Pharmacology, Semester 1 Exam 3

Front 1

angiotensin 2 agonist on AT1 receptor

Back 1

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

Front 2

angiontension 2 agonist on the AT2 receptors

Back 2

keep in mind that no drugs target AT2
cellular growth, differentiation, repair, apoptosis,
protection against ischemia
development of the urinary tract/kidneys
vasodilatation

Front 3

ACE inhibitors

Back 3

just remember -pril
all -prils have poor absorption, and so excluding enalaprilat they were all converted into pro drug esters

Front 4

Benazapril or lotensin

Back 4

ACE inhibitor

Front 5

benzapril

Back 5

ACE inhibitor
lotensin

Front 6

lotensin

Back 6

ACE inhibitor
benzapril

Front 7

catopril or capoten

Back 7

ACE inhibitor
first developed, and has shortest half life making it good for beginning treatment

Front 8

catopril

Back 8

ACE inhibitor
capoten

Front 9

capoten

Back 9

ACE inhibitor
catopril

Front 10

enalapril or vasotec or enalaprilat

Back 10

ACE inhibitor
a pro drug which is not well absorbed, but it becomes metabolized into the active drug.

Front 11

enalapril

Back 11

ACE inhibitor
vasotec

Front 12

vasotec

Back 12

ACE inhibitor
enalapril

Front 13

fisinopril or monopril

Back 13

ACE inhibitor

Front 14

fisinopril

Back 14

ACE inhibitor
monopril

Front 15

monopril

Back 15

ACE inhibitor

Front 16

lisinopril or prinivil

Back 16

ACE inhibitor

Front 17

prinivil

Back 17

ACE inhibitor
lisinopril

Front 18

lisinopril

Back 18

ACE inhibitor
prinivil

Front 19

moexipril or univasc

Back 19

ACE inhibitor

Front 20

univasc

Back 20

ACE inhibitor
moexipril

Front 21

MOExipril

Back 21

ACE inhibitor
univasc

Front 22

quinapril or accupril

Back 22

ACE inhibitor

Front 23

accupril

Back 23

ACE inhibitor
quinapril

Front 24

perinodopril

Back 24

ACE inhibitor
aceon

Front 25

aceon

Back 25

ACE inhibitor
perinodopril

Front 26

ramipril or altace

Back 26

ACE inhibitor

Front 27

ramipril

Back 27

ACE inhibitor
altace

Front 28

altace

Back 28

ACE inhibitor
ramipril

Front 29

trandolapril or mavik

Back 29

ACE inhibitor

Front 30

trandolapril

Back 30

ACE inhibitor
mavik

Front 31

mavik

Back 31

ACE inhibitor
trandolapril

Front 32

angiotensin 2 receptor blockers

Back 32

very selective to AT1 and remember that they end in -sartan

Front 33

candesartan or atacand

Back 33

ARB

Front 34

candesartan

Back 34

ARB
atacand
has the highest affinity along with olmesartan

Front 35

atacand

Back 35

ARB
candesartan

Front 36

olmesartan or benicar

Back 36

ARB

Front 37

olmesartan

Back 37

ARB
benicar

Front 38

benicar

Back 38

ARB
olmesartan

Front 39

eprosartan or tevetan

Back 39

ARB

Front 40

eprosartan

Back 40

ARB
tevetan

Front 41

tevetan

Back 41

ARB
eprosartan

Front 42

valsartan or diovan

Back 42

ARB

Front 43

valsartan

Back 43

ARB
diovan

Front 44

diovan

Back 44

ARB
valsartan

Front 45

irbesartan or avapro

Back 45

ARB

Front 46

irbesartan

Back 46

ARB
avapro

Front 47

avapro

Back 47

ARB
irbesartan

Front 48

telmisartan or micardis

Back 48

ARB

Front 49

micardis

Back 49

ARB
telmisartan

Front 50

telmisartan

Back 50

ARB
micardis

Front 51

losartan or cozar

Back 51

ARB

Front 52

losartan

Back 52

ARB
cozar

Front 53

cozar

Back 53

ARB
losartan

Front 54

aliskiren or tekturna

Back 54

direct renin inhibitor

Front 55

aliskiren

Back 55

direct renin inhibitor
tekturna

Front 56

tekturna

Back 56

direct renin inhibitor
aliskerin

Front 57

organic nitrates

Back 57

nitroglycerin
isosobride dinitrate or isordil
isosorbide 5 mononitrate or imdur

