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32 Cards in this Set

  • Front
  • Back
Predisposing factors for Hyperlipidemias
athersclerosis
coronary artery disease.
Predisposing factors for Hypertriglyceridemia
Pancreatitis
Role of Drug Therapy for Hypolipidemic Agents.
1. ↓cholesterol in lipoprotein fractions which deliver cholesterol to peripheral tissues (vLDL, LDL, IDL, ...)
2. ↑lipoprotein fractions which extract cholesterol from peripheral tissues (HDL)
3. ↓circulating triglycerides when indicated.
Cholestryamin
(QUESTRAN)
Bile Acid-Binding Resin
Colestipol
(COLESTID)
Bile Acid-Binding Resin
Colesevelam
(WELCHOL)
Bile Acid-Binding Resin
Bile Acid-Binding Resins

-MOA
-Adminstration
MOA
-Non-absorbable cationic exchange resins which bind to bile acid
-Interfer with enterohepatic circulationg of bile acids →→→ cholesterol-lowering effect

Administration
-Take it with meals (time when bile acid secretion is optimal)
[Meal → colocystokinins → bile acid release stimulated → bile acids emulsify fats for absorption]
Niacin
[Nicotinic acid]

-MOA
MOA
-↓cholesterol & ↓triglycerides at high doses compared to vitamin requirement.
-↓hepatic esterification of triglycerides and ↓vLDL (↓Tg liver → ↓vLDL → ↓Tg in ciruclation)
gemfibrozil
(LOPID)
Fibric acid derivative

Primarily excreated unchanged in the urine
fenofibrate
(TRICOR)
Fibric acid derivative

hydrolyzed by esterases in the gut and absrobed. Major fractions excreted include urinary glucuronide and in teh feces.
Fibric Acid Derivatives

-MOA
-Ligand of PPAR-α (Peroxisome proliferator-activated receptor)
- Reduces vLDL particle secreation

-↑Lipoprotein lipase activity
-↓vLDL triglycerides

-↓lipolysis in adipose tissue → reflex ↑HDL →→ ↓development of atherscloerotic plaque
Fibric Acid Derivative

-Problems
-↑biliary cholesterol may induce cholelithiasis.

↑hepatotoxity and myopathy
-hepatotoxicty due to interferance with PPAR-alpha
Atorvastatin
(LIPITOR)
HMG-CoA Reductase Inhibitor
Fluvastatin
(LESCOL)
HMG-CoA Reductase Inhibitor
Lovastatin
(MEVACOR)
HMG-CoA Reductase Inhibitor
Pravastatin
(PRAVACHOL)
HMG-CoA Reductase Inhibitor
Rosuvastatin
(CRESTOR)
HMG-CoA Reductase Inhibitor
Simvastatin
(ZOCOR)
HMG-CoA Reductase Inhibitor
HMG-CoA Reductase Inhibitors
Atorvastatin (LIPITOR)
Fluvastatin (LESCOL)
Lovastatin (MEVACOR)
Pravastatin (PRAVACHOL)
Rosuvastatin (CRESTOR)
Simvastatin (ZOCOR)
Statins: Disposition

-Admin, metabolism, excreation.
-CYP 3A4 & 2C9 metabolism (↑DDI risk)
-High First pass extraction
-Administration in evenings for optimum effect upon cholesterol synthesis.
-Drugs and metabolites excreted primarily in bile
Statins:

-Side-effects, additional MOA, counteridication
-↑myopathy risk (as compared to other agents)
-Hepatotoxicity may be dose independent

-anti-inflammatory effect (add to statin effect)

Counterindication: pregnant women and nursing mothers
Counterindication for all hypolipidemic agents
Pregnant women OR
Nursing mothers
Ezetimibe
(ZETIA)

-MOA
Cholesterol Absorption Inhibitors

-Inhibits cholesterol absorption from the small intestine.
-↓circulating cholesterol, LDL, & Tg
-↑HDL
Combo Therapies

Fibric Acid & Resin
FA ↓vLDL associated TG and Re can ↑vLDL as a reflexive response (one will offset the vLDL associated TG reflex). Net benefit of both ↓LDL and ↓vLDL cholesterol
Combo Therapies

Statin & Resin
Resin are gonna take away bile acids, liver may respond by stimulating the uptake of LDL but also the synthesis of cholester (by ↑HMG-CoA) ← statin offsets this response
Combo Therapies

Niacin & Resin
sever hypertiglyceridemia along with elevelated LDL/vLDL. Niacin: good job with ↓triglycerides; if resin causes reflex ↑in TG, niacin will get rid of this reflex.

i. Resin ↑TG, and pt already has ↑TG, couple this with niacin, to prevent TG reflex ↑. (may want to use FA with Resin) ← remember niacin and FA are cousins (they go after vLDL associated TG).
Combo Therapies

Niacin & Statin
CAUTION: it tends to ↑(ability to lower LDL cholesterol), but also ↑hepatotoxicty (2 hepatotoxins in the hepatocyte)
Combo Therapies

Resin & Niacin & Statin
Sever hyperlipoproteimia: Resin (block reuptake of bile acids) → ↑HMG-CoA r (block with Statin). And than reduce over all amt of LDL (hit it with niacin).

i. Problem with hepatotixicty
ii. Resins: ↓in solubalization ability. Statins: abiliy to ↓introhepatic cholesterol
Combo Therapies

Statin & Ezetimibe
hyperportenemia: inhibit uptake of cholesterol and synthesis of cholesterol. (in this case ur staying away from a resin)
Combo Therapies

Fibric Acid & Statin
DON’T USE: FA and Statins: presents the most problems with hepatoxicities
Bile Acid-Binding Resins

-SideEffects
-Counterindication
SideEffects
-DDI due to entric binding of other drugs
-GI disconformation
-May cause hypertriglyceridemia

Counterindication
-Pre-existing hepato-biliary tract disease [BABR ↓entrohepatic circulation of bile acids and effecti fluidity of the bile acids]
Niacin
[Nicotinic acid]

-Kinetics
-SideEffects
-Montoring
-Counterindication
Kinetics: inactive metabolite and unchanged drug in urine.
SideEffects
-cutaneous vasodilation (→ itching mediated by prostaglandins). Prevent with aspirin or ibuprofen.
-Hepatotoxicity is dose-dependent
-GI upset and Ulcerations
-Hyperglycemia
Monitor: Liver function tests
Counterindication: Pregnancy