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Pharmacology > Hyperlipidemia/Dyslipidemia > Flashcards

Hyperlipidemia/Dyslipidemia Flashcards

1
Q

hypercholesterolemia

A

high LDL, normal TG and HDL

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2
Q

mixed or combined dyslipidemia

A

high LDL and TG and possibly low HDL

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3
Q

hypertriglyceridemia

A

high TG, normal LDL and possible low HDL

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4
Q

where is most cholesterol produced

A

75% in liver

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5
Q

what does cholesterol make?

A

hormones
Vit D
bile salts

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6
Q

first line conventional tx for hyperlipidemia

A

statins

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7
Q

Statins MOA

A

HMG-CoA reductase inhibitors (this enzyme catalyzes the rate-limiting step in cholesterol synthesis) –> liver increases cholesterol uptake from the blood stream by increasing the number of LDL receptors (PCSK9 up regulation)

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8
Q

Statin indications

A

first-line therapy for primary and secondary prevention of ASCVD; familial hypercholesterolemia

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9
Q

Statin C/I

A

active liver dz (not absolute), pregnancy (category X), or breat feeding

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10
Q

Statin s/e

A

myopathy, increase in liver enzymes, nausea, HA

if someone is predisposed to DM, these can make dz more likely

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11
Q

Statin pharmacokinetics

A

1) onset: variable, peak effect in a few weeks
2) T1/2 = 1-20 hr
3) metabolism: variable, usu. involves CYP enzyme
4) variable bioavailability

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12
Q

How is atorvastatin metabolized?

A

CYP34A

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13
Q

How is fluvastatin metabolized?

A

CYP2C9 (major)

CYP34A (20%)

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14
Q

How is lovastatin metabolized?

A

CYP3A4

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15
Q

How is pitavastatin metabolized?

A

glucoronidation (major)

CYP2C9 and CYP2C8 (minor)

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16
Q

How is rosuvastatin metabolized?

A

not extensively metabolized; the major metabolite is formed by CYP2C9 and CYP2C19

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17
Q

How is simvastatin metabolized?

A

CYP3A4

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18
Q

Interactions between statins and natural therapies

A

1) Red yeast rice - duplication of therapy, incr. risk of myopathy
2) Niacin - might interact but is also used purposefully s/t when TG are high or HDL is low
3) Alcohol - hepatotoxicity
4) Grapefruit - CYP3A4 inhibitor, OATP inhibitor
5) Hypericum - CYP3A4 inducer
6) Sweet orange - OATP inhibitor

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19
Q

A person on atorvastatin drinks up to 1 quart of grapefruit juice per day. (1) How might their levels of artorvastatin be effected. (2) What s/e would be of concern? (3) What alternative statins could they take?

A

1) Grapefruit juice inhibits CYP3A4, which metabolizes atorvastatin
2) myalgia; have pt. self monitor b/c juice doesn’t significantly affect all pt.
3) **pravastatin, pitavastatin, rosuvastatin

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20
Q

Ezetimibe (Zetia) MOA

A

prevents absorption of dietary and biliary cholesterol –> upregulates LDL receptors in the liver lowering plasma LDL-C

**inhibits cholesterol GI absorption

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21
Q

Ezetimibe (Zetia) indications

A

adjunctive therapy in homozygous familial hypercholesterolemia and primary hyperlipidemia; typically used when statin intolerant

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22
Q

Ezetimibe (Zetia) cautions

A

1) C/I in pregnancy (category C) and breast feeding

2) may incr. liver enzymes; higher likelihood of this when administered w/ statin than as a monotherapy

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23
Q

Ezetimibe (Zetia) efficacy

A

on small reduction in ASCVD when used WITH a statin

minor reduction in LDL; even smaller increase in HDL and decrease in TG

24
Q

Ezetimibe (Zetia) pharmacokinetics

A

1) onset = 1 wk
2) T1/2 = 22 hr
3) metabolism = ~30 undergoes glucuronide conjugation in SI and liver, active metabolite; ~80% excreted in feces

25
Q

Ezetimibe (Zetia) interactions with natural products

A

1) b/c it inhibits sterol absorption in the gut, it will lower effectiveness of green tea, omega-3 FA, sitostanol, and beta-sitosterol
2) numerous meds w/ moderate interactions that effect liver toxicity or drug absorption

**no interactions w/ niacin or red yeast rice

26
Q

Fenofibrate (fibric acid) class

A

fibrate

27
Q

Gemfibrozil class

A

fibrate

28
Q

Fibrates MOA

A

lower production and increase clearance of VLDL, increase HDL production

ultimately lowers TG and increased HDL, but has variable effect on LDL

29
Q

Fibrates indications

A
  • hypercholesterolemia or mixed dyslipidemia as adjunct therapy or monotherapy in pt. who cannot tolerate statins
  • hypertriglyceridemia first-line pharmacotherapy (TG > 1000 mg/dL)
30
Q

Fibrates cautions

A

1) C/I = active liver dz, severe renal impairment or ESRD, pre-existing GB dz, breast feeding
2) s/e = dyspepsia, gallstones, myopathy (incr risk w/ statins, esp. gemfibrozil)

31
Q

Fibrate pharmacokinetics

A

1) onset = 2-3 days
2) T1/2 = 20 hrs
3) Inactived by glucuronidation in the liver or kidney; ~60% excreted in urine as metabolites

32
Q

Fibrates interactions w/ natural therapies

A

1) if combined w/ red yeast rice might incr. risk of myopathy
2) niacin might incr. hepatoxicity
3) alcohol - hepatoxicity
4) other meds that cz liver toxicity

33
Q

Gemfibrozil increases the risk for what s/e when used with statin therapy?

