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ACEI MOA
inhibit ACE, less angiotensin II produced (less vasoconstriction), less aldosterone secretion (less reabsorption), more bradykinin (vasodilation).
-
ACEI kinetics (DOA)
intermediate (12-24 hr) duration of action (except captopril).
-
ACEI indication
HTN, CHF, MI, diabetic neuropathy
-
ACEI contraindications
absolute hx of angioedema, pregnancy (cat D)
-
ACEI interactions
lithium (increased toxicity), azathioprine (increased toxicity). caution with NSAIDS in pts with poor kidney function (NSAIDS constrict, AA, ___ constrict EA).
-
ACEI SE
cough (>women), angioedema (>blacks, women, smokers), hyperkalemia, proteinuria, dysguesia
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lisinopril brand
Prinivil, Zestril
-
lisinopril class/dosing
ACEI, 10-80mg PO qd (>40 rarely effective)
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benazepril brand
Lotensin
-
benazepril class/dosing
ACEI, 10-80mg PO qd (may give BID)
-
-
enalapril class/dosing
ACEI, 5-40mg PO qd (lower with diuretic)
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captopril class/info
ACEI. dosed BID/TID on empty stomach, is not a prodrug (hepatic impairment). Additional SE rash.
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ACEI/ARB monitoring
monitor K and SrCr as they begin or increase dose
-
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ARB MOA
blocks binding of angiotensin II to AT1 receptor (less vasoconstriction)
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ARB kinetics (DOA)
intermediate (12-24 hr) duration of action
-
ARB indications
HTN, CHF, pts who require an ACEI but cannot tolerate cough
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ARB contraindications
absolute pregnancy (cat D). caution with volume depletion.
-
ARB SE
dizziness, hypotension, hyperkalemia, renal failure. [cough/angioedema less frequent]
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-
valsartan class/dosing
ARB, 80-320mg PO qd (lower with diuretic)
-
-
olmesartan class/dosing
ARB, 20-40mg PO qd
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Direct Renin Inhibitor drugs
aliskiren (Tekturna)
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DRI MOA
inhibit renin, less angiotensin I produced, less angiotensin II produced (less vasoconstriction), less aldosterone secretion (less reabsorption), more bradykinin (vasodilation).
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DRI kinetics (T1/2)
long (40 hr) half life
-
-
DRI contraindications
absolute pregnancy (cat D). caution with volume depletion, hyponatremia.
-
DRI SE
diarrhea, GERD, hyperkalemia.
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DRI misc
renin concentrations will likely increase during administration (ATII negative feedback loop)
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Sodium Channel Blockers class
class 1a - procainamide, disopyramide, quinidine. Class 1b - lidocaine, mexitetene. Class 1c - propafenone, flecainide.
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SCB - Class 1a
moderate Na+ channel blockers, increased ERP
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SCB - Class 1b
weak Na+ channel blockers, decreased ERB
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SCB - Class 1c
strong Na+ channel blockers, no ERB effect
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SCB MOA
block sodium channels, decreasing ion mvmt during phase 0. results in slower conduction, wider QRS. Phase 3 (and therefore QT interval) can be longer or shorter. also helps prevent after-depolarizations.
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SCB indications
cardiac arrhythmia
-
SCB contraindications
pt does not have a life-threatening arrhythmia. lots of drug interactions (leading to QT prolongation, arrhythmias, other toxicities).
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SCB SE
cardiac arrhythmias, including torsades de pointes
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procainamide class/SE
SCB class 1a. SE drug-induced lupis.
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disopyramide class/SE
SCB class 1a. SE anticholinergic.
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quinidine class/SE
SCB class 1a. SE GI, bitter taste, cinchonism (vertigo, headache, tinnitus, psychosis)
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mexiletine class/info
SCB class 1b. orally active form of lidocaine (lidocaine is IV due to short half life).
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propafenone class
SCB class 1c
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flecainide class
SCB class 1c
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Beta Blockers class/drugs
class 2, "lols"
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BB MOA
competitively antagonize the action of chatecholamines at beta receptors (beta-1 stimulation at SA/AV nodes leads to an increase in sodium currents/chronotropy/ionotropy). this reduces HR, contractility, and prevents after-depolarizations. can also block any compensatory increases in sympathetic activity.
