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Pharmacology > Chapter 8: Hyperlipidemia treatment > Flashcards

Chapter 8: Hyperlipidemia treatment Flashcards

1
Q

HMG-CoA Reductase Inhibitors are also called

A

Statins

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2
Q

Is cholesterole water or lipid soluble?

A

Lipid

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3
Q

Major lipoproteins

(chylomicrons)

A

​

  • Very low density lipoprotein (VLDL)
  • intermediate lipoprotein (ILP)
  • Low density lipoprtein (LDL)
  • High density lipoprotein (HDL)
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4
Q

Which is the “bad cholesterol” and what does it do?

A

LDL

It carries cholesterol from the liver to the rest of the body

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5
Q

Which is the “good” cholesterol and what does it do?

A

HDL

it carries cholesterol from the body to the liver

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6
Q

What does VLDL do?

A

carries fat from liver to adipose tissue

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7
Q

LDL goal

A

< 100mg/dL

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8
Q

Total cholesterol goal

A

<200 mg/dL

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9
Q

HDL goal

A

> 40mg/dL

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10
Q

Preffered drug type for lowering LDL

A

statins

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11
Q

Which drug class is the first-line treatment for hyperlipidemia and why?

A

Statins

Reduces the risk of MI, stroke, and cardiovascular death

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12
Q

what labs should be monitored when a patient is on statins?

A

LFTs, creatinine kinase, lipids

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13
Q

If a patient taking a statin develops persistent muscle weakness/discomfort or brown urine what labs should be done and why?

A

Creatinine kinase (CK) to assess for rhabdomyolysis

value will be increased

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14
Q

Assessing for signs of myopathy with statin use

A

6-12 weeks after begining regimen and every visit thereafter

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15
Q

When can peak effect for statins be seen?

A

After approximately 4 weeks

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16
Q

What do statins do?

A

decrese total cholesterol, LDL, triglycerides

Increase HDL

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17
Q

How do statins work?

A

block the enzyme that catalyzes early cholesterol synthesis

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18
Q

Statin drug names

A

​

  • lovastatin (Mevacor)
  • pravastatin (Pravachol)
  • simvastatin (Zocor)
  • fluvastatin (Lescol)
  • atorvastatin (Lipitor)
  • rosuvastatin (Crestor)
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19
Q

Statins: Absorption

A

Rapid with 24% bioavailability due to first pass metabolism

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20
Q

Statins: Distribution

A

Highly protein bound

enter breast milk, placenta, and blood-brain barrier

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21
Q

Statins: metabolism/excretion

A

Metabolized in liver with minimal excretion in urine

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22
Q

Statin: half-life

A

Varies

See page 125

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23
Q

Rule of 6

A

Statins are most effective at starting dose, longer dosing times only 6%

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24
Q

Patient education for statins

A
  • symptoms of myopathy
  • grapefruit juice increases levels (rhabdo risk)
  • photosensitivities
  • diet restriction and exercise
  • report any muscle pain/weakness
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25
Q

Statin: pregnancy category

A

X

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26
Q

Statin side effects: CV

A

chest pain

peripheral edema

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27
Q

DERM side effects: Statins

A

rash

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28
Q

EENT side effects: statins

A

rhinitis

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29
Q

Statin side effects: GI

A

abdominal cramps

diarrhea/constipation

gas

heart burn

altered taste

liver toxicity (elevation in LFTS)

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30
Q

Statin side effects: MS

A

SERIOUS myopathy

(rhabdomyolysis, depletion of CoQ10, mylagias)

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31
Q

Statin side effects: NEURO

A

dizziness

insomnia

headache

weakness

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32
Q

drugs that increase serum concentration of Statins

A

CYP450 enzyme inhibitors

grapefruit juice

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33
Q

drugs that decrease effectiveness of statins

A

St. John’s wort

bile acid sequestrants

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34
Q

why would you coadminister statins and CoQ10

A

decrease muscle symptoms

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35
Q

When a patient is on statins, which drugs should you be extremely cautious with?

A
  • gemfibrozil
  • protease inhibitors
  • niacin
  • cyclosporine
  • amiodarone
  • erythromycin
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36
Q

Purpose of bile acid sequestrants

A

lower LDL, not triglycerides

(may worsen if triglycerides elevated)

lowers LDL by only 13-30%

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37
Q

How do bile acid sequestrants work?

