Exam 5 - Anti-Hyperlipidemic Drugs Hockerman Flashcards

1
Q

which is described below?

-essential component of cell membranes
-precursor to sterols and steroids

a. cholesterol
b. triglyceride (triacylglycerol)

A

a. cholesterol

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2
Q

which is described below?

-storage form of fuel to support generation of high energy compounds
-component of structural lipids

a. cholesterol
b. triglyceride (triacylglycerol)

A

b. triglyceride (triacylglycerol)

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3
Q

true or false: both cholesterol and triglyceride (triacylglycerol) are transported in blood macromolecular aggregates known as lipoproteins

A

true

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4
Q

what is the lipoprotein core made of? (2 things)

A

triglyceride & cholesterol ester

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5
Q

which is the main cholesterol form in blood?

a. chylomicrons
b. VLDL
c. IDL
d. LDL
e. HDL

A

d. LDL

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6
Q

which is involved in transport of dietary lipids from gut to liver & adipose tissue?

a. VLDL
b. IDL
c. LDL
d. HDL
e. chylomicrons

A

e. chylomicrons

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7
Q

which apolipoprotein is structural in HDL and mediates reverse cholesterol transport?

a. ApoA-I
b. ApoB-100
c. ApoB-48
d. ApoE
e. ApoCII

A

a. ApoA-I

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8
Q

which apolipoprotein is structural in chylomicrons and produced in the intestine?

a. ApoA-I
b. ApoB-100
c. ApoB-48
d. ApoE
e. ApoCII

A

c. ApoB-48

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9
Q

____ ____ synthesis is the major source of cholesterol. _____ synthesis is most critical to total body burden

A

De novo; liver

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10
Q

ratio of total cholesterol to HDL-cholesterol is key in assessing risk of CVD. Ratio of > ___ is associated with increased risk of CVD

A

4.5

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11
Q

consequences of hypertriglyceridemia (3 of them)

A

-pancreatitis
-xanthomas (fat build up under surface of skin)
-inc risk of CHD

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12
Q

bile acid sequestrants mechanism (2)

A

-inhibit reabsorption of bile acids from intestine by binding bile acids to form insoluble complex excreted in feces
-up-regulate LDL receptors in liver

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13
Q

two bile acid sequestrant drugs from class

A

cholestyramine (Questran)
colestipol (Colestid)

(colesevelam is another one that Chaudry talked about)

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14
Q

basic mechanism for upreg of LDL receptors by statins

A

statin is ingested, it goes to liver, inhibits HMG-CoA reductase, thus lowering cholesterol production. The dec in liver cholesterol activates SREBP processing

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