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CPR II Exam 1 > Lecture 5: Drugs for Lipid Disorders > Flashcards

Lecture 5: Drugs for Lipid Disorders Flashcards

1
Q

Dietary measures the management of hyperlipoproteinemia are initiated first unless the pt has evidence of what?

A

Coronary or peripheral vascular disease

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2
Q

The HMG-CoA reductase inhibitors used in management of lipid disorders end in which suffix?

A

-statin

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3
Q

What are the most effective agents in reducing LDL levels and best tolerated class of lipid lower agents?

A

HMG-CoA reductase inhibitors (statins)

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4
Q

Which HMG-CoA reductase inhibitor (statin) is almost completely absorbed when taken orally?

A

Fluvastatin

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5
Q

Statin absorption is enhanced by what?

A

Food

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6
Q

Which 3 HMG-CoA reductase inhibitors (statins) have the longest plasma half-lives of 19, 14, and 12 hours?

A
  • Rosuvastatin (19 hrs)
  • Atorvastatin (14 hrs)
  • Pitavastatin (12 hrs)
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7
Q

Which HMG-CoA reductase inhibitor is not metabolized by CYP450’s?

A

Pravastatin

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8
Q

What is the MOA of HMG-CoA reductase inhibitors (statins)?

Leads to what changes and overall net effect?

A
  • Inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis
  • Depletes intracellular supply of cholesterol –> cell then ↑ the # of cell-surface LDL-receptors = ↑ internalization of circulating LDL
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9
Q

List the HMG-CoA reductase inhibitors in descending order of potency starting with the most potent.

i.e., simvastatin, rosuvastatin, atovastatin, pitavastatin, lovastatin, pravastatin and fluvastatin

A

Atorvastatin = Rosuvasatin > Simvastatin > Pitavastatin = Lovastatin = Pravastatin > Fluvastatin

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10
Q

List the 4 therapeutic benefits of HMG-CoA reductase inhibitors (statins)?

A
  • Plaque stabilization
  • Improvement of coronary endothelial function
  • Inhibition of platelet thrombus formation
  • Anti-inflammatory effects
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11
Q

When does the majority of cholesterol synthesis occur, thus, is when statins are taken for therapeutic effects?

A

Nightime

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12
Q

Statins are effective at lowering plasma cholesterol levels in all types of hyperlipidemia and can be used alone, or in combo with what 3 other agents?

A
  • Resins
  • Niacin
  • Ezetimibe
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13
Q

What may be seen in pt’s with liver disease or a hx of alcohol abuse if they taken a statin?

A

Elevations of serum aminotransferase activity (up to 3x normal)

*Levels decrease upon suspension of drug therapy

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14
Q

What may be seen in the muscle of patients who take a statin, especially in those with high level of physical activity?

A

Creatine kinase activity levels may increase

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15
Q

Which AE associated with the muscle can occur rarely and lead to renal injury in those on statins?

A

Rhabdomyolysis (leading to myoglobinuria)

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16
Q

There is an increased incidence of what AE in pt’s concomitantly taking statins and fibrates?

A

Myopathy

*Can also occur with monotherapy

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17
Q

Statins increase the levels of which anti-coagulant?

A

Warfarin

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18
Q

Statins are contraindicated in which subset of patients?

A

Women who are pregnant, lactating, or likely to become pregnant

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19
Q

Use of statins is not recommended in pt’s with what 2 underlying diseases?

A
  • Liver disease
  • Skeletal muscle myopathy
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20
Q

Use of statins in children is restricted to those with what?

A

Homozygous familial hypercholesterolemia and some pt’s w/ heterzygous disease

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21
Q

Niacin (nicotinic acid, Vit B3) decreases levels of which 3 lipids and increases what?

A
  • Decreases = TG’s, LDL, and Lp(a)
  • Increases = HDL
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22
Q

Niacin is converted to nicotinamide and incorporated into NAD, which is well absorbed, and is mainly distributed to which 3 tissues?

A
  • Hepatic
  • Renal
  • Adipose tissue
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23
Q

What is the MOA of niacin in reducing levels of lipids?

Net effect on FFA’s, LDL, VLDL, and HDL?

A
  • Inhibits lipolysis of TG’s in adipose tissue = ↓ circulating FFA’s
  • Reduced hepatic synthesis of VLDL and LDL
  • Catabolic rate for HDL is ↓
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24
Q

What is the effect of niacin on levels of tPA and fibrinogen?

A
  • Fibrinogen levels are decreased
  • tPA levels are increased
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25
Q

What can be taken before the administration of niacin to reduce the AE of nicain cutaneous flushing?

A

Aspirin or 1x daily ibuprogen

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26
Q

Niacin may cause toxicity of which organ as an AE?

