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209 Cards in this Set
- Front
- Back
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what does sympathomimetics mean
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mimic sympath nerv. system
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what produces epi
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adrenal medulla
hypothalamus brainstem |
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adrenal medulla releases epi and it is then released into the blood what happens next
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tissues>extracellullar>postsynaptic (a1 and a2)
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the epi that is released from the hypothalamus and brainstem works on what system
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CV
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which is more potent L or D
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L isomer
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what does epi activate
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a1
a2 b1 b2 |
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t/f
epi is active orally |
f
broken down in GI tract |
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how does epi increase cardiac contractility
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it activate PKA dependent phosphorylation of L type channels to increase Ca entry
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epi activates --- dependent phosphorylation of -- type channels to increase Ca entry
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PKA
L |
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what does Ca act on in the heart
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myocin
cardiac muscle |
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the more --- the stronger the heart contraction
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Ca
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how does epi increase rate of relaxation
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activates PKA dependent phosphorylation of Ca ATPase
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to increase releaxation epi activates PKA dependent ------ of Ca ------
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phosphorylation
ATPase |
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how does epi increase HR
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increase rate of depolarization of SA node
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epi increases HR by increasing rate of ------ of -- node
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depolarization
SA |
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epi will ---- time btw depolarization to increase HR
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shorten
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which receptors do epi work on to increase cardiac contractility
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B1
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which receptors do epi work on to increase HR
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B1
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what are the vascular effects of epi
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contract and relax depending on receptor
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which receptors will increase BP
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a1
a2 |
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which receptors will decrease bp
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b2
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will epi increase or decrease the following:
lipolysis glycongenolysis insulin release metabolic release |
increase lipolysis
increase glycongenolysis decrease insulin release increase metabolic rate |
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the purpose of metaboic effects of epi
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to increase O2 to brain and muscles
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will epi relax/contract bronchi
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relax
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epi also stablizes ------ cells
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mast
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stabilizing mast cells will decrease an ---- response cuz they contain ----
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allergic
histamine |
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epi will constrict/relax sphincters
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constrict
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epi will increase/decrease peristalsis thru which receptor
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decrease
b2 |
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epi will relax/contract uterine sm muscle
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relax
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what will contract uterine muscles
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a1
expressed closer to term |
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epi will increase/decrease intraocular pressure
how |
decrease
dilates vessels, so it will increase outflow |
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epi works on which muscle to cause mydriasis
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radial
a1 receptor! |
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how will epi prolong local anesthetics
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by contricting the vessels, so there'll be a slower diffusion of lido
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pt's having V Fib why will you give epi
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cardiac stimulant
increases HR, contractility, conduction |
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t/f
ok to mix epi and vasopressin |
f
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t/f
epi usu recommended for asthma why |
f
cuz has a lot of side effects |
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therapeutic uses of epi
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anaphylactic shock
cardiac stimulant bronchial asthma gluacoma prolong local anesthetics |
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why's it bad to overuse primatene mist
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due to side effects
(used for asthma) acts on b2 |
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side effects of epi
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tachycardia
arrhythmias elevated bp tremors contraindicated in hyperthyroidism |
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why is epi contraindicated w/ gen anesthetics
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it works on receptors on the heart which can cause arrhythmias
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what helps regulate the # of b receptors
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thyroid
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why the contraindication w/ hyperthyroidism and epi
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will lead to an exaggerated response due to regulation of b receptors of thyroid
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name some other meds hat will have interactions w/ epi
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tricyclics and cocaine: block reuptake: so exaggerated response
MAO inhibitors: blocks metabolism |
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name an epi drug
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adrenalin
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what does norepi activate
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a1
a2 b1 b3 limited b2 |
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thru which route is norepi given
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iv only!
