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Pharm > HLD drugs > Flashcards

HLD drugs Flashcards

1
Q

High triglycerides can eventually result in what condition?

What is the recognized threshold (serum mg/dL)?

A

Pancreatitis

> 500 mg/dL

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2
Q

List the presently accepted values for desirable, borderline and high serum LDL-cholesterol.

A
  • Desireable: < 100 mg/dL
  • Borderline: 100-159 mg/dL
  • High: >190 mg/dL
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3
Q

List the presently accepted values for desirable serum HDL-cholesterol. (men vs. women).

A
  • Men: > 40 mg/dL
  • Women: > 50 mg/dL
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4
Q

List the presently accepted values for desirable, borderline, and high triglyceride levels. (Also, what is considered very high?)

A
  • Desirable: < 150 mg/dL
  • Borderline: 150-199 mg/dL
  • High: > 200 mg/dL (> 500 very high)
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5
Q

NCEP lipoprotein treatment goals: VERY HIGH RISK:

  • CV risk factors?
  • LDL goal?
A
  • Current CHD + other factors
  • < 70 mg/dL
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6
Q

NCEP lipoprotein treatment goals: HIGH RISK:

  • CV risk factors?
  • LDL goal?
A
  • Previous CHD, diabetes, > 2 risk factors
  • < 100 mg/dL (optional < 70)
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7
Q

NCEP lipoprotein treatment goals: MODERATELY HIGH RISK:

  • CV risk factors?
  • LDL goal?
A
  • > 2 risk factors. 10-20% ten-year risk
  • < 130 mg/dL (optional < 100 mg/dL)
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8
Q

NCEP lipoprotein treatment goals: MODERATE RISK:

  • CV risk factors?
  • LDL goal?
A
  • > 2 risk factors, < 10% ten-year risk
  • < 130 mg/dL
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9
Q

NCEP lipoprotein treatment goals: LOWER RISK:

  • CV risk factors?
  • LDL goal?
A
  • 0-1 risk factors
  • < 160 mg/dL
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10
Q

What’s the DOC for treating pts w/elevated LDL-C?

A

Statins

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11
Q

Name the 6 different statins.

A
  1. Lovastatin
  2. Simavastatin
  3. Atorvastatin
  4. Fluvastatin
  5. Rosuvastatin
  6. Pravastatin
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12
Q

Statins: MoA?

A

Inhibits HMG-CoA reductase & triggers SREBP ts factor –> increased LDL-R expression and increased LDL clearance

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13
Q

Statins: indications?

A

High LDLs

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14
Q

Statins: toxic/adverse effects?

A

A. Myalgia/myopathy.

B. ***Rhabdomyolysis***

C. hepatitis.

D. Small risk T2DM.

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15
Q

What are some lab and physical signs that a pt has rhabdomyolysis?

A
  • Fever, malaise, diffuse myalgia and/or tenderness,
  • Marked elevation of serum [CK]
  • Myoglobin present in the urine (dark)
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16
Q

When are statins contraindicated?

A

Severe liver disease, pregnancy (teratogenic)

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17
Q

Which statins are metabolized by CYP3A4?

Which statins do not undergo CYP450 metabolism?

Which statins are glucuronidated in the liver?

A

ASL: atorvastatin, simvastatin, lovastatin

Pravastatin only

All statins

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18
Q

CYP3A4 inhibitors ___________ levels of Lovastatin, Simvastatin & Atorvastatin (ASL).

CYP3A4 inhibitors associated with increased risk of what disease?

A

Increase

Rhabdomyolysis

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19
Q

Describe the effect of statins on serum lipids.

A

v LDL (20-60%)

v TG (10-20%)

^ HDL (5-10%)

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20
Q

Give some eg’s of CYP3A4 inhibitors.

A

Eric’s red grape kept its clear fluid

  • Immunosuppressants: cyclosporin & tacrolimus
  • Macrolide antibiotics: clarithromycin & erythromycin
  • Ca2+-channel blockers: diltiazem & verapamil
  • Anti-arrhythmia drugs: amiodarone
  • Azole anti-fungals: itraconazole & ketoconazole
  • HIV protease inhibitors: ritonavir, indinavir & nelfinavir
  • Anti-coagulants: warfarin
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21
Q

Name some eg’s of CYP3A4 inducers.

