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Pharmacology- Test 3 > Hyperlipidemias > Flashcards

Hyperlipidemias Flashcards

1
Q

What are lipoproteins made of?

A
  • Have a central core of lipids (triglycerides and cholesterol esters)
  • An outer case of phospholipids, free cholesterol and proteins (called apoproteins)
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2
Q

What are the classes of lipoproteins?

A

(1) Chylomicrons
(2) VLDL
(3) IDL
(4) LDL
(5) HDL
- They all differ in size, density and relative proportion of the core lipids and type of apoproteins-

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3
Q

Hyperlipidemia

A

An increase in plasma lipids in general

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4
Q

Hypercholesterolemia

A

An increase in plasma cholesterol, indicated by an increases in LDL (familial, hypothyroidism, corticosteroids)

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5
Q

Hypertriglyceridemia or Hyperlipemia

A

An increase in triglycerides, indicated by an increase in VLDL (familial, diabetes, centripetal obesity, alcohol use, corticosteroids, estrogens)

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6
Q

Mixed hyperlipidemia

A

An increase in both cholesterol and triglycerides (LDL & VLDL)

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7
Q

What contributes to increased risk of coronary artery disease?

A

(1) High LDL cholesterol
(2) Low HDL cholesterol
(3) Hypertriglyceridemia (increased VLDL)

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8
Q

Which lipoproteins are rich in triglycerides? Cholesterol? Apoproteins?

A

VLDLs, LDL, HDLs respectively

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9
Q

Which lipoproteins are large/small in size?

A

Chylomicrons very large in size, VLDLs smaller in size than chylomicrons, HDLs very small in size,

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10
Q

What are desirable levels of Total Cholesterol and LDL Cholesterol? Borderline high? High?

A

(1) Desirable- 240, >160

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11
Q

What are the desirable LDL levels for moderate and high risk patients?

A
  • Moderate risk: LDL <70
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12
Q

What are the 5 classes of Lipid-lowering drugs?

A

(1) HMG-CoA reductase inhibitors (Statins)
(2) Niacin (Nicotinic acid)
(3) Fibric acid derivatives
(4) Bile acid binding agents
(5) Inhibitors of intestinal sterol absorption

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13
Q

What do you have to make sure of with drugs that alter plasma lipoprotein concentrations?

A

They may require adjustment of warfarin doses

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14
Q

What are the HMG-CoA Reductase inhibitors?

A

(1) Lovastatin

(2) Atorvastatin

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15
Q

What drug is the most effective in reducing LDL?

A

Statins (HMG-CoA reductase inhibitors)

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16
Q

Lovastatin/Atorvastatin- Mechanism of Action

A

(1) Reduce cholesterol synthesis by inhibition of HMG Co A reductase
(2) Increases LDL receptors (indirect effect), thus increasing the extraction of LDL by the liver and decreasing LDL in the plasma

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17
Q

Statins- Uses

A

(1) Hypercholesterolemia (increased LDL)
(2) Mixed hyperlipidemia (LDL and VLDL increase)
(3) First line of treatment after M.I.

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18
Q

Statins- Adverse effects

A

(1) Hepatitis (increase of hepatic enzymes such as serum amino transferase)
(2) Myalgia

19
Q

When should statins be discontinued?

A

If serum levels of creatine phosphokinase are elevated of if myopathy occurs (rhabdo, myoglobinuria)

20
Q

Niacin- Mechanism of Action

A

(1) Reduces VLDL secretion from liver and in turn, decreases production of LDL
(2) Inhibits lipolysis in adipose tissue, decreasing FFA supply to the liver and VLDL synthesis
(3) Increases VLDL clearance in the plasma by increasing LPL activity
(4) Decreases catabolism of HDL and increases HDL

21
Q

Niacin- Uses

A

(1) Useful in mixed hyperlipidemia because of its favorable effects of VLDL, LDL, and HDL
(2) combined with other drugs for hypercholesterolemia and hypertriglyceridemia

22
Q

Niacin- Adverse Effects

A
  • Useful only in large doses which produce vasodilation
    (1) cause skin flushing
    (2) pruritis (usually goes away within first few days)
  • increase in serum transaminase level, gastric distress, glucose intolerance, and hyperuricemia
  • Avoid in liver disease, peptic ulcer, gout, diabetes
23
Q

What is used with Niacin to reduce adverse effects?