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BB cardioselective (beta-1 only)
atenolol, metoprolol selectivity
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BB non-cardioselective (beta-1 and beta-2)
propanalol selectivity
-
BB mixed alpha/beta
labetalol, carvedilol selectivity
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BB least lipophilic, most water soluble, least CNS side effects
atenolol, (labetalol) distribution
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BB most lipophilic, easily cross membranes, most CNS side effects (anhedonia, but could also help calm hyperenergetic brain)
propranolol, (metoprolol) distribution
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BB indications
HTN, CHF, angina, cardiovascular event protection, post-MI
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BB contraindications
absolute non-selective + asthma, 2nd degree heart block, bradycardia, acute heart failure. many cautions/interactions.
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BB SE
hypotension, Raynaud's, impotence, fatigue, hypoglycemia, insomnia, depression. **d/c taper (rebound HTN)
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atenolol class/dosing
BB, 50-200mg PO qd
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metoprolol tartrate brand
Lopressor
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metoprolol tartrate (IR) class/dosing
BB, 50-200mg PO BID
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metoprolol succinate brand
Toprol XL
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metoprolol succinate (XL) class/dosing
BB, 25-400mg PO qd
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carvedilol (short-acting) class/dosing
BB, 6.25-25mg PO BID
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carvedilol ER (Coreg CR) class/dosing
BB, 20-80mg PO qd
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sotalol class/info
BB with class 2 and class 3 antiarrhythmic properties. start in hospital due to potential for serious arrhythmias/interactions/issues. CrCl prior to start.
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Potassium Channel Blockers class/drugs
class 3, amiodarone (also shows class 4 properties), dronedarone, ibutilide, dofetilide, azimilide
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PCB MOA
blocking K channels in phase 3 of the action potential slows the efflux of K, increasing the refractory period.
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PCB EKG
prolonged QT interval
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PCB interactions
"darones" are inhibitors of CYP3A4/P-glycoprotein, so numerous interactions.
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amiodarone kinetics
very long half-life (58 days), variable and slow elimination from plasma/tissues (so proarrhythmic effect, potential for interactions is prolonged). requires a loading dose.
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dronedarone kinetics
shorter half-life than other "darone" (loading dose not needed). Is also less lipophilic, and lacks an iodine group.
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PCB indications
treat/prevent a-fib/flutter, VF/VT
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PCB contraindications
absolute with 2/3 degree heart block (suppresses conduction/escape beats). caution with amiodarone in pts with hypotension.
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PCB SE
fatal pulmonary toxicity (report SOB/cough), eye issues, hepatotoxicity, blue-grey skin, thyroid issues. "beta blocker blues"
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Calcium Channel Blockers class/drugs
class 4 = verapamil, diltiazem. also in this category are the "pines"(dihydropyridines)
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CCB MOA
binds to various sites on L-type calcium channels (V, D, or N) blocking Ca influx. non-DHPs are cardiac depressants (chronotropy/ionotropy) with some vasodilator activity. DHPs are primarily vasodilators, which can lead to a potential reflex increased chronotropy/ionotropy.
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amlodipine kinetics (T1/2/info)
much longer (40 hr) half life than nifedipine (4 hr), helping to mitigate reflex tachycardia.
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felodipine kinetics (info)
has the highest affinity of the dipines, therefore causes the most dilation but also the most side effects
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CCB indications
non-DHPs angina, tachycardia, HTN (diltiazem only). DHPs HTN, vasospasm (eg. Prinzmetal's).
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CCB contraindications
non-DHPs end stage CHF. DHPs conditions where tachycardia might be undesirable.
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CCB interactions
metabolized by CYP3A4, so numerous potential interactions. grapefruit is also an issue (except with amlodipine).
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CCB SE
verapamil constipation (blocks Ca channels in bowel), diltiazem less so. DHPs HA, hypotension, peripheral edema.
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verapamil class/dosing
CCB, 80-120mg PO TID
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diltiazem class/dosing
CCB, 120-480mg PO qd
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amlodipine class/dosing
CCB, 5-10mg PO qd
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cleviprex info
IV CCB, avoid in pts allergic to soy/eggs
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anticholinergic drugs
atropine (cardiac), glycopyrrolate (surgical), scopolamine (surgical, motion sickness)
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anticholinergic MOA
block activity of ACh on parasympathetic muscaric receptors. in heart, SA/AV nodes increase pacemaker rate, sometimes increase conduction through blocks
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anticholinergic indications
SB with hypotension, 2 degree heart block with bradycardia (can be tried in 3 degree).