A

myopathy

34
Q

How can we assess severity of myopathy?

A

creatinine kinase

*rarely, pt. can have really high creatinine kinase w/out sx of myalgia, so it might be good to get a baseline and monitor them a few mo. into tx

35
Q

Niacin MOA

A

somewhat unclear

increases lipoprotein lipase (LPL) activity, enhancing removal of TG from plasma; reduces TG synthesis; incr. HDL levels

36
Q

Niacin indications

A

hypercholesterolemia or mixed dyslipidemia

  • as adjunct therapy in pt. that don’t tolerate fibrates or omega-3 FA
  • as monotherapy in pt. that don’t tolerate statins, BAS, fibrates
37
Q

Niacin cautions

A

1) C/I = active liver dz (esp. w/ sustained release), gout, or PUD
2) s/e = hepatotoxicity (enhanced SR formulation), hyperglycemia, hyperuricemia, upper GI distress, flushing**, itching

38
Q

Niacin efficacy

A

studies haven’t panned out for using niacin as ASCVD preventative

moderate reduction in LDL and TG, moderate incr. in HDL

39
Q

Niacin pharmacokinetics

A

1) onset = immediate
2) T1/2 = 30 min
3) quickly converted to NAD+ in liver, but pathways become saturated at doses need to tx hyperlipidemia
4) ~70% excreted in urine

40
Q

Niacin interactions with natural therapies

A

1) Red yeast rice - depends on dose
2) alcohol
3) other meds that increase hepatoxicity

41
Q

Niacin causes flushing, the ER form has less flushing as a s/e. However, it is not used very often because of an increased risk for what s/e?

A

hepatotoxicity

42
Q

What is the largest benefit of omega-3 FA?

A

lowering TG

43
Q

What is the therapeutic dose of omega-3 FA?

A

2-4 grams of EPA + DHA (high!)

44
Q

omega-3 FA MOA

A
  • inhibits release of FA from adipose tissue
  • inhibits beta oxidation of hepatic FA
  • inhibits FA synthesis
  • increased VLDL clearance
  • *lowers TG and increases HDL
45
Q

omega-3 FA indications

A

hypertriglyceridemia second-line tx (TG > 1000 mg/dL)

46
Q

omega-3 FA cautions

A

1) C/I = hypersensitivity to fish oil
2) s/e = eructation, nausea, dyspepsia, taste change
3) may incr. bleeding time (use w/ caution in pt. on anticoagulants and antiplatelets)

47
Q

omega-3 FA efficacy

A

no benefit in ASCVD risk has been shown

small incr. in HDL, 20-50% decease in TG

48
Q

omega-3 FA

A

1) onset = 2 wks
2) T1/2 = 140 hr
3) 100% bioavailability
4) metabolized by lipid enzymes in liver and tissues

**high bioavail. and long T1/2 is impt to consider in terms of bleeding effects

49
Q

Bile acid sequestrants (BAS) MOA

A

they are resins that bind bile acids in the intestine –> reduces enterohepatic recycling –> increases hepatic conversion of cholesterol to bile acid

upregulates LDL receptors on liver

50
Q

Bile acid sequestrants (BAS) indications

A

hypercholesterolemia for high risk pt. who are statin-intolerant or are on maximal tolerated doses of a statin

51
Q

Bile acid sequestrants (BAS) cautions

A

1) C/I = TG over 300 mg/dL, complete biliary obstruction
2) s/e = constipation, abdominal discomfort, intestinal gas, dyspepsia, heartburn, diarrhea
3) b/c it’s an absorbent, it can bind onto other medications that the pt. is taking

52
Q

Bile acid sequestrants (BAS) pharmacokinetics

A

1) onset = 21 days to peak effect
2) T1/2 = variable
3) 100% excreted in feces, not absorbed

53
Q

What other drugs shares the intestine as a site of action?

A

ezemtimibe (Zetia)

54
Q

BAS and Ezetimibe both work to lower GI absorption of cholesterol. What changes occur in the liver to lower LDL?

A

increased LDL receptors (so that more LDL is taken up from the blood)

55
Q

Bile acid sequestrants (BAS) interactions with natural therapies

A

1) Niacin absorption might be inhibited

2) Only moderate interactions, mostly d/t changes in absorption profiles

Pharmacology (14 decks)

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