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Cardio > Pharm Hyperlipidemias > Flashcards

Pharm Hyperlipidemias Flashcards

1
Q

What is the MOA of statins?

A

HMG-CoA reductase inhibitor that blocks the rate-limiting step in cholesterol synthesis

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2
Q

What is the primary effect of statin therapy?

A

lowers LDL by 25-60%

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3
Q

What is the MOA of bile acid resins? Name them.

A

binds to bile acid to prevent re-absorption and re-use of bile acid cholesterol

Colestipol, cholestyramine, and colesevelam

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4
Q

What is the primary effect of bile acid resins?

A

lowers LDL by up to 20%

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5
Q

What is the MOA of ezetimibe?

A

prevents the aborption of dietary cholesterol

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6
Q

What is the primary effect of ezetimibe?

A

lowers LDL by up to 20%

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7
Q

What is the MOA of niacin?

A

inhibits VLDL secretion, in turn decreasing production of LDL. Increased clearance of VLDL via the LPL pathway contributes to reduction of triglycerides.

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8
Q

What is the primary effect of niacin?

A

Decreases LDL levels by about 20% and TGs. It often increases HDL levels significantly.

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9
Q

Where does micelle formation occur?

A

in the small interstine

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10
Q

Where are micelles absorbed to make chylomicrons?

A

intestinal mucosal cells

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11
Q

What are the 4 components of a nascent chylomicron?

A 
o	Phospholipids
o	Triacylglycerols (80-95%)
o	Cholesterol
o	Apoprotein B-48
* 10:1 TG: cholesterol ratio
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12
Q

Where do nascent chylomicrons enter the blood?

A

thoracic duct

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13
Q

What happens when nascent chylomicrons come in to contact with HDL in the blood?

A

HDL donates ApoCII and ApoE to the nascent chylomicron which is then called a mature chylomicron.

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14
Q

What is the fate of a mature chylomicron?

A

The ApoCII on mature chylomicrons binds to Lipoprotein Lipase on tissues which allows TGs in the lipoprotein to be broken down. The free fatty acids and diglycerides are taken in to the adjacent tissue cell to be utilized or stored.

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15
Q

How is a chylomicron remnant formed?

A

ApoCII is given back to HDL and the chylomicron is now called a remnant.

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16
Q

What is the fate of a chylomicron remnant?

A

The remnant is then further acted upon by LPL and Hepatic lipase to form a particle that is taken up by the liver via an ApoE receptor.

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17
Q

What are remnant components used for in the liver?

A

The remnant’s components are then used to synthesize nascent VLDL

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18
Q

How does nascent VLDL mature?

A

Nascent VLDL comes into contact with HDL in the blood and acquired the ApoCII and ApoE to become mature

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19
Q

What are the components of VLDL?

A 
•	Apoprotein B100 (backbone of lipoprotein)
•	TGs (55-80%)
•	Cholesterol
•	Phospholipids
*5:1  TG: cholesterol ratio
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20
Q

How is IDL formed?

A

The ApoCII on mature VLDL binds to Lipoprotein Lipase on tissues which allows TGs in the lipoprotein to be broken down. VLDL then donates ApoCII back to HDL and becomes IDL

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21
Q

What is the TG: cholesterol ratio of IDL?

A

1:1

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22
Q

How is LDL formed?

A

As IDL loses TGs and becomes less dense, it is considered to be a LDL

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23
Q

What is the fate of LDL?

A

LDL is then catabolized by hepatocytes and other cells via receptor-mediated endocytosis (LDL receptor) BUT usually goes to periphery and stores (in things like arteries—causing problems)

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24
Q

What makes up LDL?

A

(low TG content, high cholesterol content).

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25
Q

Describe HDL synthesis? *he didn’t talk about this is class

A
  • Early HDL (with ApoA1) is generated in liver. It is released from the liver and picks up free cholesterol from periphery (via ABCG1 and ABCA1)
  • This cholesterol in the core of the HDL is esterified by LCAT to form cholesteryl esters
  • Cholesterylester transfer protein (CETP) facilitates the transfer of cholesterol esters (in HDLs) with TAGs (in VLDLs and LDLs). This makes the HDL larger and more susceptible to uptake by the liver.
  • These HDL particles can be taken up by Scavenger Receptor-B1 (on liver)
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26
Q

What causes Primary chylomicronemia?