A

Phen-phen rifled St. John’s glowing pink cars.

Phenytoin, Phenobarbitol, Rifampin, St. John’s wort, Glucocorticoids, Pioglitazone, Carbamezapine.

Also: barbiturates and thiazolidnediones

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22
Q

CYP3A4 inducers ___________ levels of Lovastatin, Simvastatin & Atorvastatin (ASL).

A

Decrease (and therefore decrease their clinical efficacy)

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23
Q

Which of the statins are metabolized by CYP2C9?

Give some eg’s of CYP2C9 inhibitors.

(less important than 3A4)

A

FR (France): fluvastatin, rosuvastatin

Ketoconazole, itraconazole, metronidazole, sulfinpyrazone

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24
Q

What transporter do statins use to enter the liver?

A

OATP2

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25
Q

What is the only statin that is FDA-approved for concurrent use w/cyclosporine in cancer tx?

A

Pravastatin

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26
Q

*How does gemfibrozil relate to statin use?

*What is the mech behind this?

A
  • Strongly associated with an increased risk of statin-induced myopathy and rhabodmyolysis
    1. Inhibits OATP2 transporter-mediated uptake of statins into the liver- can increase statin systemic bioavailability >2X
    2. Inhibits the glucuronidation of statins, which is involved in the metabolism and ultimate excretion of all statins (including Pravastatin) - can cause an increase in the systemic levels of ALL STATIN drugs.
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27
Q

Which is the safest statin to sue when a pt has a weakned liver and why?

A

Pravastatin (due to dual hepatic/renal elimination)

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28
Q

Name the 3 bile acid-binding resins.

A

Cholestyramine, colestipole, colesevelam

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29
Q

Bile acid-binding resins: MoA?

A

Binds bile acids and prevents reabsorption –> increased cholesterol 7alpha-hydroxylase (rate-limiting enzyme in bile acid synthesis) –> decreased chol –> increased LDL-R –> increased LDL clearance.

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30
Q

When would a bile acid-binding resin be used in combination with a statin?

When instead of a statin?

A
  • Combo: increase LDL-lowering effect or to allow for lower statin dose to avoid drug interactions
  • When statins are contraindicated (e.g. pregnancy)
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31
Q

Bile acid-bindign resins: adverse effects?

A
  • Generally safe
  • Can increase TG levels in hypertriglyceridemia.
  • At high concentrations, Cholestyramine and Colestipol, but not Colesevelam, impair the absorption of the fat soluble vitamins A, D E & K
32
Q

Bile acid-binding resins: contraindications?

A

TG > 400 mg/dL

Type III Dysbetalipoproteinemia

33
Q

Bile acid-binding resins: effects on serum lipids?

A

v LDL (10-25%)

Small increase in TG

34
Q

What’s the name of the drug that inhibits cholesterol absorption?

35
Q

Ezetimibe: effects on serum lipids?

How is this the same/different compared to bile acid-binding resins?

A

Effect on serum lipids: v LDL (~18%)

Note: unlike Bile acid-binding resins, Ezetimibe does not raise triglyceride levels

36
Q

Bile acid-binding resins: indications?

37
Q

Ezetimibe: indications?

38
Q

Ezetimibe: MoA?

A

Inhibits intestinal absorption of chol (via NPCL1, small int) –> decreased hepatic chol (therefore reduced VLDLs, LDLs) –> increased LDL-R expression –> increased LDL clearance

39
Q

What are the therapeutic uses for ezetimibe?

A
  1. Reduces LDL-C in patients with primary hypercholesterolemia
    1. i.e. not completely dependent upon intact LDLR
  2. Can induce a significant further LDL-C lowering effect when combined with a STATIN
    1. Allows the use of a lower STATIN dose to avoid adverse effects
40
Q

Ezetimibe: toxicity?

A

Generally well-tollerated

41
Q

Name 2 PCSK9 inhibitors.

A

Alirocumab

Evolocumab

42
Q

PCSK9 inhibitors: MoA?

