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62 Cards in this Set

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  • Back
Name the antilipemic drugs
simvastatin, pravastatin, atorvastatin, rosuvastatin, ezetimibe, cholestyramine, colestipol, colesevelan, niacin, gemfibrozil, fenofibrate
Statin drugs
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)
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
Cholestyramine, Colestipol, Colesevelan
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)**
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
Gemfibrozil and Fenofibrate
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
Antiangina drugs
atenolol, propanolol, nitroglycerin, isosorbide mononitrate/dinitrate, diltiazem, verapamil, amlodipine
Atenolol and propanolol (antiangina)
beta blockers; dec HR, contractility, DBP; incr flow to endocardium
SE: bronchoconstriction, exacerbates heart failure, sudden withdrawl precipitates MI
Nitroglycerin, Isosorbide dinitrate/mononitrate
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
Diltiazem, Verapamil
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,
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
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
Abciximab, Tirofiban, Eptifibatide
blocks IIb/IIIa receptors so fibrin cant bind and there is no platelet aggregation
- T & E cleared by the kidney
Ticlopidine and Clopidogrel
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
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
Dalteparin and Enoxaparin
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
Contraindications and adverse effects of heparin and LMW heparin
Contraindication: spinal anesthesia, LP, bleeding
SE: bleeding, HIT, osteoporosis, elevated K due to inhibited aldosterone synthesis
Danaproid and Fondaparinux
indirect inhibitors of factor Xa (requires ANTIII)
- used in pt with HIT
Lepirudin and Argatroban
direct inhibitor of IIa (thrombin); incr aPTT (A can incr PT in overdoase)
- A reversibly inhibits, L irreversibly inhibits
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
factors that cause warfarin resistance and those that increase response
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
recombinant tPA -> activates plasminogen -> plasmin inhibitors are overwhlemed and plasmin degrades systemic thrombin and factors 5&8
binds plasminogen and changes its conformation so it can activate itself and other plasminogens -> overwhelm inhibitors and get degradation of factors 5&8
Aminocaproic Acid
binds to plasmin and plasminogen and prevents their binding to thrombin
cleaves plasminogen to form plasmin; tPA binds fibrin and its activity is increased 200X
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
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)
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
Atenolol, Propanolol, Esmolol (antidysrhythmic)
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
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
Class III - blocks K channels -> delays repolarization -> incr ERP -> incr QT interval
- cardioversion of Afib
SE: torsade de pointe
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
Verapamil, Diltiazem
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
- 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
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
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
captopril, enalapril, lisinopril
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
Losartan and Valsartan
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
Nifedipine, Amlodipine, Felodipine
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
Atenolol, metoprolol, propanolol, timolol
MOA: beta blocker; dec TPR
PE: fall in renal perfusion -> Na/H2O retention -> limits anti-HTN effect -> pseudotolerance
TX: works best with a thiazide
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
MOA: acts centrally
TX: used to treat HTN in children and PG
SE: sedation, drymouth, rebound HTN, pos Coombs test
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
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
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)
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
Sodium Nitroprusside
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
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)
Isorbide mononitrate/dinitrate
MOA: donate NO to dilate venules -> dec EDVP
Captopril, Enalapril, Lisinopril
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
SE: can have a neg effect on renal funct so must monitor serum K and cretinine
Losartan and Valsartan
MOA: ARB -> balanced vasodilation -> incr EF & SV -> dec congestion sx and remodeling
Isorbide dinitrate + hydralazine
inc SV & EF, dec LEDV/P & wall stress
- decr mortality and remodeling
- use in pt with poor response to ACEI or diuretics
Spironolactone, Eplerenone
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
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
- 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
MOA: dec SNS activity -> dec preload & afterload ->inc SV; dec HR/automaticity; dec O2 demand
- higher mortality if have STEMI
-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
MOA: stim B1 and B2, eneantiomers prevent Areceptor effects -> inc SV, dec TPR/DBP, dec VR
TX: pt w MI and NOT hypotensive
MOA: inhibits PDEase -> inc cAMP -> inc dp/dt; faster relaxation; balanced vasodilation (dec pre and afterload) -> inc SV
- does not dec mortality
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
Sodium Nitroprusside
converted to NO -> balanced vasodilation -> inc SV/CO and dec wall tension
Method of treatment for acute coronary syndrome/MI
M Morphine
O Oxygen
N nitroglycerin
A aspirin