A

Defective removal of CM (apoCII, LPL defect)

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27
Q

What is the effect of primary chylomicronemia?

A

Chylomicrons elevated, VLDL elevated, pancreatitis

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28
Q

What does serum of a patient with primary chylomicronemia look like?

A

creamy layer and clear infranate

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29
Q

What causes Familial hypertriglyceridemia?

A

Defective metabolism of VLDL (LPL defect)

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30
Q

What is the primary effect of Familial hypertriglyceridemia?

A

VLDL elevated, Hypertriglyceridemia, pancreatitis

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31
Q

Who do you typically see with Familial hypertriglyceridemia? How do you treat it?

A

Classic in people with T2D with low insulin! Develop LPL defect. Treat the diabetes, and put patient on low calorie diet.

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32
Q

What does serum of a patient with Familial hypertriglyceridemia look like?

A

Will see creamy layer with cloudy infranate

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33
Q

What causes Familial dysbetalipoproteinemia?

A

Defective metabolism of VLDL, Chylomicrons, ApoE defect (E2/E2 alleles that are not as good at binding to ApoE receptor!).

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34
Q

What is the primary effect of Familial dysbetalipoproteinemia?

A

VLDL and CM remnants (IDL) elevated. Cholesterol and TG elevated 1:1, atherosclerosis

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35
Q

What causes Familial Combined Hyperlipidemia (FCH)?

A

Overproduction of apoB (VLDL)

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36
Q

What is the primary effect of Familial Combined Hyperlipidemia (FCH)?

A

Variable phenotype, elevated VLDL, LDL, or Both. Premature atherosclerosis

37
Q

Who will you see with Familial Combined Hyperlipidemia (FCH)?

A

people with a VERY strong family history of heart disease

38
Q

What causes Familial Hypercholesterolemia (FH)?

A

LDL receptor, ApoB defect. Decreased receptor mediated removal of LDL from plasma

39
Q

What is the primary effect of Familial Hypercholesterolemia (FH)?

A

LDL increased, premature atherosclerosis

40
Q

What is a desirable cholesterol level?

A

<200

41
Q

What is a desirable LDL?

A

< 70

42
Q

What is a desirable HDL in men and women?

A

> 40 men

>50 women

43
Q

What is a desirable TG level?

A

< 120

44
Q

What statins are inactive lactone prodrugs?

A

Lovastatin, Simvastatin

45
Q

Are lactone prodrugs lipid soluble?

A

YES

46
Q

How are lactone prodrugs metabolized?

A

CYP3A4

47
Q

How potent are the inactive lactone prodrugs?

A

intermediate potency and efficacy

48
Q

What statin has an active, open lactone ring?

A

Pravastatin

49
Q

Is pravastatin lipid soluble?

A

NO, water soluble

50
Q

What is the consequence of pravastatin being water soluble?

A

it does not cause as severe of myopathy

51
Q

How potent is pravastatin?

A

low potency, low efficacy

52
Q

List the synthetic, flourine containing congeners?

A

Atorvastatin, Rosuvastatin

53
Q

What is unique about the flourine containing congeners?

A

1) active as given
2) long plasma T/2 (14-19 hr)
3) have very high affinity for pocket of HMG-CoA reductase enzyme

54
Q

How potent are the fluorine containing congeners?

A

high potency, high efficacy

55
Q

What should persons age > 75 yr, or with safety concerns for ASCVD take?

A

moderate intensity statin

56
Q

What should you give patients <75 yr after an MI to prevent recurrence?

A

high intensity statin

57
Q

What do you give a patient >21 yr with LDL-C level > 190 mg/dl ?

A

high intensity statin

May consider adding non-statin LDL lowering drugs to further reduce LDL

58
Q

What statins are metabolized by CYP3A4?

A

lovastatin, simvastatin, atorvastatin (also oxidation)→

59
Q

What statins are metabolized by CYP2C9?

A

fluvastatin, rosuvastatin

60
Q

What statin has NO CYP interactions and is metabolized by sulfation?

A

Pravastatin

61
Q

What type of metabolism is experienced by EVERY statin?

A

glucaronidation by UGT1A1

62
Q

What drug should be avoided in people taking statins due to its effect on UGT1A1?

A

gemfibrozil

63
Q

What are drugs that should be avoided with CYP3A4 statins?