A

Inhibits PCSK9 (secreted) –> blocks nl targeting of LDL-R to lysosome –> increased LDL-R expression –> increased LDL clearance

43
Q

PCSK9 inhibitors (alirocumab, evolocumab): indications?

A

Hetero FH

High LDL not controlled w/statins or statin-intollerant

44
Q

PCSK9 inhibitors: effect on serum lipids?

A

v LDL (> 50%)

45
Q

Name 2 drugs that are indicated for homozygous familial hypercholesterolemia (FH).

A

Lomitapide

Mipomersen

46
Q

Lomitapide: MoA?

A

Inhibits MTP (microsomal triglyceride transfer protein) in both erythrocytes and liver –> decreased production of chylomicrons, VLDL, and LDL

47
Q

Mipomersen: MoA?

A

Antisense oligonucleotide specific for apoB48/100 –> decreased expression of apoB48/100 –> decreased VLDL & LDLs.

48
Q

Lomitpide: toxicity?

Mipomersen: toxicity?

A

Hepatotoxicity

Hepatotocity

49
Q

Lomitpide: contraindications?

Mipomersen: contraindications?

A

Lomitipide: pregnancy

Mipomersen: Mild/mod hepatic impairment

50
Q

Lomitapide: effect on serum lipids?

Mipomersen: effect on serum lipids?

A

Lomitapide: v chylomicrons, v VLDL, v LDL

Mipomersen: v VLDL, v LDL

51
Q

Elevated serum triglycerides are often a/w what other lipoprotein?

A

Decrease in HDLs (“good cholesterol”)

52
Q

Name all 3 of the drugs whose main action is to lower triglycerides.

A

Niacin, fibrates (gemfibrozil + fenofibrate)

53
Q

Treatment options for Hypercholesterolemia

  1. For moderate hypercholesterolemia with low cardiovascular risk:
A

Therapeutic lifestyle change

  • Dietary reduction of cholesterol intake
  • Exercise/Weight reduction (improves lipoprotein metabolism)
54
Q

Treatment options for Hypercholesterolemia

  1. For severe hypercholesterolemia and/or a high cardiovascular risk
A

i. e. - LDL levels > 190 mg/dL (or > 70 mg/dL with Diabetes)
- Current clinical evidence of CVD
- New: 10 yr CVD risk > 7.5% (controversial)

Answer:

Drug therapy is indicated.

  • the initial goal is to reduce LDL - decrease risk of atherosclerosis
  • the initial drug of choice is typically a STATIN
55
Q

Treatment Options for Hypertriglyceridemia:

  1. When serum triglycerides are borderline high (150-199 mg/dL)
A
  • Lifestyle change is indicated
  • Low fat diet, exercise & cessation of smoking/alcohol
56
Q

Treatment Options for Hypertriglyceridemia:

  1. When serum triglycerides are very high (>500 mg/dL)
A
  • The initial goal is to to prevent pancreatitis by lowering triglyceride levels with either niacin or a fibrate
  • Once triglycerides are <500 mg/dL then any LDL-C goals should be addressed
57
Q

What are 2 other names for niacin?

A

Nicotinic acid/vitamin B3

58
Q

Niacin: effects on serum lipids?

A

v TG (30-80%), v LDL (10-20%), ^ HDL (10-30%)

59
Q

Niacin: indications?

A

High VLDL, high LDL, low HDL

  • Lowers both plasma cholesterol and triglycerides–Useful in the treatment of familial combined hyperlipidemias (­VLDL & ­LDL) and familial dysbetalipoproteinemia (­IDL), i.e. where both cholesterol and triglycerides are elevated.
  • Low HDLs
  • In patients with a history of previous MI, NIACIN has been shown to reduce the incidence of:
    • Re-infarctions, CVAs, overall mortality
  • Combo therapy w/statins (esp. if low HDLs)
60
Q

What’s the most effective drug at reducing HDL levels?

61
Q

Niacin: MoA? (6)

A

A. Gi agonist in fat: Decreased lipolysis in adipocytes –> decreased FFA –> decreased VLDL.

B. Inhibits DGAT2 (diacylglycerol transferase, rate-limiting enzyme in hepatic triglyceride synth) –> decreased VLDL synthesis.

