Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
111 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
5 major side effects for hydrochlorothiazide
|
hypOkalemia, slight hyperlipidemia, hyperuricemia, hypercalcemia, hyperglycemia hyperGLUC
|
HyperGLUC
|
|
|
4 major side effects for loop diruetics
|
potassium wasting, metabolic alkalosis, ototoxicity, hypotension
|
|
|
|
clonidine side effects (2)
|
dry mouth, severe rebound hypertension
|
|
|
|
methyldopa side effects (2)
|
sedation, positive Coombs test
|
|
|
|
hexamethonium side effects (4)
|
severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction
|
|
|
|
reserpine side effects (4)
|
sedation, depression, nasal stuffiness, diarrhea
|
|
|
|
guanethidine side effects (4)
|
orthostatic/exercise hypotension, sexual dysfunction, diarrhea
|
|
|
|
prazosin side effects (3)
|
1st-dose orthostatic hypotensoin, dizziness, headache
|
|
|
|
beta-blocker major side effects (6)
|
asthma, impotence, sleep problems, bradycardia, CHF, AV block
|
|
|
|
hydralazine side effects (4)
|
lupus like syndrome, reflex tachycardia, angina, salt retention
|
|
|
|
minoxidil side effets (5)
|
hair, pericardial effusion, reflex tachycardia, angina, salt retention
|
|
|
|
vasodilator: calcium blocker side effects (3)
|
flushing, constipation, nausea
|
|
|
|
nitroprusside major side efect
|
cyanide toxicity
|
|
|
|
captopril side effects (8)
|
hyperkalemia, cough, angioedema, proteinuria, taste changes, hypotension, pregnancy problems (fetal renal damage), rash
|
|
|
|
ARB side effect (losartan)
|
fetal renal toxicity, hyperkalemia
|
|
|
|
two drugs that cause hyperkalemia
|
losartan and captopril
|
|
|
|
what do you have to do with hydralazine and minoxidil?
|
use beta blockers to treat reflex tachy, diuretic to block salt retention
|
|
|
|
mechanism of hydralazine
|
increase cGMP, smooth muscle relaxation, vasodilation, afterload reduction
|
|
|
|
hydralazine selectively dilates which vessels?
|
arterioles
|
|
|
|
clinical use for hydralazine (2)
|
severe hypertension, CHF, first-line therapy for HTN in pregnancy
|
|
|
|
mechanism for clonidine
|
alpha2 agonist
|
|
|
|
mechanism for methyldopa
|
alpha2 agonist
|
|
|
|
mechanism for prazosin
|
alpha1 blocker
|
|
|
|
mechanism for reserpine
|
blocks re-uptake of NE, E and Serotonin back into pre-synaptic vesicles --> allows degradation by MAO
|
|
|
|
mechanism for guanethidine
|
blocks the release of catecholamines from the presynaptic terminal by inhibiting Mg/ATPase dependent pump
|
|
|
|
what is the mechanism of hexamethonium?
|
it is a neronal ACh receptor antagonist in autonomic ganglia
|
|
|
|
name 3 calcium channel blockers
|
nifedipine, verapamil, diltiazem
|
|
|
|
mechanism of calcium blockers
|
block voltage-dependent calcium channels on cardiac/smooth muscle and reduce muscle contractility
|
|
|
|
rank vascular smooth muscle block by calcium blocker
|
nifedipine>diltiazem>verapamil
|
|
|
|
rank heart smooth muscle block by calcium blocker
|
verapamil>diltiazem>nifedipine
|
|
|
|
use for calcium blockers
|
hypertension, angina, arrhythmia (not nifedipine)
|
|
|
|
calcium blocker toxicity (3)
|
cardiac depression, peripheral edema, flushing,
|
|
|
|
mechanism for nitro drugs
|
vasodilate by releasing nitric oxide, increase cGMP, smooth muscle relaxation, decrease preload
|
|
|
|
rank the preference for dilation of vascular beds in nitro drugs
|
veins >> arterioles
|
|
|
|
clinical use for nitro drugs (4)
|
angina, pulmonary edema, aphrodisiac, erection enhancer
|
|
|
|
name side effects for nitro (4)
|
tachycardia, hypotension, headache, monday disease
|
|
|
|
define monday disease
|
build tolerance to nitro during occupational exposure, resensitize on weekend and get tachy and dizziness
|
|
|
|
goal of antianginal therapy
|
reduce myocardial oxygen consumption
|
|
|
|
name 5 determinants of antianginal therapy
|
end diastolic volume, blood presure, heart rate, contractility, and ejection time
|
|
|
|
how do nitrates effect end diastolic volume, blood pressure, contractility, heart rate, and ejection time
|
decrease EDV, decrease BP, increase contractility (reflex), increase HR (reflex), decrease Ejection time
