarin resistance and those that increase response
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Resistance: induction of CYP2C9, hypoalbuminemia, anion exchange resin, incr intake of vitK
Incr Response: CYP2C9 inhibitors, destruction of gut bacteria, decr synthesis of factors due to hepatic dysfuncion |
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Alteplase
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recombinant tPA -> activates plasminogen -> plasmin inhibitors are overwhlemed and plasmin degrades systemic thrombin and factors 5&8
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Streptokinase
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binds plasminogen and changes its conformation so it can activate itself and other plasminogens -> overwhelm inhibitors and get degradation of factors 5&8
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Aminocaproic Acid
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binds to plasmin and plasminogen and prevents their binding to thrombin
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tPA
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cleaves plasminogen to form plasmin; tPA binds fibrin and its activity is increased 200X
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Quinidine
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Class IA
blocks Na channels -> suppresses phase 4, inc threshold for depolarization, dec conduction velocity -> wide QRS block K channel -> prolongs AP, incr ERP -> long PR and QT blocks musc. receptors-> tachycardia, attenuated by other affects blocks A-receptors -> dilates arterioles and venules - control ventricular rate in Afib; suppress PVCs - SE: torsade de pointe; Vtach (large dose, musc.block); cinchonism; reduces clearance of digoxin |
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Procainamide
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Class IA
blocks Na & K channels -> wide QRS, long PR and QT interval - control vent rate, PVCs SE: hypotension, torsade de pointe, SLE in slow acetylators (SHIP drug) |
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Lidocaine
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Class IB
blocks Na channels in ventricles only -> suppress automaticity in partially depolarized tissues (ischemia, digoxin); abolishes ventricular reentry dysrhythmia (2 way blockade in retrograde tissue); no EKG effect - suppress PVCs immediatley after MI or digoxin induced PVC; V tach in healed MI SE: CNS depression, seizures |
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Atenolol, Propanolol, Esmolol (antidysrhythmic)
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Class II
block B-receptors -> suppress catecholamine automaticity; reduce conduction velocity and incr ERP of AV node; decrease rate of discharge of SA node - incr PR interval - reduce post MI sudden death; prevent PVCs due to emotional stress; suppress tachycardia due to hyperthyroidism; control Vrate in Afib; DOC for Vtach in pt w/ congenitally prolonged QT interval; suppress AVnode reentry |
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Amiodarone
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Class III - blocks Na & K channels, AandB receptors
- prolong PR, QRS, QT; reduce rate of SA firing - cardioversion of Afib; reduce vent rate in Afib; chronic therapy to prevent/tx Vtach, Vfib - seldomly causes torsade de pointe SE: pneumonitis leading to pulm fibrosis; purple skin; hypothyroidism |
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Dofetilide
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Class III - blocks K channels -> delays repolarization -> incr ERP -> incr QT interval
- cardioversion of Afib SE: torsade de pointe |
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Sotalol
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combined class II & III
-Lisomer blocks Breceptor -> dec HR, incr APD/ERP - D&L isomers block K channel -> incr APD/ERP - cardioversion of Afib; prevent Vtach SE: torsade de pointe, dec ventricular contractility in HF; AV block |
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Verapamil, Diltiazem
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Class IV block Ca channel -> dec HR, conduction velocity, incr ERP, dec contractility
- prolong PR interval - converts AVnodal reentry tachycardia SE: hypotension, sinus bradycardia, heart block |
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Digoxin
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- increases vagal activity and decreases sympathetic and inhibits Na/K ATPase
- dec HR, conduction velocity in AV, block of Na/K causes incr contractility and incr SV - control vent-rate in Afib in the presence of HF due to systolic dysfunction; increase contractility in pt w/ HF from systolic dysfunction overdose: PAC & PVC (due to Na/K block); inc symp. activity (due to dec ERP in presence of Ca); AV block |
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Adenosine
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incr K conductance to hyperpolarize the AVnode; inhibits ability of symp. to stimulate AV node
- AVnode: dec conduction, inc ERP, dec transmission - DX of AVNRT (if tach goes away with tx); produce coronary vasodilation SE: short burning sensation; transient asystole; flushing; dyspnea |
