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D&T3 Test 1 > Drug Therapy for Hyperlipidemia > Flashcards

Drug Therapy for Hyperlipidemia Flashcards

1
Q

what are the primary causes of hyperlipidemia

A

diet or genetic

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2
Q

what are secondary causes of hyperlipidemia

A

drug or presence of disease

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3
Q

what is the first line of therapy for hyperlipidemia

A

diet

  • decrease fat intake
  • restrict alcohol and carbohydrate intake
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4
Q

Name Bile acid resins drugs

A

Cholestyramine
Colesevelam
Colestipol

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5
Q

MOA for Cholestyramine, Colesevelam, Colestipol? what does this cause

A
  1. bind bile acids in the GI
    - increases fecal bile acid excretion
    - diminishes bile acid enterohepatic recirculation
    - enhances hepatic conversion of cholesterol to bile acids
  2. increased number of hepatic LDL receptors
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6
Q

Where in the body do Bile acid resins go

A

stay in GI

- do not enter systemic circulation

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7
Q

bile acids have a negative feedback on what enzyme

A

7alpha-hydroxylase

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8
Q

what are therapeutic uses for Cholestyramine, Colesevelam, Colestipol

A

Lowers only cholesterol

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9
Q

When does maximum effect occur with bile acid resins

A

4 weeks

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10
Q

what form does Cholestyramine, Colesevelam, Colestipol come in

A

powder, must be mixed with liquids and taken with meal

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11
Q

what is Colesvelam specifically

A

capsule

- turns to gel in stomach with liquids, less GI effects

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12
Q

What are adverse effects of bile acid resins

A
  • GI: constipation, bloating, abdominal pain

- interfere with absorption of fat soluble vitamins/drugs

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13
Q

what happens if a patient is taking Cholestyramine, Colesevelam, Colestipol with another medication

A
  • stagger drug 1 hour before or 4 hours after resin
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14
Q

who can take bile acid resins

A

pregnant patients

children 6yrs and older

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15
Q

Who are the HMG CoA reductase inhibitors

A

Statins

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16
Q

MOA for statins

A

competitive inhibitor of HMG CoA reductase
- inhibits endogenous cholesterol synthesis
increases hepatic LDL receptors

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17
Q

Where is the site of primary action for statins

A

liver

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18
Q

what are all statins used for

A

lower cholesterol

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19
Q

which statins can lower both cholesterol and triglycerides

A

Atorvastatin and Rosuvastatin

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20
Q

What are the 2 major adverse effects of taking statins

A
  1. elevated serum transaminase
  2. muscle weakness, mylagia and/or dark brown urine
    - increased creatine phosphate CPK levels
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21
Q

if you take statin with either cyclosporine, azole antifungals, gemfibrozil, nicotinic acid, or erythromycin what risks are present

A

increase risk of serum transaminase

- increase risk with higher doses

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22
Q

who is statins contraindicated in

A
  • pregnant women
  • nursing mothers
  • acute liver disease
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23
Q

when does maximum endogenous cholesterol synthesis occur? so when should statin be taken

A

at night

- before going to bed

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24
Q

What statins are taken at night

A

Fluvastatin
Pravastatin
Rosuvastatin

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25
Q

when do statins have maximum effect when a person starts taking them

A

less than 2 weeks

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26
Q

statins have good absorption but not good

A

bioavailability

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27
Q

what is the pediatric guideline for giving statins

A
  • Pravastatin greater than 8 yrs

- other statins greater than 10 years

28
Q

food increases the absorption of food with which statin

A

Lovastatin

29
Q

food decreases the absorption of food with which statin

A

Pravastatin

Pitavastatin

30
Q

which statins are prodrugs? what metabolizes them?

A

Lovastatin and Simvastatin

- intestinal carboxyesterase and CYP3A4 activate

31
Q

what home food alters CYP3A4

A

grape fruit

32
Q

CYP3A4 metabolizes what stain

A

Atorvastatin
Lovastatin
Simvastatin

33
Q

CYP2C9 metabolizes what stain

A

Rosuvastatin and Fluvastatin

34
Q

CYP2D6 metabolizees what statin

A

Simvastatin

35
Q

wrong metabolism of Simvastatin can cause what?

