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Pharmacology > Hyperlipidemia/Dyslipidemia > Flashcards

Hyperlipidemia/Dyslipidemia Flashcards

1
Q

definition hypercholesterolemia

A

increased LDL, normal TG and HDL

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2
Q

define mixed or combined dyslipidemia

A

increased LDL and TG and possibly low HDL

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3
Q

define hypertriglyceridemia

A

increased TG, normal LDL and possibly low HDL

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4
Q

define low HDL cholesterol

A

low HDL and normal LDL and TG

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5
Q

natural products for hyperlipidemia

A 
niacin
omega 3 fatty acids
red yeast rice (mevinolin = lovastatin)
green tea
sitostanol
beta-sitosterol
EDTA chelation
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6
Q

statins MOA

A

HMG-CoA reductase inhibitors (vital step in cholesterol synthesis)
liver then increases cholesterol uptake from blood stream by increasing LDL receptors
PCSKP up regulation

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7
Q

which statins fall into high intensity

A

Atorvastatin 40-80mg

Rosuvastatin 20-40mg

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8
Q

which statins are moderate-intensity

A 
Atorvastatin 10-20mg*
Rosuvastatin 5-10mg*
Pravastatin 40-80mg*
Lovastatin 40mg*
PItavastatin 2-4mg
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9
Q

which statins are low-intensity

A

Pravastatin 10-20mg

Lovastatin 20mg

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10
Q

statin contraindications

A

active liver dz
pregnancy
breast feeding

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11
Q

side effects

A

myopathy
increase in liver enzymes
nausea
HA

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12
Q

potential interactions btwn statins and natural therapies

A

red yeast rice
niacin (altho sometimes used with TG high or HDL low)
alcohol, grapefruit, St John’s wort, and Sweet Orange area ll major interactions

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13
Q

Ezetimibe (Zetia) MOA

A

Ezetimibe prevents absorption of dietary and biliary cholesterol —> interrupts enterohepatic circulation of cholesterol as well as chylomicron assembly –> upregulates LDL receptors in liver, lowering plasma LDL

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14
Q

Ezetimibe uses **

A

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

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15
Q

contraindications to Ezetimibe

A

pregnancy

breast feeding

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16
Q

side effects Ezetimibe

A

increase liver enzymes when given with statin

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17
Q

Ezetimibe onset/metabolism

A

onset: within 1 week
metabolism: 30% undergoes glucuronide conjugation in small intestine and liver

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18
Q

interactions with ezetimibe and natural therapies

A

ezetimibe inhibits sterol absorption in the gut and would lower the effectiveness of green tea, omega 3 fatty acids, stiostanol and betasitosterol

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19
Q

fibrates MOA

A

lower production and increase clearance of VLDL
increased HDL production
lowers TG** and increases HDL but has has variable effects on LDL

20
Q

fibrate indications

A

hypercholesterolemia or mixed dyslipidemia as adjunct therapy or monotherapy in patients who can not tolerate statins
hypertriglyceridemia first-line pharmacotherapy

21
Q

contraindications to fibrates

A

active liver dz
severe renal impairment or ESRD
pre-existing gallbladder dz
breast feeding

22
Q

side effects fibrates

A

dyspepsia
gallstones
myopathy (increased with statins, esp gemfibrozil)

23
Q

onset and metabolism of fibrate

A

onset: 2-3 days (quicker than statins)
metabolism: inactivated by glucuronidation in liver or kidneys

24
Q

What is phase 1 detox

A

Oxidation reduction and hydrolysis (CYP450)

25
Q

What is phase II detox

A

Chemically change the drug (or P1 metabolite) into compounds that are soluble enough to be excreted in urine

26
Q

Potential interactions between fibrates and natural therapies

A

Combined with red yeast rice might increase risk of myopathy (same as statins and fibrates)
Niacin might increase the hepatoxicity of fibrates
No interaction with green tea, omega-3 FA, sitostanol and beta-sitosterol

27
Q

Two drug names of Fibrates

A

Fenofibrate

Gemfibrozil

28
Q

Gemfibrozil increases the risk for what side effect when used with statin therapy?

A

Myopathy

29
Q

Can we assess severity of this adverse effect?

A

Yes through creatine kinase

30
Q

Niacin MOA

A

Niacin is converted to nicotinamide then to NAD+ and NADH
Increases lipoprotein lipase activity enhancing removal of triglycerides from plasma
Reduces TG synthesis
Increases HDL levels

31
Q

Niacin indications

A

Hypercholesterolemia or mixed dyslipidemia as an adjunct therapy for patients who do not tolerate fibrates or omega-3 FAs
Monotherapy for patients who do not tolerate statins, BAS, or fibrates

32
Q

Contraindications to Niacin

A

Active liver disease, gout or peptic ulcer dz

33
Q

Potential side effects of Niacin

A

Hepatotoxicity (enhanced in SR formula), hyperglycemia, hyperuricemia, upper GI distress, flushing, itching

34
Q

Niacin onset

A

Immediate

35
Q

Potential interactions between niacin and other natural therapies

A

Hyperlipidemia: red yeast rice might interact

Alcohol

36
Q

Niacin causes flushing, the extended release form has less flushing as a side effect. However, it is not used very often because of an increased risk for what major side effect?

A

Hepatoxicity

37
Q

What is the largest benefit of omega-3 FA’s?

A

Lowering TG’s

38
Q

Omega-3 FA MOA

A 
Inhibits release of FA from adipose tissue
Inhibits beta oxidation of hepatic FA
Inhibits FA synthesis 
Increases VLDL clearance 
Lowers TG and increases HDL
39
Q

Omega 3 FA indications

A

Hypertriglyceridemia second line pharmacotherapy

40
Q

Contraindications omega 3-FA

A

Hypersensitivity to fish oil

41
Q

Potential side effects omega 3 FA

A

Eructation, nausea, dyspepsia, taste changes

May increase bleeding time (use with caution with anticoagulants and antiplatelets)

42
Q

Onset and metabolism of Omega 3 FA

A

Onset 2 weeks

Metabolized by lipid enzymes in liver and tissues

43
Q

What effect does omega 3 FA have on bleeding

A

May impair platelet function and increasing bleeding times

44
Q

Bile acid sequestrants

A

Resins that bind bile in intestine
Reduces enterohepatic recycling
Increases hepatic conversion of cholesterol to bile acid
Upregulates LDL receptors on the liver

45
Q

BAS indications and contraindications

A

Indications: hypercholesterolemia for high risk patients who are stain-intolerant or are on maximal tolerated doses of statin

46
Q

What two drugs share intestine as site of action?

A

Ezetimibe and BAS

Work in lower intestine to lower absorption of cholesterol

47
Q

What change occurs in the liver to lower LDL

A

Increase in LDL receptors –> more uptake on blood

Pharmacology (6 decks)

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