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Hydrochlorothiazide
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MOA: unknown; fall in BP is dependent on maintaining a neg NA balance
PE: initially lowers ECF vol and therefore CO and BP; CO eventually returns to normal and fall in BP is due to decr TPR; PRA elevated; HR unchanged; reduces LVH by 5% TX: small doses work; salt restriction allows small doses and less K effect; 2-aldosteronism; doesnt work if GFR<30; prevent/reverse Na/water retention caused by other drugs SE: hyperuricemia, hyperglycemia, hypokalemia (predisposes to digoxin arrythmias); hyperlipoproteinemia; lower hypoK by cotx w Ksparing diuretic, ARB, ACEI, beta blocker, K supplement |
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captopril, enalapril, lisinopril
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MOA: ACE inhibitors; plasma aldost. is maintained by ACTH; prevents the breakdown of bradykinin
PE: dec TPR ->dec MAP; incr compliance of arteries-> further fall in SBP; dec SBP, DBP, MAP; balanced vasodilation at kidney prevents Na/H2O retention; prevent/reduce cardiac remodeling caused by ANGII TX: normally used with a thiazide; malignant HTN; renovascular HTN; HTN crisis of scleroderma; DOC for pts with HF, LVH, DM, syst dysfnct; every type 2 DM should be on ACEI; prevent or reverse hypokalemia and lipid profile caused by thiazides SE: first dose hypotension; renal insufficiency; hyperkalemia if on Ksparing diuretic too; dry cough; angioedema, rash; aguesia and dysguesia |
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Losartan and Valsartan
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MOA:AngII receptor antagonist; blcok AngI receptor; does not effect bradykinin
PE: incr compliance of both small and large arteries; other affects are the same as ACEI TX: HTN; dose-response curve is small so better to use a small dose and add another drug SE: dont use in PG or lactating women; angioedema, hypotension, hyperkalemia; NO dry cough |
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Nifedipine, Amlodipine, Felodipine
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MOA: block Ltype Ca channels in heart and vessels
PE:dilate afferent arterioles -> inc GFR; NO change in renin; promote Na/H2O excretion; dec proteinuria in DM; dilates arterioles and not venules -> dec TPR -> dec DBP; dec SBP, DBP, MAP TX: mild-mod HTN; lowers SBP>DBP SE: excessive vasodilation -> hypotension, pounding bulse, pedal edema (decr'ing the dose helps); GERD; paradoxical angina from coronary steal |
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Atenolol, metoprolol, propanolol, timolol
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MOA: beta blocker; dec TPR
PE: fall in renal perfusion -> Na/H2O retention -> limits anti-HTN effect -> pseudotolerance TX: works best with a thiazide |
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Labetolol
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MOA: blocks B1 in heart; A1 in arterioles & venules; partial agonist at B2
PE: dec TPR -> dec MAP; balanced vasodilation -> no CO change; basal HR dec; dec renal perfusion -> Na/H2O retention; PRA & AngII dont change TX: hypertensive emergency SE: orthostatic hypotension, HA, fatigue, reduced sexual function |
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a-methyldopa
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MOA: acts centrally
TX: used to treat HTN in children and PG SE: sedation, drymouth, rebound HTN, pos Coombs test |
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Clonidine
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MOA: lipid soluble -> enters brain and is an A2 agonist in RVLM -> dec sympathetics
PE: standing -> dec TPR -> dec BP; seated -> venodilation -> dec VR -> CO; dec renal pefusion -> incr FF -> Na/H2O retention; PRA & AngII suppressed TX: hypertension (pseudotolerance) SE: sedation, drymouth, CNS depression, orthostatic intolerance, slows AV conduction; withdrawl syndrome |
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Hydralazine
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MOA: dec Ca -> relaxes VSM of aterioles -> lowers TPR -> dec BP; degraded to NO -> hyperpolarize SM by opening Kchannel
TX: only used for severe HTN; never used as single angent b/c of tachycardia and ECF expansion SE: tachy; edema; angina; SLE (SHIP drug); pyroxidine responsive polyneuropathy |
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Minoxidil
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MOA: dec Ca -> relaxes VSM of aterioles -> lowers TPR -> dec BP; mioxidil sulfate incr Kconductance and hyperpolarizes cells
TX: only used for severe HTN; never used as single angent b/c of tachycardia and ECF expansion SE: tachy; edema; angina; global hypertrichosis (hair in weird areas) |
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Diazoxide
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MOA: dec Ca -> relaxes VSM of aterioles -> lowers TPR -> dec BP; hyperpolarizes cells by incr gK
TX: only used in HTN emergency SE: hyperglycemia; tachy, edema, angina; relaxes uterine SM and may arrest labor if given to tx preeclampsia |
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Sodium Nitroprusside
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MOA:when contacts RBC NO is released -> vasodilation and inhibits platelet aggregation via stimulation of guanyl cyclase
