Anti Lipid Flashcards

1
Q

_____ million Americans have elevated cholesterol. Dyslipidemias have been classified into 5 major subtypes. ____ causes half of all deaths in US. The incidence of CHD correlates with high levels of _____cholesterols and triacylglycerols and low levels of HDL cholesterol.

A

40; Coronary heart disease (CHD); LDL

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2
Q

What do the most common types of dyslipidemias involve

A
  1. elevated LDL (IIa) –> genetic component
  2. VLDL (IV)
  3. Both LDL and VLDL (IIb)
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3
Q

What are risk factors for CHD

A
  1. cigarette smoking
  2. hypertension
  3. obesity
  4. family history
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4
Q

what do lipid lowering therapies aim to do

A
  1. decrease carrier production
  2. increase degradation
  3. decrease absorption
  4. increase removal
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5
Q

when is the patient borderline for total high cholesterol levels

A

220-240

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6
Q

when is patient borderline for LDL cholesterol

A

130-160

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7
Q

when is patient borderline for HDL cholesterol

A

35-60; want it greater than 60

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8
Q

What are the lipid lowering therapeutics

A
  1. HMG CoA Reductase Inhibitors (Statins)
  2. Fibrates
  3. Niacin (Vitamin B3)
  4. Cholesterol Absorption Inhibitors
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9
Q

What is the suffix of HMG CoA reductase inhibitors

A

“-statin”

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10
Q

Red rice yeast contains _____

A

lovastatin

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11
Q

Which statin’s have adverse effects in the CNS

A
  1. Lovastatin

2. Simvastatin

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12
Q

What is the indication for Atorvastatin

A
  1. Dyslipidemia

2. CVD Prevention

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13
Q

What is the mechanism of action of Atorvastatin

A
  1. Competitively inhibits HMG-CoA reeducates which is responsible for an early, rate limiting step in cholesterol biosynthesis.
  2. Increases hepatic LDL receptors, enhancing catabolism.
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14
Q

What are common adverse effects of Atorvastatin

A
  1. nasopharyngitis

2. myalgia (muscle pain)

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15
Q

what are skeletal AE of atorvastatin

A

myopathy

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16
Q

what are hepatic AE of atorvastatin

A
  1. impaired function associated with elevated serum transaminase levels –> jaundice
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17
Q

what are CNS AE of atorvastatin

A

amnesia

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18
Q

what are ocular AE of atorvastin

A
  1. dipolopia
  2. ptosis
  3. pseudo - CME
  4. blurred vision
  5. elevated IOP
  6. IOP hemorrhage
  7. cataracts
19
Q

What are drug interactions of atorvastatin

A

cyclosporine, erythromycin, azole antifungals cause myopathy exacerbation.

20
Q

What are contraindications of atorvastatin

A

azole antifungals

21
Q

What are the indication of fibrates

A
  1. hypertriglyceridemia

2. hypercholesterolemia

22
Q

when are fibrates prescribed

A

with statins or to statin intolerant patients; its a second line therapy, unless problems are severe and PCP decides to put them on both.

23
Q

what is the MOA of fenofibrate

A
  1. stimulates nuclear receptor PPAR which modulates transcription of insulin sensitive genes in liver, muscle and adipose tissue.
  2. enhances HDL production; inhibits triglyceride synthesis and stimulates catabolism of triglyceride rich lipoproteins.
24
Q

There is also an integral relationship between PPAR receptor and_______management and lipid level regulations in the body.

A

diabetes

25
Q

What are the endogenous ligands for PPARs?

A

free fatty acids and eicosanoids.

26
Q

What are common AE of fenofibrate

A
  1. headache
  2. rhinitis
  3. flu syndrome
27
Q

What are serious AE of fenofibrate

A
  1. hypersensitivity: SJS, TEN (toxic epidermal necrolysis)
  2. Hepatitis, cirrhosis
  3. CV: thromboembolism
  4. Muscular: Mysotitis, myopathy, rhabdomyolysis
28
Q

What are drug interactions of fenofibrate

A
  1. Acyclovir, Amicoglycosides, cyclosporine, ganciclovir: cause impaired renal elimination
  2. Impaired metabolism of Sulfonylureas (drugs used to treat diabetes –> pt can become hypoglycemic as a result of being on fenofibrate).
29
Q

What is the indication of Niacin

A
  1. hypertriglyceridemia
  2. hypercholesterolemia
  3. mixed dyslipidemia
30
Q

What is the MOA of niacin

A

inhibits lypolysis in adipose tissue, resulting in reduced hepatic VLDL synthesis and production of LDLs in the plasma.

31
Q

where does niacin act?

A

in the adipose tissue

32
Q

what are common AE of niacin

A
  1. headache
  2. pseudo cystoid macular edema
  3. flushing
  4. pruritus
  5. hyperpigmentaiton
  6. jaundice
  7. xeroderma
  8. toxic amblyopia (impt!)
  9. orthostatic hypotension
33
Q

what are serious AE of niacin

A
  1. hepatotoxicity

2. arrhythmias

34
Q

what are drug interactions of niacin

A
  1. alpha blockers
  2. beta blockers
    - both additive
35
Q

When are you supposed to caution with use of niacin

A
  1. diabetes (elevates blood sugar)

2. surgery (anti platelet effects)

36
Q

What is a cholesterol absorption inhibitor

A

Ezetimibe

37
Q

what is the indication for ezetimibe

A

dyslipidemia

38
Q

what is the MOA of ezetimibe

A

inhibits dietary and biliary cholesterol absorption at small intestine brush border.

39
Q

what are common AE of ezetimibe

A
  1. sinusitis
  2. influenza
  3. diarrhea
40
Q

what are serious AE of ezetimibe

A
  1. angioedema
  2. anaphylaxis
  3. hepatitis
  4. thrombocytopenia
41
Q

The most common thing to note among anti lipid drugs is that patient needs to have a healthy _____

A

liver

42
Q

what are drug interactions of ezetimibe

A

cyclosporine; may increase levels of both drugs (the cyclosporine, and the ezetimibe)

43
Q

when are you supposed to caution when using ezetimibe

A

hepatic impairment