A

microlides, azoles, SSRIs, grapefruit, HIV PIs

64
Q

What are the 8 adverse effects of statins?

A

1) Generally well tolerated
2) Mild transient gastrointestinal distress
3) Increased liver enzymes (hepatitis rare)
4) Sleep disturbance, reduced daytime vigilance, memory loss
5) Teratogenic Potential: Pregnancy Category X!
6) Myalgia: muscle pain/weakness, no CPK rise
7) Myositis: muscle weakness + increased CPK
8) Rhabdomyolysis (marked increase CPK, renal failure,death)

65
Q

Why are statins so well tolerated?

A

cleared almost completely by first pass metabolism

66
Q

How do bile acid sequestrants get into the systemic circulation?

A

TRICK QUESTION- they don’t get absorbed!

67
Q

Are bile acid sequestrants safe?

A

YES! can be used in children and people with liver disease

68
Q

When is a bile acid sequestrant typically used?

A

usually in adjunct with statins or in people intolerate of statins

69
Q

Why do you not want to give someone with high TGs a bile acid sequestrant?

A

TGs can increase if someone has high TGS

70
Q

What are the adverse effects of bile acid sequestrants ?

A

GI problems (bloating and constipation)

71
Q

Why do you need to take bile acid sequestrants with water?

A

fecal impaction

72
Q

What type of drugs do bile acid sequestrants prevent the uptake of?

A

digoxin, b-blockers, thyroxine, coumadin (take other medications 1 hour before or 3-4 hours after bile acid sequestrant)

73
Q

When do you use Ezetimibe?

A

as a complementary effect with statin therapy that you cannot incrase more (additional 18% lowering of LDL on top of the effects of statin!)

74
Q

Does Ezetimibe reduce risk of CHD?

A

NOT yet proven

75
Q

List the 2 fibric acid inhibitors?

A

Gemfibrozil and Fenofibrate

76
Q

What is the MOA of fibric acid inhibitors?

A

Ligand for the ligand-activated PPARa nuclear receptor
Make more LPL (VLDL and chylomicrons broken down quicker
Supress synthesis of ApoCIII (which inhibits LPL)
Increases HDL

77
Q

What is the effect of fibric acid inhibitors?

A

Reduces VLDL, Increases HDL
Triglyceride reduced up to 50%
HDL-C increased up to 15%
LDL-C unchanged or decreased modestly (may increase).

78
Q

What are the adverse effects of fibric acid inhibitors?

A

gastroesophageal reflux, diarrhea, increased liver enzymes

79
Q

What are some weird adverse effects of fenofibrate?

A

ncreased creatinine (reversible), paradoxical HDL lowering

80
Q

What are contraindications of fibric acid inhibitors?

A

NOT with gallstones

NOT with pregnancy

81
Q

Which fibric acid inhibitor can you use in renal failure?

A

gemfibrozil (cannot use fenofibrate, because it is metabolized to an active metabolite in the liver and is excreted through the kidney)

82
Q

What is niacin?

A

Vitamin B3 in HUGE doses

83
Q

Why do people like using extended-release niacin?

A

because it causes less flushing

84
Q

What is the MOA of niacin?

A

reduces TG synthesis
decreases VLDL production
activates LPL
Increase plasma ApoA1 to increase transfer of cholesterol from macrophages to HDL

85
Q

What are the primary effects of niacin?

A 
Increases HDL-C by 15-35%.
Reduces LDL-C levels by 5-25%.
Reduces triglyceride by 20-50%.
Shifts LDL density to larger particles.
Reduces Lp(a) by 30%  (unique feature).
86
Q

What is the primary adverse effect of niacin?

A

Increases PGD2 and leads to flushing (give aspirin, take at night, etc.)
Hyperuricemia/gout.
Conjunctivitis, cystoid macular edema, retinal detachment.
Myositis (rare).
Dry skin, pruritis, icthyosis, acanthosis nigricans.

87
Q

When is niacin contraindicated?

A

history of gout
history of peptic ulcer disease
insulin resistance worsened (be sure to really control diabetes)
Pregnancy category C

88
Q

If you have high TGs, what should you take to decrease your risk of CHD?

A

doesn’t matter, want to use a high-dose statin

89
Q

What has been shown to reduce the risk of CHD (other than statins)?

A

diets high in N-3 PUFAs

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