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Pharm II > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

what are the 3 major classes of lipoproteins?

A

LDLs
HDLs
very low density lipoproteins (VLDLs)

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2
Q

where is synthesis of lipids greatest?

A

liver

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3
Q

what does the intestinal mucosa secretes?

A

VLDL (TG-rich)

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4
Q

what do triglycerides break down into?

A

FFA + phospholipids (transferred to HDL)

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5
Q

what enzyme breaks down cholesterol?

A

HMG-CoA reductase (rate limiting step)

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6
Q

what type lipidemia is from a single inherited gene defect or caused by combo of genetic and environmental factors

A

primary hyperlipidemia

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7
Q

what type lipidemia is result of generalized metabolic disorders ie., DM, excessive ETOH, hypothyroidism, primary biliary cirrhosis

A

Secondary hyperlipidemia

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8
Q

what is due to dysfunctional or absent LDL receptors and leads to increased LDL (250-450)

A

Familial hypercholesterolemia (FH)

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9
Q

What id due to a decreased LPL activity leading to decreased TG removal. manifests as TG of 200-500

A

Familial hypertriglyceridemia (FHTG)

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10
Q

Defect with increased HDL catabolism. Will have isolated HDL <35.

A

Hypoalphalipoproteinemia

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11
Q

what are 3 drugs that may alter lipid profiles

A 
Thiazide diuretics (increase TGs)
Beta blockers (Increase TGs, decrease HDL) 
OCPs (increase cholesterol and TGs)
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12
Q

what do macrophages due to LDL

A

Oxidize LDL and then take up the LDL creating foam cells which makes the cell surface more adhesive

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13
Q

What does HDL promote?

A

Reverse cholesterol transport

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14
Q

what is Preventing the development of atherosclerosis and cardiovascular disease

A

primary prevention

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15
Q

Prevent the progression of cardiovascular disease and recurrence of cardiovascular events

A

secondary prevention

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16
Q

what is the optimal LDL level?

A

<100

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17
Q

what is the desirable total cholesterol level?

A

<200

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18
Q

what should HDL be between?

A

40-60

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19
Q

what should triglycerides be less than?

A

<150

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20
Q

what should antihyperlipidemic drugs be combined with?

A

diet
exercise
weight reduction

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21
Q

after antihyperlipidemia drugs are started when should you get labs?

A

4-8 weeks after starting therapy

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22
Q

What is the MOA of Niacin?

A

Inhibits mobilization of FFA’s from adipose tissue => results in decreased VLDL synthesis by the liver

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23
Q

therapeutic uses for niacin?

A

mixed hyperlipoporteinemias
increase HDL (most effective)
decrease TG

24
Q

ADRs with niacin

A

Vasodilation –> Flushing, itching, HA
GI- activation of PUD
hepatotoxicity (LFTs 3X ULN) (get LFTs q 6-8 weeks)

25
Q

contraindications w/ niacin

A

DM (worse glucose tolerance), gout, peptic ulcer

liver dz

26
Q

what is an anithyperlipidemic drug that is a fibrate?

A

Gemfibrozil (main one)

fenofibrate

27
Q

MOA of gemfibrozil

A

inhibits lipolysis and increases liporprotein lipase. Decrease serum VLDL and increase HDL

28
Q

what is gemifibrozil approved for?

A

Lowering TG in patients with hypertriglyceridemia

used for combined increased cholesterol and TG (in combo)

29
Q

ADRs with gemfibrozil

A 
GI (most common, decrease with time)
myopathy 
hepatotoxicity
neutropenia
gallstones and pancreatitis (avoid in high risk patients)
30
Q

What are 2 bile acid binding resins?

A

Cholestyramine

Colestipol

31
Q

MOA of bile acid binding resins

A

inhibit enterohepatic recycling of bile acids and salts

liver stimulated to convert stores cholesterol to bile acids

32
Q

What do bile acid binding resins lower?

A

Total cholesterol
LDL in dose dependent area
(may increase TGs)

33
Q

ADRs of bile acid binding resins

A

primarily GI

can increase triglycerides

34
Q

what three drugs should you not give w/i 2 hours of bile acid binding resins?

A

warfarin, thyroid, digoxin

35
Q

Contraindications with bile acid binding resins

A

Biliary obstruction, fasting TG >500

relative is fasting TG >200

36
Q

MOA of HMG-COA reductase inhibitors

A

Competitively inhibit the rate-limiting enzyme (HMG-CoA Reductase) necessary for cholesterol synthesis results in an increase in hepatic LDL receptors

37
Q

effects of HMG-CoA reductase inhibitors

A

Decrease LDL, TG, increases HDL

38
Q

Other CV benefits with statins

A

Stabilize atherosclerotic plaques
enhance vascular nitric oxide production
attenuate inflammation due to vascular injury
decrease oxidative stress

39
Q

What drug class also inhibit bone resorption, modulate inflammatory precess in glomerular mesangial.

A

statins

40
Q

when do statins have their greatest efficacy?

A

dinner or at bedtime to coincide with peak cholesterol biosynthesis

41
Q

Most common ADRs with statins

A

HA, myalgias, dyspepsia
Hepatotoxicity (LFTs)
myopathy and CPk >10 x normal

42
Q

Biggest contraindications with statins

A 
grapefruit juice
macrolides
triazole antifungals
fluoroquinolones
diltiazem
verapamil
amoidarone
omperzole
protease inhibitors
43
Q

What does lovastatin due to warfarin?

A

increases warfarin effects

44
Q

what is a drug that combines Niacin ER and lovastatin?

A

advicor

45
Q

ADRs with advicor

A

increased risk of myopathy

monitor LFTs

46
Q

drug that inhibits absorption of choelsterol at the brush border of the small intestine and there is decreased delivery of cholesterol to the liver.

A

Ezetimbe (cholesterol absorption inhibitor)

47
Q

ADRs with ezetimbe

A

HA
GI
arthralgia
sinusitis

48
Q

what is simvastatin + ezetimbe

A

Vytorin

49
Q

when should vytorin be used?

A

only is other drugs aren’t working well enough

50
Q

is there any CV benefit for replacing estrogen for women going into menopause?

A

No, not recommended to use estrogen to prevent CAD

51
Q

what is fish oil effective at lowering

A

Triglycerides

52
Q

side effects of lovaza (Rx fish oil drug)

A

can effect bleeding time (more thinning of blood)
may impair insulin secretion
GI

53
Q

What does metamucil help lower

A

LDL

54
Q

What are OTC things that help with hyperlipidemia

A

Garlic
olestra
red yeast rice

55
Q

what can moderate alcohol consumption help with

A

Increase HDL
decreased LDL oxidation
decreased platelet aggregation

Pharm II (16 decks)

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