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Pharmacology Exam II > Antihyperlipidemics > Flashcards

Antihyperlipidemics Flashcards

1
Q

Chylomicrons mainly consist of (2)

Ratio?

A

Dietary triglycerides
Cholesteryl esters

10:1

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2
Q

VLDL primarily consists of (2)

Ratio?

A

Endogenous triglycerides
Cholesteryl esters

5:1

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3
Q

IDL primarily consists of (2)

Ratio?

A

Endogenous triglycerides
Cholesteryl esters

1:1

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4
Q

LDL primarily consists of (1)

A

Cholesteryl esters

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5
Q

HDL primarily consists of (2)

A

cholesteryl esters

phospholipids

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6
Q

Major Apolipoproteins of CHYLOMICRONS (4)

A

B-48, C, E, and A

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7
Q

Major apolipoproteins of VLDL (3)

A

C, B-100, and E

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8
Q

Major apolipoproteins of LDL (1)

A

B-100

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9
Q

Major Apolipoproteins of HDL (5)

A

A-I, A-II, C, E, and D

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10
Q

What is the important transporter for cholesterol in intestines?

A

NPC1-L1

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11
Q

Chylomicron Synthesis Steps

A

Formed in small intestine - Apo-B48 attached

Enter circulation - Apo-CII and Apo-E attached

LPL breaks down triglycerides through activation by Apo-CII

Chylomicron remnants lose Apo-CII to HDL

Reuptaken by liver through Apo-E protein

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12
Q

VLDL Synthesis Steps

A

Formed in Liver

Apo-B100 attached

Received Apo-E and Apo-CII in circulation

LPL removes TG’s

IDL forms and loses Apo-CII and Apo-E

LDL finally forms - Apo-B100 allows uptake into liver and extrahepatic tissue

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13
Q

Where is the only place to get rid of excess cholesterol?

A

Liver

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14
Q

Reverse cholesterol transport is performed by what molecule?

What apolipoprotein is important in the process?

A

HDL

Apo-AI

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15
Q

Apo-AI on HDL increases activity of what?

Also binds to what in the liver?

A

LCAT

SR-B1 - to allow exchange of cholesterol

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16
Q

Primary chylomicronemia associated with?

Manifests as?

A

decreased LPL activity

Increased chylomicrons/VLDL

17
Q

Familial Hypertriglyceridemia associated with?

Manifests as

A

impaired VLDL/chylomicron removal

Increased VLDL (moderate)

18
Q

Familial Combined Hyperlipoproteinemia associated with?

Manifests as?

A

Increased VLDL production

high conversion of VLDL to LDL

Increased VLDL and LDL

19
Q

Familial Hypercholesterolemia associated with?

Manifests as?

A

LDLR impairments

Increased LDL

20
Q

Familial Ligand-defective Apo-B associated with?

Manifests as?

A

mutated apo-B100

results in impaired endocytosis of LDL

Increased LDL

21
Q

Familial Dysbetalipoproteinemia associated with?

Manifests as?

A

decreased clearance of VLDL, IDL, and chylomicrons due to DEFECT OF APO E

Increased IDL, Chylomicrons

22
Q

HMG-CoA reductase inhibitors end in?

A

statin

23
Q

Fibrates MOA

A

activate PPAR

increases Apo-AI and A-II

Decreases Apo-CIII

Increases LPL expression

ultimately leads to increased plasma HDL and decreased Plasma triglycerides

24
Q

Fibrates (2)

A

gemfibrozil

fenofibrate

25
Q

Bile acid-binding resins (3)

A

cholestyramine
colesevelam
colestipol

26
Q

Bile-acid binding resins MOA

A

bind up bile acids and lead to excretion

causes liver to increase bile synthesis which uses more cholesterol

leads to decreased LDL

27
Q

Bile-acid binding resins shouldn’t be used in

A

Hypertriglyceridemia patients

can cause increase in TG’s

28
Q

Niacin MOA

A

decreases LPL activity in fat tissue

increases HDL production

decreases free fatty acids in plasma which decreases VLDL synthesis by liver

29
Q

Niacin useful in?

A

all hypertriglyceridemias and hypercholesterolemias

30
Q

Bile-acid binding resins useful in?

A

Moderately effective drugs in hypercholesterolemia treatment

Treatment of hypercholesterolemia in patients for whom statins do not provide sufficient LDL reduction

familial hypercholesterolemia

31
Q

Niacin adverse effects

A

cutaneous flushing/itching

hyperuricemia

hepatotoxicity

increased risk of statin-induced myopathy

32
Q

Ezetimibe MOA

A

inhibits NPC-L1 cholesterol transporter in intestines

leads to decreased Chylomicron size, decreased LDL, and Increased VLDL

33
Q

Ezetimibe useful in

A

treatment of all types hypercholesterolemia

34
Q

Statins MOA

A

inhibit HMG-CoA reductase

prevents formation cholesterol

leads to increased LDL receptor expression

leading to decreased LDL

35
Q

Most potent statins?

least?

A

atorvastatin and rosuvastatin

Fluvastatin

36
Q

Adverse effects of Statins

Contraindicated in?

A

Myopathy/myositis

Rhabdomyolysis

Liver toxicity

PREGNANCY

Pharmacology Exam II (5 decks)

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