Antihyperlipidemic Drugs Flashcards

1
Q

_____________ is a recessive trait that is correlated with a high incidence of acute pancreatitis

A

Chylomicronemia

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2
Q

How is chylomicronemia managed?

A

managed by restriction of total fat

intake

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3
Q

Alcohol raises ______ and ________ levels, it should be avoided by patients with hypertriglyceridemia

A

TG

VLDL

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4
Q

The drugs that are most effective at lowering LDL cholesterol include?

A

Statins
Niacin
Resins
Ezetimibe

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5
Q

What drugs are most effective at lowering triglyceride and VLDL concentrations and raising HDL cholesterol concentrations

A

Fibrates
Niacin
Marine omega 3 fatty acids

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6
Q

Elevated ______ concentration is associated with atherosclerosis

A

LDL

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7
Q

_________ is target of the fibrate drugs and omega-3 fatty acids

A

Proliferator-activated receptor-alpha (PPAR-α)

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8
Q

__________ is the member of a family of nuclear transcription regulators that participate in the regulation of metabolic processes

A

PPAR-α

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9
Q

HMG-CoA reductase inhibitors lowers _________

A

LDL-C

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10
Q

What are the other functions of HMG-CoA reductase inhibitors?

A

Atherosclerotic plaque stabilization
Improvement of coronary endothelial function
Inhibition of platelet thrombus formation
Vascular anti-inflammatory activity

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11
Q

All statins are _______ (competitive/noncompetetive) inhibitors of HMG CoA reductase

A

competitive

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12
Q

__________ and ____________ are the most potent LDL-C lowering statins

A

Rosuvastatin and atorvastatin

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13
Q

he HMG CoA reductase inhibitors also __________ (increase/decrease) triglyceride levels in some patients

A

decrease

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14
Q

Patients who are homozygous for familial hypercholesterolemia lack LDL receptors and, therefore, benefit much _______ (more/less) from treatment with these drugs

A

less

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15
Q

Lovastatin and simvastatin are lactones that are hydrolyzed to the __________ (active drug/inactive metabolite)

A

active drug

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16
Q

All statins are metabolized by cytochrome P450 (CYP450) isoenzymes in the liver, except _________

A

pravastatin

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17
Q

What are the half lives of

  1. Rosuvastatin
  2. Atorvastatin
  3. Pitavastatin
A
  1. Rosuvastatin = 19 hrs
  2. Atorvastatin = 14 hrs
  3. Pitavastatin = 12 hrs
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18
Q

What are the half lives of statins other than Rosuvastatin, Atorvastatin, and Pitavastatin?

A

1-3 hrs

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19
Q

Elevated _______ enzymes may occur with statin therapy

A

liver

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20
Q

Hepatic insufficiency can cause _____ accumulation

A

drug

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21
Q

Risk factors for rhabdomyolysis, include renal insufficiency, vitamin D _______ (deficiency/excess), _________ (hyperthyroidism/hypothyroidism), advanced age, ________ (male/female) sex, and use of drugs

A

vitamin D deficiency
hypothyroidism
female

22
Q

What drugs increase the risk of muscle adverse effects?

A
Azole antifungals
protease inhibitors
cyclosporine
erythromycin
gemfibrozil
niacin
23
Q

Simvastatin is metabolized by ___________, and

inhibitors of this enzyme may increase the risk of rhabdomyolysis

A

CYP450 3A4

24
Q

Plasma ___________ levels should be

determined in patients with muscle complaints

A

creatine kinase

25
Q

The HMG CoA reductase inhibitors may also ________ (increase/decrease) the effect of warfarin so it is important to evaluate the INR

A

increase

26
Q

What are the conditions in which use of statins is contraindicated?

A

pregnancy
lactation
active liver disease

27
Q

Which statin is the best when it comes to LDL reduction?

A

Rosuvastatin (60%)

Atorvastatin (55%)

28
Q

Which statin is the best when it comes to triglyceride reduction?

A

Atorvastatin (29%)

Pravastatin (24%)

29
Q

Which statin is the best when it comes to HDL increase?

A

Pravastatin (12%)

Simvastatin (12%)

30
Q

Which statin has the least renal excretion?

A

Atorvastatin (2%)

31
Q

Which statin has the greatest renal excretion?

A

Pravastatin (20%)

32
Q

Name the statins which can penetrate BBB?

A

Lovastatin
Pitavastatin
Simvastatin

33
Q

What are the adverse effects of statins?

A

Liver failure

Myopathy

34
Q

Niacin reduces LDL-C by _________

A

10% to 20%

35
Q

Niacin is the most effective agent for ____________ (increasing HDL-C/decreasing TG)

A

increasing HDL

36
Q

Niacin also lowers triglycerides by __________ at typical doses of 1.5 to 3 g/day

A

20% to 35%

Dose is important

37
Q

The addition of niacin to statin therapy _________ (has/has not) been shown to reduce the risk of ASCVD events

A

has not

38
Q

At gram doses, niacin strongly inhibits ________ in adipose tissue

A

lipolysis

39
Q

What does niacin do to the levels of triglycerides?

A

Niacin strongly inhibits lipolysis in adipose tissue, thereby reducing production of free fatty acids. If less FFAs then liver can’t make more triglycerides

40
Q

Reduced liver triglyceride levels decrease hepatic _______ production, which in turn reduces LDL-C plasma concentrations

A

VLDL production

41
Q

What are the therapeutic uses of niacin?

A
Familial hyperlipidemia (because it decreases both TG and cholesterol)
Severse hypercholesterolemia (w/ other agents)
42
Q

Administration of nicotinamide alone ________ (does/ does not) decrease plasma lipid levels

A

does not

43
Q

Niacin is administered ________ (orally/systematically)

A

orally

44
Q

What are the adverse effects of niacin?

A
Intense cutaneous flush
Feeling of warmth
Pruritis
N/Abd pain
Hyperuricemia, gout
Impaired glucose tolerance
hepatotoxicity
45
Q

What are the conditions in which niacin should be avoided?

A

Active hepatic disease

Active peptic ulcer

46
Q

Administration of aspirin _____ (prior/after) to taking niacin decreases the flush, which is prostaglandin-mediated

A

prior

47
Q

Fenofibrate is ______ (more/less) effective than gemfibrozil in lowering triglyceride levels

A

more

48
Q

Fibrates also increase HDL-C by increasing the

expression of apo ___ and apo ____

A

apo AI

apo AII

49
Q

What is the mechanism of action of fibrates?

A

Fibrates bind to peroxisome proliferator–activated receptors (PPARs)
The complex then bind to peroxisome proliferator response elements → ↑lipoprotein lipase → decreased triglyceride concentrations

50
Q

Fibrates are particularly useful in treating _______________, in which IDL particles accumulate.

A

Type III hyperlipidemia (dysbetalipoproteinemia)

51
Q

Fenofibrate is a prodrug, which is converted to the active moiety _____________

A

fenofibric acid