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Pharmacology 2 Final Dr. Balqees Ikhmais > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

What are the two main types of lipids?

A

Cholesterol and triglycerides.

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2
Q

Why do lipids need transporters (such as lipoproteins) to move around the body?

A

They are water-insoluble.

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3
Q

What are lipoproteins?

A

Spherical macromolecules of lipid and apolipoprotein.

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4
Q

Where is each type of lipoprotein synthesized?

A
  • Chylomicron: intestine.
  • VLDL and LDL: liver.
  • HDL: peripheral tissues.
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5
Q

What is the function of chylomicrons?

A

Carry exogenous triglycerides and cholesterol from the gut to blood circulation.

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6
Q

What does VLDL transport?

A

Endogenous triglycerides from the liver to blood circulation.

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7
Q

What is the role of LDL?

A

Carry endogenous cholesterol from the liver to blood circulation.

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8
Q

What does HDL do?

A

Carries cholesterol from peripheral tissues and blood to the liver for metabolism and/or secretion.

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9
Q

What are the three lipid-related factors correlated with coronary heart disease (CHD)?

A

Elevated LDL-C, elevated triglycerides, low HDL-C.

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10
Q

What do plasma lipids mostly consist of?

A

Lipoproteins.

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11
Q

What are lipoproteins a combination of?

A

Triglyceride or cholesterol with apoprotein.

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12
Q

List the clinically important lipoproteins in decreasing order of atherogenicity.

A

LDL > VLDL > chylomicrons > HDL.

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13
Q

What is the primary effect of HMG CoA reductase inhibitors on LDL-C?

A

Lower elevated LDL-C.

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14
Q

What is the result of lowering LDL-C with HMG CoA reductase inhibitors?

A

Reduction in coronary events and death from CHD.

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15
Q

How are HMG CoA reductase inhibitors commonly known?

A

Statins.

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16
Q

Name some common statins.

A

Lovastatin, Simvastatin, Pravastatin, Atorvastatin, Fluvastatin, Pitavastatin, Rosuvastatin.

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17
Q

Which statin is the most effective?

A

Rosuvastatin.

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18
Q

How do HMG CoA reductase inhibitors (statins) lower LDL cholesterol?

A

Statins competitively inhibit HMG CoA reductase, the rate-limiting step in cholesterol synthesis, depleting intracellular cholesterol. This increases cell surface LDL receptors, which bind and internalize circulating LDLs, leading to increased LDL catabolism.

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19
Q

What additional effects do HMG CoA reductase inhibitors have?

A

Decrease triglyceride levels, increase HDL cholesterol levels in some patients.

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20
Q

What is the primary treatment option for hypercholesterolemia?

A

Statins.

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21
Q

For which patients are statins considered first-line treatment?

A

Patients with elevated risk of atherosclerotic cardiovascular disease (ASCVD).

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22
Q

What is the effect of statins on plasma cholesterol levels?

A

They lower plasma cholesterol levels in all types of hyperlipidemias.

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23
Q

When should statins be administered and why?

A

In the evening, because major cholesterol synthesis happens in the early morning.

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24
Q

What are the common adverse effects of statins?

A

Elevated liver enzymes (hepatotoxicity), myopathy, and rhabdomyolysis.

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25
Q

How can statins affect warfarin?

A

They may increase the effect of warfarin by inhibiting its metabolism.

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26
Q

Why are statins contraindicated during pregnancy and lactation?

A

Due to potential adverse effects on the fetus and infant.

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27
Q

By what percentage does niacin reduce LDL-C?

A

20%.

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28
Q

By what percentage does niacin lower triglycerides?

A

35%.

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29
Q

What is niacin the most effective agent for?

A

Increasing HDL-C.

30
Q

How does niacin reduce the production of free fatty acids?

A

By inhibiting lipolysis in adipose tissue.

31
Q

What does the liver use circulating free fatty acids for?

A

As a major precursor for triglyceride synthesis.

32
Q

How does reduced liver triglyceride levels affect hepatic VLDL production and LDL-C plasma concentrations?

A

Decreases hepatic VLDL production, which reduces LDL-C plasma concentrations.

33
Q

What plasma levels does niacin lower and what condition is it used to treat?

A

Lowers plasma levels of both cholesterol and triglycerides; used in the treatment of familial hyperlipidemias.

34
Q

What is the most common side effect of niacin?

A

Intense cutaneous flush and pruritus.

35
Q

What causes the cutaneous flush and pruritus from niacin, and how can it be managed?

A

Production of prostaglandins; managed by taking NSAIDs before administering niacin and taking it at night.