A

Bind to bile acids and form an insoluble complex that is excreted in the feces

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38
Q

Bile acid sequestrant drug names

A

cholestryramine (Questran, Prevalite)

colestipol (Colestid)

colesevelam (Welchol)

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39
Q

Contraindications for statins

A

liver disease/alcoholism

persistent unexplained elevated LFT

pregnancy

hypersensitivities

asians

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40
Q

Pregnancy category of bile acid sequestrants

A

Category B

safe

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41
Q

Common side effect of cholestyramine

A

Pruritus

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42
Q

Bile resin side effects: EENT

A

irritation of tongue

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43
Q

BIle resin side effects: GI

A

nausea

constipation

gas/bloating

fecal obstructionn

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44
Q

Bile acid sequestrants can lead to deficiencies in what vitamins?

A

A, D, E, K

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45
Q

Bile acid sequestrant side effects: NEURO

A

lightheadedness, weakness, insomnia

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46
Q

Why do patients often stop using bile acid sequestrants?

A

GI side effects

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47
Q

Bile resins and triglyceride levels

A

Not for monotherapy if triglycerides > 400mg/dL

OK as monotherapy if triglycerides < 200mg/dL

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48
Q

Patien education of bile resins

A

Powder: how to prepare

Tablets: swallow dont chew

increase fiber to avoid constipation/bloating

more effective if taken before meals

49
Q

Bile resins prevention absorption of which medications?

A

fat soluble vitamins

digoxin

warfarin

thyroxin

thiazides

beta blockers

folic acid

50
Q

How can interactions between bile resins and other medications be avoided?

A

take 1 hour before or 4 hours after meals

51
Q

Bile resin contraindications

A

liver disease

biliary obstruction

caution with history of constipation or bowel obstruction

52
Q

Nicotinic acid is also known as

A

Vitamin B3

Niacin

53
Q

When is use of B3 indicated for cholesterol treatment?

A

High LDL

low HDL

elevated triglycerides

54
Q

What is the benefit of combining B3 with a statin?

A

decreased progression of atherosclerosis

reduce CHD events

55
Q

Maximum dose of Niacin

A

2mg for ER

5mg for immediate release

56
Q

Ways to reduce flushing with Niacin

A

ASA or NSAID 30 minutes prior

take with food

avoid hot liquids

avoid alcohol

57
Q

A patient taking Niacin long term should be instructed to report

what symptoms

A

darkening of urine

light colored stools

anorexia

severe stomach pain

jaundice

(signs of hepatotoxicity)

58
Q

How does niacin work?

A

inhibits fatty acid release from adipose tissue

inhibits fatty acid ang triglyceride synthesis in the liver

59
Q

decreases LDL

prevents recurrent MI

reduces atherosclerosis

60
Q

Niacin: absorption

A

rapid and extensive

61
Q

Niacin: distribution

A

widely distributed after converted to niacinamide

62
Q

Niacin: metabolism

A

must be converted to niacinamide, which concentrates in liver, kidneys, and adipose tissue

63
Q

Niacin: excretion

64
Q

Niacin half-life

A

45 minutes

65
Q

side effects of niacin: CV

A

orthostatic hypotension

cardiac arrhythmias

pakpitations

syncope

66
Q

side effects of niacin: DERM

A

flushing

pruritus

67
Q

side effects of niacin: EENT

A

blurry vision

68
Q

side effects of niacin: GI

A

upper GI distress

hepatotoxicity with long term use

69
Q

side effects of niacin: HEM

A

Niaspan ER is associated with platelet count reduction

70
Q

side effects of niacin: META

A

can interefere with BG in diabetics

can exacerbate gout

71
Q

side effects of niacin: NEURO

A

nervousness

panic

72
Q

Niacin contraindications

A

liver disease

caution with diabetes, peptic ulcer disease, hyperuricemia

73
Q

Cholesterol absorption inhibitor:

drug names

A

ezetimbe (zetia)

estetrol

74
Q

What does Zetia do?

A

reduce total cholesterol, LDL, apo B, and triglycerides

increase HDL

75
Q

How does Zetia work?

