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82 Cards in this Set
- Front
- Back
4 therapies for essential HTN
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Diuretics
ACE inhibitors AII receptor blockers Ca-channel blockers |
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4 treatments for CHF-induced HTN
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Diurectics
ACEI/ARBs B-blockers (compensated CHF) K-sparing diuretics |
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In a patient with CHF, when are b-blockers
a. indicated b. contraindicated |
a. compensated CHF
b. decompensated CHF |
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5 treatments for Diabetes Mellitus-induced HTN
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ACEI/ARBs
Ca-channel blockers Diuretics B-blockers a-blockers |
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What type of drugs are protective against diabetic nephropathy, used as an antihypertensive in DM
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ACE inhibitors
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Drug to use for
-severe HTN -CHF -First line drug for hypertension in pregnancy (given with methyldopa) what is the drug and what is it often co-administered with? |
hydralazine, often coadministered with a b-blocker to prevent reflex tachycardia
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Hydralazine
MOA |
increases cGMP --> smooth muscle relaxation
vasodilates arterioles > veins --> lowers afterload |
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Adverse effects of what antihypertensive drug
Compensatory tachycardia Fluid retention Nausea Headache Angina Lupus-like syndrome |
Hydralazine
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what are 2 contraindications of hydralazine?
why? |
angina, coronary artery disease
the drug vasodilates --> can cause compensatory tachycardia |
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Nifedipine, verapamil, diltiazem
class MOA How does the effectiveness of each drug differ in vascular vs. cardiac muscle |
Ca-channel blockers
block voltage-gated L-type Ca channels of cardiac and smooth muscle --> reduce contractility Vascular: nifedipine > diltiazem > verapamil Heart: verapamil > diltiazem > nifedipine |
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5 clinical uses of Ca channel blockers
which one do you NOT use nifedipine for |
HTN, angina, arrhythmias, Prinzmetal's, Raynaud's
no nifedipine for arrhythmias |
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Cardiac depression
AV block peripheral edema flushing dizziness constipation adverse effects of which drugs |
Ca channel blockers = nifedipine, diltiazem, verapamil
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2 drgus that are used in angina, pulmonary edema, and as an erection enhancer/aphrodesiac
MOA? |
Nitroglycerin, isosorbide dinitrate
Releases NO in smooth muscle --> increase in cGMP --> smooth muscle relax; dilates veins a lot, reduces preload |
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Reflex tachycardia, hypotension
flushing headache -workers who work with these substances develop tolerance during the week, lose it over the weekend, and come back to work on monday with tachycardia, dizziness, and headache |
Nitroglycerin, isosorbide dinitrate
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A short-acting treatment for malignant HTN that can cause CN toxicity
MOA? |
Nitroprusside
Increases cGMP by directly releasing NO |
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a treatment for malignant HTN that works as a D1 (dopamine) receptor agonist
where does it act? |
Fenoldopam
Relaxes renal vascular smooth muscle |
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Treatment for Malignant HTN that acts by opening K channels, leading to hyperpolarization and relaxation of vascular smooth muscle
what is the side effect |
diazoxide
hyperglycemia (reducees insulin release) |
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What is the fundamental goal of anti-anginal therapy
what are 5 possible targets |
decrease myocardial oxygen consumption
need to reduce 1. end diastolic volume 2. BP 3. HR 4. Contractility 5. Ejection time |
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Nitrates vs. B-blockers
which affects preload? afterload? |
Nitrates = preload (dilates veins)
B-blockers = afterload (dilates arteries) |
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Effect of nitrates on
a. end diastolic volume b. BP c. Contractility d. HR e. ejection time f. Myocardial O2 consumption |
a. down
b. down c. up (reflex) d. up (reflex) e. down f. down |
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What are the effects of b-blockers on
a. end diastolic volume b. bp c. contractility d. hr e. ejection time f. myocardial O2 consumption |
a. up
b. down c. down d. down e. up f. down |
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What are the effects of using b-blockers AND nitrates on
a. end diastolic volume b. bp c. contractility d. hr e. ejection time f. myocardial O2 consumption |
a. no effect or down
b. down c. no effect d. down e. no effect f. way down! |
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Ca channel blockers
a. which one acts more similarly to nitrates b. which one acts more similarly to b-blockers |
a. Nifedipine more like Nitrates
b. verapamil more like b-blockers |
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2 beta blockers contraindicated in angina and why?
