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59 Cards in this Set
- Front
- Back
o2 demand depends on
|
cardiac contractility
hr wall tension |
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meds that will control cardiac contractility and hr
|
bb
ccb ndhp |
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meds that will control wall tension
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ccb
nitrates dhp |
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load put on heart
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preload
|
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load to pump against
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afterload
|
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o2 supply depend on
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o2 extraction
coronary bl flow regional bl flow |
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meds that will control coronary bl flow
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ccb
vasodilators |
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which nitrate is squeezed and inhaled
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amyl nitrate
|
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peak of ntg
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4 min
|
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t1/2 of ntg
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1-3 min
|
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peak of isorsorbide dinitrate
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6 min
|
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t1/2 life of isosorbide dinitrate
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45 min
|
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isosorbide 5 mononitrate t 1/2
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3-6 hrs
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nitrates release---- and/or -----
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NO
nitrothiols |
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nitrites/nitrates activate ---- ----- to form -----
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cytosolic guanylate cyclase
cGMP |
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cGMP activation of --- ----- phosphorylates -----
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protein kinase
proteins |
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decrease in ------ light chain kinase causes dephoshorylation of ---- relaxes -----
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myosin
myosin vessels |
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----- doesn't release ---; it just activates it
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thiol
|
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nitrates more effects on veins/arteries
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veins
|
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nitrates lead to reduced --- and veno----
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preload
venodilation |
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nitrates dilate the --- vessels
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coronary
|
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nitartes decrease --- and co
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tpr
tpr and co reduction depend on dose |
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nitrates reduces ---demand
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o2
|
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nitrates decrease --- adhesion
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platelet
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nitrates cause reflex
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tachycardia
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nitrates balance ---- ------
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O2 supply w/ demand
|
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how will reduced preload help the heart
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keep bl in veins instead of going to heart. . . so less O2 demand
|
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nitrates undergo bio-activation w/ ---- group
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sulfhydryl
|
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what causes tolerance w/ nitrates
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continued use of nitrates depletes sulfhydryl groups
|
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t/f
once tolerance develops w/ nitroprusside can't use other nitrates |
f
no cross tolerance w/ NO |
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what can reverse tolerance
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N-Acetylcysteine
sulfhydryl-reducing agents |
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tolerance can also develop due to ---- mechanism
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counter-regulatory
(due to decrease in CO and TPR. . . ang 2, etc activated) |
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what can interfere w/ the endothelium that can cause tolerance
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free radicals
peroxynitrate (O2 + NO ---> ONOO-) |
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to prevent free radical and counterregulatory actions what do you do
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remove patch for 8-12 hrs/day
|
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se of nitrates
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ha
postural hypotension reflex tachycardia overdose: elevated methemoglobin oral agents cause: nausea pathches: skin rxns. . . move them around |
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hemoglobin that carries less O2
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methemoglobin. . . suffocate
|
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what combo is best in african americans
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isosorbide dinitrate
hydralazine |
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blacks have less active
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renin-Ang system
|
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blacks have lower --- of NO
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bioavailabilty
|
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sildenafil inhibits cGMP-phosphodiesterase ---- and ---
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5
6 |
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w/ silden once NO released where does it go and what does that allow
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released into the corpus carvenosum
allows bl inflow and erection |
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NO activates --- --- to make cGMP
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gyanylate cyclase
|
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other than erection what is silden used for
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pulmonary htn
|
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se of silden.
|
ha
flushing dyspepsia priapism visual disturbances |
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why visual disturbances w/ sildena
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cuz have pde6 in eyes
|
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sild potentiates actions of ----- and NO donor up to 24 hrs after use
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nitrates
this may induce severe ischemia |
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no will increase acid production leading to
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dyspepsia
|
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which ed med has duration of 36 hrs
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tadalafil
|
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which hasa slower onset of aciton
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tadalafil
|
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which ed med is more selective for pde5
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tadalafil
|
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se of tada
|
ha
flushing dyspepsia priapism |
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tada ci w/
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alpha blockers
cuz too much vasodilation |
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nitro and --- may potentiate effects of ed meds
|
etoh
|
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t/f
since tada is pde5 selective there will be no visual disturbances |
f
some, but small |
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which ed med can be given q day or prn
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tada
|
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which ed med has faster onset of duration
|
vardenafil
|
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varden blocks pde-
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5
6 |
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se of vardena
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ha
flushing dsypepsia priapism visual disturbances |
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durantion of vardenafil
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same as sildenafil
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