A
  • muscle pain
  • CYP2D5*4 allel
  • SCLO1B1 SNP
36
Q

MOA for Ezetimibe

A

inhibits cholesterol absorption at the enterocytes of small intestines

  • Inhibits NPC1L1 transporter protein
  • targets dietary cholesterol
37
Q

what is a therapeutic advantage of Ezetimibie

A

better reduction of cholesterol when combined with statin than doubling statin dose

38
Q

Ezetimibe is not often combined with that drug

A

resins

39
Q

contraindications of Ezetimibe

A

liver disease

- undergoes enterohepatic recirculation

40
Q

Adverse affects of Ezetimibe

A

diarrhea

myalgia when combined with Statins

41
Q

name 2 PCSK9 drugs

A

Alirocumab

Evolocumab

42
Q

MOA for PCSK9? results in?

A

inhibit PCSK9 binding to LDL-receptor on hepatocytes to promote receptor degradation

  • increases hepatocyte LDL receptor number
  • lower LDL levels
43
Q

What is PCSK9 used for and what drug can you combine it with?

A
  1. lower cholesterol

2. used with statin

44
Q

how often does a patient take PCSK9 and how is it administered

A

sub-cutaneous injection biweekly or monthly

45
Q

Adverse effect of PCSK9

A

hypersensitivity

46
Q

What is the mechanism of action for fibrates gemfibrozil, Fenofibrate, Clofibrate

A
  • decreases hepatic VLDL triglyceride production

- increase lipoprotein lipase activity

47
Q

Fibrates Gemfibrozil, Fenofibrate, and Clofibrate actions are mediated by what? effects?

A

PPAR alpha, stimulates lipoprotien lipase synthesis

  • diminishes expression of APO CII
  • increases APO I and II expression which increases HDL-C
48
Q

what are 3 therapeutic uses of Fibrates gemfibrozil, fenofibrate and clofibrate

A

hypertriglyceridemia

Increasing HDL

49
Q

rate the effectivness of Fibrates gemfibrozil, fenofibrate, and clofibrate

A

fenofibrate and gemfibrozil more effective than clofibrate

50
Q

what are adverse effects of fibrates gemfibrozil, fenofibrate, and clofibrate

A
  1. clofibrate- increase risk of gallstones

2. myopathy - when combined with statin and worse with clofibrate,

51
Q

why is clofibrate cause myopathy

A

it inhibits OATP2 and competes with glucuronidation enzymes

52
Q

which fibrate is best choice for combination with statin

A

fenofibrate

53
Q

contraindications of fibrates

A
  • liver dysfunction
  • renal disease
  • preexisting gallbladder disease
54
Q

MOA of Niacin or nicotinic acid

A
  • decreased triglyceride synthesis, lower delivery of free fatty acids to liver
  • Diminsh hepatic VLDL and LDL production
  • increase lipoprotein lipase activity
55
Q

therapeutic uses for niacin and nicotininc acid

A
  1. lowers triglycerides
  2. lowers cholesterol, combine with resin
  3. increasing HDL, combine with statin or fibric
56
Q

Niacin and Nicotinic acid does not interact with what

A

PPARalpha

57
Q

how is dosing of niacin or nicotinic acid given to a patient

A

extended release must be tapered

58
Q

what are adverse effects of Niacin and Nicotinic acid

A
  • flushing
  • peptic ulcers
  • hyperuricemia
  • worsen glucose tolerance ( elevate transaminases ALT/AST)
  • itching
  • monitor creatine kinase when combined with statins
59
Q

contraindication of Niacin and Nicotininc acid

A
  • active liver disease
  • active peptic ulcer
  • bleeding disorder
60
Q

how can a patient relieve flushing from niacin or nicotininc acid

A

baby aspirin before taking drug

61
Q

Familial lipoprotein lipase deficiency (type I)

A

elevated chylomicrons after 12 hr fast

  • high triglycerdies
  • defect in lipoprotein lipase of APO C-II
62
Q

treatment for Familial lipoprotein lipase deficiency (type I)

A

Diet therapy critical

- use fibrates (Gemifibrozil) and nicotininc acid

63
Q

Familial hypercholesterolemia (IIa)

A
  • elevated cholesteroal and LDL
  • increase risk heart disease
  • decrease LDL clearance
64
Q

Familial hypercholesterolemia (IIb)

A

-elevated triglycerides and cholesterol

65
Q

cholesteroal is often elevated in what diseases

A
  • biliary disease
  • renal disease
  • hypothyroidism
  • diabetes mellitus
66
Q

tirglyceride levels are elevated in what disease

A
  • diabetes mellitus
  • alcoholism
  • renal disease
67
Q

what drugs can cause hyperlipidemia

A
  • thiazide diuretics
  • b-blockers ( non-specific)
  • oral contraceptives (estrogen+progesterone)

D&T3 Test 1 (11 decks)

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