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Pharm: Pre Midterm 1 > Antihyperlipidemic Drugs > Flashcards

Antihyperlipidemic Drugs Flashcards

1
Q

What is hyperlipidemia?

A

Elevation of plasma cholesterol and or triglycerides

Low HDL levels

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2
Q

Increased risk of cardiovascular mortality is most closely linked to elevated levels of LDL cholesterol and?

A

Decreased levels of HDL cholesterol

–in addition TAGs present an independent risk factor

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3
Q

What are other risk factors for cardiovascular disease?

A

Cigarette Smoking
Hypertension
Obesity
Diabetes

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4
Q

Primary cause of hyperlipidemia includes what?

A

Monogenic Disease
Genetic Polymorphism
Gene Environment Interactions

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5
Q

What are the classifications of lipid disorders?

A

Type I: Familial Hyperchylomicronemia: increased chylomicrons: Deficiency in LPL or apoCII (Rare)
Type IIA: Familial Hypercholesterolemia: Increased LDL: Decreased or non functional LDL receptor expression
Type IIB: Familial Combined Hyperlipidemia: Increased LDL and increased VLDL. Overproduction of VLDL by the liver (common)
Type III: Familial Dysbetalipoproteinemia: Increased IDL: abnormal apoE
Type IV: Familial HyperTAGs: Increased VLDL. Overproduction and/or impaired catabolism of VLDL (common)
Type V: Familial Mixed TAGs: increased chylomicrons and Increased VLDL. Increased production or decreased clearance of VLDL and chylomicrons

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6
Q

Now secondary hyperlipidemia is common in the adult population. What are the secondary causes in developed countries?

A

Sedentary lifestyle with excessive dietary intake of saturated fat, cholesterol, and trans fatty acids
OTHER FACTORS:
–alcohol (leads to increased VLDL production)
—type 2 DM (increased VLDL synthesis and reduced chylomicron and VLDL catabolism by LPL. ApoCIII levels are increased) – all due to the insulin resistance
–hypothyroidism

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7
Q

What are the signs and symptoms of hyperlipidemia?

A

No symptoms
–can lead to symptomatic vascular disease (coronary artery disease and peripheral arterial disease)
High TGs
–can lead to acute pancreatitis

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8
Q

Lipoprotein disorders are detected by measuring serum lipids after a 10 hour fast. What are these values?

A

Total Cholesterol, TGs, and HDL are measured directly
–LDL are calculated: LDL= TC-(HDL + TG/5)
–only works if TGs are less than 400mg/dl
LDL can be measured directly using plasma ultracentrifugation

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9
Q

Moving on to the drugs, what are the first choice in management of hyperlipidemia?

A

Statins

–decrease the incidence of major coronary events and death in such patients

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10
Q

Addition of a nonstain lipid lowering agent to a stain can reduce what?

A

LDL levels further than a statin alone

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11
Q

What are the 5 main classes of drugs available for the treatment of hyperlipidemia?

A
  1. HMG-CoA reductase inhibitors
  2. Niacin
  3. Bile acid binding resins
  4. Fibric acid derivatives
  5. Cholesterol absorption inhibitors
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12
Q

HMG-CoA reductase inhibitors (statins) include atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin and simvastatin. What is their MOA?

A

Competitive Inhibitors of HMG-CoA reductase

  • -the enzyme that catalyzes the first committed step of cholesterol biosynthesis
  • -blocking this inhibits cholesterol synthesis which causes the cell to up-regulate LDL receptors.
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13
Q

Statins are the most effective drug at lowering LDL. what is the most potent statin?

A

Rosuvastatin followed by Atorvastatin followed by simvastatin followed by Lovastatin/pravastatin

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14
Q

What are the clinical uses for statins?

A 
Drug class of choice for LDL reduction and are most widely used class of lipid lowering drugs 
--reduce cardiovascular mortality
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15
Q

Which patients benefit the least from statins?

A

Homozygous for familial hypercholesterolemia

–lack functional LDL receptors

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16
Q

Which group of patients should not receive statins?

A

pregos

17
Q

What are the four major statin benefit groups?

