Hyperlipidemia Flashcards

1
Q

What are the LDL-C goals?

A

Low risk: <160 mg/dL, moderate to moderately high risk: <130, high risk: <100

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2
Q

What are the goals of other lipoprotein levels?

A

total C: 50, TG: <150, HDL-C: >50

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3
Q

What are the dietary guidelines for treating hyperlipidemia?

A
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4
Q

What is the non-HDL-C (VLDL-C + LDL-C) goal?

A

LDL-C goal + 30 mg/dl

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5
Q

Which drug classes are effective in lowering LDL-C?

A

statins

bile acid resins

niacin

cholesterol absorption inhibitors

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6
Q

What is the mechanism of action of statins (simvistatin)?

A

Partially inhibits HMG-CoA reductase, the rate-limiting step of cholesterol synthesis, lowering intracellular cholesterol. This induces LDL receptor formation and removal of LDL-C from the circulation

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7
Q

What are the benefits of statins?

A

Lowers LDL-C 25-50%, raises HDL-C 10%, lowers TG 15-25%

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8
Q

What are the side effects of statins?

A

abnormal LFTs (increased transaminase), myositis/myalgias

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9
Q

Concomitant use of which drug class increases the risk of myalgia/myositis with simvistatin?

A

fibrates

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10
Q

What is the MOA of bile acid resins?

A

interrupts bile acid reabsorption, requiring bile acid synthesis from cholesterol; this upregulates LDL receptor synthesis, resulting in removal of LDL and VLDL from the blood

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11
Q

What is an example of a bile acid resin?

A

cholestyramine

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12
Q

What are the benefits of cholestyramine?

A

lowers LDL-C 10-15%

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13
Q

What are the side effects of cholestyramine (and other bile acid resins)?

A

GI: constipation, bloating, abdominal pain

Drug interactions (affects absorption): warfarin, beta-blockers, thyroid hormone

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14
Q

What is the MOA of niacin?

A

reduces hepatic production of VLDL and apo B, which results in decreased catabolism to LDL

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15
Q

What are the benefits of niacin?

A

best agent to raise HDL-C, lowers LDL-C and TG 10-30%

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16
Q

What are the side effects of niacin?

A

flushing, hepatotoxicity, hyperuricemia (uric acid), hyperglycemia and reduced insulin sensitivity, activation of peptic ulcer

17
Q

What are the contraindications for niacin?

A

active liver disease, peptic ulcer disease

18
Q

What causes niacin-induced flushing?

A

release of PGD2 from tissue macrophages in the skin (minimize with aspirin)

19
Q

What is the MOA of cholesterol absorption inhibitors?

A

blocks the uptake of micelles into the brush border of the duodenum and jejunum

20
Q

What is an example of a cholesterol absorption inhibitor?

A

ezetimibe

21
Q

What are the benefits of ezetimibe?

A

decreases delivery of intestinal cholesterol to the liver, reducing hepatic stores; increases clearance from the blood; reduces LDL-C by 18%

22
Q

What are the adverse effects of ezetimibe?

A

relatively well-tolerated with few side effects

23
Q

Which drug classes are effective in lowering TG?

A

fibrates

niacin

Omega-3 fatty acids

24
Q

In patients with very high TG, what is the primary aim of therapy?

A

reduce risk of pancreatitis by lowering TG

25
Q

What is an example of a fibrate?

A

gemfibrozil

26
Q

What are the benefits of fibrates?

A

best TG-lowering drugs: decreases 25-50%; increases HDL-C 15-25%

27
Q

What are the side effects of fibrates?

A

GI upset, cholelithiasis, myositis, abnormal LFTs

28
Q

What are the contraindications for fibrates?

A

hepatic or renal dysfunction, gallbladder disease

29
Q

What is the MOA of omega-3s?

A

inhibits hepatic TG synthesis, augments chylomicron TG clearance