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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
when do statins have maximum effect when a person starts taking them
less than 2 weeks
26
statins have good absorption but not good
bioavailability
27
what is the pediatric guideline for giving statins
- Pravastatin greater than 8 yrs | - other statins greater than 10 years
28
food increases the absorption of food with which statin
Lovastatin
29
food decreases the absorption of food with which statin
Pravastatin | Pitavastatin
30
which statins are prodrugs? what metabolizes them?
Lovastatin and Simvastatin | - intestinal carboxyesterase and CYP3A4 activate
31
what home food alters CYP3A4
grape fruit
32
CYP3A4 metabolizes what stain
Atorvastatin Lovastatin Simvastatin
33
CYP2C9 metabolizes what stain
Rosuvastatin and Fluvastatin
34
CYP2D6 metabolizees what statin
Simvastatin
35
wrong metabolism of Simvastatin can cause what?
- muscle pain - CYP2D5*4 allel - SCLO1B1 SNP
36
MOA for Ezetimibe
inhibits cholesterol absorption at the enterocytes of small intestines - Inhibits NPC1L1 transporter protein - targets dietary cholesterol
37
what is a therapeutic advantage of Ezetimibie
better reduction of cholesterol when combined with statin than doubling statin dose
38
Ezetimibe is not often combined with that drug
resins
39
contraindications of Ezetimibe
liver disease | - undergoes enterohepatic recirculation
40
Adverse affects of Ezetimibe
diarrhea | myalgia when combined with Statins
41
name 2 PCSK9 drugs
Alirocumab | Evolocumab
42
MOA for PCSK9? results in?
inhibit PCSK9 binding to LDL-receptor on hepatocytes to promote receptor degradation - increases hepatocyte LDL receptor number - lower LDL levels
43
What is PCSK9 used for and what drug can you combine it with?
1. lower cholesterol | 2. used with statin
44
how often does a patient take PCSK9 and how is it administered
sub-cutaneous injection biweekly or monthly
45
Adverse effect of PCSK9
hypersensitivity
46
What is the mechanism of action for fibrates gemfibrozil, Fenofibrate, Clofibrate
- decreases hepatic VLDL triglyceride production | - increase lipoprotein lipase activity
47
Fibrates Gemfibrozil, Fenofibrate, and Clofibrate actions are mediated by what? effects?
PPAR alpha, stimulates lipoprotien lipase synthesis - diminishes expression of APO CII - increases APO I and II expression which increases HDL-C
48
what are 3 therapeutic uses of Fibrates gemfibrozil, fenofibrate and clofibrate
hypertriglyceridemia | Increasing HDL
49
rate the effectivness of Fibrates gemfibrozil, fenofibrate, and clofibrate
fenofibrate and gemfibrozil more effective than clofibrate
50
what are adverse effects of fibrates gemfibrozil, fenofibrate, and clofibrate
1. clofibrate- increase risk of gallstones | 2. myopathy - when combined with statin and worse with clofibrate,
51
why is clofibrate cause myopathy
it inhibits OATP2 and competes with glucuronidation enzymes
52
which fibrate is best choice for combination with statin
fenofibrate
53
contraindications of fibrates
- liver dysfunction - renal disease - preexisting gallbladder disease
54
MOA of Niacin or nicotinic acid
- decreased triglyceride synthesis, lower delivery of free fatty acids to liver - Diminsh hepatic VLDL and LDL production - increase lipoprotein lipase activity
55
therapeutic uses for niacin and nicotininc acid
1. lowers triglycerides 2. lowers cholesterol, combine with resin 3. increasing HDL, combine with statin or fibric
56
Niacin and Nicotinic acid does not interact with what
PPARalpha
57
how is dosing of niacin or nicotinic acid given to a patient
extended release must be tapered
58
what are adverse effects of Niacin and Nicotinic acid
- flushing - peptic ulcers - hyperuricemia - worsen glucose tolerance ( elevate transaminases ALT/AST) - itching - monitor creatine kinase when combined with statins
59
contraindication of Niacin and Nicotininc acid
- active liver disease - active peptic ulcer - bleeding disorder
60
how can a patient relieve flushing from niacin or nicotininc acid
baby aspirin before taking drug
61
Familial lipoprotein lipase deficiency (type I)
elevated chylomicrons after 12 hr fast - high triglycerdies - defect in lipoprotein lipase of APO C-II
62
treatment for Familial lipoprotein lipase deficiency (type I)
Diet therapy critical | - use fibrates (Gemifibrozil) and nicotininc acid
63
Familial hypercholesterolemia (IIa)
- elevated cholesteroal and LDL - increase risk heart disease - decrease LDL clearance
64
Familial hypercholesterolemia (IIb)
-elevated triglycerides and cholesterol
65
cholesteroal is often elevated in what diseases
- biliary disease - renal disease - hypothyroidism - diabetes mellitus
66
tirglyceride levels are elevated in what disease
- diabetes mellitus - alcoholism - renal disease
67
what drugs can cause hyperlipidemia
- thiazide diuretics - b-blockers ( non-specific) - oral contraceptives (estrogen+progesterone)

D&T3 Test 1 (11 decks)

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