A

inhibits absorption of cholesterol in small intestine. This lowers the amount of cholesterol available to the liver which reduces circulating cholesterol and hepatic stores

76
Q

Zetia: absorption

A

easily absorbed and conjugated to an active phenolic complex (ezetimibe-glucuronide)

77
Q

Zetia: distribution

A

highly distributed bound to plasma protein

78
Q

Zetia: metabolism

A

in intestine and liver

79
Q

Zetia: excretion

A

biliary and fecal

80
Q

Zetia: half-life

81
Q

Coadministration of zetia and statins or fenofibrates

A

May be taken at the same time

82
Q

Coadministration of Zetia and bile resins

A

2 hours before or 4 hours after bile resin is taken

83
Q

Side effects of zetia: DERM

84
Q

side effects of zetia: GI

A

elevated LFT

abdominal distress

cholecystitis

cholelithiasis

nausea

85
Q

side effects of zetia: HEM

A

MAY CAUSE ANGIOEDEMA

86
Q

side effects of zetia: META

87
Q

side effects of zetia: MS

A

arthralgia

back pain

88
Q

when is zetia most effective?

A

when given with statins

89
Q

which medications does zetia interact with?

A

antacids

cholestyramine

cyclosporin

90
Q

zetia contraindications

A

zetia/statin combo is contraindicated with liver disease or unexplained elevated LFT

91
Q

What do fibric acids do?

A

decrease triglycerides

increase HDL

increase size and decrease density of LDL

92
Q

What is the most effective type of drug for lowering triglycerides?

A

Fibric acids

93
Q

Why is fenofibrate preferred when used in combination with a statin?

A

Because of better renal clearance

94
Q

Fibric acid drug names

A

gemfibrozil (Lopid)

fenofibrate (TriCor)

clofibrate (Atromind-S)

95
Q

benefits of fibric acids

A

prevents cardiovascular disease

96
Q

how do fibric acids work?

A

activate a nuclear receptor which inhibits triglyceride synthesis

(also facilitates liver uptake of LDL)

97
Q

What is heightened with coadministration of fibric acids and statins?

A

risk for rhabdomyolysis

98
Q

fibric acids: absorption

A

reduced by bile resins

99
Q

fibric acids: distribution

A

unknow: upt to 99% protein bound

100
Q

fibric acids: metabolism

A

converted to fenofibric acid (active metabolite) which is metabolized in the liver

101
Q

fibric acids: excretion

102
Q

fibric acid side effects: CV

A

arrhythmias

103
Q

fibric acid side effects: DERM

104
Q

fibric acid side effects: GI

A

dyspepsia, abdominal pain, diarrhea, gas, liver dysfunction, gall bladder disease, pancreatitis

105
Q

when are GI side effects of fibric acids increased?

A

when coadministered with statins

106
Q

fibric acid side effects: MS

A

muscle pain, myopathy, rhabdomyolysis

107
Q

fibric acid side effects: NEURO

A

fatigue, weakness, headache

108
Q

coadministration of a fibrate and warfarin

A

increased bleeding risk

109
Q

coadminstration of a fibrate and statin

A

increased risk of rhabdomyolysis

110
Q

fibric acid contraindications

A

gall bladder, liver, or kidney dysfunction

breastfeeding women

111
Q

fibric acids in pregnancy

A

safety not determined use only if necessary

112
Q

When is combination therapy indicated?

A

when goals are not reached with statin monotherapy and lifestyle modifications

113
Q

which 2 drugs make up Vytorin?

A

Ezetimibe/simvastatin

114
Q

Considerations with Vytorin

A

slightly increased risk of rhabdomyolysis

64% reduction in LDL

adjunt to diet

115
Q

What 2 drugs make up Simcor?

A

Niacin/simvastatin

116
Q

Considerations with Somcor

A

watch for flushing. pruritis, GI distress

single dose at half strength with low fat snack

used in patients with hypercholesterolemia and dyslipidemia

117
Q

NCEP guidelines: screening

A

should be done with fasting labs every 5 years in patients over 20

118
Q

NCEP guidelines: goal for LDL (all patients)

A

<100 mg/dL

119
Q

NCEP guidelines: LDL goal for those at risk for or with coronary or vascular disease

Pharmacology (28 decks)

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