|
|
|
|
how does beta-blocker affect end-diastolic volume, blood pressure, contractility, heart rate, ejection time
|
increase EDV, decrease BP, decrease contractility, decrease HR, increase ejection time
|
|
|
|
name 3 factors that combo beta-blockers + nitrates will decrease
|
blood pressure, heart rate, and overall myocardial oxygen consumption
|
|
|
|
for calcium channel blockers, what drug is similar to nitro
|
nifedipine
|
|
|
|
for calcium channel blockers, what durg is similar to beta-blockers
|
verapamil
|
|
|
|
define bioavailability, protein bound percentage, where excreted, and 1/2 life for digoxin
|
75% availability, 20-40% bound, excreted in kidney, 40 hours t(1/2)
|
|
|
|
mechanism for digoxin
|
block Na/K ATPase, increase Na, slow Na/Ca antiport, increases Ca in ECM, positive inotrope
|
|
|
|
how does digoxin affect ECG readings
|
vagal effects increase PR, decrease QT, T wave inversion on ECG, and scooping of ST segment
|
|
|
|
name 2 uses for digoxin
|
CHF (increase contractility) and A-Fib (decrease conduction at AV node)
|
|
|
|
5 major general digoxin side efects
|
nausea, vomiting, diarrhea, blurry yellow vision, arrhythmia
|
|
|
|
name 3 contraindications with digoxin
|
renal failure, quinidine (will displace dig on protein, potentiate effect), hypokalemia (potentiate effect)
|
|
|
|
what is the antidote for digoxin
|
slowly normalize K, lidocaine, cardiac pacer, anti-dig Fab fragments
|
|
|
|
describe function that all class I antiarrhythmics have
|
decrease slope of phase 4 depolarization by blocking Na channels
|
|
|
|
define state dependency and state what drugs are state dependent
|
class I antiarryhtmics. selectively depress tissue that is depolarized
|
|
|
|
name 4 class Ia antiarrhythmics
|
Queen Amy Proclaims Diso's pyramid: quinidine, amiodarone, procainamide, disopyramide
|
|
|
|
name 3 mechanisms of class Ia antiarrhythmics
|
increase AP duration, increase ERP, increase QT interval
|
|
|
|
what do you use class Ia antiarrhythmics for?
|
atrial and ventricular arrhythmias
|
|
|
|
quinidine toxicities
|
cinchonism: headache, tinnitisum, thrombocytopenia plus torsades
|
|
|
|
procainamide toxicity
|
reversible lupus like side effect
|
|
|
|
name 3 class IB antiarrhythmics
|
lidocaine, mexiletine, tocainide
|
|
|
|
mechanism for class IB
|
decrease AP duration by blocking Na channel
|
|
|
|
where does class IB affect?
|
affect ischemic or depolarized purkinje and ventricular tissue.
|
|
|
|
what is class IB useful for?
|
acute ventricular arrhythmias (post-MI) and digitalis induced arrhythmia
|
|
|
|
name 4 side effects of class IB
|
local anesthetic, cns stimulation, cns depression, cardiovascular depression
|
|
|
|
name 3 class IC antiarrhythmics
|
flecainide, encainide, propafenone
|
|
|
|
name mechanism of class IC
|
no effect on AP
|
|
|
|
what is class IC sueful for?
|
v-tach that progress to V fib and also for SVT. usuaully only last resort for refractory tachyarrhythmias
|
|
|
|
class IC toxicities
|
proarrhythmitic, especially post-MI (contraindiciated)
|
|
|
|
name 5 class II antiarrhythmics
|
propanolol, esmolol, metoprolol, atenolol, timolol
|
|
|
|
mechanism of class II antiarrhythmics
|
Beta-blockers; decrease cAMP, decrease Ca currents, decrease slope phase 4, increase PR interval at AV node
|
|
|
|
what is a short acting class II
|
esmolol
|
|
|
|
name 5 side effects of class II drugs
|
mask hypoglycema, impotence, asthma, CV effects (bradycardia, av block, chf). sleep alterations
|
|
|
|
name 4 class III antiarrhythmics
|
sotalol, ibutilide, bretylium, amiodarone
|
|
|
|
mehcanism of class III
|
block K channels; increase AP duration, increase ERP, increase QT, used when others fail
|
|
|
|
sotalol toxicity
|
torsades, excessive beta-block
|
|
|
|
ibutilide toxicity
|
torsades
|
|
|
|
bretylium toxicity
|
new arrhythmias, hypotension
|
|
|
|
amiodorone toxicity
|
hypothyrodism/hyperthyrodism, pulmonary fibrosis, hepatic toxicity, corneal deposits, skin deposits (photodermatitis), neurologic defects, constipation, bradycardia, heart block, chf
|
|
|
|
what 3 tests to do before using amiodarone?