Levels of what should be monitored at baseline?

A
  • Hepatotoxicity
  • Monitor liver function (aminotransferases)
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27
Q

Niacin should be avoided in pt’s with what 2 underlying diseases?

A
  • Hepatic disease
  • Active peptic ulcer
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28
Q

Why should niacin be used with caution in pt’s with diabetes mellitus?

A

Due to niacin-induced insulin resistance –> hyperglycemia

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29
Q

Which cutaneous AE’s may be associated with the use of niacin?

A
  • Pruritus
  • Acanthosis nigricans
  • Rashes
  • Dry skin or mucous membranes
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30
Q

How many times is niacin doses per day?

A

2-3x daily (half-life is ~60 mins)

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31
Q

Which enzyme inside of adipose tissues is inhibited by Niacin?

A

Hormone-sensitive lipase

32
Q

What are the 2 Fibric acid derivatives (fibrates) used for lipid disorders?

A
  • Fenofibrate
  • Gemfibrozil
33
Q

Dietary changes suffice for lipid management can only be made after weight has stabilized for how long?

34
Q

Dietary management of hyperlipoproteinemia includes limiting total calories from fat to what % of daily intake?

Saturated fats < what %?

Cholesterol less than how many mg/day?

A
  • Limit total calories from fat to 20-25%
  • Saturated fats to <8%
  • Cholesterol <200 mg/day
35
Q

Which fibric acid derivtive (fibrate) has the longest half-life (20 hours)?

A

Fenofibrate

36
Q

Fibric acid derivatives (fibrates) act as agonists for which receptor?

When activated what is the function of this receptor?

A
  • Agonists for nuclear receptor, PPARα —> binds DNA
  • ↑ expression of genes for lipoprotein lipase, apo A-I, apo A-II
  • ↓ expression of apo C-III
37
Q

What are the major effects of fibric acid derivatives (fibrates) on levels of lipids (TG’s, LDL, VLDL, and HDL)?

A
  • Major effect = ↑ oxidation of FA’s in liver and striated MUSCLE
  • ↑ lipolysis of TG via lipoprotein lipase, while intracellular lipolysis in adipose tissue is ↓
  • VLDL and LDL levels ↓ and TG’s ↓ ↓ ↓
  • HDL levels ↑ moderately
38
Q

Fibrates are useful in the management of which 3 lipid disorders?

A
  • Hypertriglyceridemias where VLDL predominates
  • Dysbetalipoproteinemia
  • Hypertriglyceridemia resulting from tx w/ viral protease inhibitors (i.e., saquinavir, indinair, or nelfinavir for HIV therapy)
39
Q

What are the common GI AE’s of fibrates?

A
  • Mild GI disturbances are most common AE’s
  • ↑ risk of cholelithiasis (due to ↑ in cholesterol content of bile)
40
Q

Due to the possible GI AE’s (cholelithiasis) fibrates should be used with caution in which patients?

A
  • Pt’s w/ biliary tract disease
  • Those at high risk (i.e., women, obese, and Native Americans)
41
Q

AE of fibrates in the liver?

A

Increased serum transaminases (up to 3x normal)

42
Q

AE’s of the muscle associated with Fibrates?

Should evaluate pt for what?

A
  • Myositis can occur (evaluate for muscle weakness and tenderness)
  • Myopathy and rhabdomyolysis (↑ risk when fibrates and statins combined)
43
Q

Fibrates may potentiate the actions of what class of drugs?

A

Anti-coagulants (i.e., Warfarin)

44
Q

Fibrates should be avoided in pt’s with what underlying dysfunctions?

Safe for pregnancy?

A
  • Avoided in pt’s with hepatic or renal dysfunction
  • Safety has NOT been established in pregnant or lactating women
45
Q

What are the 3 bile acid sequestrants (resins) used for lipid disorders?

A
  • Colestipol
  • Cholestyramine
  • Colesevelam
46
Q

Which class of drugs used for lipid disorders are insoluble in water; neither absorbed nor metabolically altered by the intestine; and totally excreted in the feces?

A

Bile acid sequestrants (resins)

47
Q

What is the MOA of bile acid sequestrants (resins) used for lipid disorders?

A
  • Bind to negatively charged bile acids and ↑ bile acid excretion up to ten-fold
  • ↑ excretion of bile acids enhances converstion of cholesterol –> bile acids in the liver via 7α-hydroxylation
48
Q

How does the decline in hepatic cholesterol caused by bile acid sequestrants (resins) lead to decreased levels of LDL?

A

Stimulates an ↑ in hepatic LDL receptors —> ↑ LDL clearance

49
Q

Why is the combined use of a statin w/ a bile acid sequestrant (resin) useful?

