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89 Cards in this Set

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lovostatin and atorvastatin
HMG-CoA reductase inhibitors causing upreg of hepatic LDL receptors. Decreases: LDL (20-55), Tri (10-35)
used for high chol or LDL, atherosclerosis, prevent coronary HD
AE: FDA-X, renal damage from myopathy after inhibition of p450 or use with fibric acid or niacin
cholestyramine
bile acid resin binding that prevents re-uptake of bile acids, so chol excret is up 10 fold, forcing upreg of hepatic LDL receptors. Decreases LDL (10-35), but can INCREASE TRIs!! Has F=zero
give with ezetimibe and/or statin
used for high LDL
AE constipation, decreased absorb of fat sol vit, hypertrigly, increase coag from decreased Vit K absorb. Also messes with absorb of warfarin, statins, thiazides, aspirin, thyroxine
niacin
inhibits lipolysis in adipose tissue. Decreases LDL (15-25), VLDL (15-40), Tris (30-50) and increases HDL (15-30). Only drug with large increase in HDL.
used for high VLDL/LDL, low HDL
AE: stim of histamine, flushing, decreased glu tolerance, rhabdomyolysis when with statin. Contra in peptic ulcer, DM, gout, liver disease, bleeding disorder. DO NOT give with statin
gemfibrozil
fibric acid that activates transcription leading to increase in lipoprotein lipase synth, so VLDL is removed. Decreases Tri (30-60), VLDL (20-30), increases HDL (5-10).
used for type 3 hyperlipoproteinemia and high Tris
AE: cholelithiasis, DO NOT give with statin (chance of rhabdomyolysis)
ezetimibe
localizes at small intestine brush border inhibiting chol and sterol absorp. Decrease in LDL (15-20) and Apo-B (16). Give with ezetimibe for statin
used for hyperlipid
AE: diarrhea, hypersens rxn. Contra in hepatic disease
Amy nitrite
decrease O2 demand by reducing preload (main action) and increase O2 delivery my relieving coronary spasm. Duration is 3-5min. Converted to NO, increasing cGMP, increases dephos MLC via activation of kinase G. Thereby stim guanylyl cyclase in platelets and decreasing availability of tissue -SH groups. Marked relaxation of large veins. Rapid appearance and disappearance of tolerance.
used for cyanide poisoning
AE: throbbing headache, profound hypotension
contra in hypertrophic cardiomy, constrictive pericarditis, hypotension, hyperthyroid, heptic disease
nitroglycerin
decrease O2 demand by reducing preload (main action) and increase O2 delivery my relieving coronary spasm. Duration is 3-5min. Converted to NO, increasing cGMP, increases dephos MLC via activation of kinase G. Thereby stim guanylyl cyclase in platelets and decreasing availability of tissue -SH groups. Marked relaxation of large veins. Rapid appearance and disappearance of tolerance.
used for angina, exertional, variant, and unstable, heart failure, MI, and cyanide poisoning
AE: throbbing headache, profound hypotension
contra in hypertrophic cardiomy, constrictive pericarditis, hypotension, hyperthyroid, heptic disease
isosorbide mononitrate
decrease O2 demand by reducing preload (main action) and increase O2 delivery my relieving coronary spasm. Duration is 3-5min. Converted to NO, increasing cGMP, increases dephos MLC via activation of kinase G. Thereby stim guanylyl cyclase in platelets and decreasing availability of tissue -SH groups. Marked relaxation of large veins. Rapid appearance and disappearance of tolerance.
used for angina, exertional, variant, and unstable, heart failure, MI, and cyanide poisoning
AE: throbbing headache, profound hypotension
contra in hypertrophic cardiomy, constrictive pericarditis, hypotension, hyperthyroid, heptic disease
propranolol
decrease O2 demand by reducing contract and rate, increase myocardial perfusion due to increased dyastole
used for MI and exertional angina. NOT for variant angina
AE: increased EDV, increased ejection time, withdrawl effect, bad for asthmatics and DM
metoprolol
decrease O2 demand by reducing contract and rate, increase myocardial perfusion due to increased dyastole
used for MI and exertional angina. NOT for variant angina
AE: increased EDV, increased ejection time, withdrawl effect, bad for asthmatics and DM
nifedipine and nimodipine
blocks Ca channels in vasculature. Decreases O2 demand by decreasing afterload through decreased TPR through vasodilation.
