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Pharmacology > Anti Hyperlipidemia > Flashcards

Anti Hyperlipidemia Flashcards

1
Q

EPA, DHA, Lovaza class

A

omega 3 fatty acids

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2
Q

EPA, DHA, Lovaza description/mechanism

A

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

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3
Q

Ezetimibe class

A

Cholesterol Absorption Inhibitors

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4
Q

Ezetimibe description

A

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

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5
Q

Ezetimibe mechanism

A

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

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6
Q

Ezetimibe adverse

A

Impaired hepatic function (reversible)
Myositis
Increases cholesterol synthesis

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7
Q

Cholestyramine, Colestipol, Colesevelam class

A

Bile acid binding resins

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8
Q

Cholestyramine, Colestipol, Colesevelam description

A

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

Completely excreted in the feces

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9
Q

Cholestyramine, Colestipol, Colesevelam mechanism

A

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

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10
Q

Cholestyramine, Colestipol, Colesevelam indication

A

only useful in patients with isolated high LDL

Use in combination with statins or niacin

DOC for pregnant women (category B) and children

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11
Q

Cholestyramine, Colestipol, Colesevelam adverse

A

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

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12
Q

Gemfibrozil, Fenofibrate class

A

Fibrate derivatives

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13
Q

Gemfibrozil, Fenofibrate description

A

Decrease TAG
Modest decrease of VLDL
Increase HDL

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14
Q

Gemfibrozil, Fenofibrate mechanism

A

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

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15
Q

Gemfibrozil, Fenofibrate indication

A

Hypertriglyceridemia

Dysbetalipoproteinemia

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16
Q

Gemfibrozil, Fenofibrate adverse

A

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

17
Q

Niacin (nicotinic acid) description

A

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

18
Q

Niacin (nicotinic acid) mechanism

A

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
Q

Niacin (nicotinic acid) indication

A

Adjuvant therapy with statins

20
Q

Niacin (nicotinic acid) adverse

A

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
Q

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

A

HMG-CoA reductase inhibitor “Statins”

22
Q

Statins description

A 
Analogs of HMG
Pleiotropic effects:
Increased endothelial function
Decreased platelet aggregation
Decreased Inflammation
Decreased plasma CRP
Decreased LDL
23
Q

Statin mechanism

A

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
Q

Statin indication

A

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
Q

Statin adverse

A

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
Q

Five phenotypic groups of primary hyperlipidemias

A

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

Pharmacology (24 decks)

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