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name a norepi drug
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levophed
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cardiac effects of norepi
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vasoconstriction
increase CO decrease HR |
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norepi will increase/decrease CO
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increase
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norepi will increase/decrease HR
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decrease
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how is the HR decreased w/ norepi
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via baroreceptors
ACH acts on SA Node to decreased HR |
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increased or decreased contractions w/ norepi
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increased
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tx use of norepi/levophed
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increase bp
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SE of norepi
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vasoconstriction
increased cap filtration contraindicated in CVA and aneurysm |
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what can occur due to excessive vasoconstrict.
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decrease O2: tissue damage
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what can occur due to cap filtration
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edema: more fluid out of bl vessels
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why's norepi contraindicated in cva/aneurysm
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increased bp can increase chances of cva and bursting aneurysm
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what does isoproterenol work on
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b1
b2 |
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med w/ isoproterenol
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isuprel
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t/f
isoproterenol works on both a and b receptors |
B adrenergic receptors only,
nonselective |
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isoproteronol has positive --- and ---- effects on the heart
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inotropic
chronotropic |
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how does isorpoterenol vasodilate
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decrease TPR
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t/f
isoproterenol vasoconstricts |
f
vasodilates |
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isoproterenol bronch------
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dilates
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isoproterenol is metabolized rapidly by --- and ---
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COMT
MAO |
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why no binding of isoproterenol to alpha receptors
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cuz of the extra two CH3 groups
difference w/ epi |
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tx uses of isoproteronol
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cardiac arrest
cardiogenic shock bronchodilation |
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how does isuprel help cardiogenic shock
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increase contraction
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thru which route does isuprel work to bronchodilate
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inhalation
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meds w/ dopamine
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intropin
dopastat |
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da active orally
|
f
not active orally IV adminis only |
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receptors for Dopamine
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D1
D2 a1 b1 b2 |
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da has positive --- and --- effects
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inotropic
chronotropic |
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why give a brain dead person da
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dilates renal/mesenteric arteries will maintain perfusion to save kidneys for organ donation
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why use da instead of norepi
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norepi works everywhere; will constrict even kidney vessels which can lead to renal failure
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da given for circulatory shock. why?
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increases bp
it works on both b and a |
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at low conc what does da work on
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D1
D2 |
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at higher conc what does Da work on
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a1
b1 b2 |
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which works to increase hr by increasing rate of depolarization of sa node
epi or iso |
epi
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will the hr increase or decrease w/ epi
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increase
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what receptors will increase hr in epi
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B1
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will TPR increase or decrease w/ epi
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decrease
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what will decrease the TPR w/ epi
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B2
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what's competing w/ b2 to increase TPR
which is stronger |
a1 and a2
but b2 is stronger |
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t/f
due to epi there's an increase in bp |
f
no change cuz alpha receptors are working to constrict, but b2 is working to relax. this mean bp stays about the same |
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t/f
baroreceptors are working due to epi |
f
there's no change in bp, so no need for baroreceptors |
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will hr in norepi decrease or increase
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decrease
due to baroreceptors |
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will tpr w/ norepi increase or decrease
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increase
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receptor that increase tpr w/ norepi
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a1
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bp w/ norepi
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increase
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how will the baroreflex decrease hr
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due to an increase in bp
para will act on ACH on M2 in SA node |
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what receptor will usu cause reflex bradycardia
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a1
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hr will increase/decrease w/ isoproterenol
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increase
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thru which receptor will hr increase w/ isoproterenol
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b1
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will there be increase or decrease tpr w/ iso
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decrease
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what causes decrease tpr in iso
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b2
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why will there be a slight increase in iso
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to compensate for the increase in hr; to help w/ perfusion/pumping of blood
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overall what's the effect on bp w/ iso
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decrease
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does DA increase or decrease hr
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increases
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thru which receptor will DA increase HR
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B1
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is there any decrease in hr in DA
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y
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how's there an decrease in hr in DA
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due to a1 increasing the bp, reflex brady
however, there's less decrease than there's increase |
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overall decrease or increase in tpr
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decrease
due to stronger effect from D, B2 |
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what will increase tpr
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a1
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if you pretreat w/ a1 blocker, but then give norepi what will happen
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no change in baseline of tpr or bp
however, no baroreflex, so HR will increase |
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if you pretreat w/ b blockers and then give iso what happens
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no change in baseline
so iso will not increase hr, etc anymore than the baseline |
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if you pretreat w/ an alpha blocker then give epi what will happen
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the graphs will look like iso because alpha's removed
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pretreat w/ beta blocker and epi
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look like norepi
might have bigger decrease in hr cuz beta's no B there to block |
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atropine plus norepi
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increase in hr due to block of baroflex
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ephedrine aka
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pretz-d
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pseudoephedrine aka
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sudafed
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how many isomers in ephedrine/pseudoephedrine
name them |
4
+/- ephedrine +/- pseudoephedrine |
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natural product for ephedrine/pseudo
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ma huang
natural alkaloid |
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what does ephedrine/pseudo activate?