used for extertiona and variant angina, HTN, and Raynaud's phenom
AE hypotension, tachy, aggravation of myocardial ischemia via coronary steal, contra in AV block, WPW, vent tachy, systolic failure
verapamil and diltiazem
blocks Ca channels in vasculature and heart. Decreases O2 demand by decreasing afterload through decreased TPR through vasodilation and increases O2 supply by relieving coronary spasms.
used for extertiona and variant angina, HTN, and Raynaud's phenom
AE hypotension, tachy, aggravation of myocardial ischemia via coronary steal, contra in AV block, WPW, vent tachy, systolic failure
digoxin (MOA and use)
steriod glycoside, inhibits Na/K pump, so intracellualar Na in increased, so Ca in increased as well. More Ca leads to increased contract
used for acute or chronic systolic heart failure, atrial flutter, atrial fibrilation, atrial/nodal tachy
AE-many, see other card
digoxin (AE)
very narrow theraputic index!! toxicity is dose dep and cumulative due to long half life (40hrs). Can lead to arrhytmias (vent tachy is lethal), N/V, CNS disturbances (digitalis delirium), green-yellow halos, hyperkalemia. Tx with Digibind, and/or lidocaine/phenytoin (for vent tachy). Contra in hyperCa, hypoK, hyperK, hypoMg.
digoxin (contras)
digoxin contra in hypertrophic cardiomy, diastolic dysfunction, cor pulmonale, WPW syndrome, vent arrhythmias, AV blocks, MI, myocarditis, amyloid cardiomy
digoxin drug interactions
amiodarone/verapamil (increase serum lvl of digoxin)
macrolides, tetracyclines, aminoglycosides (decrease bact that biotransform digoxin)
spironolactone (increases serum lvl of digoxin up to 30%)
dopamine
low dose is D1 receptor agonist, mid-dose is B1 agonist, high dose is a1 and d2 agonist. Therefore low dose has vasodilation in renal, middose has pos inotropic effect, high dose can cause HTN
tx of cardiac failure when poor renal perfusion contributes
AE tolerance, arrhythmias, anginal pain, vasospasm
dobutamine
b1-agonst. (no change in TPR/BP)
tx for acute cardiac failure with depressed left vent function
milrinone
phosphodiesterase inhibitor of isozyme 3, leading to increase in cAMP. In cardiac there is increased Ca, in smooth muscle MLCK is inactivated, therefore in heart there is positive inotropic effect, peripheral effect is vasodilation
used fro acute decompensated heart failure or cardiogenic shock in pts where other therapy is not working, they are on beta blockers
AE hypotension, vent arrythmias, thrombocytopenia!!!
diuretics for HTN name
HCTZ, indapamide, furosemide, spironolactone
central sypathetics for HTN name
clonidine, methydopa
a1 blockers for HTN name
Prazosin
b-blockers for HTN name
Propranolol, Labetalol, Esmolol
ACE inhibitors for HTN name
Captopril, Enalapril
AT2R blockers for HTN name
Losartan
Ca Channel blocker (name
nifedipine and Nicardipine (only vascular).