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anticholinergic ACLS
symptomatic bradycardia, slow PEA, asystole
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anticholinergic contraindications
caution in situations where tachycardia can be dangerous
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anticholinergic side effects
tachycardia, hyperthermia, delirium, other decreased parasympathetic issues
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atropine class/dosing
anticholinergic, 0.5mg IV q5min max 3mg
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atropine OD
quartet: red, hot, dry, confused
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adenosine MOA
stimulates A1 receptors in AV note, decreasing K efflux, Ca influx, and Na influx. Hyperpolarization renders the cell refractory (essentially causing a 3 degree heart block for a few seconds).
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adenosine outcomes
1) reentry circuits terminated and NSR resumes, 2) QRS eliminated so atrial tachycardias can be more easily diagnosed
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adenosine kinetics (T1/2)
half life of 10 seconds, so double-push.
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adenosine interactions
caffiene acts on the same receptors and can block its action.
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adenosine indications
SVT
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adenosine SE
short-lived angina/extreme discomfort (endogenous adenosine is typically released with ischemia: decreased o2 --> decreased ADP change to ATP --> increased adenosine levels)
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adenosine dosing
6-12 mg IV q1-2min, max 3 doses. pts taking carbamazepine, dipyridamole, heart transplant, central line initial dose is 3mg.
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Cardiac Glycoside drugs
digoxin, digitalis (foxglove plant, longer T1/2)
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digoxin MOA1
decreased Na/K pump action. Increased intracellular Na decreases electrochemical gradient for Na-Ca exchanger, less Ca exits cell and intracellular levels rise. Net result is increased contractility. Indirectly decreases need for sympathetic compensation.
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digoxin MOA2
direct increase in parasympathetic tone via baroreceptors/brainstem vagal nuclei. net result is a decrease in HR (also useful in pts with a-fib due to increased PNS tone at AV node)
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digoxin kinetics (T1/2)
half-life is 30 hrs
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digoxin toxicity
therapeutic index 0.8-2ng/mL, 2.6 probable toxicity, 3 guaranteed toxicity (higher in children). Draw levels away from dose administration. 20% will experience toxicity, especially those with hypokalemia/electrolyte imbalances.
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digoxin indications
CHF, a-fib
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digoxin contraindications
absolute in pts with VF. relative in pt with ventricular arrhythmias/PVCs (exacerbate them).
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digoxin interactions
diuretics (spironolactone), antiarrhythmics (quinidine), calcium antagonists (verapamil), statins (atorvastatin) increase levels
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digoxin SE
GI (N/V/D, anorexia), CNS (confusion, dizziness, agitation), CV (arrhythmias/blocks), visual (orange-tinted vision, visual disturbances)
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digoxin EKG
long PR interval, AV block, scooping of ST-segment, upslope into R wave
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statin MOA
inhibit HMG-CoA reductase, mediator in the first step in the biosynthesis of cholesterol. reduced synthesis increases number of LDL receptors (via SREBPs), increasing catabolic rate of LDL and liver extraction of LDL precursors.
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statin effects
major LDL. minor HDL/trigs.
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statin kinetics (prodrugs)
lovastatin/simvastatin/atorvastatin/rosuvastatin have active metabolites
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statin interactions
cyclosporine, macrolides, anti-fungals. pravastatin is the only one not metabolized by CYP450 enzymes (reduced risk of interactions)
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statin contraindications
absolute pregnancy (cat X), liver disease
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statin SE
generally well tolerated. myalgia 10%. rare include myositis/rhabdomyolysis, hepatotoxicity. possibly increase glucose.
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simvastatin dose
10-80mg PO qd
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atorvastatin brand
Lipitor
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atorvastatin dose
10-80mg PO qd
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pravastatin brand
Pravachol
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pravastatin dose
10-80mg PO qd
-
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lovastatin dose
20-80mg PO qd
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rosuvastatin brand
Crestor
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rosuvastatin dose
5-40mg PO qd
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simbastatin/ezetimibe brand
Vytorin
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simbastatin/ezetimibe (Vytorin) dose
20-40mg/10mg PO qd
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statin monitoring
monitor liver enzymes, blood sugar
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fibrates drugs
gemfibrozil, fenofibrate, clofibrate
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fibrates MOA
activate transcription factors (PPARs). reduces production of VLDL and speeds up removal of triglycerides, increases HDL levels (apo A1/A2 expression increased).
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fibrates effect
major HDL/trigs. minor LDL.