|
PFT, LFT, TFT
|
|
|
|
name 2 class IV antiarrhytmics
|
verapamil, diltiazem
|
|
|
|
mechanism for class IV antiarrhythmics
|
blocks Ca channels; affect AV nodal cells, decrease conduction velocity, incrase ERP, increase PR.
|
|
|
|
what are class IV antiarrhythmics used for
|
prevent nodal arryhtmias (SVT)
|
|
|
|
what are 4 general side effects for class IV
|
constipation, flushing, edema, cv (chf, av block, sinus node depression)
|
|
|
|
bepridil toxicity
|
torsades
|
|
|
|
adenosine function
|
hyperpolarizes cells by facilitating K movement out of cells. drug of choice in diagnosing/abolishing AV nodal arryhtmias
|
|
|
|
potassium function
|
depress ectopic pacemaker, esp in dig toxicity
|
|
|
|
magnesium function
|
torsades and dig toxicity use
|
|
|
|
what are the adverse effects of nifedipine and verapamil? (5)
|
dizziness, flushing, nausea (verapamil also has constipation and AV block)
|
|
|
|
adverse effects of Diazoxide?
|
hypoglycemia - reduces insulin release
|
|
|
|
what is the first-line treatment of hypertension in pregnancy?
|
hydralazine with methyldopa
|
|
|
|
what is the mechanism of minoxidil?
|
K channel opener --> hyperpolarizes and relaxes vascular smooth muscle
|
|
|
|
what is the toxicity of minoxidil?
|
hypertrichosis, pericardial effusion
|
|
|
|
what is the treatment for malignant hypertension?
|
nitroprusside, fenoldopam and diazoxide
|
|
|
|
what is the mechanism of action of fenoldopam?
|
Dopoamine D1 receptor agonist --> relaxes renal vascular smooth muscle
|
|
|
|
what is the mechanism of diazoxide?
|
K channel opener --> hyperpolarizes and relaxes vascular smooth muscle
|
|
|
|
what are the HMG-CoA reductase inhibitors?
|
lovastatin, pravastatin, simvastatin, atorvastatin
|
|
|
|
What effects do the statins have on LDL, HDL and TGs?
|
greatly decreases LDL, increases HDL and decreases TGs
|
|
|
|
what is the mechanism of action of the Statins?
|
inhibit cholesterol precursor, mevalonate
|
|
|
|
side effects of statins?
|
reversible increase in LFTs and myositis
|
|
|
|
What effect does Niacin have on LDL, HDL and TGs?
|
decreases LDL, increases HDL, lesser decrease in TGs
|
|
|
|
what is the mechanism of action of niacin?
|
inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation
|
|
|
|
what effect do the Bile acid resins have on LDL, HDL, and TGs?
|
decrease LDL, slight increase in HDL, slight increase in TGs
|
|
|
|
what are the bile acid resins?
|
cholestyramine, colestipol
|
|
|
|
what is the mechanism of action of cholestyramine and colestipol?
|
prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more
|
|
|
|
what are side effects of cholestyramine and colestipol?
|
bad taste, causes GI discomfort, decreased absorption of fat-soluble vitamins
|
|
|
|
What effect does ezetimibe have on LDL, HDL and TGs?
|
decreases LDL; no effect on others
|
|
|
|
what is the mechanism of action of ezetimibe?
|
prevents cholesterol reabsorption at small intestine brush border
|
|
|
|
What are the Fibrates?
|
gemfibrozil, clofibrate, bezafibrate, fenofibrate
|
|
|
|
what effect do the fibrates have on LDL, HDL and TGs?
|
mainly decrease TGs, lesser decrease LDL and increase HDL
|
|
|
|
what is the mechanism of action of the fibrates?
|
upregulate LPL --> increase TG clearance
|
|
|
|
what are the side effects of fibrates?
|
myositis, and increase in LFTs
|
|
|
|
what Beta blockers are contraindicated in angina and why?
|
labetalol, pindolol and acebutolol, due to partial agonist effects
|
|