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pindolol and acebutolol
partial b-agonists |
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Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin
class? MOA? inhibits what compound? side effects? |
HMG-CoA reductase inhibitors, inhibit cholesterol precursor, mevalonate
Hepatotoxicity (inc. LFTs), rhabdomyolysis |
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Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin
Effect on a. LDL b. HDL c. TGs |
a. way down
b. up c. down |
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Niacin
MOA? Side effects? (3) |
Inhibits lipolysis of adipose tissue, reduces hepatic VLDL secretion into circulation
1. Red, flushed face (dec. by aspirin) 2. hyperglycemia (acanthosis nigricans) 3. hyperuricemia (exacerbates gout) |
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Niacin
Effect on a. LDL b. HDL c. TGs |
a. down
b. up c. down |
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Cholestyramine, colestipol, colesevalam
class? MOA? adverse? (4) |
bile acid resin
prevents intestinal reabsorption of bile acids, so liver must use more cholesterol 1. tastes bad 2. GI discomfort 3. decreases absorption of fat-solube vitamins 4. cholesterol gallstones |
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Cholestyramine, colestipol, colesevelam
Effect on a. LDL b. HDL c. TGs |
a. down
b. slightly up c. slightly up |
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Ezetimibe
class MOA Side effects |
Cholestrol absorption blockers
Prevents cholesterol reabsorption at small intestine brush border rare increase in LFTs |
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gemifibrozil, clofibranate, fenofibrate
class MOA side effects (3) |
"fibrates"
upregulate LPL --> increases TG clearance Myositis, hepatotoxicity (high LFTs), cholesterol gallstones |
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Ezetimibe
Effect on a. LDL b. HDL c. TGs |
a. down
b. none c. none |
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gemifibrozil, clofibranate, fenofibrate
Effect on a. LDL b. HDL c. TGs |
a. down
b. up c. way down |
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6 structures of cardiac excitation contraction coupling (start with Na/K ATPase)
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1. Na/K ATPase sends Na out, K in
2. Na/Ca exchanger sends Ca out, Na in 3. L-type Ca channel (voltage gated) brings Ca in 4. Ca pump in wall of SR (closely coupoled to L-type Ca channel) 5. Ryanodine receptors and Ca-release channels in wall of SR 6. Ca interaction in troponin-tropomyosin system |
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Where does digoxin work
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Na/K ATPase channel in cardiac cell membrane
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Where do Ca channel blockers and b-blockers work
effect |
L-type Ca channels in cell membrane
Decrease cardiac contraction |
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Where does ryanodine work
effect? |
Inhibits ryanodine receptor in SR
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Where do "Ca sensitizers" work in the cardiac excitation-contraction coupling
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increases Ca binding to troponin/tropomysoin
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How do B1 receptors increase contractility
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B1 receptor --> Gs --> ^cAMP --> PKA --> phosphorylates L-type Ca channel and phospholamban (SR Ca-Channel inhibitor) --> increases intracellular Ca during contraction
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Digoxin
a. bioavailability b. % protein bound c. t (1/2) = d. Mechanism of excretion |
a. 75%
b. 20-40% c. 40hrs d. urinary excretion |
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Drug used to treat CHF (increases contractility), atrial fibrillation (decreases conduction at AV node, depresses SA node)
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Digoxin
-cardiac glycoside |
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Drug that is used to increase contractility, treat atrial fibrillation
Adverse: -anti-cholinergic -ECG - high PR, low QT, Twave inversion, arrhythmia, hyperkalemia |
Digoxin
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Digoxin
MOA (2) |
1) inhibits Na/K ATPase (Na builds up inside) --> directly inhibits Na/Ca exchanger (Na can't enter cell so Ca can't leave) --> increases Ca --> positive intropy
2) also stimulates vagus |
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3 contraindications of digoxin
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-renal failure (dec. excretion)
-hypokalemia -quinidine (decreases digoxin clearance, displaces digoxin from tissue-binding sites |
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antidote to digox poinsong
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-slowly normalize K
-lidocaine -cardiac pacer -anti-dig Fab fragments -Mg |
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What is the MOA of drugs that serve as local anesthetics
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Na channel blockers (class I antiarrhythmics)
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class I antiarrythmics
3 effects |
Na channel blockers
1. slows/blocks conduction i(n depolarized cells especially) 2. decreases slope of phase 0 depol. (slows HR) 3. increases threshold for firing abnormal pacemaker cells |
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What does it mean that Na-channel blockers (class I antiarrhythmics) are state dependent
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selectivly depress tissue that is frquently depolarized (ex. fast tachycardia)
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Quinidine
Procainamide DisoPYRAMIDe class? 3 effects? |
Class IA antiarrhythmic (Na channel blocker)
"the Queen Proclaims Disco's Pyramid" (Quinidine, procainamide, disopyramide) 1. increases AP duration 2. increases effective refractory period 3. increases QT interval |
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Drugs to use for
