Usmle - Pharmacology - Other Cv Drugs

Front 1

Atorvastatin

Back 1

HMG analog; inhibits rate limiting step of de novo cholesterol synthesis; increased expression of LDL receptors

Hint 1

Hyperlipidemias

Front 2

Fluvastatin

Back 2

HMG analog; inhibits rate limiting step of de novo cholesterol synthesis; increased expression of LDL receptors

Hint 2

Hyperlipidemias

Front 3

Lovastatin

Back 3

HMG analog; inhibits rate limiting step of de novo cholesterol synthesis; increased expression of LDL receptors

Hint 3

Hyperlipidemias

Front 4

Pravastatin

Back 4

HMG analog; inhibits rate limiting step of de novo cholesterol synthesis; increased expression of LDL receptors

Hint 4

Hyperlipidemias

Front 5

Rosuvastatin

Back 5

HMG analog; inhibits rate limiting step of de novo cholesterol synthesis; increased expression of LDL receptors

Hint 5

Hyperlipidemias

Front 6

Simvastatin

Back 6

HMG analog; inhibits rate limiting step of de novo cholesterol synthesis; increased expression of LDL receptors

Hint 6

Hyperlipidemias

Front 7

Fenofibrate

Back 7

Impact PPAR activity
Decreased TAG concentration, increased lipoprotein lipase, decreased apoCII
Increase HDL via increased apoCI and apoCII

Hint 7

Hypertriglyceridemias

Front 8

Gemfibrozil

Back 8

Fibrate
Impact PPAR activity
Decreased TAG concentration, increased lipoprotein lipase, decreased apoCII
Increase HDL via increased apoCI and apoCII

Hint 8

Hypertriglyceridemias

Front 9

Niacin

Back 9

Inhibits lipolysis in adipose tissue leading to decreased liver VLDL production and subsequently, decreased LDL
Significantly increases HDL levels
Boosts production of plasminogen activator

Hint 9

Particularly useful in treatment of familal hypercholesterolemias; specifically increasing HDL levels

Front 10

Colesevelam

Back 10

Bile acid sequestrant
Binds bile acids in gut, leading to increased bile acid excretion in feces
Increased cholesterol synthesis by liver, associated with increased LDL receptor expression

Hint 10

DOC in type Iia and type Iib hyperlipidemias

Front 11

Colestipol

Back 11

Bile acid sequestrant
Binds bile acids in gut, leading to increased bile acid excretion in feces
Increased cholesterol synthesis by liver, associated with increased LDL receptor expression

Hint 11

DOC in type Iia and type Iib hyperlipidemias

Front 12

Cholestyramine

Back 12

Bile acid sequestrant
Binds bile acids in gut, leading to increased bile acid excretion in feces
Increased cholesterol synthesis by liver, associated with increased LDL receptor expression

Hint 12

DOC in type Iia and type Iib hyperlipidemias; can relieve pruritus in those with biliary obstruction

Front 13

Ezetimibe

Back 13

Inhibits intestinal absorption of cholesterol
Decreases serum LDL and triacylglycerides; Increases HDL

Hint 13

Hyperlipidemias

Front 14

Nitroglycerin

Back 14

Organic Nitrates

Hint 14

Angina pectoris

Front 15

Aliskiren

Back 15

Renin Inhibitor

Hint 15

Hypertension

Front 16

Amlodipine

Back 16

Ca2+ Channel Blocker, 2nd generation dihydropyridine
Selective for vascular smooth muscle

Hint 16

Hypertensive patients with asthma, diabetes, angina, and/or peripheral vascular disease

Front 17

Diltiazem

Back 17

Ca2+ Channel Blocker, Benzothiazepine
Relatively non-selective; affects both cardiac and smooth muscle receptors

Hint 17

Hypertensive patients with asthma, diabetes, angina, and/or peripheral vascular disease

Front 18

Felodipine

Back 18

Ca2+ Channel Blocker, 2nd generation dihydropyridine
Selective for vascular smooth muscle

Hint 18

Hypertensive patients with asthma, diabetes, angina, and/or peripheral vascular disease

Front 19

Isradipine

Back 19

Ca2+ Channel Blocker, 2nd generation dihydropyridine
Selective for vascular smooth muscle

Hint 19

Hypertensive patients with asthma, diabetes, angina, and/or peripheral vascular disease

Front 20

Nicardipine

Back 20

Ca2+ Channel Blocker, 2nd generation dihydropyridine
Selective for vascular smooth muscle

Hint 20

Hypertensive patients with asthma, diabetes, angina, and/or peripheral vascular disease

Front 21

Nifedipine

Back 21

Ca2+ Channel Blocker, 2nd generation dihydropyridine
Selective for vascular smooth muscle

Hint 21

Hypertensive patients with asthma, diabetes, angina, and/or peripheral vascular disease

Front 22

Nisoldipine

Back 22

Ca2+ Channel Blocker, 2nd generation dihydropyridine
Selective for vascular smooth muscle

Hint 22

Hypertensive patients with asthma, diabetes, angina, and/or peripheral vascular disease

Front 23

Verapamil

Back 23

Ca2+ Channel Blocker, Diphenylalkylamine
Relatively non-selective; affects both cardiac and smooth muscle receptors

Hint 23

Hypertensive patients with asthma, diabetes, angina, and/or peripheral vascular disease

