Pharm Final - Drugs For Hyperlipidemia

Front 1

chylomicrons are made up of Tg derrived from _______

Back 1

Diet

--intestines-->blood-->periphreal cells

Front 2

VLDL is made up of Tg from_______

Back 2

Hepatocytes

--Licer-->blood-->periphreal cells

Front 3

LDL is made up of ________derrived from _________ and is taken _________

Back 3

1) made up of cholesterol
2) it is a VLDL remnant (after Tg is removed)
3) LDL --> Blood --> liver and periphreal cells

Front 4

HDL does what

Back 4

takes Cholesterol from the periphery to the liver


-- periphreal cells --> blood -->liver

Front 5

measure serum lipids after how many hours of fasting?

Back 5

10

Front 6

term used to describe elevated LDL

Back 6

hypercholesterolemia

Front 7

term used to describe elevated chylomicrons or VLDL

Back 7

hypertriglyceridemia

Front 8

low HDL puts you at rick for_______

Back 8

heart disease

Front 9

list 6 primary lipoprotein disorders

Back 9

1) hypertriglyceridemia (Type IV)
2) chylomicronemia
3) combined hyperlipidemia (type IIb)
4) dysbetalipoprotinemia (TYpe III)
5) hypercholesterolemia (type IIa)
6) ligand defective apolipoprotein B

Front 10

characteristics of hypertriglyceridemia (Type IV)

Back 10

overproduction of VLDL or low LPL activity

Front 11

characteristics of chylomicronemia

Back 11

LPL and cofactor deficiency

Front 12

characteristics of combined hyperlipidemia (IIb)

Back 12

increased VLDL production and increased conversion to LDL

Front 13

characteristics of Dysbetalipoproteinemia (Type III)

Back 13

Lack of Apo E3,4

Front 14

Characteristics of Hypercholesterolemia (IIa)

Back 14

LDL receptor defect

Front 15

characteristics of Ligand defective apolipoprotein B

Back 15

defect in ligand domain of apoB100

Front 16

secondary causes of lipoprotein disorders

Back 16

1) drug induced
--diuretics
--BB
--isotretinoin
--OCP
2) Other diseases
--diabetes
--hypothyroidism
--alcoholism
--renal disease
--Liver disease

Front 17

describe the therapudic lifestyle change to treat lipoprotein disorders

Back 17

1) therapudic diet
--total fat 20-25% of total callories
--saturated fat <7% of callories
--cholesterol <200mg/day
--soluble fiber
2) weight reduction
3) physical activity

Front 18

drugs used to tx hyperlipidemia

Back 18

1) statins
2) niacin
3) bile acid binding resins
4) fibrates

Front 19

list 6 statins

Back 19

1) lovastatin
2) simvastatin
3) pravastatin
4) atorvastatin
5) fluvastatin
6) rosuvastatin

Front 20

what is the MOA for all statins

Back 20

inhibits HMG-CoA reductase -->
decrease hepati Cholesterol synthesis-->
upregulate hepatic LDL receptors-->
increase uptake of LDL cholesterol-->
decrease serum and total cholesterol

Front 21

which of the statins are inactive lactone prodrugs?

Back 21

1) Lovastatin
2) Simvastatin

Front 22

which of the statins has an open, active lactone ring?

Back 22

pravastatin

Front 23

which of the statins is active, and fluorine containing

Back 23

1) atorvastatin
2) fluvastatin
3) rosuvastatin

Front 24

most statins have short half lifes (2-3 hours) so when must they be given?

Back 24

1) administered in evening so peak effect occurs during nocturnal peak of cholesterol synthesis

Front 25

which statin has absorption increased when taken with food?

Back 25

lovostatin

Front 26

which statins have a long half life?

Back 26

atorvastatin (11-14 hours)
Rosuvastatin

--therefore can be administered antime...not just the evening

Front 27

most statins are metabolized by________

Back 27

CYP 3A

Front 28

which statin is not metabolized by CYP 3A?