36
Q

How does niacin affect uric acid secretion and what does this predispose to?

A

Inhibits tubular secretion of uric acid, predisposing to hyperuricemia and gout.

37
Q

Why should niacin be avoided in hepatic disease and used with caution with statins?

A

Due to the risk of hepatotoxicity.

38
Q

What are fenofibrate and gemfibrozil derivatives of?

A

Fibric acid.

39
Q

What effects do fenofibrate and gemfibrozil have on lipid levels?

A

Lower serum triglycerides and increase HDL levels.

40
Q

Which agents are most efficacious in lowering triglycerides?

A

Niacin and fibric acid derivatives.

41
Q

What receptors do fibrates activate to regulate lipid metabolism?

A

Peroxisome proliferator-activated receptors (PPARs).

42
Q

How do fibrates decrease triglyceride concentrations?

A

By increasing the expression of lipoprotein lipase.

43
Q

What is the clinical use of fibrates?

A

Treatment of hypertriglyceridemias.

44
Q

What are the most common adverse effects of fibrates?

A

Mild gastrointestinal (GI) disturbances.

45
Q

What risk is associated with the increased biliary cholesterol excretion caused by fibrates?

A

Predisposition to form gallstones.

46
Q

What serious adverse effects may occur when gemfibrozil is taken with statins?

A

Myopathy and rhabdomyolysis.

47
Q

What is the primary effect of bile acid sequestrants (resins) on LDL cholesterol?

A

Significant LDL cholesterol-lowering effects.

48
Q

How do the benefits of bile acid sequestrants compare to those of statins?

A

The benefits are less than those observed with statins.

49
Q

What do cholestyramine, colestipol, and colesevelam bind to in the small intestine?

A

Bile acids and bile salts.

50
Q

How is the resin/bile acid complex excreted from the body?

A

Excreted in the feces.

51
Q

What is the effect of lowering bile acid concentration on hepatocytes?

A

Increases conversion of cholesterol to bile acids.

52
Q

What is the consequence of increased conversion of cholesterol to bile acids?

A

Decreased intracellular cholesterol concentrations.

53
Q

For what conditions are bile acid-binding resins useful?

A

Treating type IIA and type IIB hyperlipidemias.

54
Q

In what combination are bile acid-binding resins often used?

A

In combination with diet or niacin.

55
Q

For what additional condition is colesevelam indicated and why?

A

Type 2 diabetes due to its glucose-lowering effects.

56
Q

What is the solubility and molecular weight characteristic of bile acid sequestrants?

A

Insoluble in water and have large molecular weights.

57
Q

How are bile acid sequestrants processed after oral administration?

A

They are neither absorbed nor metabolically altered by the intestine.

58
Q

How are bile acid sequestrants excreted from the body?

A

Totally excreted in feces.

59
Q

What are the most common side effects of bile acid-binding resins?

A

GI disturbances such as constipation, nausea, and flatulence.

60
Q

How do bile acid-binding resins affect the absorption of vitamins and drugs?

A

They may impair the absorption of fat-soluble vitamins (A, D, E, K) and interfere with the absorption of many drugs.

61
Q

Why are bile acid-binding resins contraindicated in patients with significant hypertriglyceridemia?

A

Because they may raise triglyceride levels.

62
Q

What is the mechanism of action of ezetimibe?

A

Selectively inhibits absorption of dietary and biliary cholesterol in the small intestine.

63
Q

How does ezetimibe affect LDL and HDL cholesterol levels?

A

Lowers LDL cholesterol and increases HDL.

64
Q

Why does ezetimibe increase HDL levels?

A

Due to increasing the clearance of cholesterol from the blood.

65
Q

How common are adverse effects with the use of ezetimibe?

A

Adverse effects are uncommon.

66
Q

What are omega-3 polyunsaturated fatty acids (PUFAs) used for?

A

Triglyceride lowering.

67
Q

What is a potential adverse effect of omega-3 PUFAs on cholesterol?

A

May raise LDL-C.

68
Q

How do essential fatty acids affect VLDL and triglyceride synthesis?

A

Inhibit VLDL and triglyceride synthesis in the liver.

69
Q

What are the primary sources of omega-3 PUFAs eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)?

A

Marine sources such as tuna, halibut, and salmon.

70
Q

What are the most common side effects of omega-3 PUFAs?

A

GI effects (abdominal pain, nausea, diarrhea) and a fishy aftertaste.

71
Q

In which patients can the bleeding risk be increased with omega-3 PUFAs?

A

Those concomitantly taking anticoagulants or antiplatelets.

Pharmacology 2 Final Dr. Balqees Ikhmais (6 decks)

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