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63 Cards in this Set

  • Front
  • Back
2 mechs by which ACEi's works
1. blocks production of AII (and therefore aldosterone
2. blocks breakdown of bradykinin
Indications for ACEi's
1. HTN
2. CHF
3. post-MI
what is ACEi's effect on preload? afterload? SVR?
decrease afterload and SVR thru vasodilatory effects

decrease preload b/c block aldosterone and therefore reabsorption of water
contraindications for ACEi's
1. pregnancy - hypotension
2. renal failure
side effects of ACEi's
dry cough
renal failure
angioedema - due to effects of increased bradykinin
captopril is a prototype of what class?
losartan is a prototype of...
ARBs work on what receptor?
Angiotensin 1 receptor
indications for ARBs
for pts that cna't tolerate ACEi's b/c of the cough
SE's of ARBs
m/c = dizziness, hypotension

-renal failure
does ARB have an effect of cough?
nope. probably due to the fact that it doesn't affect bradykinin
do ARB's work upstream or downstream from teh ACEi's?
downstream - step after!
prazosin is a prototype for
what drug initially results in compensatory SNS response such as renin release and tachycardia? (later these subside, and you get the vasodilatory effect you aimed for)
alpha antagonists
SE of alpha antagonist that stands out?
first dose hypotension
B1 cardioselective B blockers: prototypes
metoprolol, atenolol
non-cardioselective B blockers:
propranolol, timolol, nadolol
mixed alpha and beta receptor B-blockers
carvedilol, labetolol
B blockers: partial agonists
pindolol, acebutalol
B1 antagonism due to b-blockers will cause waht?
reduction in renin secretion --> causes vasodilation
do b-blockers have direct inhibitory effects on the SNS?
what is the main problem with propranolol
low bioavailability due to first pass effects
main SE's of B blockers
-lipid profile changes - increased triglycerides, and increasesd HDl, without a change in total cholesterol
-carb metabolism - reduced carb metabolism and glu mobilization
-raynaud's phenom.
indications of B blockers
heart failure
non-cardio (migrain, stage fright, anxiety, flaucoma)
what is a drug that is dangerous to stop abruptly due b/c of receptor upregulation?
why are b-blockers risky to use in diabetics?
b/c they mask the tachycardia that usually signals to diabetics that they are hypoglycemic
prototype of calcium channel blcokers (DHP)
MOA of ca-channel blockers
L type receptor blockers - inhibit contraction of smooth muscle
main diff b/w DHP and non-DHP?
DHP is more selective for vasculature (less cardio effects)
how are Ca-channel blockers metabolized?
indications for ca-channel blockers (DHP)
hypertension (not as first line)
stable angina (not as first line)

variant (Printzmetal's) - to control spasms
contraindications for Ca-channel blockers?
conditions in which tachycardia is harmful (mitral/aortic stenosis, CAD)

why are Ca-channel blockers not used as a first line Tx in pts with hypertension
b/c it has been found dto have increased incidence of heart failure c.f. thiazides or ACEi's
what is one of the main consequences of DHPs having a greater effect on vasculature than the heart?
reflex tachycardia
digoxin is classified as a cardiac ________
in addition to being an inotrope, digoxin is loosely classified as a(n) ______
2 MOAs of digoxin
1. blocks Na/K ATPase --> increases intracellular concentration of Na --> blocks the gradient for outflow of Ca from teh myoctye --> Ca stays in myocyte --> increased contractility, SV, CO

2. direct effect on parasympathetic system - incresases sensivity of baroreceptors - fire more readily to vagal nuclei - decreases HR, causes vasodilation
digoxin has a ________ (direct/indirect) effect on the SNS and a _______ (direct/indirect) effect on teh parasympathetic
indirect, direct
indications for digoxin
CHF (3rd line for adults, 1st line for kids)

atrial flutter - decreases AV node conduction, and therefore regulated ventricular contractions
what is the MAJOR concern with digoxin
what is one factor that increases digoxin sensitivity
SE's of digoxin (toxicity) (4)
increased automaticiy (PAC/PVC) by:
-increasing P4 slope
-decreasing phase 0 slope

Long PR or AV block


ST "scooping"
list the prototypical inotropes and pressors
what is the sequence of steps in teh synthesis of catecholamines?
tyr --> dopamine + OH --> norepi + CH3 --> epi
which of the inotropes and pressors are synthetic compounds?
which is the only inotrope/pressor to act on a receptor different than the alpha or beta?
dopamine - acts on dopaminergic receptor - results in mesenteric and renal vasodilation
what is the cascade of events that occurs when an alpha 1 receptor is stimulated?
IP3 --> increased intracellular calcium --> contraction
which of teh inotrope/pressors is/are inotrope(s) but not pressors?
which of the inotrope/pressors is/are both inotrop(s) AND pressor(s)?
dopamine and epi
which of the inotrope/pressors is/are primarily pressors (not inotropes)
phenylephrine and norepi
what is one inappopriate use of inotropes/pressors?
using them to correct hypotension/shock, when the underlying problem is a preload problem (i.e. hypovolemia) - MUST CORRECT PRELOAD FIRST before afterload is manipulated
what are teh 2 vasodilators we talk about in the handout?

sodium nitroprusside (SNP)
MOA of hydralizine
a vasodilator
-no effects on coronary arteries
-no effects on veins (not a venodilator)
will hydralizine have an effect on preload?
no b/c its not a venodilator
vasodilator (moderate venodilator properties)
What are the breakdown products of SNP
cyanide and NO
indications for SNP and hydralazine
this drug can provoke an systemic lupus erythromatosus effect (immunological effect)- causing glomerulonerphritis
this drug can cause cyanide poisoning
what is SNP?
prototype for anticholinergic
MOA of anticholinergic
blocks activity of Ach at M receptors
where are the effects of anticholinergics most pronounced?
at the SA and AV nodes - result in increased pacemaker rates of the SA node and increased conduction through AV
indciations of anticholinergic?
sinus bradycardio with hypotension