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Cardio Exam 2 > Dyslipidemia Pharmacology > Flashcards

Dyslipidemia Pharmacology Flashcards

1
Q

Define Dyslipidemia

A

Hypercholeserolemia
Hyper TG
Low HDL

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2
Q

Dyslipidemia is a major cause of

A

increased atherogenic risk and atherosclerosis-associated conditions: ischemic HD, CVD, PVD

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3
Q

Dyslipidemia is recognized as

A

risk facotr for CVD and lipid-lowering thearpy is very beneficial

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4
Q

Primary goal of drug therapy of dyslipidemia

A

Reduce LDL levels

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5
Q

Other goals of drug therapy of dyslipidemia

A

Elevate HDL and reduce TG levels

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6
Q

Acetyl CoA is used to form what via what?

A

Mevalonic Acid via HMGCoA reductase

RATE LIMITING STEP

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7
Q

Cholesterol is used in the making of?

A

steroid hormones like glucocorticoids, mineralcorticoids and sex hormones
Cell membranes
Bile acids

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8
Q

Statins

A 
Mevastatin (first)
Lovastatin (most common)
Simvastatin
Pravastatin
Fluvastatin
Atorvastatin (Lipitor)
Rosuvastatin (no generic)
Pitavastatin
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9
Q

Statin structure is based on?

A

Trying to find a compound that would inhibit the rate limiting step

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10
Q

Statin MOA

A

competitive inhibitors of HMGCoA reductase and block synthesis of cholesterol

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11
Q

Effects of Statins

A

Synthesis is blocked in the liver –> increased LDL receptors –> increased removal of LDL from blood –> reduction of LDL levels

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12
Q

Statin + TGs

A

Leads to increased LDL receptors which leads to increased removal of LDL precursors (IDL, VLDL) which reduces TGs and the overall reduction of cholesterol leads to decreased synthesis of VLDL which decreases TGs

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13
Q

What else can statins do?

A

Increase HDL by 7.5%

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14
Q

Statin Pleiotropic Effects

A

Improve endothelial function and enhanced NO production
Down regulate AT1 receptor
Increased plaque stability (inhibit SMC proliferation and migration and inhibit monocyte infiltration)
Anti-inflammatory (Athero)
Antioxidant (CV)
Anti-platelet effect (Clots)

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15
Q

Define pleiotropic

A

Beneficial but have nothing to do with lipid lowering effects of statins

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16
Q

Statins PK

A

Poor bioavailability
Large first pass effect
Excreted by liver and eliminated in feces

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17
Q

Pro-drug Statins?

A

Lovastatin and Simvastatin

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18
Q

Provastatin CYP

A

NOT cyp

3 day half life

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19
Q

Fluvastatin CYP

A

75% 2C9

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20
Q

CYP3A4

A

Atorvastatin
Lovastatin
Simvastatin

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21
Q

Inhibitors of 3A4

A 
Clarithro
Erthro
Keto
Itra
HIV PIs
Grapefruit juice
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22
Q

Inducers of 3A4

A

Rifampin

Efavirenz

23
Q

Inhibitors of 2C9

A

Gemfibrozil which is the enzyme that metabolizes Fluvastatin!!!

24
Q

Statin AEs

A

Hepatotoxicity
Myopathy –> rhabdomyolysis (breakdown of muscle fibers)
Cognitive effects (reversible)
Hyperglycemia (increase glc and A1c; but benefit still outweighs the risk in DM pts)
TSH (falsely lowers the TSH levels

25
Q

Rhabdomyolysis

A

Can be indicated by elevated CK levels but not always

26
Q

AEs in statins are

A

concentration dependent

27
Q

Statins are cautioned with:

A 
Drug combinations
Hepatic/renal dysfunction
Perioperative period
Advanced age
Multisystem disease
Small body size
Gemfibrozil
28
Q

Gemfibrozil does what?

