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Block 4: Pharm > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q 
HMG-CoA Reductase Inhibitors (Statins)-
All of the drugs in this class end in \_\_\_.
A

statins

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2
Q

Statins: MOA
Statins are Competitive inhibitors of 3-hydroxy-3-methylglutaryl (HMG) coenzyme A (CoA) reductase. HMG-CoA is involved in the synthesis of ______in the liver

A

cholesterol

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3
Q

Statins: MOA
Statins are Competitive inhibitors of 3-hydroxy-3-methylglutaryl (HMG) coenzyme A (CoA) reductase. HMG-CoA is involved in the synthesis of cholesterol in the liver.

Bottom line: less cholesterol made in cells results in a compensatory increase in the expression of___ receptors on hepatocyte membranes and a stimulation of LDL catabolism

A

LDL

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4
Q

We have LDL receptors on hepatocytes. When The body senses we need more ______, it makes more LDL receptors that will trap LDL out of the blood.

A

cholesterol

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5
Q

Statins: ADRs

A
  1. Hepatic: range from increased transaminases to toxicity
  2. MSK: strains, sprains, myalgias
  3. CNS: cognitive dysfunction including memory loss, confusion
  4. Cataracts
  5. small increase risk in developing diabetes
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6
Q

increased transaminases to hepatic toxicity is an ADR of statins, what should be monitored in the patients because of this?

A

Monitor liver enzymes- need to order CMP

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7
Q

strains, sprains, myalgias is an ADR of statins. There is an Increased risk of this if pt also has______ or is taking what kind of medications?

A

renal disease

fibrates, macrolides, “azole”, niacin- these are 3A4 drugs

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8
Q

strains, sprains, myalgias is an ADR of statins, what should be monitored in the patients because of this?

A

Check creatine kinase (CK) (also called creatine phosphokinase or CPK) levels with pt complaints

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9
Q

if your patients is on a statin and has cognitive dysfunction,memory loss, or confusion what should you do?

A

stop statin to see if memory gets better

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10
Q

Statins are Major substrate of _____and also weak inhibitor of _____,

A

CYP3A4

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11
Q

Common drugs that can have major interactions with statins?

A

Warfarin, protease inhibitors, macrolides, fibrates

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12
Q

If you need a macrolide to treat pneumonia, but macrolides have DDIs with statins, what should you do?

A

If you need macrolide to treat pneumonia or something, STOP THE STATIN. Because the statin can be started again after.

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13
Q

Statins: CI

3

A
  1. Pregnancy- DO NOT USE ON PREGNANCY, the developing baby needs cholesterol, if you block it is can cause birth defects or death of the fetus.
  2. Breast feeding
  3. Active liver disease
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14
Q

For statin monitoring, what baseline levels should you get?

A

o Creatine kinase
o Liver enzymes
o Lipid panel
o Renal function

Thereafter depending on clinical situation
o Lipids q4-8 wk until stable then at least q 6 months

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15
Q

some statins work better if dosed in the ______.

A

evening, Most dose daily at bedtime

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16
Q

Alternate-day dosing of statins has been shown to be useful and effective if patients have ______.

A

myalgias (mild muscle pain)

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17
Q

Niacin (nicotinic acid) MOA:

Niacin Inhibits lipolysis in adipose tissue which liver normally uses to produce _____

A

VLDL/LDL

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18
Q

Niacin (nicotinic acid) MOA:

Niacin Inhibits lipolysis in adipose tissue which liver normally uses to produce VLDL/LDL.This results in Fat cells that won’t break down

It also Increases secretion of tissue plasminogen activator and lowers level of plasma ______

A

fibrinogen

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19
Q

What is the Most potent agent to raise HDL

A

statin

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20
Q

Statin Increases secretion of tissue plasminogen activator and lowers level of plasma fibrinogen. this Can potentially cause _____ issues.

A

bleeding

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21
Q

Are niacin RX products the same as the OTC niacin products?

A

NO,
Rx products different than OTC vitamin forms

o OTC: <20 mg/day
o Rx: 1000-2000 mg/day (depends on formulation)

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22
Q

Rx Niacin products are often what kind of formulations?

A

sustained-release

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23
Q

Due to ADRs, Niacin is usually dosed at bedtime, with _____.