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fibrates interactions
gemfibrozil inhibits glucoronidation of statins (increased liklihood of muscle breakdown/pain with coadministration). Interact with warfarin (potentiate anticoag - monitor INR).
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fibrates SE
rash, gallstones, liver enzyme elevation. rare pancreatitis, reversable decreased renal function, myositis/myopathy/rhabdomyositis.
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fenofibrate brand
Fenoglide
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fenofibrate class/dose
fibrate, 50-200mg PO qd
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gemfibrozil class/dose
fibrate, 600-1200mg PO qd
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Bile Acid Sequestrants drugs
cholestyramine, colestipol, colesevelam
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BAS MOA
bile acids facilitate fat digestion/absorption, and are normally enterohepatically recycled. sequestrants are large and carry a positive charge, so they bind negatively charged bile acids and are excreeted together. the body needs to create more bile acids (which takes cholesterol) and less fat is absorbed.
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BAS effect
major LDL. no HDL. hurt trigs.
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BAS kinetics
never leave GI tract, so are OK to use in disease/pregnancy. reduce absorption of fat-soluble vitamins (A,D,E,K)
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BAS contraindications
hypertriglyceridemia (interruption of enterohepatic recycling increases enzyme activity of phospatidic acid phosphatase, which is involved in triglyceride formation)
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BAS interactions
bind to negatively charged molecules, so interfere with absorption of thiazides, furosimide, propranolol, digoxin, warfarin, OCPs (can be overcome simply by seperating administration)
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BAS SE
GI. rare hyperchloremic acidosis (bile acid resins are chloride salts, can result in increased chloride/decreased bicarb levels)
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cholestyramine brand
Questran
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cholestyramine class/dose
BAS, 8g powder dissolved in liquid PO TID
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BAS combo
most often used in combo with statins because their use alone results in upregulation of HMG-CoA reductase
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Nicotinic Acid (a B-complex vitamin)
Niacin
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Niacin MOA
unknown. does reduce liver synthesis of VLDL.
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Niacin effect
major HDL/trigs. moderate LDL.
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Niacin contraindications
arterial bleeding (can cause slight decrease in platelets/increased prothrombin times), hepatic issues (increased LFTs dose related)
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Niacin effects
skin flushing, itching, dryness, rash (offset with ASA/ibuprofin 30 min prior). hyperglycemia, hyperuricemia, upper GI distress (offset by taking with food).
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Niacin class/dosing
nicotinic acid, 0.5-2g PO TID
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Cholesterol Absorption Inhibitors drugs
ezetimibe
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CAI MOA
selectively inhibit absorption of cholesterol by small intestine (NPC1L1 transporter) by up to 50%
-
CAI effect
moderate LDL. no HDL/trigs.
-
-
ezetimibe class/dosing
CAI, 10mg PO qd
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Essential Fatty Acid drugs
omega-3 fatty acids (eicosapentaenoic acid/docosahexaenoic acid; EPA/DHA)
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EFA MOA
thought to inhibit triglyceride synthesis in the liver.
-
EFA effect
Major trigs. No HDL, hurt LDL.
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EFA contraindication
caution with anticoagulation (can inhibit platelet aggregation)
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omega-3 fatty acid brand
Lovaza
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Lovaza class/dosing
EFA, (EPA 465mg/DHA 375mg) 4g PO qd (can divide dose)
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Ionotrops/Pressors drugs
dobutamine; norepinephrine, phenylephrine; epinephrine, dopamine
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I/P MOA
act on adrinergic receptors. alpha-1 receptors increase IP3 which increases vascular tone (vasoconstriction). beta-1 receptors activate G proteins that increase cAMP levels, resulting in increased myocardial contractile force.
-
beta1-selective ionotropes
dobutamine (also a vasodilator)
-
alpha1-selective pressors
norepinephrine, phenylephrine (pure)
-
combo pressors and ionotropes (alpha and beta)
epinephrine, dopamine
-
I/P kinetics (T1/2)
very short half lives, so IV infusions (or boluses in ACLS)
-
I/P indications
hypotension, shock, acute CHF (dobutamine/dopamine)
-
epinephrine dosing
1mg IV q3-5min
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PDE-3 Inhibitors drugs
amrinone/inamrinone, milrinone
-
PDE-3 MOA
PDE breaks down cAMP/cGMP. Inhibitors increase cAMP/cGMP, causing increased intracellular Ca. Cardiac tissue = stronger contraction, smooth muscle = decreased afterload due to smooth muscle relaxation. Also theoretically improves diastolic functioning (decreased end diastolic pressure).