Front 58

nitroglycerin

Back 58

organic
sublingual tablets/spray, and patches acute angina
half life 5 min
path, ointment chronic

Front 59

isosorbide dinitrate or isordil

Back 59

organic
oral, half life of 1 hour

Front 60

isosorbide dinitrate

Back 60

organic isordil
oral, half life of 1 hour

Front 61

isordil

Back 61

organic isosorbide dinitrate
oral, half life of 1 hour

Front 62

isosorbide 5 mononitrate or imdur

Back 62

a metabolite of isordil
oral, half life of 4 hours

Front 63

direct vasodilators

Back 63

nitroprusside
hydralazine
minosidil
diazoxide
natercor

Front 64

nitroprusside

Back 64

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.

Front 65

hydralazine

Back 65

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

Front 66

minoxidil

Back 66

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.

Front 67

diazoxide

Back 67

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)

Front 68

natrecor

Back 68

direct vasodilator
however, used more for it's effects on heart failure than vaso dilation

Front 69

synthetic prostacyclin analogs

Back 69

ventavis or iloprost
must be inhaled

Front 70

ventavis

Back 70

synthetic prostacyclin analog

Front 71

iloprost

Back 71

synthetic prostacyclin analog

Front 72

endothelin receptor antagonist

Back 72

bosentan
ambrisentan

Front 73

bosentant

Back 73

endothelin receptor antagonist
non selective antagonist blocking both ETa ETb

Front 74

ambrisentan

Back 74

endothelin receptor antagonist
selective ETa receptor antagonist

Front 75

sildenafil or revatio or viagra

Back 75

PDE 5 inhibitor
for pulmonary artery HTN
will inhibit metabolism of cyclic AMP/GMP ?????

leads to vaso dilation and also called viagra

Front 76

phosphodiesterases

Back 76

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.

Front 77

sildenafil or viagra

Back 77

metabolized by CYP 3A4?
this drug is a PDE 5 inhibitor and will cause an increase in cGMP... dilation comes next and it goes

Front 78

sildenafil

Back 78

or viagra
remember that it is metabolized by CYP 3A4?
viagra is a PDE5 inhibitor
sildenafil will cause an increase in cGMP

Front 79

viagra

Back 79

or sildenafil
cyp 3A4 metabolizm ?
PDE 5 inhibitor
will cause an increase in cGMP

Front 80

tadalafil or cialis

Back 80

these drugs are PDE 5 inhibitors
they will cause an increase in cGMP
and are metabolized by CYP 3A4

Front 81

tadalafil

Back 81

cialis

Front 82

cialis

Back 82

tadalafil

Front 83

vardenafil or levitra

Back 83

PDE 5 inhibitors
will cause an increase in cGMP which will lead to smooth muscle vaso dilation
levitra will he inhibited by CYP 3A4

Front 84

drugs used to treat ED

Back 84

yohimbine
papaverine
alprostadil or caverject

Front 85

papaverine

Back 85

a non selective PDE inhibitor.
used through an intracavernosal injection

Front 86

alprostadil or caverject

Back 86

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

Front 87

alprostadil

Back 87

caverject

Front 88

caverject

Back 88

alprostadil

Front 89

drugs classes in treatment of dyslipidemia

Back 89

HMG-COA reductase inhibitors or statins...
bile acid sequestrates
fibrates
niacin
cholesterol absorption inhibitors

Front 90

atorvastatin

Back 90

lipitor

Front 91

rosuvastatin

Back 91

crestor

Front 92

prevastatin

Back 92

pravachol

Front 93

simvastatin

Back 93

zocor

Front 94

fluvastatin

Back 94

lescol

Front 95

lovastatin

Back 95

mevacor

Front 96

statins will increase HDL how ?
how do statins decrease TG levels

Back 96

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.

