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42 Cards in this Set

  • Front
  • Back
beta blocker effects on body
decrease HR and inotropy
decrease renin
decrease PVR via CNS
All lead to decrease PVR
ISA
what is it?
when used?
when NOT used?
intrinsic sympathomimetic activity
some BBs at high concentrations will activate B1 receptos while blocking them also. useful in ppl exhibiting excessive bradycardia with sustained BB treatment
NOT used in Post MI
What drug used acute and post MI
what does it do?
BBs, recommended in all patients if tolerated, continue indefinitely
reduces chance to go into arrythmia, reduces M&M
major side effects of BBs
bradycardia, during exercise no rise in HR
av conduction abnormatities - AV blocks
bronchospasms
nightmares, depression
sexual dysfunction
increase TGs and decrease HDL
GLUCOSE intoelrance
Unopposed vasoconstriction in ppl w/ peripheral vascular disease
what other conditions to watch for when giving BBs
asthma, copd, diabetes, peripheral vasc. disease, bradycardia, AB block
hyperlipidemic stable angina
CCBs, how do we know them
non dhps - verapamil, diltiezem
dhps - -idipines
how do CCBs work
block calcium channels on vacular smooth muscle, relax, decrease PVR
Non DHPs on heart, show down and make less contractile
which CCB is selective for cerebral arteries, good for what condition
nimodipine
subarachnoid hemorrhage
side effects of CCBs
sinus bradycardia
av block
!!!!exacerbation of heart failure or pulmonary edema!!!!
**CONSTIPATION**
and those related to vasodilation
what to give to treat peripheral edema caused by CCBs
WHY?
ace inhibitors

CCBs preferentially dilate arterioles and veins stay constricted
what does ang II affect
constrict arterioles > venules , but both
facilitate SNS activity
constrict efferent renal arteriole
releases aldosterone _> Na H20 retention
Stimulate thirst
other effects of Ang II
Stime thirst
stimulates vasopressin release
hypertrophy/hyperplasia of vasc SMC, mesengial cells, cardiac myocytes
myocyte apoptosis
inflamm mediator
help regulate GFR
Uses for Ace Inh
acute and post MI, give within 24 hrs of MI
Diabetic and non diabetic nephropathy - to decrease pressure on glomerulus
major S.E. of Ace Inh.
Possible renal insufficiency
hypotension
hyperkalemia
Heme effects - neutropenia, agranulocytosis
CAPTOPRIL - loss of taste, metal taste
skin rash
ANGIOEDEMA/COUGH - swith to arbs
MOA for ace inhibitors, what do they also block
blocks formation of ANG II and also blocks the degradation of bradykinin so we get its vasodilitory effects
ABSOLUTE CONTRAINDICATIONS FOR ACE INHIBITORS
stenosis of renal arteries, or one side
PREGNANCY
what to be careful of when iving Ace Ings to a person with diabetic kidney disease
hyperkalemia - from the decrease in aldosterone
increase in serum creatinine - B/c we are decreaseing hydrostatic pressure in glom.
Why use arbs
if ppl cannot tolerate the effects of ace inhibitos, angio edema
because we still allow bradykinin to break down
why use aliskiren
to inhibit renin, same as arbs.
can be monotherapy
where do alpha blockers work
on veins and arteries!!
acute effects of Alpha blockers

2 reflexes!

then what?
decrease PVR
but reflex tachycardia
reflex renin release

chronic use - CO and plasma renin return to normal and vasodilation stays
what line drug is alpha blocker
2nd
side effects from alpha blockers
orthostatic hypotension - FIRST DOSE EFFECT
reflex tach
edema b/c of reflex renin release
what do we use to counter act one of the major side effects of alpha blockers
edema - use diuretics, from reflex renin
how does labetalol work

what is it used for
alpha and beta blocker

blocks A1 on vessels
blocks B1 on heart
++ B2 on vessels (less effect)
But little effect on Heart also

USED FOR HYPERTENSIVE URGENCIES
what are the centrally acting Alpha 2 agonists
clonidine
methyldopa
side effects: dry mouth

what other side effects
what can we use for one of these side effects
clonidine

depression, sedation, impotence,
NA/H20 retention (compensetory use diuretic with clonidine)
problem with clonidine
Rebound HTN !!!!!
nervousness, tachycardia, headache
Side effects:
positive coombs test
methyldopa
side effect of HTN drug:
hepatotoxicity
methyldopa
name all the direct vasodilators that we should use for HTN
hydralazine
minoxidil
fenoldapam
nitroprusside
MOA of minoxidil
activates the K+ channels on areriolar vascular SMCells
hyperpolarize
relaxation
decrease PVR
problem with minoxidil
REFLEXES
decrease in PVR causes increase renin, Na/H2O retention leads to increase CO
also causes a reflex SNS response --> tachy --> up CO
and SNS and ANGII constrict vessels --> up BP
what do we use with minoxidil
why?
BB to block HR, SNS effects and maybe even Ang II
and use diuretic to treat the water retention
side effect of a HTN drug: lupus like rash

what drug and what other SE
hydralazine
execessive vasodilation
tachycardia can lead to angina
side effect: hypertrichosis
minoxidil
MOA: activate D1 receptors

where does it work?
when used?
fenoldapam

vasodilates arteries and renal arteries

used in HTN emergency - only IV
MOA of nitroprusside
increase NO --> increase cGMP --> vasodilate arteries and veins
what drugs dilate veins and arteries
ace inhibitors, nitroprusside, alpha blockers
side effect of nitroprusside
cyanide toxicity
hypotension
Drugs to use for HTn urgency
ACEI?
alpha2 agonist?
Alpha and beta blocker?
CCB? why possible baD?
captopril?
clonidine
labetalol
nifedipine
drugs for HTN emergency
CCB?
ACEI?
Alpha blocker?
BB?
alpha and beta blocker?
direct Vasodilators?
CCB - nicardipine and clevidipine
ACEI - enalaprilat
ABlock - phentolamine
BB- esmolol, propanolol
A&B block - labetaolo
DVD - hydralazine, minoxidil, sodium nitroprusside