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49 Cards in this Set
- Front
- Back
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 |
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methyldopa SE? (2)
|
sedation
positive Coombs test |
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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 |
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name two mixed antagonists (i.e. block both a and B blocker)
|
labetolol
carvedilol |
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a1 selective blockers? (3)
name a use of these besides antiHTN |
prazosin
terazosin doxazosin BPH symptoms (i.e. relax urethra to decrease urinary retention) |
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SE of prazosin (3)
|
1st dose orthostatic hypotension
dizziness headache |
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nonselective a blockers (3)
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phentolamine
tolazoline phenoxybenzamine |
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Name two adrenergic blockers and their MOA?
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reserpine
(blocks uptake of NT into synaptic vesicles) guanethidine (inhibits release of stored NE) |
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reserpine SE and drug interaction
|
depression
antidepressants |
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what agents will block the action of guanethidine
|
any reuptake inhibitor
|
|
hexamethonium, trimethaphan, mecamylamine
MOA? |
ganglionic blockers that block the nicotinic receptors
|
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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 |
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Minoxidil SE
|
hypertrichosis (i.e. grows hair)
|
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Nitroprusside MOA?
SE? |
via NO
cyanide toxicity (nausea, psychosis,spasms, tissue hypoxia) (give nitrites to control cyanide and Hb interaction) |
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Name 3 Ca channel blockers
|
verapamil
diltiazem nifedipine (all 3 decrease TPR but the first two can also slow AV conduction) |
|
verapamil SE
|
constipation
|
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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 |
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Antiarrhythmic classes:
name all 4 |
I: Na channel blockers
II: B blockers III: K channel blocker (i.e. prolong AP) IV: Ca channel blockers |
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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 |
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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 |
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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
|
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Name 4 Class III
MOA use |
amiodarone bretylium
sotalol ibutilide block K thus increase repol used when other antiarrhythmics fail |
|
ibutilide SE
|
torsades
|
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sotalol SE
|
torsades and excessive B block
|
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bretylium SE
|
causes new arrhythmias
|
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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 |
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antidote for digoxin (4)
|
K
lidocaine cardiac pacer anti-dig Fab fragments |
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Drugs that increase digoxin toxicity
|
verapamil
quinidine thiazides K wasting diuretics |
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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 |
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Statins MOA
Lipids? SE? |
HMG CoA Reductase inhibitors
same as niacin but major effect on LDL rhabdomyosarcoma |