Front 97

Rho and Rac

Back 97

explain rho and racs

Front 98

effects of statins 4 major effects

Back 98

endothelial cells will have better fxn
plaques will become more stable and less likely of rupturing
less platelet activation
decrease in vascular inflammation

Front 99

effects of statins, more details about platelets, monocytes/macrophages, and vascular inflammation

Back 99

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.

Front 100

metabolism of statins
name all 6 statins and what metabolizes each.

Back 100

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

Front 101

the metabolism of crestor

Back 101

or rosuvastatin is metabolized by CYP2C9 ,
crestor has a half life of 19 hours
Rosuvastatin is the most potent of the 6 statins

Front 102

the metabolism of lipitor

Back 102

atorvastatin is metabolized by CYP3A4
lipitor has a half life of about 15 hours
atorvastatin is the 2nd most potent of the 6 statins

Front 103

the metabolism of Zocor

Back 103

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

Front 104

the metabolism of mevacor

Back 104

lovastatin is metabolized by CYP3A4
mevacor has a half life of about 3 hours
lovastatins is the 4th most potent of the 6 medications

Front 105

the metabolism of pravachol

Back 105

pravastatin is metabolized by sulfation
pravachol has a half life of about 3 hours
pravastatin is the 5th most potent statin medicaiton

Front 106

the metabolism of fluvastatin

Back 106

lescol is metablized by CYP2C9
fluvastatin has a half life of about 1 hour
lescol is the lest potent of the 6 statin medications

Front 107

side effects of statins

Back 107

hepatic dysfunction and elevations of amiontransferase levels.
myopathy, myalgia, myositis, rhabodmyolysis

Front 108

bile acid sequestrates
the second class

Back 108

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

Front 109

cholestyramine or questran

Back 109

a bile acid sequestrant

Front 110

cholestyramine

Back 110

questran

Front 111

questran

Back 111

cholestyramine

Front 112

colestipol or colestid

Back 112

a bile acid sequestrant

Front 113

colespitol

Back 113

colestid

Front 114

colesevalem or welochol

Back 114

a bile acid sequestrant

Front 115

colesevalem

Back 115

welochol

Front 116

welochol

Back 116

colesevam

Front 117

fibrates
the 3rd class

Back 117

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

Front 118

effects of fibrates

Back 118

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

Front 119

niacin
the 4th class

Back 119

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.

Front 120

Niacin side effects

Back 120

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.

Front 121

what are the adverse effects of ACEi compared to the adverse effects of ARBs

Back 121

? you tell me

Front 122

fen fen

Back 122

a drug that lead to lsot of pulmonary artery HTN... what was it composed of?

Front 123

what are the 3 pathways for treatment of pulmonary artery HTN.

Back 123

the NO pathway
the prosticyclin pathway
and the endothelin pathway

Front 124

what are the synthetic prostacyclin analogs

Back 124

their the PGI2??
used to heart used to treat pulmonary arteriole HTN?

Front 125

flolan or epoprostenol

Back 125

a derivative of prosticyclin (PGI2)
half life of 3 min, and infused ith a pump

Front 126

flolan

Back 126

epoprostenol
a prosticyclin derivative

Front 127

epoprostenol

Back 127

flolan
a prosticycylin derivative, the infusion one

Front 128

remodulin or treprostinil

Back 128

prosticyclin or PGI2 derivatives
can be administered SQ or IV is more stable than epoprostenol

Front 129

remodulin

Back 129

treprostinil
the prostacyclin derivative PGI2

Front 130

treprostinil

Back 130

remodulin
the PGI2 derivative, more stable than flolan

Front 131

ventavis and iloprost

Back 131

a derivative of the PGI2, but can be inhaled