verapamil and dilitazem (caridac and vascular)
Vasodilators for HTN (name)
nitroprusside, hydralazine, minoxidil, diazoxide, fendolapam
diuretics for HTN function
initial effects are volume reduction, but longterm effects are arterolar vasodilation
in HTN, thiazides are most effective with intact renal function, often given with K sparring, and note that spirololactone is used for hyperaldosteroniam
central sypathetics for HTN function (Clonidine)
a2-antagonist, reducing symp output
2nd choice for HTN due to toxicity
AE drowsiness, sudden withdrawl leads to hypertensive crisis, xerostomia, postural hypotension
central sypathetics for HTN function (methydopa)
converted to methylNE that acts on a2
used to treat HTN in PREG
AE postural hypotension, drowsiness, sudden withdrawl leads to hypertensive crisis, xerostomia
can cause hemolytic anemia
a1 blockers for HTN function (prazosin)
blocks a1 leading to vasodilation in periphery
used as 2nd choice for HTN
AE postural hypotension, nasal stuffiness, sexual dysfun, peripheral edema after chronic tx
b-blockers for HTN function (propranolol, labetalol, esmolol)
reduces HR, contract, and renin release
used for HTN in young, supravent arryth, hypertrophic cardiac, angina, post MI, hypertensive emerg (labetalol)
AE DM, asthmaics, can give postural hypotension, cardiogenic shock in pheochromocytoma
ACE inhibitors for HTN function (captopril, enalapril)
block ACE, also leads to decrease in bradykinin breakdown
decrease in venous tone, slight postural hypotension
1st choice in HTN, good for MI for HF pts, CHF
AE dry cough, postural hypotension, hypokalemia
Conta in PREG, renal/aortic stenosis,
AT2R blockers for HTN function (lorsartan, valsartan)
blocks AT1 recceptor, more complete inhibition that ACE-Is, no effect on bradykinin
used for HTN, no cough or angioedema
AE contra in PREG and renal/aortic stenosis
nifedipine and nicardipine
vascualar selective Ca channel blocker, limits contration by blocking L-type Ca channel, decreases TPR, slight increase in HR
used for mild/moderate HTN when angina, tachy, or broncospastic disease present
AE hypotension. Contra in cardiac failure pts
verapamil
vascualar and cardiac Ca channel blocker, limits contration by blocking L-type Ca channel, decreases TPR
used for mild/moderate HTN when angina, tachy, or broncospastic disease present
AE hypotension. Contra in cardiac failure pts
diltiazem
vascualar and cardiac Ca channel blocker, limits contration by blocking L-type Ca channel, decreases TPR
used for mild/moderate HTN when angina, tachy, or broncospastic disease present
AE hypotension. Contra in cardiac failure pts
nitroprusside
metabolized into NO in smooth muscle cells, strong decrease in TPR, reflex increase in HR. When RBCs metabolize, cyanide is produced
used for hypertensive emergy, NOT for chronic use
AE strong postural hypotension, accumulation of cyanide (tx with amyl nitrite), thiocyanate has CNS toxicity. Contra in intracranial pressure
hydralazine
unk, but thought to limit Ca release from SR, leads to arteriolar vasodilation, decrease in TPR, increase in HR, can undergo tolerance
used to HTN
AE nausea, dizziness, palpitations, sweating, flushing. Can create lupoid syndrome
minoxidil
opens K channels in smooth muscle, vasodilation is mostly arteriolar vasodilation, prodrug transformed by liver
rarely used for HTN due to toxicity, but is used for hair growth
AE na/water retention, pericardial effusion, cardiac failure w/ LVH, hypertrichosis (hair growth), adn allergic rxns
diazoxide
opens K channels in smooth muscle, vasodilation is mostly arteriolar vasodilation,
used in HTN crisis and hypoglycemia secondary to insulinoma
AE na/water retention, hyperglycemia (50% of pts), hypertrichosis, sulf rxns, contra in angina
