Anti Hyperlipidemia Flashcards Preview

Pharmacology > Anti Hyperlipidemia > Flashcards

Flashcards in Anti Hyperlipidemia Deck (26):
1

EPA, DHA, Lovaza class

omega 3 fatty acids

2

EPA, DHA, Lovaza description/mechanism

With long term use, they can increase HDL

Decrease TAG synthesis and increase fatty acid oxidation in the liver

Adverse-> may increase total LDL as they decrease TAG

3

Ezetimibe class

Cholesterol Absorption Inhibitors

4

Ezetimibe description

Inhibits absorption of cholesterol -> increase synthesis
Decrease LDL; Increase HDL
-Complementary actions to statins

5

Ezetimibe mechanism

Inhibits intestinal transport protein which takes up cholesterol from the lumen, decrease absorption -> decrease chylomicrons -> upregulation of LDL-r and increased clearance

6

Ezetimibe adverse

Impaired hepatic function (reversible)
Myositis
Increases cholesterol synthesis

7

Cholestyramine, Colestipol, Colesevelam class

Bile acid binding resins

8

Cholestyramine, Colestipol, Colesevelam description

H2O insoluble
Charged, high MW -> NOT absorbed or metabolized

Completely excreted in the feces

9

Cholestyramine, Colestipol, Colesevelam mechanism

Binds the anionic bile acids in the intestine -> prevents reabsorption -> increased produciton in the liver -> decreased production in the liver -> decreased intracellular cholesterol -> upregulate LDL-r -> increased plasma clearance of LDL

Modest increase in HDL

10

Cholestyramine, Colestipol, Colesevelam indication

**only useful in patients with isolated high LDL**

Use in combination with statins or niacin

**DOC for pregnant women (category B) and children**

11

Cholestyramine, Colestipol, Colesevelam adverse

GI (bloating, cramps, nausea, constipation)
Colesevelam has less AE

**Contraindicated with increased TAGs -> may increase TAGs and VLDL**

Non specific binding -> may decrease absorption of some drugs and fat soluble vitamins

12

Gemfibrozil, Fenofibrate class

Fibrate derivatives

13

Gemfibrozil, Fenofibrate description

Decrease TAG
Modest decrease of VLDL
Increase HDL

14

Gemfibrozil, Fenofibrate mechanism

Activates PPAR-alpha (peroxisome proliferator activated receptor) which is expressed in the liver and brown adipose tissue

In combined disease: increase LDL with a decrease in TAG

15

Gemfibrozil, Fenofibrate indication

Hypertriglyceridemia
Dysbetalipoproteinemia

16

Gemfibrozil, Fenofibrate adverse

Mild GI disturbance
Myositis (patients with renal insufficiency)
Rhabdomyolysis
Cholelithiasis due to increased cholesterol excretion

17

Niacin (nicotinic acid) description

Increase HDL
Decrease VLDL, LDL and La(a)
Only one that decreases Lp(a)

18

Niacin (nicotinic acid) mechanism

Activates Gi -> decreases cAMP -> decreases PKA -> Inhibits HSL: decreased plasma FFA sent to liver -> decreases TAG synthesis -> decreases VLDL production/release

Activates LPL -> increase uptake of LDL, Decrease HDL catabolism

Decrease fibrinogen, increase t-PA -> reverses endothelial dysfunction

19

Niacin (nicotinic acid) indication

Adjuvant therapy with statins

20

Niacin (nicotinic acid) adverse

Intense cutaneous flush: PG-mediated so it can be blocked by prior administration of aspirin

Pruritis, rash, dry skin
*Acanthosis nigricans*

*Hepatotoxicity* (increased serum tansaminase levels)
Insulin resistance -> severe *hyperglycemia*
Increase uric acid -> gout

21

Rosuvastatin, Atorvastatin, Simvastatin, Fluvastatin, Lovastatin, Pravastatin class

HMG-CoA reductase inhibitor "Statins"

22

Statins description

Analogs of HMG
Pleiotropic effects:
Increased endothelial function
Decreased platelet aggregation
Decreased Inflammation
Decreased plasma CRP
Decreased LDL

23

Statin mechanism

Competitive inhibition of HMG-CoA reductase (rate limiting step in cholesterol synthesis) -> decrease synthesis and intracellular depletion -> upregulation of LDL-r -> increase clearance of LDL from blood

Inhibit cholesterol synthesis and increase absorption

24

Statin indication

*DOC for LDL reduction*
Decrease CV mortality

Not as good of an effect for patients homozygous for FH due to lack of functional LDL-r
Best when used in combination with resins, niacin, or ezetimibe

25

Statin adverse

Elevated aminotransferase (LFTs increase > 3x is bad)

Myopathy and rhabdomyolysis (muscle pain) -> incidence increase when combined with a fibrate
Myoglobinuria -> renal injury (serum CK)

*Contraindicated in pregnancy -> Category X*

26

Five phenotypic groups of primary hyperlipidemias

Hyperchylomicronemia
A: hypercholesterolemia (LDL) B: combined hyperlipidemia (LDL and VLDL)
Dysbetalipoproteinemia (IDL)
Triglyceridemia (VLDL)
Mixed hypertriglyceridemia (chylomicrons and VLDL)