what do they release |
activate: a1, b1, b2
releases: NE |
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what do you remove from ephedrine to get amphetamines
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OH
CH3 |
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t/f
ephedrine only acts directly on receptors |
f
direct and indirect direct: acts on receptors indirect: releases norepi |
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t/f
ephredrine/pseudo is inactive orally |
f
active orally |
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t/f
ephredine/pseudo has a long duration of action |
t
it's not as easily metabolized |
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what can develop due to use of ephedrine/pseudo. . . like tolerance
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tachyphylaxis
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an advantage ephedrine/pseudo have over epi/norepi
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orally active
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ephedrine/pseudo have --- actions
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stimulant: CNS
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indication for ephedrine
pseudo |
eph: weight loss
pseudo: nasal decongestant |
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amphetamine aka
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benzedrine
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amphe is indirect/direct
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indirect
has to release NE, DA |
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what does amphe release
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NE
DA |
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which isomer of amph most potent
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D isomer
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dexedrine isomer
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D isomer
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amph decrease/increase food intake
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decrease
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a paradoxical effect of amphe
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increase attention
used in ADD/ADHD |
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amph is used to help people stay awake in which disease
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narcolepsy
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phenylephrine aka
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neo-synephrine
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phen is orally active/inactive
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orally active; goes thru 1st pass
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other than oral, what other route can phen be administered
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IV
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t/f
phen is a substrate for COMT so it will have a short life |
f
not a substrate, OH not in "correct" place so, it has a longer duration |
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phenly will vaso-
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constrict
it used w/ spinal anesthesia |
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why use phenly w/ spinal anesthesia
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to localize where anesthetic occurs
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uses for phenly
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vasoconstriction
decongestant mydriasis reflex dependent bradycardia |
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t/f
phenyl is a cyclopegia |
f
not it vasoconstricts used in eye to reduce redness |
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side effects of phenly
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excessive vasoconstriction
rebound hyperemia contraindicated in CVA and aneurysm |
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when will a pt have rebound hyperemia
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when using phenyl for a long time, overproduction of NE
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which muscle will phenyl activate
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radial: mydriasis
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why use phenl over atropine
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cuz atropine will affect accomadation
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can you use phenl to decrease hr
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yes
increase bp and thru that barorecetors activated |
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other a1 agonist
|
methoxamine
tetrahydrozoline oxymethazoline |
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methoxamine aka
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vasoxyl
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what's methoxamine used for
|
vasoconstrictor
pressor agent maintains bp watch out for renal failure |
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tetrahydrozoline aka
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visine
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what's tetrahydrozoline used for
|
bloodshot eyes
redness due to vasodilation, so this drug will constrict |
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oxymetazoline aka
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afrin
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what's wrong w/ oxymetazoline
good |
wrong: overuse can cause damage to nasal mucosa
good: long duration |
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clonidine aka
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catapres
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clonidine is a --- selective agonist
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a2
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receptors for clonidien
|
a2 selective agonist
imidazoline |
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t/f
clonidine orally inactive |
f
orally active |