fenoldpoam
D1 agonist, vasodilates the kidney
used for HTN crisis
AE reflex tachy, flushing, increased intraocular pressure, so CONTRA in glaucoma
Acetazolamide
carbonic anhydrase inhibit
up excreation of Na, K, HCO3
down excretion of NH4, H
used for open angle glaucoma, altitude sickness, made urine alkaline
AE: sulf sens, nephrolithiasis, hyperuricemia, hypokalemia
contra in COPD
Dorzolamide
a topical carbonic anhydrase inhibit
up excreation of Na, K, HCO3
down excretion of NH4, H
used for open angle glaucoma,
contra in COPD
hydrochlorothiazide
blocks Na/Cl symport, decreasing diluting capacity, long term arteriolar vasodilation, is a sulfa
up excret of Na, K, H, Cl, HCO3, acidifies urine
down excret of Ca (unique) and NH4
used to HTN, edema, nephrolithiasis, nephrogenic diabetes
AE hpercalcemia (unique), hypokalcemia, metabolic alkalosis , impaired glu toler, postural hypotension
contra in PREG, DM
Indapamide
blocks Na/Cl symport, decreasing diluting capacity, long term arteriolar vasodilation, is a sulfa
up excret of Na, K, H, Cl, HCO3, acidifies urine
down excret of Ca (unique) and NH4
used to HTN, edema, nephrolithiasis, nephrogenic diabetes
AE hpercalcemia (unique), hypokalcemia, metabolic alkalosis , impaired glu toler, postural hypotension
contra in PREG, DM
Furosemide
blocks Na/K/Cl triport decreasing lumen potential, conc ability, and inhibition of macula densa, works with low GFR, urine Osm=blood Osm
up excret of Na, K, H, Ca, Cl
down excret of urates, acidifies pH of blood
used for pul edema, heart failure, renal failure edema, HTN with renal insufficiency
AE hypocalcemia, hypokalemia, hypochloremia, post hypotension, tinnitus
contra in DM pts, is a sulfa drug
Ethacrynic acid
NOT a sulfa. blocks Na/K/Cl triport decreasing lumen potential, conc ability, and inhibition of macula densa, works with low GFR, urine Osm=blood Osm
up excret of Na, K, H, Ca, Cl
down excret of urates, acidifies pH of blood
used for pul edema, heart failure, renal failure edema, HTN with renal insufficiency
AE hypocalcemia, hypokalemia, hypochloremia, post hypotension, tinnitus
contra in DM pts
Triamterene
Blocks Na channels directly in DCT, sparring K
up excret of Na, Cl
down excret of K, H
used to counteract K loss of other diuretics
AE hyperkalemia
Amiloride
Blocks Na channels directly in DCT, sparring K
up excret of Na, Cl
down excret of K, H
used to counteract Li-induced nephrogenic DI
AE hyperkalemia
Spironolactone
Blocks aldosterone receptors in DCT, sparring K
up excret of Na, Cl
down excret of K, H
used to counteract Li-induced nephrogenic DI
AE hyperkalemia, sexual dysfunct, and steriod side effects (gynocomastia, menses irregularites)
Mannitol
increases Osm of tubular fluid
increases excretion of everything, urine is acidic but blood is normal, can cause extracellular volume expansion, then extracellular volume reduction
used for cerebral edema and reduce intraocular pressure in closed angle glaucoma
AE if renal failure, excess fluid can not be removed so leads to pulm edema
Class 1a
Quinidine, Procainamide
blocks activated Na and K channels
Class 1b
Lidocaine, Mexiletine, Pheytoin
blocks inactivated Na channels
Class 1c
Flecainide
blocks activated Na and K channels
Class 2
Metoprolol, Propranolol, Esmolol
b-blocker
Class 3
Amiodarone (K channel blockade and inactivated Na channels)
Ibutilde (blocks K and activates inward Na)
Sotalol (blocks K and B activity)
Class 4
Verapamil and Diltiazem (Ca channel blocker: activated and inactivated)
quiidine
Class 1a, blocks act Na and K. increase in phase 0 and prolonged repol
seldomly used for a-fib, recurrent supravent tachy
AE: Torsade de pointes, cinchonism, thrombocytopenia, digitalis tox, increases QT interval!!
