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MHD1/Pharm1 Exam 4 > (THER) Hyperlipidemia I and II > Flashcards

(THER) Hyperlipidemia I and II Flashcards

1
Q

Define Hyperlipidemia

A

Abnormal/elevated levels of cholesterol/triglycerides in the blood. Increased LDL or low levels of HDL

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2
Q

Increase in what lipid can lead to pancreatitis?

A

Triglycerides

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3
Q

What is the relationship between LDL and atherosclerosis?

A

Increased cholesterol leads to increased LDL, which ultimately enters into the arterial wall. This damage ultimately leads to atherosclerosis because it causes monocytes to enter and to eventually form foam cells.

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4
Q

What is the role of foam cells in atherosclerosis? (2)

A
  1. Foam cells secrete proteases and growth factors that promote smooth muscle cell migration and proliferation contributing to atherosclerotic plaque
  2. Necrotic foam cells release cholesterol and other debris that contributes to the formation of a fatty streak
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5
Q

Protective roles of HDL in atherosclerosis (4)

A
  1. Inhibit the oxidation of LDLs
  2. Inhibit expression of adhesion molecles on the endothelium (monocyte recruitment)
  3. Inhibit formation of FOAM cells
  4. REVERSE CHOLESTEROL TRANSPORT
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6
Q

Optimal vs high LDL levels

A

Optimal:

Very high: > 190 mg/dL

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7
Q

Optimal vs very high Triglyceride levels

A

Optimal:

Very High: >500 mg/dL

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8
Q

At what point do you treat hypercholesterolemia with drugs? What do you do prior?

A

Once it hits the point of being “severe”. (LDL > 190; LDL w/diabetes > 70; CVD or risk for it)

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9
Q

What is the initial goal of drug therapy for hypercholesterolemia? What is the initial drug of choice?

A

Goal: reduce LDL

Drug: STATINs

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10
Q

What is the most prescribed class of drug in the US?

A

STATINs

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11
Q

Name the STATINs from most potent to least potent (6)

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

Indication(s) for STATIN use

A

High LDL

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13
Q

MOA of STATINs

A
  1. Inhibits HMG-CoA Reductase
  2. Triggers SREBP transcription factor

Both lead to increased LDL-R expression and resulting increased LDL clearance.

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14
Q

Effect of STATINs on serum lipids

A

Decreased LDL and TG

Increased HDL

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15
Q

What is the main adverse effect associated with STATINs?

A

Rhabdomyolysis

Otherwise they are generally well tolerated

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16
Q

STATINs are contraindicated in what groups?

A

Individuals with severe liver disease and pregnant/nursing mothers

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17
Q

Name the (4) Drug interactions associated with STATINs

A
  1. CYP3A4 inhibitors (increased adverse effects)
  2. CYP3A4 inducers (decreased efficacy)
  3. CYP2C9 inhibitors
  4. Gemfibrozil (decreased glucoronidation)
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18
Q

Name the Bile Acid binding resins (3)

A
  1. Cholestyramine
  2. Colestipol
  3. Colesevelam
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19
Q

Indication for Bile Acid binding resins

A

High LDL

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20
Q

MOA for Bile Acid binding resins

A
  1. Binds bile (negative charge) and prevents reabsorption, leading to…
  2. Increased bile production via chol 7a-hydroxylase, leading to…
  3. Decreased cholesterol and INCREASED LDLR, leading to…
  4. increased LDL clearance
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21
Q

Effect of Bile Acid Binding Resins on serum lipids

A

decreased LDL

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22
Q

Adverse effects of Bile Acid Binding Resins

A

Can increase TG levels in hypertriglyceridemia

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23
Q

Contraindications for Bile Acid Binding Resins

A

Contraindicated if TG > 400 mg/dL

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24
Q

Bile Acid Binding Resin Drug Interactions

A

Cholestyramine/ Colestipol interfere with absorption of a number of drugs (warfarin, digoxin, phenobarbital and tetracycline).

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25
Q

Ezetimibe indication(s)

A

High LDL

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26
Q

Ezetimibe MOA

A

Inhibits intestinal absorption of cholesterol (via NPCL1), leading to decreased hepatic cholesterol, and increased LDL-R expression/ LDL clearance.

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27
Q

Effect of Ezetimibe on serum lipids

A

Decreased LDL

28
Q

Niacin Indications

A

High VLDL (aka TGs) and LDL, Low HDL

29
Q

Niacin effect on serum lipids

A

Dec. TG and LDL

Inc. HDL

30
Q

Main adverse effects of Niacin (3)

A
  1. Skin flushing
  2. Risk of Gout (inhibits uric acid secretion)
  3. Exacerbates peptic ulcers
31
Q

Name the Fibrates (2)

A
  1. Gemfibrozil
  2. Fenofibrate
32
Q

Fibrate MOA

A

Act as ligands for the nuclear hormone TF PPARa. Leading to

  • Increased plasma HDL
  • Decreased plasma triglycerides (inc. peripheral VLDL clearence, decreased TG synthesis and VLDL secretion)
33
Q

Effect of Fibrates on serum lipids

A

Dec. TG and LDL

Inc. HDL

34
Q

Adverse effects of Fibrates (2)

A
  1. Increased gallstones
  2. Rhabdomyolysis (rare- more common with gemfibrozil)
35
Q

Contraindications of Fibrates

A
  • Severe Renal/hepatic disease
  • Patients with pre-existing gallbladder disease
  • Pregnant women
36
Q

Drug interactions for Fibrates

A

It interacts with

  1. strong protein binders (warfarin/sulfonylureas)
  2. STATINs (causes Rhabdomyolysis)
37
Q

Name the PC SK9 Inhibitors

A

Alirocumab

Evolocumab

38
Q

PC SK9 Inhibitor Indications

A

Hetero FH/ High LDL not controlled with maximum STATIN or STATIN intolerant

39
Q

PC SK9 Inhibitor MOA

A

Human antibodies which bind to PC SK9 and prevent it from binding to the LDL-R.