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t/f
the predominant inhibition of clonidine is presynaptic |
f
postsynaptic: it works centrally |
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tx effects of clonidine
|
antiHTN
supplement to anesthesia drug withdrawal ADD |
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clonidine supplement to anesthesia cuz
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unknown
but seems to be a2 receptors on pain fibers so less anesthesia can be used |
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how does clonidine work for drug withdrawal
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w/ drug withdrawal the pt's s/s are an overactivity of the sympathetic system
clonidine inhibits this |
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other a 2 agonist meds
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guanfacine
guanabenz |
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t/f
receptors on a2 agonist are a2 and imidazoline, just like clonidine |
f
no imidazoline activity |
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guanfacine aka
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tenex
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guanabenz aka
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wytensin
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common side effect of all a1 agonist
|
sedation
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s/e of other a2 agonist
|
sedation
caution in DM |
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dobutamine aka
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dobutrex
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t/f
dobutamine is effective orally |
f
ineffective orally; should be given IV |
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isomers of dobutamine
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+ isomer B agoinst, a1 antagonist
- isomer weak B agonist, a1 agonist |
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effects on heart w/ dobutamine
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+ inotropic
no chronotropic the isomers block the HR effect |
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what's dobutamine used for
|
Heart Failure
increases force of contraction to help w/ perfusion thru body |
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dobutamine is given as an rx
|
f
it can only be given via IV so stabilize pt w/ it then d/c and start on an oral med |
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terbutaline aka
|
brethine
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terbutaline is a ---- agonist
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B2
|
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t/f
terbutaline is active orally |
t
|
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what other routes can terbutaline be given
|
inhalation
injection |
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t/f
terbutaline is resistant to COMT |
t
so long use |
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tx use of terbutaline
|
relaxes bronchial sm. muscle
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t/f
terbutaline used for acute asthma attacks |
t
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s/e of terbutaline
|
nervousness
tremors tachycardia |
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albuterol aka
|
proventil
ventolin |
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albuterol receptor
|
b2 agonist
|
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route of albuterol
|
oral
inhalation |
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tx use of albuterol
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relaxes bronchial sm. muscle
|
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another tx use of terbutaline
|
relaxes vaginal sm muscle for premature labor
|
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s/e of albuterol
|
nervousness
tremors tachycardia |
|
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metaproterenol aka
|
alupent
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|
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receptor for metaproterenol
|
B2 agonist
|
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route for metaproterenol
|
oral
inhalation |
|
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t/f
albuterol affected by COMT |
f
not affected |
|
|
alubent is long term use for asthma
|
f
rescue inhaler for acute asthma attack |
|
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tx use of metaproterenol
|
relaxes bronchial sm muscle
|
|
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s/e of metaproterenol
|
nervousness
tremors tacycardia |
|
|
salmeterol aka
|
serevent
w/ fluticasone in advair |
|
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receptor for salmeterol
|
B2 agonist
|
|
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route of administration for salmeterol
|
inhalation
|
|
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t/f
salmeterol has a slow onset |
t
so, used as for long term control |
|
|
--- hour duration of salmeterol
|
12
|
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is there receptor down regulaiton in salmeterol
|
possibly, so watch out for inefficacy
|
|
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what's salmeterol used for
|
nocturnal asthma
COPD asthma |
|
|
s/e of salmeterol
|
nervousness
tremors tachycardia |
|
|
what's the prob w/ taking salmeterol during an asthma attack
|
long onset of action
it will occupy the receptors and when an acute med is used it won't be as effective possible suffocation : ( |
|
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formoterol aka
|
foradil
|
|
|
receptor for formoterol
|
B2
|
|
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route for formoterol
|
inhalation
|
|
|
duration of formoterol
|
12 hrs
|
|
|
formoterol has a slower onset of action than slameterol
|
f
faster |
|
|
is there concern for receptor down regulation in formoterol
|
yes
|
|
|
tx for fomoterol
|
nocturnal asthma
COPD |
|
|
s/e of formoterol
|
nervousness
tremors tacycardia |
|
|
t/f
formoterol used for rescue |
F!
for long term use |