A

ASA and/or small meal

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24
Q

Niacin ADRs

A
  1. Cutaneous flushing/pruritus: can be severe and very uncomfortable
  2. GI: n/v
  3. Endo: increases risk of gout, Impaired glucose tolerance
  4. Hepatic disease is rare possibility
  5. Caution if used with statin
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25
Q

niacin Inhibits tubular secretion of uric acid so increases risk of__.

A

gout

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26
Q

niacin can cause Impaired glucose tolerance- can cause glucose to go up and down (usually up), so caution with ____ patients

A

diabetes

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27
Q
  • Fenofibrate (Antara, TriCor, many others)
  • Fenofibric acid (Fibricor, TriLipix)
  • Gemfibrozil (Lopid)

these belong in what drug class?

A

Fibrates

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28
Q

FIBRATES MOA:
Agonist for peroxisome proliferator-activated receptor-alpha (PPAR-alpha) which Downregulates What?

and up regulates what?

A

Downregulates:
apoprotein C-III (an inhibitor of lipoprotein lipase)

Upregulates:
lipoprotein lipase, apolipoprotein A-I, fatty acid oxidation, and elimination of TG-rich particles

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29
Q

Fibrates cause decrease in VLDL, TG, and increase in ___.

A

HDL

30
Q

Fibrates are often used in patients with what disease?

A

ISOLATED HYPOTRIGLYCERIDEMIA

31
Q

Fibrates: ADRs

A
  • GI: n/v/d/c (usually lessen as therapy progresses)

- Gallstones (these drugs increase biliary cholesterol excretion) fibrates probably not best to use in this situation

32
Q

Fibrates: DDI (2)

A

o Statins: use together increase risk of myopathy/rhabdomyolysis
o Warfarin: competes for PPB so need to check INR frequently until dose stable

33
Q

Fibrates: CI (4)

A

o Severe liver/kidney disease
o Gallbladder disease
o Biliary disease
o Pregnancy/breast feeding (not studied well so better to avoid)

34
Q

Bile Acid Sequestrants (Resins) MOA:

anion-exchange resins that bind bile acids and bile salts in _________.

A

small intestine

o Complex is excreted in feces
o Liver increases conversion of cholesterol to bile acids and increases its LDL-receptors
o Some modest rise in HDL can occur

35
Q

Colestipol (Colestid) is a Bile Acid Sequestrants (Resins) that comes in what form?

A

o Tablet form

36
Q

Colesevelam (Welchol) is a Bile Acid Sequestrants (Resins) that comes in what form?

A

o Tablet form

37
Q

Colesevelam (Welchol) is Also indicated for what other disease?

A

DIABETES TYPE II

38
Q

Cholestyramine resin (Questran, et al.) is a Bile Acid Sequestrants (Resins) that comes in what form?

A

o Powder form

39
Q

All Bile Acid Sequestrants (Resins) are insoluble in ____ and have very large molecular weights

A

water

40
Q

Bile Acid Sequestrants (Resins) are totally eliminated in _____.

A
  • Totally eliminated in feces
41
Q

Bile Acid Sequestrants (Resins) ADRs

A

GI are most common complaints
o Constipation and flatulence
o n/v

Impaired absorption: can bind with drugs and fat-soluble vitamins(A,D, and K)

42
Q

Bile Acid Sequestrants (Resins) inhibit absorption of many drugs such as?

A

digoxin, warfarin, statins, TCN, ASA, thiazides

43
Q

how are Bile Acid Sequestrants (Resins) dosed?

A

usually taken 1-2 hours before or 4-6 hours after other meds

44
Q

Cholesterol Absorption Inhibitor (CAI)

drug name

A

Ezetimibe (Zetia)

45
Q

Ezetimibe (Zetia)

belongs in what drug class?

A

Cholesterol Absorption Inhibitor (CAI)

46
Q

Ezetimibe (Zetia) Also comes in combo with _____.

A

atorvastatin or simvastatin

47
Q

Cholesterol Absorption Inhibitor (CAI) MOA: inhibits absorption of cholesterol at brush border of small intestine. This decreases?

