Cardiovascular Pharm

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clonidine and methyldopa class? MOA? which one works both peripherally and centrally?: antihypertensive

a2 agonist thus decreases symp outflow

clonidine
clonidine SE (3): dry mouth
sedation
severe rebound hypertension after witdrawal
methyldopa SE? (2): sedation
positive Coombs test
clonidine and methyldopa drug interaction: antidepressant

(they cancel each other)
when are B1 selective blockers used: in pts with severe pulmonary disease b/c nonselective B blockers could cause fatal bronchoconstriction
B1 selective blockers (5) HINT: A BEAM: acebutolol
betaxolol
esmolol
atenolol
metoprolol
name two mixed antagonists (i.e. block both a and B blocker): labetolol
carvedilol
a1 selective blockers? (3) name a use of these besides antiHTN: prazosin
terazosin
doxazosin

BPH symptoms (i.e. relax urethra to decrease urinary retention)
SE of prazosin (3): 1st dose orthostatic hypotension
dizziness
headache
nonselective a blockers (3): phentolamine
tolazoline
phenoxybenzamine
Name two adrenergic blockers and their MOA?: reserpine
(blocks uptake of NT into synaptic vesicles)

guanethidine
(inhibits release of stored NE)
reserpine SE and drug interaction: depression

antidepressants
what agents will block the action of guanethidine: any reuptake inhibitor
hexamethonium, trimethaphan, mecamylamine MOA?: ganglionic blockers that block the nicotinic receptors
Name 3 smooth muscle vasodilators used to treat HTN that are not ca channel blockers: hydralazine
minoxidil
Nitroprusside
hydralazine: usually taken with (2) SE: B blocker to prevent reflex tach
diuretic to prevent salt/water retension

lupus like syndrome
(note procainamide has the same SE)
Hydralazine/nitrate used for?: CHF

this is an alternative to ACE inhibitors
Minoxidil SE: hypertrichosis (i.e. grows hair)
Nitroprusside MOA? SE?: via NO

cyanide toxicity
(nausea, psychosis,spasms, tissue hypoxia)

(give nitrites to control cyanide and Hb interaction)
Name 3 Ca channel blockers: verapamil
diltiazem
nifedipine
(all 3 decrease TPR but the first two can also slow AV conduction)
verapamil SE: constipation
Name two ACE inhibitors name one contraindication: Captopril
enalapril

renal artery stenosis
Captopril SE Remember mnemonic: Cough (very imp- Losartan does not)
Angioedema
Proteinuria
Taste changes
hypOtenstion
Preg problems (fetal renal problems)
Rash
Increased renin
Lowers AII
Antiarrhythmic classes: name all 4: I: Na channel blockers
II: B blockers
III: K channel blocker (i.e. prolong AP)
IV: Ca channel blockers
Name 4 Class 1A (mnemonic) agents MOA? arrhythmias?: Quinidine Amiodarone
Procainamide Disopyramide
(Queen Amy Proclaims Diso's pyramid)

slows phase 0 depolarization
(increases AP duration)

atrial and ventricular
procainamide SE: reversible SLE-like syndrome
(remember increased anti-histone Ab)
quinidine SE (3): cinchonism
(headache and tinnitus)
thrombocytopenia
torsades de pointes
Class IB agents (3) MOA?: Lidocaine mexiletine
tocainamide

shortens phase 3 repolarization
Class IB best use of these agents (2): hypoxic - post-MI

depolarized - digitalis toxicity
Class IC (name 3) MOA? main use? SE?: felcainide encainide
propafenone

severe phase O depression

fatal ventricular arrhythmias

proarrhythmic
Class II agents (5) MOA: propanolol esmolol
metoprolol atenolol
timolol

inhibit AV node conduction
Class II SE of importance: they may mask signs hypoglycemia
Name 4 Class III MOA use: amiodarone bretylium
sotalol ibutilide

block K thus increase repol

used when other antiarrhythmics fail
ibutilide SE: torsades
sotalol SE: torsades and excessive B block
bretylium SE: causes new arrhythmias
amiodarone SE (4) remember mnemonic: pulmonary fibrosis
hepatotoxicity
hypo/hyperthyroidism
grey man syndrome (smurf skin)

(always check the PFTs, LFTs, TFTs)
Class 4 agents (2) MOA what agent is not used b/c it causes torsades: Verapamil Diltiazem

slows conduction through AV node

bepridil
Nmae two other agents imp in digoxin toxicity: K
Mg
MOA of cardiac glycosides (digoxin) use (2): inhibit Na-K ATPase, increses intracellular Na, slows Na-Ca exchanger, thus increases intracellular ca

CHF
atrial fibrillation
SE of cardiac glycosides (4) what increases these se (3): nausea vomiting blue-yellow vision (van Gogh)
life threatening arrhythmias

renal failure
hypokalemia
quinidine
antidote for digoxin (4): K
lidocaine
cardiac pacer
anti-dig Fab fragments
Drugs that increase digoxin toxicity: verapamil
quinidine
thiazides
K wasting diuretics
Name 3 classes of drugs used to treat angina: organic nitrates
Ca channel blockers
B blockers
Nitroglycerin MOA SE: increses NO

Monday disease (headache, tachycardia, dizziness)
Niacin MOA Lipids? SE?: decrease VLDL synthesis

decreases LDL, TG
increases HDL (the best at this)

red flushed face
Gemfibrozil and Clofibrate MOA (fibric acid derivatives) Lipids? SE?: inhibit lipoprotein lipase

same as niacin but major decrease in TGs

LFTs and myositis
Cholestyramine and colestipol MOA Lipids? SE?: bind bile acids

decreases LDL

bad taste and GI discomfort
Statins MOA Lipids? SE?: HMG CoA Reductase inhibitors

same as niacin but major effect on LDL

rhabdomyosarcoma

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