A
  • Bile acid resins cause an ↑ in the conversion of cholesterol to bile acids for excretion, which ↓ cholesterol levels
  • ↓ cholesterol leads to upregulation of HMG-CoA reductase, which enhances cholesterol synthesis, but can be reduced with a statin
50
Q

What are 3 therapeutic uses for bile acid sequestrants (resins)?

A
  1. Pt’s w/ primary hypercholesterolemia (↓ LDL by 20%)
  2. Monotherapy or in combo w/ niacin for tx of Type IIa and IIb hyperlipidemias
  3. Relief of pruritus in pt’s who have bile salt accumulation (i.e., biliary tract obstruction)
51
Q

Most common AE’s of bile acid sequestrants (resins)?

A

GI effects (i.e.m constipation, nausea, and flatulence)

52
Q

High doses of bile acid sequestrants (resins) impair the absorption of what?

Which drugs specifically?

A
  • Absorption of fat-soluble vitamins (ADEK)
  • Numerous drugs, including tetracycline, phenobarbital, digoxin, warfarin, pravastatin, fluvastatin, aspirin, and thiazide diuretics
53
Q

As a result of impaired absorption of other meds with bile acid sequestrants (resins) excpet for niacin, when should other drugs be dosed?

A

1 hour before or at least 2 hours after

54
Q

Bile acid sequestrants (resins) should be avoided or used with caution in pt’s with what 3 underlying diseases?

A
  • Diverticulitis
  • Preexisting bowel disease
  • Cholestasis
55
Q

What is the cholesterol absorption inhibitor used for lipid disorders?

56
Q

What is the MOA of Ezetimibe?

A
  • Selectively inhibits intestinal absorption of cholesterol and phytosterols (plant sterols)
  • Thru inhibition of NPC1L1 transport protein in intestinal brush border
57
Q

Why is Ezetimibe effective even in the absence of dietary cholesterol?

A

Inhibits reabsorption of cholesterol excreted in bile

58
Q

How much Ezetimibe is absorbed and what is the half-life?

A
  • Highly water insoluble; majority excreted in feces
  • 22-hour half-life
59
Q

Which lipoproteins does Ezetimibe have an affect on?

A
  • ↓ LDL (18%) and TG’s (6%)
  • ↑ HDL (1.3%)
60
Q

Ezetimibe can be used for primary hypercholesterolemia how?

A
  • As a monotherapy
  • In combo with HMG-CoA reductase inhibitors
61
Q

Ezetimibe can be used for homozygous familial hypercholesterolemia in combo with?

A

Atorvastatin or Simvastatin

62
Q

Ezetimibe can be used in combo with what other drug to treat mixced hyperlipidemia?

A

Fenofibrate

63
Q

Avoid administration of ezetimibe with what class of drug due to impaired ezetimibe absorption?

A

Bile acid sequestrants

64
Q

Which class of drugs will lower LDL levels the greatest?

65
Q

Which class of drugs causes the greatest increase in HDL?

66
Q

Which class of drugs causes the greatest decrease in TG’s?

67
Q

What is the MOA of lomitapide as a drug for homozygous familial hypercholesterolemia?

A
  • Directly binds to and inhibits MTP in the lumen of ER.
  • Prevents assembly of apo-B containing lipoproteins in entorocytes and hepatocytes —> ↓ chylomicrons and VLDL
  • ↓ plasma LDL-C concentrations
68
Q

Lomitapide is a substrate and inhibitor of what?

69
Q

AE’s of Lomitapide?

A
  • GI sx’s
  • Elevated liver aminotransferase levels
  • Hepatic fat accumulation
70
Q

What is the MOA of Mipomersen used for tx of homozygous familial hypercholesterolemia?

A

Antisense oligonucleotide that targets apoB-100 mRNA and disrupts its function

71
Q

AE’s associated with Mipomersen?

A
  • Injection site rxns (administered SQ 1x/week)
  • Flu-like sx’s
  • HA
  • Elevation of liver enzymes >3x the upper limit (discontinue if elevations persist or accompanied by clinical sx’s, such as hepatic steatosis)
72
Q

What are the 2 PCSK9 inhibitors used as lipid-lowering agents?

A
  1. Alirocumab
  2. Evolocumab
73
Q

What is the MOA of the PCSK9 inhibitors (-mab’s)?

A
  • Inhibits the catabolism of LDL-receptor
  • ↑ amount of LDL removed from blood stream
74
Q

What is the clinical indication for use of PCSK9 inhibitors?

A

Familial hypercholesterolemia not responsive to oral therapy

75
Q

What are some of the AE’s associated with the PCSK9 inhibitors?

A
  • Myalgia
  • Neuro effects: delirium, dementia
  • Nasopharyngitis, flu-like sx’s

CPR II Exam 1 (25 decks)

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