A
  1. Patients with clinical atherosclerotic cardiovascular disease
  2. Patients with LDL 190 or higher
  3. Patients age 40-75 years of age with diabetes and LDL 70-189
  4. Patients without ASCVD or diabetes with LDL 70-189 with an estimated 10 year risk of ASCVD of 7.5% or higher.
18
Q

In addition to LDL reduction what are other effects of statins?

A

Improve endothelial function
Decrease platelet aggregation
Stabilize atherosclerotic plaque
Reduce inflammation

19
Q

What are the side effects of statins?

A
  1. Elevation of aminotransferases: needs to be baseline measured then monitored
  2. Myopathy and rhabdomolysis: causes myoglobinuria leading to renal injury
20
Q

The next lipid lowering drug is Niacin (nicotinic acid). What affects does this drug have on the lipid profile?

A

Decrease VLDL, LDL and Lp(a)

–increases HDL levels significantly (most significant)

21
Q

What is the MOA for Niacin?

A

Inhibits Adenylyl Cyclase in adipocytes

  • -leads to inhibition of hormone sensitive lipase which reduces transport of fatty acids to the liver and decreases hepatic TG synthesis
  • -as a consequence there is a decrease in hepatic VLDL production and release leading to a reduction in LDL levels
  • in addition there is increased LPL activity as well as HDL
22
Q

What are the uses for Niacin?

A
  1. Most effective drug for raising HDL levels
  2. For patients with combined hyperlipidemia and low HDL levels
  3. Effective in combo with statins
23
Q

What are the adverse effects of Niacin?

A
  1. Intense cutaneous flush
    - -admin of aspirin 30 minutes prior reduces this side effect
  2. Hepatotoxicity and hyperglycemia
  3. Niacin induced insulin resistance causes severe hyperglycemia
  4. elevates uric acid levels and may precipitate gout
  5. Acanthosis nigricans
24
Q

Moving on to the Fibrates, Gemfibrozil and Fenofibrate. What effect do they have on the lipid profile?

A

Lower serum TG and increase LDL levels

25
Q

What is the MOA for Fibrates?

A

Activate the nuclear receptor
–peroxisome proliferator-activated receptor-alpha (PPAR-alpha)
Decrease in plasma TG levels is caused by increased expression of lipoprotein lipase, decreased hepatic expression of apoC-III and increased hepatic oxidation of fatty acids

26
Q

What are the uses for fibrates?

A

Fibrates are the drugs of choice in severe hypertriglyceridemia

27
Q

What are the adverse effects of fibrates?

A

Mild GI disturbances
Myositis can occur
Should be avoided in patients with hepatic or renal dysfunction
Lithiasis: increase biliary cholesterol excretion

28
Q

What are the drug interactions associated with fibrates ?

A

Gemfibrozil: inhibits hepatic uptake of statins, thus increasing plasma concentrations of statins.
-competes for the same glucuronosyl transferases that metabolize most statins
–therefore levels of both drugs may be increased which increases the risk of rhabdomyloysis
Fenfibrate: does not inhibit statin metabolism

29
Q

The next lipid lowering drugs are the Bile Acid Binding Resins, Cholestyramine, Colestipol and Colesevelam. What are these agents useful for?

A

Hyperlipoproteinemias involving isolated increases in LDL

–in patients who have hypertriglyceridemia as well as elevated LDL levels

30
Q

What is the MOA for the Bile Acid Binding Resins?

A

Bind to anionic bile acids in the intestinal lumen and prevent their reabsorption
–the resin-bile acid complex is excreted in feces
Reduction in bile acid concentration causes hepatocytes to increase conversion of cholesterol to bile acids
–therefore cholesterol decreases which leads to up regulation of LDL receptors in the liver, which leads to a decrease LDL
This effect is partially offset by the increased cholesterol synthesis

31
Q

What are the uses for bile acid binding resins?

A

Used in combo with statins or niacin to increase LDL reduction
Drug of choice for children and women planning to become pregnant
Little effect in patients who lack functional LDL receptors

32
Q

What are the adverse effects of Bile Acid Binding Resins?

A

Bloating, nausea, cramping and constipation
Colesevelam is better tolerated than cholestyramine or colestipol
Increase TG so contraindicated in hyperTAG
Impaire absorption of liposouble vitamins (A,D,E,K)

Pharm: Pre Midterm 1 (30 decks)

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