A

o Decreases hepatic cholesterol stores
o Decreases serum LDL

has Smaller effect on TG, TC, HDL

48
Q

Cholesterol Absorption Inhibitor (CAI) ADRs

A
  • Some GI affects (mainly diarrhea)
  • Hepatic transaminase/myopathy increase with statin
  • Rarely used alone unless patient can’t tolerate other meds
49
Q

IMPROVE-IT trial findings in late 2014 showed a reduction in ______ in those who took Cholesterol Absorption Inhibitor (CAI) with high risk when combined with a statin

A

CV Death Reduction

50
Q

Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors (PCSK9) binds to LDL receptors on hepatocyte surfaces to promote _____ degradation within the liver

A

LDLR

51
Q

LDLR is the primary receptor that clears circulating ___

A

LDL

52
Q

PCSK9 Inhibitors MAIN RESULT? what does it do to LDL?

A

increased number of LDLRs available to clear LDL

Drastically clears LDL

53
Q

Alirocumab (Praluent) and Evolocumab (Repatha) belong to what drug class?

A

PCSK9 Inhibitors

54
Q

PCSK9 Inhibitors has what 2 drugs?

A

Alirocumab (Praluent) and Evolocumab (Repatha)

55
Q

Both Alirocumab (Praluent) and Evolocumab (Repatha) are indicated for _______ who have failed max statin therapy or for those who can’t tolerate high statin therapy

A

familial hyperlipidemia

56
Q

______ Can also be used for those without familial hyperlipidemia but with ASCVD and max statin therapy

A

PCSK9 Inhibitors

57
Q

Omega-3 Fatty Acids MOA

A

decrease VLDL-TG synthesis with unknown exact mechanism

58
Q

Omega-3 Fatty Acids use

A

hypertriglyceridemia

59
Q

o Icosapent ethyl (Vascepa)
o Omega-3-acid ethyl esters (Lovaza, Omtryg)
o Omega-3-carboxylic acid (Epanova)

the drugs above belong to what drug class?

A

Omega-3 Fatty Acids

60
Q

Mipomersen (Kynamro) and Lomitapide (Juxtapid) are ONLY used to treat _______.

A

homozygous familial hypercholesterolemia

61
Q

what two drugs are only used to treat homozygous familial hypercholesterolemia

A

Mipomersen (Kynamro) and Lomitapide (Juxtapid)

62
Q

Mipomersen (Kynamro) and Lomitapide (Juxtapid) inhibit synthesis of ______.

A

apo-B

63
Q

Mipomersen (Kynamro) and Lomitapide (Juxtapid) are Both restricted products due to ________.

A

hepatotoxicity

64
Q

Best drugs to lower LDL

A

STATINS
BILE ACID SEQUESTRANTS
(niacin also but not as well as the above)

65
Q

Best drug to increase HDL

A

Niacin

66
Q

Best drugs to lower triglycerides

A

Fibrates
Niacin
(statin also but not as well as the above)

67
Q

THERE ARE 4 PEOPLE THAT SHOULD GET STATINS, who are they?

A

Individuals with clinical ASCVD that already have vascular problems (1st patient)

Individuals with primary elevations of LDL–C ≥190 mg/dL (2nd patient)

Individuals 40 to 75 years of age with diabetes and LDL–C 70 to 189 mg/dL without clinical ASCVD (3rd patient)

Individuals without clinical ASCVD or diabetes who are 40 to 75 years of age with LDL–C 70 to 189 mg/dL and have an estimated 10-year ASCVD risk of 7.5% or higher (4th patient)

68
Q

Individuals with clinical ASCVD that already have vascular problems should be prescribed a statin, over what age should the statin prescribed be a moderate intensity dose instead of a high dose?

A

75

Age <75:  high-intensity dose
Age >75:  moderate-intensity dose
69
Q

Individuals with primary elevations of LDL–C ≥190 mg/dL should be given a statin with what intensity dose?

A

high intensity dose

70
Q

Individuals 40 to 75 years of age with diabetes and LDL–C 70 to 189 mg/dL without clinical ASCVD should be given a moderate intensity dose. unless they have _________, and they should be given a high intensity statin dose.

A

10-year ASCVD risk >7.5%: high-intensity dose

71
Q

Individuals without clinical ASCVD or diabetes who are 40 to 75 years of age with LDL–C 70 to 189 mg/dL and have an estimated 10-year ASCVD risk of 7.5% or higher should be given what kind of statin dose?

A

moderate to high intensity

72
Q

what are the are the most potent statins on market?

A

Atorvastatin and rosuvastatin

Block 4: Pharm (7 decks)

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