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131 Cards in this Set
- Front
- Back
angiotensin 2 agonist on AT1 receptor
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vaso constriction in the renal artery, preferentially coronary, and cerebral locations
greater re-uptake of Na and water suppression of ADH release increased adrenal drive and the sympathetic NS increase in BP with greater inotropic contractions |
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angiontension 2 agonist on the AT2 receptors
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keep in mind that no drugs target AT2
cellular growth, differentiation, repair, apoptosis, protection against ischemia development of the urinary tract/kidneys vasodilatation |
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ACE inhibitors
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just remember -pril
all -prils have poor absorption, and so excluding enalaprilat they were all converted into pro drug esters |
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Benazapril or lotensin
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ACE inhibitor
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benzapril
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ACE inhibitor
lotensin |
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lotensin
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ACE inhibitor
benzapril |
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catopril or capoten
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ACE inhibitor
first developed, and has shortest half life making it good for beginning treatment |
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catopril
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ACE inhibitor
capoten |
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capoten
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ACE inhibitor
catopril |
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enalapril or vasotec or enalaprilat
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ACE inhibitor
a pro drug which is not well absorbed, but it becomes metabolized into the active drug. |
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enalapril
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ACE inhibitor
vasotec |
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vasotec
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ACE inhibitor
enalapril |
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fisinopril or monopril
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ACE inhibitor
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fisinopril
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ACE inhibitor
monopril |
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monopril
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ACE inhibitor
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lisinopril or prinivil
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ACE inhibitor
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prinivil
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ACE inhibitor
lisinopril |
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lisinopril
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ACE inhibitor
prinivil |
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moexipril or univasc
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ACE inhibitor
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univasc
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ACE inhibitor
moexipril |
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MOExipril
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ACE inhibitor
univasc |
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quinapril or accupril
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ACE inhibitor
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accupril
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ACE inhibitor
quinapril |
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perinodopril
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ACE inhibitor
aceon |
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aceon
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ACE inhibitor
perinodopril |
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ramipril or altace
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ACE inhibitor
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ramipril
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ACE inhibitor
altace |
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altace
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ACE inhibitor
ramipril |
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trandolapril or mavik
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ACE inhibitor
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trandolapril
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ACE inhibitor
mavik |
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mavik
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ACE inhibitor
trandolapril |
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angiotensin 2 receptor blockers
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very selective to AT1 and remember that they end in -sartan
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candesartan or atacand
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ARB
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candesartan
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ARB
atacand has the highest affinity along with olmesartan |
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atacand
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ARB
candesartan |
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olmesartan or benicar
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ARB
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olmesartan
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ARB
benicar |
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benicar
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ARB
olmesartan |
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eprosartan or tevetan
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ARB
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eprosartan
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ARB
tevetan |
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tevetan
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ARB
eprosartan |
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valsartan or diovan
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ARB
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valsartan
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ARB
diovan |
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diovan
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ARB
valsartan |
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irbesartan or avapro
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ARB
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irbesartan
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ARB
avapro |
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avapro
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ARB
irbesartan |
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telmisartan or micardis
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ARB
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micardis
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ARB
telmisartan |
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telmisartan
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ARB
micardis |
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losartan or cozar
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ARB
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losartan
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ARB
cozar |
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cozar
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ARB
losartan |
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aliskiren or tekturna
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direct renin inhibitor
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aliskiren