Front 24

Clonidine

Back 24

α2-agonist that decreases central adrenergic output
Does not decrease RBF or GFR

Hint 24

HTN complicated by renal disease or refractory to treatment with other agents

Front 25

Benazepril

Back 25

Inhibit ACE
Results in decreased Ang II-mediated vasoconstriction, increased BK-mediated vasodilation
Decreased aldosterone-mediated Na+ and fluid retention

Hint 25

Hypertension; slow progression of diabetic nephropathy; Chronic HF management

Front 26

Captopril

Back 26

Inhibit ACE
Results in decreased Ang II-mediated vasoconstriction, increased BK-mediated vasodilation
Decreased aldosterone-mediated Na+ and fluid retention

Hint 26

Hypertension; slow progression of diabetic nephropathy; Chronic HF management

Front 27

Enalapril

Back 27

Inhibit ACE
Results in decreased Ang II-mediated vasoconstriction, increased BK-mediated vasodilation
Decreased aldosterone-mediated Na+ and fluid retention

Hint 27

Hypertension; slow progression of diabetic nephropathy; Chronic HF management

Front 28

Fosinopril

Back 28

Inhibit ACE
Results in decreased Ang II-mediated vasoconstriction, increased BK-mediated vasodilation
Decreased aldosterone-mediated Na+ and fluid retention

Hint 28

Hypertension; slow progression of diabetic nephropathy; Chronic HF management

Front 29

Lisinopril

Back 29

Inhibit ACE
Results in decreased Ang II-mediated vasoconstriction, increased BK-mediated vasodilation
Decreased aldosterone-mediated Na+ and fluid retention

Hint 29

Hypertension; slow progression of diabetic nephropathy; Chronic HF management

Front 30

Moexipril

Back 30

Inhibit ACE
Results in decreased Ang II-mediated vasoconstriction, increased BK-mediated vasodilation
Decreased aldosterone-mediated Na+ and fluid retention

Hint 30

Hypertension; slow progression of diabetic nephropathy; Chronic HF management

Front 31

Quinapril

Back 31

Inhibit ACE
Results in decreased Ang II-mediated vasoconstriction, increased BK-mediated vasodilation
Decreased aldosterone-mediated Na+ and fluid retention

Hint 31

Hypertension; slow progression of diabetic nephropathy; Chronic HF management

Front 32

Ramipril

Back 32

Inhibit ACE
Results in decreased Ang II-mediated vasoconstriction, increased BK-mediated vasodilation
Decreased aldosterone-mediated Na+ and fluid retention

Hint 32

Hypertension; slow progression of diabetic nephropathy; Chronic HF management

Front 33

Candesartan

Back 33

Competitively antagonize angiotensin II receptors
Arteriolar and venous dilation
Blocks aldosterone secretion

Hint 33

Decrease nephrotoxicity in diabetics

Front 34

Eprosartan

Back 34

Competitively antagonize angiotensin II receptors
Arteriolar and venous dilation
Blocks aldosterone secretion

Hint 34

Decrease nephrotoxicity in diabetics

Front 35

Irbesartan

Back 35

Competitively antagonize angiotensin II receptors
Arteriolar and venous dilation
Blocks aldosterone secretion

Hint 35

Decrease nephrotoxicity in diabetics

Front 36

Losartan

Back 36

Competitively antagonize angiotensin II receptors
Arteriolar and venous dilation
Blocks aldosterone secretion

Hint 36

Decrease nephrotoxicity in diabetics

Front 37

Olmesartan

Back 37

Competitively antagonize angiotensin II receptors
Arteriolar and venous dilation
Blocks aldosterone secretion

Hint 37

Decrease nephrotoxicity in diabetics

Front 38

Telmisartan

Back 38

Competitively antagonize angiotensin II receptors
Arteriolar and venous dilation
Blocks aldosterone secretion

Hint 38

Decrease nephrotoxicity in diabetics

Front 39

Valsartan

Back 39

Competitively antagonize angiotensin II receptors
Arteriolar and venous dilation
Blocks aldosterone secretion

Hint 39

Decrease nephrotoxicity in diabetics

Front 40

Hydralazine

Back 40

Direct Vasodilator (Arterioles > Veins)
Activates cGMP, leading to dephosphorylation of myosin (relaxation) and increased K+ conductance (hyperpolarization)
Decreased SPR with resulting increased sypathetic reflex
Almost always administered with β-blocker and diuretic

Front 41

Isosorbide dinitrate

Back 41

Direct Vasodilators

Hint 41

Angina

Front 42

Sodium nitroprusside

Back 42

Direct Vasodilators

Hint 42

Emegency management of hypertension

Front 43

Digoxin

Back 43

Inotropic Agent
Binds to and inhibits cardiac Na+/K+ ATPase, leading to increased Na+ levels intracellularly
Increased Na+/Ca2+ activity lead to increased intracellular a2+ available for contraction
Increases cardiac output

Hint 43

Severe LV systolic dysfunction; NOT indicated in diastolic or RV dysfunction; HF with Afib

Front 44

Amrinone

Back 44

PDE inhibitor
Leads to increased cAMP, producing a greater inotropic effect in cardiac tissue
Increased MLC phosphorylation and relaxation in smooth muscle, producing vasodilation
Inotropic Agent

Front 45

Digitoxin

Back 45

Inotropic Agent

Front 46

Dobutamine

Back 46

Inotropic Agent

Front 47

Milrinone

Back 47

PDE inhibitor: leading to increased cAMP.
In cardiac tissue, produces an inotropic effect.
In vascular smooth muscle, this leads to phosphorylation of MLC, leading to smooth muscle relaxation.
Inotropic Agent