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Pharm Hyperlipidemias Flashcards

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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
Describe HDL synthesis? *he didn't talk about this is class
- 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)
26
What causes Primary chylomicronemia?
Defective removal of CM (apoCII, LPL defect)
27
What is the effect of primary chylomicronemia?
Chylomicrons elevated, VLDL elevated, pancreatitis
28
What does serum of a patient with primary chylomicronemia look like?
creamy layer and clear infranate
29
What causes Familial hypertriglyceridemia?
Defective metabolism of VLDL (LPL defect)
30
What is the primary effect of Familial hypertriglyceridemia?
VLDL elevated, Hypertriglyceridemia, pancreatitis
31
Who do you typically see with Familial hypertriglyceridemia? How do you treat it?
Classic in people with T2D with low insulin! Develop LPL defect. Treat the diabetes, and put patient on low calorie diet.
32
What does serum of a patient with Familial hypertriglyceridemia look like?
Will see creamy layer with cloudy infranate
33
What causes Familial dysbetalipoproteinemia?
Defective metabolism of VLDL, Chylomicrons, ApoE defect (E2/E2 alleles that are not as good at binding to ApoE receptor!).
34
What is the primary effect of Familial dysbetalipoproteinemia?
VLDL and CM remnants (IDL) elevated. Cholesterol and TG elevated 1:1, atherosclerosis
35
What causes Familial Combined Hyperlipidemia (FCH)?
Overproduction of apoB (VLDL)
36
What is the primary effect of Familial Combined Hyperlipidemia (FCH)?
Variable phenotype, elevated VLDL, LDL, or Both. Premature atherosclerosis
37
Who will you see with Familial Combined Hyperlipidemia (FCH)?
people with a VERY strong family history of heart disease
38
What causes Familial Hypercholesterolemia (FH)?
LDL receptor, ApoB defect. Decreased receptor mediated removal of LDL from plasma
39
What is the primary effect of Familial Hypercholesterolemia (FH)?
LDL increased, premature atherosclerosis
40
What is a desirable cholesterol level?
<200
41
What is a desirable LDL?
< 70
42
What is a desirable HDL in men and women?
>40 men | >50 women
43
What is a desirable TG level?
< 120
44
What statins are inactive lactone prodrugs?
Lovastatin, Simvastatin
45
Are lactone prodrugs lipid soluble?
YES
46
How are lactone prodrugs metabolized?
CYP3A4
47
How potent are the inactive lactone prodrugs?
intermediate potency and efficacy
48
What statin has an active, open lactone ring?
Pravastatin
49
Is pravastatin lipid soluble?
NO, water soluble
50
What is the consequence of pravastatin being water soluble?
it does not cause as severe of myopathy
51
How potent is pravastatin?
low potency, low efficacy
52
List the synthetic, flourine containing congeners?
Atorvastatin, Rosuvastatin
53
What is unique about the flourine containing congeners?
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
How potent are the fluorine containing congeners?
high potency, high efficacy
55
What should persons age > 75 yr, or with safety concerns for ASCVD take?
moderate intensity statin
56
What should you give patients <75 yr after an MI to prevent recurrence?
high intensity statin
57
What do you give a patient >21 yr with LDL-C level > 190 mg/dl ?
high intensity statin | May consider adding non-statin LDL lowering drugs to further reduce LDL
58
What statins are metabolized by CYP3A4?
lovastatin, simvastatin, atorvastatin (also oxidation)→
59
What statins are metabolized by CYP2C9?
fluvastatin, rosuvastatin
60
What statin has NO CYP interactions and is metabolized by sulfation?
Pravastatin
61
What type of metabolism is experienced by EVERY statin?
glucaronidation by UGT1A1
62
What drug should be avoided in people taking statins due to its effect on UGT1A1?
gemfibrozil
63
What are drugs that should be avoided with CYP3A4 statins?
microlides, azoles, SSRIs, grapefruit, HIV PIs
64
What are the 8 adverse effects of statins?
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
Why are statins so well tolerated?
cleared almost completely by first pass metabolism
66
How do bile acid sequestrants get into the systemic circulation?
TRICK QUESTION- they don't get absorbed!
67
Are bile acid sequestrants safe?
YES! can be used in children and people with liver disease
68
When is a bile acid sequestrant typically used?
usually in adjunct with statins or in people intolerate of statins
69
Why do you not want to give someone with high TGs a bile acid sequestrant?
TGs can increase if someone has high TGS
70
What are the adverse effects of bile acid sequestrants ?
GI problems (bloating and constipation)
71
Why do you need to take bile acid sequestrants with water?
fecal impaction
72
What type of drugs do bile acid sequestrants prevent the uptake of?
digoxin, b-blockers, thyroxine, coumadin (take other medications 1 hour before or 3-4 hours after bile acid sequestrant)
73
When do you use Ezetimibe?
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
Does Ezetimibe reduce risk of CHD?
NOT yet proven
75
List the 2 fibric acid inhibitors?
Gemfibrozil and Fenofibrate
76
What is the MOA of fibric acid inhibitors?
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
What is the effect of fibric acid inhibitors?
Reduces VLDL, Increases HDL Triglyceride reduced up to 50% HDL-C increased up to 15% LDL-C unchanged or decreased modestly (may increase).
78
What are the adverse effects of fibric acid inhibitors?
gastroesophageal reflux, diarrhea, increased liver enzymes
79
What are some weird adverse effects of fenofibrate?
ncreased creatinine (reversible), paradoxical HDL lowering
80
What are contraindications of fibric acid inhibitors?
NOT with gallstones | NOT with pregnancy
81
Which fibric acid inhibitor can you use in renal failure?
gemfibrozil (cannot use fenofibrate, because it is metabolized to an active metabolite in the liver and is excreted through the kidney)
82
What is niacin?
Vitamin B3 in HUGE doses
83
Why do people like using extended-release niacin?
because it causes less flushing
84
What is the MOA of niacin?
reduces TG synthesis decreases VLDL production activates LPL Increase plasma ApoA1 to increase transfer of cholesterol from macrophages to HDL
85
What are the primary effects of niacin?
``` 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
What is the primary adverse effect of niacin?
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
When is niacin contraindicated?
history of gout history of peptic ulcer disease insulin resistance worsened (be sure to really control diabetes) Pregnancy category C
88
If you have high TGs, what should you take to decrease your risk of CHD?
doesn't matter, want to use a high-dose statin
89
What has been shown to reduce the risk of CHD (other than statins)?
diets high in N-3 PUFAs

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