note: some anti-muscarinic activity
procainamide
Class 1a, blocks act Na and K. decrease in phase 0 and prolonged repol
used for WPW (Wolff-Parkinson-White syndrome
AE: Torsade de pointes, cinchonism, digitalis tox, increases QT interval!! Lupoid syndrome in 30%
lidocaine
Class 1b, blocks inact Na and a little act Na. Little change in phase 0, increased refractoriness in depolarized damaged cells
used for vent arrhythmias only!!! Can be used in digitalis induced issues
Contra in A-fib, heart blocks
mexiletine
Class 1b, blocks inact Na and a little act Na. Little change in phase 0, increased refractoriness in depolarized damaged cells
used for vent arrhythmias only!!! Can be used in digitalis induced issues
Contra in A-fib, heart blocks
pheytoin
Class 1b, blocks inact Na and a little act Na. Little change in phase 0, increased refractoriness in depolarized damaged cells
used for vent arrhythmias only!!! Can be used in digitalis induced issues
Contra in A-fib, heart blocks
flecainide
class 1c, blocks activated Na and K. decrease in phase 0, increase in refractoriness and repol
used for supravent arryth
AE: worsens CHF, visual disturbances, dizziness, tremor
metoprolol
class 2, b-blocker, decreases conduction, increased refractoriness
used for a-fib/flutter and supravent reentry arryth, hypertrophic cardiomy, prophylaxis of v-fib post MI
AE
propranolol
class 2, b-blocker, decreases conduction, increased refractoriness
used for a-fib/flutter and supravent reentry arryth, hypertrophic cardiomy, prophylaxis of v-fib post MI
AE
esmolol
class 2, b-blocker, decreases conduction, increased refractoriness
used for a-fib/flutter and supravent reentry arryth, hypertrophic cardiomy, prophylaxis of v-fib post MI
AE
amiodarone
class 3, K and inact (only) Na channel block,
used for most arrythmias, though has toxicity.
AE: increased QT, decreased conduction, inhibits p450, 25 day half life, 70% of pts have AE: hypotension, torsade de pointes, constipation, CNS issues, pulmonary fibrosis (can be fatal), hypothyroidism, corneal microdeposits
contra in Preg (FDA-D), heart blocks, long QT
ibutilide
class 3, blocks K and ACTIVATES inward Na channels. Leads to prolonged AP duration.
used for a-fib and flutter
AE: can lead to torsade de pointes
sotalol
class 3, blocks K and b-blocking activity.
used for supra and vent arryth
AE: can lead to torsade de pointes
verapamil
Class 4, Ca channel blocker (both inact and act). Decrease in phase 0 slope, decrease in conduction, increase in PR int
used for supravent tachy, A-fib, flutter
contra: WPW, and not effective on vent arrhythmias
diltiazem
Class 4, Ca channel blocker (both inact and act). Decrease in phase 0 slope, decrease in conduction, increase in PR int
used for supravent tachy, A-fib, flutter
contra: WPW, and not effective on vent arrhythmias
adenosine
activates K channels, leading to hyperpol. Decreased automaticity, decreased conduction.
used for paroxysmal supravent tachy
AE flushing, chest pain, hypotension
magnesium sulfate
unkn MOA
used to prevent recurring torsade de pointes and treatment of digitalis-induced arrhythmias
absolute contra for Heart failure or Hx of MI
Flecainide
absolute contra for SA, AV, nodal block ; sic sinus syndrome
Digoxin, Ca++ blockers, beta-blockers, amiodarone
absolute contra for Wolff-Parkinson-White synd
Digoxin, Ca++ blockers
absolute contra for Diarrhea
Quinidine
absolute contra for Constipation
Verapamil, diltiazem
absolute contra for Arthritis
Chronic procainamide
absolute contra for Lung disease, thyroid disorders
Amiodarone
absolute contra for Asthma,peripheral vascular disease, diabetes
beta-blockers
absolute contra for Long QT interval
Quinidine, procainamide, sotalol, amiodarone
therapy for ectopic beats
if symptomatic use beta blockers
therapy for atrial fib/flutter/tachy
to stop cardioversion: ibutilide
for rate control: b-blocker, Ca blocker, digoxin
therapy for AV nodal re-entry tachy
acute tx: vagal maneuver, adenosine, amiodarone, procainamide
chronic tx: amiodarone, procainamide, sotalol, abaltion
therapy for ventricular tachy
acute tx: amiodarone, lidocaine, procainamide
chronic : mexiletine
therapy for torsade de pointes
acute tx: cardioversion, Mg sulphate, isoproterenol
chronic: Mg sulphate
therapy for V-fib
acute tx: cardioversion then amiodarone, lidocaine
chronic: ICD, amiodarone, b-blocker