40
Q

Effect of PC SK9 Inhibitor on serum lipids

41
Q

Lomitapide indications

A

Homozygous FH (familial hypercholesterolemia)

42
Q

Lomitapide MOA

A

Inhibits MTP in both enterocytes and liver = dec. production of chylomicrons, VLDL and LDL

43
Q

Effect of Lomitapide on serum lipids

A

Dec. Chylomicrons, VLDL and LDL

44
Q

Adverse effects/ contraindications of Lomitapide

A

AE: Hepatotoxicity

Contraindications: Pregnancy

45
Q

Mipomersen indications

A

Homozygous Familial Hypercholesterolemia (FH)

46
Q

Mipomersen MOA

A

iAntisense olignucleotide specifc for apoB100 –> reduced expression of apoB100 –> dec. VLDL and LDL production

47
Q

Effect of Mipomersen on serum lipids

A

dec. VLDL and LDL

48
Q

Adverse effects and contraindications of Mipomersen

A

AE: Hepatotoxicity

Contraindication: mild/moderate hepatic impairment

49
Q

SREBP transcription factor functioning

A
  • Regulates expression of the LDL receptor gene
  • Leads to increased expression of the LDL-R at the Plasma Membrane
  • Increased LDL-R results in increased clearance of serum LDL
50
Q

Other than blocking HMG-COA reductase, what are other activites of STATINs that contribute to their anti-antherogenic effects

A
  1. Blocks proliferation and adhesion of monocytes to endothelium
  2. Stabilizes endothelium (dec. risk of plaque rupture)
  3. Blocks inflammatory responses
  4. Blocks SMC proliferation
  5. Blocks oxidation of LDLs (dec. Foam cell formation)
51
Q

What is are the drugs of choice for primary and secondary CAD (CHD) prevention? For pts with increased LDL-C?

52
Q

Increasing the dose of STATINs has the greatest effect on ___________ (efficacy/AE)

53
Q

Rhabdomyolysis

A

Muscle inflammation and disintegration due to toxic effects of STATINs

Marked elevation of serum [CK] and myoglobin present in urine

Occurs at high STATIN dose or because of drug interactions

54
Q

Rhabdomyolysis most often ocurs because of STATIN and an…

A

Interacting drug

(usually drugs which inhibit cytochrome P450 enzymes)

55
Q

Where are STATINs absorbed? How are they metabolized?

A

Absorbed in the intestine

Absorbed by CYP3A4

56
Q

How do STATINs enter the liver?

What is the bioavailability of STATINs? (generally)

A

Organic Anion Transporter 2 (OATP2)

Generally low bioavailbility (5-30%)

57
Q

What process facilitates the further metabolism and excretion which occurs for STATINs?

A

All STATINs are glucoronidated by glucurornyl transferase enzymes (UGT1A1/1A3)

58
Q

Fewer adverse effects have been observed with which STATIN? What may explain this?

A

Pravastatin

It has both hepatic and Renal excretion, so fewer opportunities to build-up and cause harm. It is also NOT METABOLIZED BY P450 ENZYMES

59
Q

What drug is strongly associated with an increased risk of STATIN-induced myopathy and Rhabodmyolysis? Why?

A

Gemfibrozil

It inhibits OATP2 and it inhibits the the glucoronidation of STATINs

60
Q

What is the function of PCSK9?

A

It is a secreted enzyme that binds to LDL-R and prevents it from recycling after internalization (by targeting it to the lysosome). This decreases the amount of receptors, thereby increasing the serum concentration of LDL, leading to increased risk of CVD.

61
Q

Elevated serum triglycerides are a risk factor for… (2)

A
  1. atherosclerosis/cardiovascular disease
  2. pancreatitis
62
Q

Elevated serum triglycerides are often associated with what effect on HDL?

A

Decreased HDL

63
Q

Value that counts as borderline high for triglycerides. What is the treatment indicated?

A

150-199 mg/dl

Lifestyle change is indicated

64
Q

Value that counts as very high for triglycerides. What is the treatment indicated?

A

>500 mg/dL

The initial goal is prevention of pancreatitis via medication (niacin or a fibrate). After this than LDL should be addressed.

65
Q

Name the drug most effective at raising HDLs

66
Q

Fibrate Indications

A
  1. Patients with hypertriglyceridemia
  2. Patients with low HDLs
67
Q

Function of FIsh Oils (Omega-3)

A

Lowers serum TG levels + some anti-inflammatory activity

Approved only as an adjunct to diet in the treatment of hypertriglyceridema.

MHD1/Pharm1 Exam 4 (26 decks)

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