PE: dec TPR -> dec DBP; venodilation -> dec VR -> dec CO; slight inc HR due to baroreflex; TX: only given to supine pts; HTN emergencies; controlled hypotension in surgery; inc CO in CHF and dec O2 demand after MI SE: VERY dangerous, used as last resort; tachy, HA, palpitations; thiocyanate intoxication |
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furosemide
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MOA: diuretic, inhibits Na/K/Cl transporter -> saluresis ->dec ECF -> dec VR
- alleviates backward HF - relieve congestive sx associated w systolic dysfunction -does NOT inprove survival, SV or reverse modeling SE: hypokalemia (tx with K sparing diuretic) |
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Isorbide mononitrate/dinitrate
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MOA: donate NO to dilate venules -> dec EDVP
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Captopril, Enalapril, Lisinopril
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MOA: ACEI -> balanced vasodilation (move to new starling curve)
PE: dec TPR, VR; incr EF, SV -> dec LVEDV and wall stress; incr RBF -> diuresis TX: incr EF&SV, dec congestion sx; reverse remodeling due to AngII; decreases mortality after MI ALL PTS w HF SHOULD BE ON ACEI SE: can have a neg effect on renal funct so must monitor serum K and cretinine |
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Losartan and Valsartan
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MOA: ARB -> balanced vasodilation -> incr EF & SV -> dec congestion sx and remodeling
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Isorbide dinitrate + hydralazine
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inc SV & EF, dec LEDV/P & wall stress
- decr mortality and remodeling - use in pt with poor response to ACEI or diuretics |
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Spironolactone, Eplerenone
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MOA: aldosterone receptor antagonist
- reverses remodeling due to Aldosterone deposition of collagen - decreases backward failure SE: hyperkalemia (esp if using ACEI); can impair renal function; spironolactone can bind sex hormone receptors |
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carvedilol
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MOA: blocks B1, B2, A1 receptors -> inc EF & SV and inhibit remodeling due to SNS; prevent Vdysrhythmia
- pt c Class II&III HF w EF<35%; give to pts on taking ACEI or diuretic - have to get rid of excess water before start tx or can get pulmonary edema - pt feels worse at first due to dec EF but with time EF increases and pt feels better |
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Digoxin
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- direct pos inotropic effect -> inhibits Na/K transporter -> incr Ca -> incr contractility
- incr vagal activity -> slows HR, dec conduction veliocity, incr ERP in AV node - dec SNS -> dec automaticity, incr ERP - NEG AFFECTS: dec phase 4 potential diff -> closer to threshold -> PAC, PVC; incr Ca -> delay after-depolarization -> triggers dysrhythmia TX: HF w systolic dysfunction when other txs not enough; HF in pt with Afib SE: side effects increased in hypokalemic state - hyperCa, hypoMg, bradycardia, sinus block, yellow/green vision -Drug interactions: loop diuretics & HCTZ indue hypokalemia; CCAs and Bblockers enhance bradycardia, dec AV conduction |
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Morphine
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MOA: dec SNS activity -> dec preload & afterload ->inc SV; dec HR/automaticity; dec O2 demand
- higher mortality if have STEMI |
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Dopamine
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-low dose: stim D1 -> dilate aff arterioles -> inc RBF -> inc Na excretion
-intermediate: stim D1 & B1 -> inc dp/dt; small inc HR; inc SV/CO -> incr GFR -large: A1 stim -> inc TPR, DBP, aterial impedance -> dec SV/CO; venoconstriction -> inc VR -> inc wall tension; inc afterload TX: pt w MI and hypotensive |
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Dobutamine
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MOA: stim B1 and B2, eneantiomers prevent Areceptor effects -> inc SV, dec TPR/DBP, dec VR
TX: pt w MI and NOT hypotensive |
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Milrinone
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MOA: inhibits PDEase -> inc cAMP -> inc dp/dt; faster relaxation; balanced vasodilation (dec pre and afterload) -> inc SV
- does not dec mortality |
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Nitroglycerin
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MOA: NO -> vasodilation
small dose -> dilate veins -> dec filling pressure/wall stress large dose -> dilate arteries and veins -> dec preload and afterload - dec size of infarct; inhibit platelet aggregation |
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Sodium Nitroprusside
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converted to NO -> balanced vasodilation -> inc SV/CO and dec wall tension
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Method of treatment for acute coronary syndrome/MI
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M Morphine
O Oxygen N nitroglycerin A aspirin |