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direct renin inhibitor
tekturna |
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tekturna
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direct renin inhibitor
aliskerin |
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organic nitrates
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nitroglycerin
isosobride dinitrate or isordil isosorbide 5 mononitrate or imdur |
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nitroglycerin
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organic
sublingual tablets/spray, and patches acute angina half life 5 min path, ointment chronic |
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isosorbide dinitrate or isordil
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organic
oral, half life of 1 hour |
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isosorbide dinitrate
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organic isordil
oral, half life of 1 hour |
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isordil
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organic isosorbide dinitrate
oral, half life of 1 hour |
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isosorbide 5 mononitrate or imdur
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a metabolite of isordil
oral, half life of 4 hours |
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direct vasodilators
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nitroprusside
hydralazine minosidil diazoxide natercor |
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nitroprusside
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direct vasodilators
no tolerance. toxic CN or lactic acidosis buildup because of its dilation on the arteriole site there will be a huge increase in HR reflex... should probably combine with a beta ant. |
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hydralazine
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direct vasodilators
has an unknown MOA. will work an arteriole side and will result in a huge reflex increase in HR... thus increasing O2 demand on heart metabolized by N acetyltransfurace... asians Vs europeans, fast and slow acetylators |
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minoxidil
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direct vasodilator
a pro drug that is metabolized into minoxidil N-O sulfate commonly used in combo with a diuretic or ace inhibitor. because of large reflex in HR we may also need to use a beta blocker keep away from women who dont want to grow a beard. |
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diazoxide
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direct vasodilator
will open both K channels in smooth muscle and beta cells causing hyper polarization. beta cells also will respond with reduce activity... hyperglycemia (inhibition of insulin) |
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natrecor
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direct vasodilator
however, used more for it's effects on heart failure than vaso dilation |
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synthetic prostacyclin analogs
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ventavis or iloprost
must be inhaled |
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ventavis
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synthetic prostacyclin analog
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iloprost
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synthetic prostacyclin analog
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endothelin receptor antagonist
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bosentan
ambrisentan |
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bosentant
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endothelin receptor antagonist
non selective antagonist blocking both ETa ETb |
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ambrisentan
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endothelin receptor antagonist
selective ETa receptor antagonist |
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sildenafil or revatio or viagra
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PDE 5 inhibitor
for pulmonary artery HTN will inhibit metabolism of cyclic AMP/GMP ????? leads to vaso dilation and also called viagra |
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phosphodiesterases
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this family of enzymes will hydrolyze cGMP and cAMP
the PDE 5 is found in vascular smooth muscle. and keep in mind that increases in cGMP will cause vasodilation. |
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sildenafil or viagra
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metabolized by CYP 3A4?
this drug is a PDE 5 inhibitor and will cause an increase in cGMP... dilation comes next and it goes |
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sildenafil
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or viagra
remember that it is metabolized by CYP 3A4? viagra is a PDE5 inhibitor sildenafil will cause an increase in cGMP |
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viagra
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or sildenafil
cyp 3A4 metabolizm ? PDE 5 inhibitor will cause an increase in cGMP |
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tadalafil or cialis
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these drugs are PDE 5 inhibitors
they will cause an increase in cGMP and are metabolized by CYP 3A4 |
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tadalafil
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cialis
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cialis
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tadalafil
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vardenafil or levitra
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PDE 5 inhibitors
will cause an increase in cGMP which will lead to smooth muscle vaso dilation levitra will he inhibited by CYP 3A4 |
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drugs used to treat ED
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yohimbine
papaverine alprostadil or caverject |
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papaverine
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a non selective PDE inhibitor.
used through an intracavernosal injection |
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alprostadil or caverject
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this drug is an analog of PGE 1 (these are loop diuretics and cause vasodilation.
like the papaverine you also inject intravavernosally. able to cause erection in the absence of sexual stimulation. meaning that there is no stimulation of PGE. keep in mind it may cause priapism |
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alprostadil
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caverject
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caverject
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alprostadil
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drugs classes in treatment of dyslipidemia
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HMG-COA reductase inhibitors or statins...
bile acid sequestrates fibrates niacin cholesterol absorption inhibitors |
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atorvastatin
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lipitor
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rosuvastatin
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crestor
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prevastatin
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pravachol
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simvastatin
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zocor
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fluvastatin
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lescol
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lovastatin
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mevacor
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statins will increase HDL how ?
