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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
The HMG CoA reductase inhibitors may also ________ (increase/decrease) the effect of warfarin so it is important to evaluate the INR
increase
26
What are the conditions in which use of statins is contraindicated?
pregnancy lactation active liver disease
27
Which statin is the best when it comes to LDL reduction?
Rosuvastatin (60%) | Atorvastatin (55%)
28
Which statin is the best when it comes to triglyceride reduction?
Atorvastatin (29%) | Pravastatin (24%)
29
Which statin is the best when it comes to HDL increase?
Pravastatin (12%) | Simvastatin (12%)
30
Which statin has the least renal excretion?
Atorvastatin (2%)
31
Which statin has the greatest renal excretion?
Pravastatin (20%)
32
Name the statins which can penetrate BBB?
Lovastatin Pitavastatin Simvastatin
33
What are the adverse effects of statins?
Liver failure | Myopathy
34
Niacin reduces LDL-C by _________
10% to 20%
35
Niacin is the most effective agent for ____________ (increasing HDL-C/decreasing TG)
increasing HDL
36
Niacin also lowers triglycerides by __________ at typical doses of 1.5 to 3 g/day
20% to 35% | Dose is important
37
The addition of niacin to statin therapy _________ (has/has not) been shown to reduce the risk of ASCVD events
has not
38
At gram doses, niacin strongly inhibits ________ in adipose tissue
lipolysis
39
What does niacin do to the levels of triglycerides?
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
Reduced liver triglyceride levels decrease hepatic _______ production, which in turn reduces LDL-C plasma concentrations
VLDL production
41
What are the therapeutic uses of niacin?
``` Familial hyperlipidemia (because it decreases both TG and cholesterol) Severse hypercholesterolemia (w/ other agents) ```
42
Administration of nicotinamide alone ________ (does/ does not) decrease plasma lipid levels
does not
43
Niacin is administered ________ (orally/systematically)
orally
44
What are the adverse effects of niacin?
``` Intense cutaneous flush Feeling of warmth Pruritis N/Abd pain Hyperuricemia, gout Impaired glucose tolerance hepatotoxicity ```
45
What are the conditions in which niacin should be avoided?
Active hepatic disease | Active peptic ulcer
46
Administration of aspirin _____ (prior/after) to taking niacin decreases the flush, which is prostaglandin-mediated
prior
47
Fenofibrate is ______ (more/less) effective than gemfibrozil in lowering triglyceride levels
more
48
Fibrates also increase HDL-C by increasing the | expression of apo ___ and apo ____
apo AI | apo AII
49
What is the mechanism of action of fibrates?
Fibrates bind to peroxisome proliferator–activated receptors (PPARs) The complex then bind to peroxisome proliferator response elements → ↑lipoprotein lipase → decreased triglyceride concentrations
50
Fibrates are particularly useful in treating _______________, in which IDL particles accumulate.
Type III hyperlipidemia (dysbetalipoproteinemia)
51
Fenofibrate is a prodrug, which is converted to the active moiety _____________
fenofibric acid

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