C. Decreases hepatic ApoCIII (LPL inhibitor) –> increased LPL –> increased VLDL breakdown –> increased VLDL clearance.

D. Increased apoAI expression –> increased HDL production.

E. Decreased Lp(a) (analog of fibrinogen) –> blocks plasmin formation –> decreased thrombosis.

F. Decreased recruitment of macrophages to atherosclerotic lesions

62
Q

Niacin: adverse effects?

A

A. Skin flushing (Tx: NSAIDs prior).

B. Risk of gout.

C. Exacerbates peptic ulcer disease.

D. Risk of hyperglycemia.

E. Hepatitis

63
Q

Niacin: contraindications?

A

a) Peptic Ulcer disease
b) Patients with a history of gout
c) Used with caution in diabetics
d) Used with caution in patients with impaired liver function

64
Q

Fibrates (fenofibrate/gemfibrozil): indications?

A

High VLDL, high LDL, low HDL

65
Q

Fibrates (fenofibrate/gemfibrozil): effects on serum lipids?

A

v TG (40-60%)

v LDL (10-20%)

^ HDL (10-20%)

66
Q

What increases HDLs more, fibrates or niacin?

67
Q

Fibrates: MoA?

A

Ligands for PPARalpha-TF.

A. Decreased ApoC3/increased LPL expression –> increased FA oxidation –> decreased VLDL synthesis –> increased VLDL clearance.

B. increased apoA1 expression –> increased HDL production

(might not need to know this that clearly except beginning and end results)

68
Q

Fibrates: therapeutic uses?

A
  • Treatment of hypertriglyceridemia associated with low HDL
    • v triglyceride levels and ^ ­HDL levels
    • Therapy of choice for patients w/Familial dysbetalipoproteniemia/Type III Hyperlipoproteinemia: ^ plasma triglycerides and IDL/VLDL remnants
  • Treatment of patients with high levels of trigylcerides (>500 mg/dL)
    • –> Risk of pancreatitis (potentially fatal)
  • Long-term fibrate usage proven to reduce the incidence of:
    • Coronary events (22%), CVA (25%), TIA (59%).
69
Q

Fibrates: indications?

A

High VLDL, low HDL

70
Q

Fibrates: adverse effects?

A

A. Increased gallstones. (inhibits cholesterol 7a-hydroxylase)

B. Hepatitis.

C. Myopathy.

D. Rhabdomyolysis (very rare, more common w/gemfibrozil). Increased w/high dose statin!

71
Q

What is the general mechanism behind fibrates drug interactions?

A

Strong protein binders, can displace others

72
Q

What are some of the drug interactions a/w fibrate

A

(Strong protein binders–increase serum conc of other drugs)

^ warfarin –> ^ risk of bleeding.

^ sulfonylureas –> (stimulate insulin) ^ hypoglycemia.

Statin interaction: ^[statins] –> ^rhabdomyolysis, esp. gemfibrozil.

73
Q

Explain the mechanism behind fibrates interaction w/statins.

Are any statins not affected?

Which of the fibrates is a/w this effect?

A

Inhibit OATP2/glucuronidation.

Affects ALL statins

Gemfibrozil (therefore use fenofibrate when combining w/statins!!)

74
Q

Fibrates: contraindications?

A
  1. Pregnant
  2. Severe hepatic disfunction
  3. Severe renal dysfunction (both fibrates renall excreted–a/w ^ risk rhabdomyolysis)
  4. Pre-existing GB disease (inhibition of cholesterol 7a-hydroxylase gene expression)
75
Q

What lipids are in fish oils?

A

Omega-3 long chain polyunsaturated fatty acids

Ethyl esters of eicosapentaenoic acid & Docosahexaenoic acid

76
Q

Fish oils: MoA?

A
  • Mechanism of action is unclear, but appears to involve inhibiting the expression of genes involved in hepatic triglyceride synthesis
  • Also posses anti-inflammatory activity- acts via GPCR expressed on macrophages
77
Q

Fish oils: effects on serum lipids?

A

Lowers TGs by 30-50%

Minor increase in HDL

Can lower LDLs in some people

Pharm (32 decks)

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