how do statins decrease TG levels |
they will stimulate pre beta-HDL synthesis, and stimulate cholesterol ester hydrolysis and HDL maturation
by lowering hepatic synthesis of VLDL and increasing hepatic reuptake of IDL and VLDL. |
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Rho and Rac
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explain rho and racs
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effects of statins 4 major effects
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endothelial cells will have better fxn
plaques will become more stable and less likely of rupturing less platelet activation decrease in vascular inflammation |
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effects of statins, more details about platelets, monocytes/macrophages, and vascular inflammation
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platelet activity will reduce, but thromboxane A2 synthesis will decrease
monocytes and macrophage growth will be reduced, and matrix metalloprotease expression will be reduced. vascular inflammation will result from a reduction in C reactive protein and leukocyte endothelial adhesion. |
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metabolism of statins
name all 6 statins and what metabolizes each. |
atorvastatin CYP3A4, 15 hours
fluvastatin CYP2C9, 1 hour lovastatin CYP3A4, 3 hours pravastatin sulfation, 3 hours simvastatin CYP3A4, 1.5 hours rosuvastatin CYP2C9, 19 hours |
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the metabolism of crestor
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or rosuvastatin is metabolized by CYP2C9 ,
crestor has a half life of 19 hours Rosuvastatin is the most potent of the 6 statins |
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the metabolism of lipitor
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atorvastatin is metabolized by CYP3A4
lipitor has a half life of about 15 hours atorvastatin is the 2nd most potent of the 6 statins |
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the metabolism of Zocor
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simvastatin is metabolized by CYP3A4
Zocor has a half life of about 1.5 hours simvastatin is the 3rd most potent of the 6 medications |
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the metabolism of mevacor
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lovastatin is metabolized by CYP3A4
mevacor has a half life of about 3 hours lovastatins is the 4th most potent of the 6 medications |
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the metabolism of pravachol
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pravastatin is metabolized by sulfation
pravachol has a half life of about 3 hours pravastatin is the 5th most potent statin medicaiton |
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the metabolism of fluvastatin
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lescol is metablized by CYP2C9
fluvastatin has a half life of about 1 hour lescol is the lest potent of the 6 statin medications |
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side effects of statins
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hepatic dysfunction and elevations of amiontransferase levels.
myopathy, myalgia, myositis, rhabodmyolysis |
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bile acid sequestrates
the second class |
cholestyramine or questran
colestipol or colestid and colesvealem or welchol a drug that has positively charged resins that bind to negatively charged bile acids and prevent their reabsorption. be careful because these drugs have many drug drug interactions |
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cholestyramine or questran
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a bile acid sequestrant
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cholestyramine
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questran
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questran
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cholestyramine
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colestipol or colestid
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a bile acid sequestrant
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colespitol
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colestid
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colesevalem or welochol
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a bile acid sequestrant
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colesevalem
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welochol
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welochol
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colesevam
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fibrates
the 3rd class |
gemfibrozil or lopid
genofibrate or tricor drugs act as ligands to PPARa nuclear receptors that affects gene expression meaning that the receptors are inside the cell where it acts as a transcription factor present in liver, adipose tissue, and kinda present in the renals, seleetals, and heart |
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effects of fibrates
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reduce vascular adhesion
reduce endothelin's vaso constriction will increase NO expression will inhibit IL-1 expression which will reduce inflammation will inhibit proliferation will inhibit TNF reduce IL-6 reduce CRP will increase HDL levels will reduce fibrous cap degradation |
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niacin
the 4th class |
niacin, or Vit B3, nicotinic acid, niacor, niaspan
niacin will inhibit lipolysis in adipose tissue, whichwill reduce circulating fatty acids in the endothelium and result in less plaques. |
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Niacin side effects
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flushing, edema, hypotension, tachycardia,
the flushing is due to prostiglandin PGD2 and PEG2 use caution when combining with Statins because of the increase of myopathy. |
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what are the adverse effects of ACEi compared to the adverse effects of ARBs
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? you tell me
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fen fen
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a drug that lead to lsot of pulmonary artery HTN... what was it composed of?
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what are the 3 pathways for treatment of pulmonary artery HTN.
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the NO pathway
the prosticyclin pathway and the endothelin pathway |
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what are the synthetic prostacyclin analogs
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their the PGI2??
used to heart used to treat pulmonary arteriole HTN? |
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flolan or epoprostenol
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a derivative of prosticyclin (PGI2)
half life of 3 min, and infused ith a pump |
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flolan
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epoprostenol
a prosticyclin derivative |
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epoprostenol
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flolan
a prosticycylin derivative, the infusion one |
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remodulin or treprostinil
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prosticyclin or PGI2 derivatives
can be administered SQ or IV is more stable than epoprostenol |
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remodulin
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treprostinil
the prostacyclin derivative PGI2 |
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treprostinil
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remodulin
the PGI2 derivative, more stable than flolan |
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ventavis and iloprost
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a derivative of the PGI2, but can be inhaled
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