-
PDE-3 kinetics (T1/2)
long half life even though administered IV, can make it tricky to find correct dose (often levels get too high) -- Swang Ganz monitoring of CO can help titrate to correct dose
-
PDE-3 containdications
CHF (increased risk of mortality)
-
PDE-3 SE
hypotension secondary to vasodilation (can last for hours due to long half life), thrombocytopenia (much less often with milrinone).
-
PDE-3 vs. beta agonists
PDE-3 not direct positive chronotropes (better for tachy pts/CAD). In CHF b-receptors are frequently down-regulated to to high endogenous chatecholamine compensatory mechanisms, so PDE-3 inhibitors are clinically much stronger.
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nitrates drugs
nitroglycerin, isosorbide dinitrate (ISDN), isosorbide-5-mononitrate
-
nitrates MOA
release NO (EDRF), inducing vasodilation primarily on venous side (reduces venous return, preload, end diastolic pressure). Lower ventricle wall tension reduces stress/o2 demand; lower intraventricular pressure means higher coronary perfusion grandient and increased o2 supply. minor effects include coronary vasodilation, arterial vasodilation (decreased SVR) decreasing afterload.
-
nitrates groups
those that release NO spontaneously (sodium nitroprusside), those that require an enzymatic process (S-nitrosothiol; organic nitrates)
-
nitrates kinetics (bioavailability)
oral availability is low (10%) due to reductase enzyme in liver. sublingual route avoids this first pass effect, as does patch/ointment.
-
nitrates kinetics (DOA)
ISDN/IS5M have a longer duration of action, thus are useful for long-term prophylaxis.
-
nitrates misc
nitrate tolerance can develop particularly with long-acting agents, therefore they need a nitrate free period to remain effective (typically 12 on, 12 off)
-
nitrates indications
angina, acute coronary syndromes, CHF, hypertensive emergencies
-
nitrates contrandications
absolute concurrent use with PDE-5 inhibitors, increased ICP, severe anemia
-
nitrates SE
HA, flushing, hypotension, dizziness
-
isosorbide mononitrate dosing
20mg PO BID
-
nitrates/beta blockers combo
prevents reflex tachlycardia, nitrates prevent coronary vasospasm of b-blockers, nitrates prevent preload increases resulting from the negative ionotropic effects produced by b-blockers
-
vasodilators drugs
sodium nitroprusside, Hydralazine
-
vasodilators MOA
dilation of arterioles. SNP (prodrug) also slighly venodilates, Hydralazine is artery selective. exact mechanism is unknown.
-
vasodilator kinetics (T1/2)
very short half life, only available IV, rapid onset
-
vasodilator indications
severe hypertensive emergencies, severe heart failure
-
vasodilator contraindications
caution where reflex tachycardia/increased contractility would be harmful (CAD,AS,MS)
-
vasodilator SE
HA, flushing, tachycardia, lupus-like syndrome (~10%)
-
Natriuretic Peptides drugs
Nesiritide (recombinant form of BNP)
-
NP MOA
endogenous serve as a counter-regulatory system for RAAS, causing vasodilation, natriuresis, and inhibition of renin and aldosterone. This reduces preload/afterload.
-
NP kinetics (T1/2)
short half life (initial bolus followed by continuous infusion)
-
NP indications
advanced decompensated acute heart failure
-
NP SE
prolonged hypotension
-
alpha-2 Agonists drugs
clonidine, guanabenz, guanfacine, methyldopa (prodrug)
-
alpha-2 agonsits MOA
agonize central alpha-2 receptors (inhibits adenylyl cyclase activity), producing a decrease in peripheral resistance, HR, BP.
-
alpha-2 agonists indications
HTN (not first line)
-
alpha-2 agonists SE
sedation, dry mucus membranes, bradycardia, hypotension, constipation, nausea
-
alpha-1 antagonists groups/drugs
selective = prazosin, terazosin, doxazosin. non-selective (used in mgmt of pts w/ pheochromocytoma) = phentolamine, phenoxybenzamine
-
alpha-1 antagonists MOA
antagonize peripheral alpha-1 adrinergic receptors (stimulate phospholipase C activity), causing vasodilation
-
alpha-1 antagonists indications
HTN (not first line), benign prostatic hypertrophy
-
alpha-1 antagonists SE
orthostatic hypotension, HA, somnolence, palpitations (reflex tachycarda), nasal congestion, dizziness
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