Hyperlipidemia Flashcards

(29 cards)

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?

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
What is an example of a fibrate?
gemfibrozil
26
What are the benefits of fibrates?
best TG-lowering drugs: decreases 25-50%; increases HDL-C 15-25%
27
What are the side effects of fibrates?
GI upset, cholelithiasis, myositis, abnormal LFTs
28
What are the contraindications for fibrates?
hepatic or renal dysfunction, gallbladder disease
29
What is the MOA of omega-3s?
inhibits hepatic TG synthesis, augments chylomicron TG clearance