-reentrant and ectopic supraventricular and ventricular tachycardia |
class IA antiarrhythmics (Na channel blockers)
quinidine, procainamide disopyramide |
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Quinidine toxicity
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cinchonism = headache, tinnitus
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prcainamide toxicity
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reversible SLE-like syndrome
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class IA antiarrhythmic toxicity
(2) |
-thrombocytopenia
-torsades de pointes (due to long QT) |
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Lidocaine
Mexiletine Tocainide class of drugs? effect? |
class IB (Na Channel blockers) antiarrhytmics
I'd Buy LIDy's MEXIcan Tacos" (can also include phenytoin) decreases AP duration |
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Drug to use in acute ventricular arrhythmias (esp. post MI) and digitalis-induced arrhythmias
what tissue do these drugs target |
Lidocaine, Mexiletine, Tocainide (class IB)
targets ischemic or depolarized Purkinje and ventricular tissue |
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3 consequences of class IB antiarrythmic toxicity
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1. local anesthetic
2. CNS depressant/stimulant 3. CV depression |
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Flecainide, Encainide, Propafenone
class of drug? effect on action potential? |
Class IC antiarrhythmic (Na channel blocker)
no effect on AP duration Chiptle's Food has Excellent Produce) |
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drug useful in
-V-tachs that progress to Vfib -intractable SVT -last resort for refractory tachyarrhytmias |
Flecainide, Encainide, Propafenone (class IC)
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What are 2 contraindications for class IC antiarrhythmics
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1. structural abnormalities
2. post MI |
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1. proarrhythmic post-MI
2. prolongs refractory period in AV node toxicities of which drug |
class IC antiarrhythmics
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Class I antiarrhytmic
a. best after MI b. contraindicated post-MI |
a. IB = best after MI
b. IC = contra after MI |
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effect of hyperkalemia on class I antiarrhythmics
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increases toxicity for all class I
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Propanolol, esmolol, metoprolol, atenolol, timolol
class? |
beta blockers (class II antiarrhythmics)
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b-blockers
MOA effect on abnormal pacemakers? effect on AV node? 2 manifestations of this |
decrease cAMP, decrease Ca currents
suppresses abnormal pacemakers and AV node --> decreased slope of phase 4, inc. PR interval |
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Drug to use for
-Vtach -SVT -slow ventricular rate during atrial fibrillation and atrial flutter |
beta blockers (class II antiarrhytmics)
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Very short acting beta blocker
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esmolol
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-Impotence
-exacerbation of asthma -bradycardia, AV block, CHF -sedation, sleep alteration -mask hypoglycemia adverse effects of what drugs |
beta blockers
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adverse effect of metoprolol
how do you treat overdose |
dyslipidemia
glucagon |
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Sotalol, ibutilide, bretylium, dofetilide, amiodarone
class of drug |
class III antiarrhythmic (K channel blocker)
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Drug to use when other antiarrhytmics fail -->
-increased AP -increased refractory time -increased QT interval |
class III antiarrhythmic (K channel blocker)
Sotalol, ibutilide, bretylium, dofetilide, amiodarone |
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class III antiarrhytmic (k channel) that has toxicity -->
-torsades de pointes -excessive beta block |
sotalol
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class III antiarrhytmic (k channel) that has toxicity -->
-new arrhytmias -hypotension |
bretylium
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class III antiarrhytmic (k channel) that has toxicity -->
-pulmonary fibrosis -hepatotoxicity -hypothyroidism / hyperthyroidism -corneal deposits -skin deposits (blue/gray) --> photodermatitis -neuro effects -constipation -bradycardia, CHF, heart block |
amiodarone
check PFTs, LFTs, and TFTs with amiodarone |
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what are the effects of amiodarone
|
alters lipid membrane --> has class I, II, III, and IV effects
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Verapamil, Diltiazem
class of drug? |
class IV antiarrhythmic (ca channel block)
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Drug used to prevent nodal arrhythmias, causes
-decreased conduction velocity -increased refractory -increased PR interval |
class IV (Ca channel blockers)
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class of antiarrhytmics that causes
-consipation -flushing -edema -CHF, AV block, sinus node depression |
Ca channel blockers (IV)
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Other antiarrhytmics
-very short acting drug that is the drug of choice in abolishing supraventrcular tachycardias MOA |
adenosine
increases K out of cells --> hyperpolarization, decreased Ca current |
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Other antiarrhytmics
3 negative effects of adenosine how can you block these |
flushing, hypotension, chest pain
blocked by theophylline |
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Other antiarrhytmics
Used to depress ectopic pacemakers in hypokalemia (ex. digoxin toxicity) |
Potassium
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Other antiarrhytmics
Used to treat torsades de pointes and digoxin toxicity |
Mg
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