Back 28

pravastatin
--therefore fewer drug interactions

Front 29

common CYP 3A inhibitors

Back 29

1) erythromycin
2) azole antifungal drugs (ketoconazole)
3) antidepressants
4) HIV protease inhibitors

Front 30

adverse effects of statins

Back 30

1) liver toxicity
2) muscle myositis (inflamed muscle)
3) muscle myalgia (muscle pain)

Front 31

name the bile acid binding resins

Back 31

1) colestipol
2) cholestyramine
3) cikesevelam

Front 32

MOA of the bile acid binding resins

Back 32

1) bind to the bile acid in the GI tract
2) prevents reabsorption of the bile acid
3) increases utilization of cholesterol to replace bile acids

Front 33

clinical use of bile acid binding resins

Back 33

1) persons not tollerating other drugs fr hypercholesterolemia
2) additive effect with other drugs

Front 34

pharmicokinetics of bile acid binding resins

Back 34

1) administered before meals and at bedtime
2) not absorbed from the gut

Front 35

drug interaction of bile acid binding resins

Back 35

1) inhibits absorption of:
--digoxin
--thyroid hormone
--other

****cholestyramine is the only one of the bile acid binding resins that can be used with any other drug

Front 36

adverse effects of the bile acid binding resins

Back 36

1) may cause constipation

Front 37

which drug inhibits intestinal sterol absorption?

Back 37

Ezetimibe

Front 38

MOA of Ezetimibe

Back 38

1) Ezetimibe localizes in the brush border of the small intestine
2) it inhibits the absorption of cholesterol

Front 39

effects of Ezetimibe on lipids

Back 39

1) decrease LDL
2) Decrease TG
3) Increase HDL

Front 40

pharmicokinetics of Ezetimibe

Back 40

1) absorbed in the small intestine
2) t1/2 = 22h
3) metabolized by conjugation w/ glucournate
4) 80% excreted in feces

Front 41

adverse effect of Ezetimibe

Back 41

few...none mentioned

Front 42

unique characteristic of Ezetimibe

Back 42

1) can be used alone or combined with a statin

--i.e. Vytorin = Ezetimibe +simvastatin

Front 43

name the fibric acid drugs

Back 43

1) Gemfibrozil
2) Fenofibrate

Front 44

MOA of the fibrates (fibric acid drug)

Back 44

1) PPAR - alpha ligand

--Bind PPAR - alpha RE (promotor region of the gene) --> transcription induction --> LPL (HDL apolipoprotein)

Front 45

effect of fibrates on the lipids

Back 45

1) increase FA catabolism
2) decrease VLDL secretion
3) increase VLDL clearance
4) decrease TG levels

Front 46

clinical use of fibrates

Back 46

1) tx hypertriglyceridemia
2) tx low HDL levels???

Front 47

adverse effect of fibrates

Back 47

1) myopathy, rhabdomyolysis
2) bone marrow supression
3) exfoliative dermatitis

Front 48

niacin is what type of acid?

Back 48

nicotinic acid

Front 49

MOA of niacin

Back 49

simular to fibrates except greater effect on LDL
--inhibit VLDL secretion
--Activate LPL (directly)

Front 50

effects of Niacin on the lipids

Back 50

1) lower LDL
2) lower TG
3) Increase HDL (more than any oter drug alone)

Front 51

clinical use of niacin

Back 51

1) hypercholesterolemia
2) hypertriglyceridemia
3) Low HDL

Front 52

adverse effects of niacin

Back 52

1) cutaneous flushing
2) hepatitis
3) increase in blood glucose (be careful in diabetics)
4) aggrevate in peptic ulcers
5) myopathy, rhabdomyolysis

Front 53

avoid the use of gemfibrozil with the use of__________

Back 53

niacin

Front 54

use statins cautiously when patient is on__________or _______

Back 54

gemfibrozil or niacin

Front 55

drugs used to tx hypercholesterolemia

Back 55

1) HMG-CoA reductase inhibitors - ‘statins’
2) Bile acid-binding resins
3) Niacin
4) Ezetimibe

Front 56

Drugs for hypertriglyceridemia and low HDL

Back 56

1) Gemfibrozil
2) Niacin