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61 Cards in this Set

  • Front
  • Back
alpha 2 agonist, treats glaucoma by blocking production of aqueous humor
alpha 1 antagonist used in the eye

reverses iatrogenically induced iris dilation
what drug can induce horner's syndrome?
dapiprazole - ocular alpha 1 antagonist
ocular musc blocker
ocular musc blocker
ocular musc blocker
use for cholinergic blockers in the eye
mainly for dilation (think tropicamide b/c it doesnt last long)

some treat uveitis inflammation of the iris and ciliary body
3 agents to decrease ocular pressure and how they work
beta blockers
cholinergic agonist
alpha 2 agonist

beta blockers decrease aq synth
cholinergic agonist increase drainage
alpha 2 agonist do both?
glaucoma and asthma - what mistake do you not want to make
dont use too much timolo :)
3 mechanism of renin release and negative feedback
1. pressure too low in the DCT
2. too little sodium in the DCT (hyponatremia or too little renal blood flow and tubule fluid going too slow)
3. sympathetic stimulation (beta 1)

AII binds to JG cells and prevents renin release
how does bradykinin cause vasodilation?
by stimulating NO production
what does ACE do to anigotensin I and bradykinin
turns AI into AII
inactivates bradykinin (it is killing off a vasodilator!!!)
cardiovascular effects of AII action at AT1R
1. increased blood pressure (vasoconstrictor)
2. decreased HR (due to BRR)
3. increaesd myocardial contractility (increases calcium uptake by cardiomyocytes)
4. no change or a slight decrease in CO (due to reflex bradycardia)
CNS effects of AII?
1. increases blood pressure
activates sympathetic efferent pathways in brainstem, increasing blood pressure
2. increases dipsogenic response (stimulates thirst in the hypothalamus)
3. increases hormone release from the anterior pituitary - ADH!!!

(ADH=vasopressin, LH, ADCH, TRH, beta-endorphin, oxytocin)
what does ADH do?
stimulates water reabsorption in the kidney

potent vasoconstrictor
adrenal cortical effect of AII?
stimulates aldosterone increase
kidney effects of AII?
vasoconstriction (decreases renal blood flow)
stimulation of Na reabsorption
SNS effects of AII?
stimulates release of catecholamines from adrenal medulla, sympathetic ganglia, and postganglionic nerve terminals
which systems does AII effect?
adrenal cortex
how does methyldopa inhibit the RAS?
It's a renin inhibitor

it decreases NE synthesis
how does clonidine inhibit the RAS?
It's a renin inhibitor

it decreases sympathetic stimulation of the JG
It's a renin inhibitor

angiotensinogen analagoue. decreases AI formation
ACE inhibitor
ACE inhibitor
longer duration of action b/c it is a prodrug ester

also enhances absorption but must be metabolized to active form
what is catapril's effect on Renin activity?
it increases Renin release b/c there is less AII to feed back on the JG cells
why do ACE inhibitors have cough as a side effect?
ACE normally decreases bradykinin levels. when you take ACE away, bradykinin goes up
how do ACE inhibitors help CHF patients?
they reduce both preload (fluid overload) and afterload (blood pressure)
why are ACE inhibitors good for people with both HTN and renal failure
less AII means increased renal blood flow and also increased sodium excretion
what is an even newer approach than ace inhibitors?
angiotensin receptor blockers!
what kind of molecule is AII?
an octapeptide
AI is a decapeptide
so is bradykinin...
how do AT1R blockers use negative feedback to their advantage?
when AT1R is blocked on the JG cells they make more Renin due to loss of negative feedback. more renin, more AI and AII. more AII binds to the unblocked AT2R and this may antagonize the effects of AT1R!!!
AT1R blocker
an enzyme in the heart that cleaves AI to AII

this one is not taken care of by ACE inhibitors but is taken care of by AT1R blockers
why don't AT1R inhibitors cause a cough?
because ACE is not inhibitted and bradykinin gets cleaved!
selectively blocks calcium channels in the heart

some blocking of calcium channels in vascular smooth muscle
selectively blocks calcium channels in the heart

some blocking of calcium channels in vascular smooth muscle
selectively blocks calcium channels in the vascular smooth muscle

doesnt block heart calcium channels
what are the 3 states of calcium channels
closed , open, inactive
selectively blocks calcium channels in the vascular smooth muscle

doesnt block heart calcium channels
which channel state does verapamil prefer?
which channel state does diltiazem prefer?
which channel state does nifedipine prefer?
what is the first pass effect on nifedipine, diltiazem, and verapamil?
verapamil and diltiazem undergo more first pass metabolism than nifedipine but are metabolized to products that still ahve some effects

nifedipine yields inactive metabolites
which calcium channel blockers have vascular effects, and what are these vascular effects?
nifedipine is vsm specific
diltiazem and verapamil are heart selective but have effects on vsm

they decrease calcium influx and promote relaxation
why are DFP's less effective in generating a hypotensive response than diltiazem and verapamil?
the hypotension induces a BRR, and reflex tachycardia and an increase in cardiac output. diltiazem and verapamil block calcium channels in the heart as well and help to decrease this effect
what are the cardiac effects of diltiazem and verapamil?
1. SA and AV nodes - decrease slow inward current (phase 0) and decrease heart rate
2. decrease conduction
3. block calcium influx in phase 2 of the action potential and this decreases cardiac contractility
do calcium channel blockers cause postural hypotension
do calcium channel blockers cause tolerance
what drug is good to treat low renin hypertensives?
calcium channel blockers
what is a side effect of verapamil?
cardiac depression
what are side effects of CCB's?
mostly related to hypotension
when are direct vasodilators used?
in hypertensive emergencies or when people arent responsive to other therapies
why aren't direct vasodilators effective solo therapies for HTN?
because of all the negative FB effects

vasodilation -> BRR -> increased symp stim of heart -> increased CO -> increased blood pressure

vasodilation -> dec BP -> decreased perfusion of kidneys -> dec sodium and fluid excretion

vasodilation -> BRR -> increased symp ->
increase in renin -> inc in ADH and aldosterone -> water and sodium retention
what are direct vasodilators used in combination with
beta blockers and diuretics to avoid the 1. BRR s/e and the 2. water/Na s/e
direct vasodilator

mech: may be K channels or may be inc NO

only dilates arterial vasculature (postural hypotension not a problem)

used in combo with beta blocker or diuretic (like all of these direct vasodilators)

not for renal failure patients because it must be excreted by the kidney!
what people are especially susceptible to hydralazine?
people with low levels of the nzm that breaks hydralazine: N-acetyltransferase
direct vasodilator

activates smooth muscle K channel -> membrane hyperpolarization

causes more venodilation than hydralazine

better than hydralazine for renal failure patients because the liver metabolizes it
which accumulates more in a renal failure patient: hydralizine or minoxidil?
hydralizine b/c the kidney must eliminate this

minoxidil is metabolized by liver
what is s/e of minoxidil
stimulates hair growth (vasodilation)
direct vasodilator (opens vascular smooth muscle K channels)

no venodilation, postural hypotension not a problem
sodium nitroprusside
direct vasodilator

acts as an NO donor and stimulates cGMP production which causes inactivation of MLCK and MLC

induces vasodilation in both arterioles AND venules!

decreases both preload and afterload, causing a decrease in myocardial oxygen demand

CAN induce postural hypotension (venous pooling)

can cause reflex tachycardia

metabolized by liver

used for hyptotensize emergencies associated with myocardial infarction and left ventricular failure

can lead to thiocyanate poisioning, thiocyanate is excreted by the kidney, so there is increased toxicity for patients in renal failure