A

Inhibits uptake of active hydroxy acid forms of statins into hepatocytes and their glucuronidation (double plasma concentration of statins

29
Q

Bile acid sequestrants

A

Cholestyramine
Colestipol
Colesevelam

30
Q

Bile acid sequestrants are the

A

safest bc they are not absorbed from the intestine

31
Q

What is the precursor of bile acids?

A

Cholesterol

32
Q

Bile acid sequestrants MOA

A

BAS have + charged and bind - charged bile acids –> not absorbed in the intestines –> eliminated in feces –> increase synthesis of bile acids (using cholesterol) –> decreased cholesterol
–> increased LDL receptors and decreased LDL levels –> reduction of LDL

33
Q

Bile acid sequestrants effects on lipid profile

A

Decreased LDL (max in 1-2 weeks)
Reduced cholesterol which upregulates HMG-CoA reductase (good with a statin)
HyperTGs
Elevated HDL by 4-5%

34
Q

Adverse effects

A

HyperTG
Interfere with absorption of sterols (digitalis), acidic drugs, fat soluble vitamins)
May cause constipation

35
Q

Niacin activity

A

Decreases TGs by 35-45% and LDL by 20-30%

BEST: Increases HDL by 30-40%

36
Q

Niacin MOA

A

Niacin + receptors in adipocytes –> reduced cAMP –> decreased breakdown of TGs –> Decreased FFA –> Decreased TG synthesis –> Decreased VLDL and reduction of LDL

37
Q

Niacin MOA for HDL increase

A

Reduced hepatic clearance of apoA-I

38
Q

Niacin Adverse Reactions

A

Hepatotocitiy
Insulin resistance
Elevated uric acid

39
Q

Fibric acid derivatives (PPARalpha agonists)

A

Clofibrate
Gemfibrozil
Fenofibrate

40
Q

Fibric acid derivatives (PPARα agonists) MOA

A

Fibrate + PPARα leads to increased FA oxidation, increased LPL synthesis which leads to increased clearance of TG rich proteins and decreased expression of apoC-III which increases clearance of VLDL
All of which decrease TG levels

41
Q

Fibric acid derivatives (PPARα agonists) MOA + HDL

A

Fibrate + PPARα Leads to increase expression of apoA-I and apoA-II which elevated HDL levels

42
Q

Fibric acid derivatives (PPARα agonists) effects of lipid profile in Mild hyperTG

A

50% decrease in TG
15% increase in HDL
LDL unchanged

43
Q

Fibric acid derivatives (PPARα agonists) effects of lipid profile in High HyperTG

A

50% TG reduction

LDL 10-30% INCREASE (YIKES)

44
Q

Fibric acid derivatives (PPARα agonists) are drug of choice in:

A

SEVERE hyperTG and chylomicronemia syndrome

45
Q

Fibric acid derivatives (PPARα agonists) caution in combo with:

A 
Oral anticoagulants (higher concentration)
Statins with gemfibrozil
46
Q

Ezetimibe is a

A

dietary cholesterol uptake inhibitor

47
Q

Ezetimibe causes ____ but doesn’t effect ____

A

synthesis in cholesterol in liver

TG absorption

48
Q

Ezetimibe MOA

A

Reduces cholesterol absorption –> decreased chylomicron formation –> increased LDL receptor expression –> increased clearance of LDL

49
Q

Ezetimibe effects on lipid panel

A

15-20% LDL reduction
5% TG reduction
1-2% HDL increase

50
Q

Omega-3-acid ethyl esters

A

Lovaza (Omacor)

Vascepa (icosapent)

51
Q

Omega-3-acid ethyl esters Use

A

Adjunct to reduce TG levels (hyperTG - >500)

52
Q

Omega-3-acid ethyl esters MOA

A

Inhibit acyl CoA acyltransferase
Increase oxidation of lipids in liver
Decreased lipogenesis
Increased LPL activity

53
Q

Difference between Lovaza and Vascepa

A

L: increase LDL
V: decreased LDL

54
Q

PCSK9

A

Induces degradation of LDL receptors –> we would want to block this in a future drug!!

Cardio Exam 2 (10 decks)

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