A

Aspirin (the effects are mediated by prostaglandins)

24
Q

What are the fibric acid derivatives?

A

Gemfibrozil and Fenofibrate

25
Q

Fibric acid derivatives- Mechanism of Action

A

(1) Decrease triglycerides (VLDL) by stimulation of LPL (hypolysis of VLDL), promote the delivery of FFA to adipose tissue
(2) May decrease VLDL synthesis in the liver

26
Q

Fibric acid derivatives- Uses

A
  • Used primarily in hypertriglyceridemia (increase in VLDL)

- May be used in mixed hyperlipidemia

27
Q

Fibric acid derivatives- Adverse Effects

A

(1) Allergic reactions, myalgia, blood cell deficiencies, hypokalemia, and an increase in serum aminotransferase
(2) Risk of myopathy increases when used with HMG-CoA reductase inhibitors
(3) Moderate increase risk in gallstones
(4) Contraindicated in hepatic or renal dysfunction

28
Q

T/F Fibric acid derivatives increase effects of warfarin.

A

TRUE because of it’s binding to plasma proteins

29
Q

What are the bile acid binding agents?

A

Colestipol, Cholestyramine

30
Q

Bile acid binding agents- Mechanism of Action

A

(1) Bind bile acids and prevent their absorption which leads to synthesis of replacement bile acids from cholesterols in the liver
- to obtain more cholesterol for this purpose, the liver increases LDL receptors leading to increased uptake of LDL from the plasma (indirect effect)
(2) May increase triglycerides and cause a small increase in HDL

31
Q

Bile acid binding agents- Uses

A

(1) Hypercholesterolemia (moderately effective)(2) Used in patients who cannot tolerate other drugs or is used in combination with other drugs

32
Q

Bile acid binding agents- Undesirable effects

A
  • annoyoing GI effects (nausea, abdominal bloating, constipation), limit their widespread use
  • interfere with absorption of fat-soluble vitamins and drugs such as digoxin, hydrocholothiazide, and warfarin
33
Q

T/F Bile acid binding agents are absorbed, leading to systemic adverse effects.

A

FALSE; they are not absorbed, no systemic adverse effects

34
Q

What does Ezetimibe do?

A

inhibits intestinal absorption of cholesterol and phytosterols

35
Q

Ezetimibe- mechanism of action

A
  • effective even in the absence of dietary cholesterol because it inhibits the absorption of cholesterol excreted in the bile
  • decreased delivery of intestinal cholesterol to the liver by chylomicron remnants stimulates expression of hepatic LDL receptor, thus enhancing clearance of LDL from the plasma (cholesterol synthesis is increased, however)
36
Q

Does Ezetimibe has a high or low incidence of toxicity?

A

Low (reversible impaired hepatic function)

37
Q

What are the indications of combined drug therapy?

A

When LDL levels are not normalized with a single agent or when LDL and VLDL levels are both elevated

38
Q

What is the effectiveness of combined drug therapy?

A
  • Statins alone decrease LDL cholesterol by 25-45%. Addition of bild acid binding resins can produce a further decrease in LDL cholesterol by 20-25%, whereas addition of nicotinic acid can produce an additional decrease of 15-20%
  • All three drugs combined can produce decreases in LDL cholesterol up to 70%
39
Q

What is Vytorin? Is it more effective than single drug therapy?

A

A combination tablet of ezetimibe and simvastatin that is approved for use; several studies show that Vytorin is no more effective than a statin at reducing heart attack risk and may increase cancer risk

40
Q

What is Advicor and Simcor?

A
  • Advicor- extended release niacin plus lovastatin

- Simcor: extended release niacin plus simvastatin

41
Q

What is Lovaza?

A

Omega 3-acid ethyl esters

42
Q

What does Lovasa do?

A
  • Lowers very high TGs
  • may reduce synthesis of TGs in the liver because EPA and DHA are poor substrates for the enzymes responsible for TG synthesis, and EPA and DHA inhibit esterification of other fatty acids
  • Has been found to increase LDL levels in some patients
43
Q

Lovasa- side effects

A

flu symptoms, infections, upset stomach and change in sense of taste

44
Q

In what is Lovasa found?

A

in plants and the oil of fish (salmon and mackerel)

Pharmacology- Test 3 (7 decks)

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