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61 Cards in this Set
- Front
- Back
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brimonidine
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alpha 2 agonist, treats glaucoma by blocking production of aqueous humor
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dapiprazole
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alpha 1 antagonist used in the eye
reverses iatrogenically induced iris dilation |
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what drug can induce horner's syndrome?
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dapiprazole - ocular alpha 1 antagonist
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homatropine
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ocular musc blocker
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cyclopentolate
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ocular musc blocker
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tropicamide
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ocular musc blocker
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use for cholinergic blockers in the eye
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mainly for dilation (think tropicamide b/c it doesnt last long)
some treat uveitis inflammation of the iris and ciliary body |
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3 agents to decrease ocular pressure and how they work
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beta blockers
cholinergic agonist alpha 2 agonist beta blockers decrease aq synth cholinergic agonist increase drainage alpha 2 agonist do both? |
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glaucoma and asthma - what mistake do you not want to make
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dont use too much timolo :)
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3 mechanism of renin release and negative feedback
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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) NEG FB AII binds to JG cells and prevents renin release |
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how does bradykinin cause vasodilation?
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by stimulating NO production
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what does ACE do to anigotensin I and bradykinin
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turns AI into AII
inactivates bradykinin (it is killing off a vasodilator!!!) |
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cardiovascular effects of AII action at AT1R
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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) |
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CNS effects of AII?
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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) |
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what does ADH do?
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stimulates water reabsorption in the kidney
potent vasoconstrictor |
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adrenal cortical effect of AII?
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stimulates aldosterone increase
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kidney effects of AII?
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vasoconstriction (decreases renal blood flow)
stimulation of Na reabsorption |
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SNS effects of AII?
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stimulates release of catecholamines from adrenal medulla, sympathetic ganglia, and postganglionic nerve terminals
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which systems does AII effect?
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vasculature
kidney CNS adrenal cortex |
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how does methyldopa inhibit the RAS?
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It's a renin inhibitor
it decreases NE synthesis |
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how does clonidine inhibit the RAS?
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It's a renin inhibitor
it decreases sympathetic stimulation of the JG |
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enalkiren
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It's a renin inhibitor
angiotensinogen analagoue. decreases AI formation |
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catopril
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ACE inhibitor
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enalapril
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ACE inhibitor
longer duration of action b/c it is a prodrug ester also enhances absorption but must be metabolized to active form |
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what is catapril's effect on Renin activity?
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it increases Renin release b/c there is less AII to feed back on the JG cells
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why do ACE inhibitors have cough as a side effect?
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ACE normally decreases bradykinin levels. when you take ACE away, bradykinin goes up
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how do ACE inhibitors help CHF patients?
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they reduce both preload (fluid overload) and afterload (blood pressure)
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why are ACE inhibitors good for people with both HTN and renal failure
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less AII means increased renal blood flow and also increased sodium excretion
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what is an even newer approach than ace inhibitors?
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angiotensin receptor blockers!
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what kind of molecule is AII?
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an octapeptide
AI is a decapeptide so is bradykinin... |
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how do AT1R blockers use negative feedback to their advantage?
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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!!!
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losartan
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AT1R blocker
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chymase
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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 |
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why don't AT1R inhibitors cause a cough?
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because ACE is not inhibitted and bradykinin gets cleaved!
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diltiazem
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selectively blocks calcium channels in the heart
some blocking of calcium channels in vascular smooth muscle |
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verapamil
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selectively blocks calcium channels in the heart
some blocking of calcium channels in vascular smooth muscle |
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nifedipine
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selectively blocks calcium channels in the vascular smooth muscle
doesnt block heart calcium channels |
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what are the 3 states of calcium channels
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closed , open, inactive
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amlodipine
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selectively blocks calcium channels in the vascular smooth muscle
doesnt block heart calcium channels |
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which channel state does verapamil prefer?
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open
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which channel state does diltiazem prefer?
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open
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which channel state does nifedipine prefer?
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inactive
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what is the first pass effect on nifedipine, diltiazem, and verapamil?
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verapamil and diltiazem undergo more first pass metabolism than nifedipine but are metabolized to products that still ahve some effects
nifedipine yields inactive metabolites |
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which calcium channel blockers have vascular effects, and what are these vascular effects?
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nifedipine is vsm specific
diltiazem and verapamil are heart selective but have effects on vsm they decrease calcium influx and promote relaxation |
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why are DFP's less effective in generating a hypotensive response than diltiazem and verapamil?
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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
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what are the cardiac effects of diltiazem and verapamil?
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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 |
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do calcium channel blockers cause postural hypotension
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no
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do calcium channel blockers cause tolerance
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no
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what drug is good to treat low renin hypertensives?
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calcium channel blockers
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what is a side effect of verapamil?
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cardiac depression
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what are side effects of CCB's?
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mostly related to hypotension
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when are direct vasodilators used?
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in hypertensive emergencies or when people arent responsive to other therapies
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why aren't direct vasodilators effective solo therapies for HTN?
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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 |
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what are direct vasodilators used in combination with
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beta blockers and diuretics to avoid the 1. BRR s/e and the 2. water/Na s/e
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hydralazine
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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! |
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what people are especially susceptible to hydralazine?
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people with low levels of the nzm that breaks hydralazine: N-acetyltransferase
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minoxidil
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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 |
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which accumulates more in a renal failure patient: hydralizine or minoxidil?
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hydralizine b/c the kidney must eliminate this
minoxidil is metabolized by liver |
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what is s/e of minoxidil
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stimulates hair growth (vasodilation)
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diazoxide
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direct vasodilator (opens vascular smooth muscle K channels)
no venodilation, postural hypotension not a problem |
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sodium nitroprusside
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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 |
