Cardio Test 5 Gotlieb

Front 1

Bile-Acid Sequestrants

Back 1

1. Cholestyramine and Colestipol (powder)
2. Colesevelam (WelChol)
Tablet

MOA:
Highly positively charged and bind negatively charged bile acids
Increase hepatic bile-acid synthesis
-Decreases Hepatic cholesterol levels
-Increases LDL receptors

ADR:
Not used in pts with Hypertriglyceridemia (causes pancreatis)
DDI:
DDI:
Interfere with the absorption of many negative drugs (since it is +)

Front 2

Ezetimibe

Back 2

MOA:
The inhibitor of dietary cholesterol uptake by jejunal enterocytes (NPC1L1)

Less incorporation of cholesterol into chylomicrons.
Less cholesterol delivered to the liver
Up regulation of LDL receptors and cholesterol biosynthesis (compensation)

DDI:
Bile acid sequestrants

Front 3

What is the function of Apo-C? what does it bind to and why is it important?

Back 3

binds to the tissues so it can deliver triglycerides to your heart, skeletal muscles, and places that require high energy or for storage

Front 4

What is the importance of Apo-E?

Back 4

delivers chylomicron and IDL to the liver

Front 5

What is the importance of Apo-A?

Back 5

major component of HDL
more Apo-A = better binding to the scavenger receptors and removing cholesterol from arteries and tissues

Front 6

What is the importance of Apo-B 100?

Back 6

have to have this in order to remove LDL out of plasma
a defect will result in high cholesterol( high LDL)

Front 7

VLDL
(lipoprotein)

Back 7

Transport endogenous lipids (TG) from liver to nonhepatic tissue

Front 8

IDL
(lipoprotein)

Back 8

Transport endogenous lipids from liver to nonhepatic tissue; also a “remnant of VLDL

Front 9

LDL
(lipoprotein)

Back 9

Transport endogenous lipids from liver to nonhepatic tissue

Front 10

Chylomicrons
(lipoprotein)

Back 10

Transport dietary lipids from intestine to peripheral tissues and liver

Front 11

Statins
MOA
Effects

Back 11

MOA:
Competitive inhibitors of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase

Rate limiting step in cholesterol metabolism

Effects:
Inhibition of cholesterol synthesis
Reduced VLDL production
Decrease LDL receptor degradation & increase in LDL receptor gene expression
LDL receptor recognize both ApoB-100 and ApoE
Effects
Reduction of LDL levels
Reduced free cholesterol content within hepatocytes
Reduce triglyceride levels
Increase HDL
-Improve vasodilation
-Less plaque formation
-Decrease in thrombosis & plaque rupture

ADR:
Myopathy & Rhabdomyolysis
Dose, age, hepatic and renal dysfunction

DDI:
Gemfibrozil

Front 12

Nicotinic Acid (Niacin)
MOA in
1. Adipose Tissue
2. Liver

Back 12

MOA Adipose Tissue:
Activates HM74a (GPCR)
Inhibit adipocyte adenyly cyclase (AC)
Inhibit lipolysis
MOA Liver:
Inhibit both the synthesis and esterification of fatty acids
Enhances LPL receptors levels
Chylomicrons and VLDL
Enhances HDL

ADR:
Flushing & Dyspepsia
HEPATOTOXICITY

Front 13

Fibric Acid Derivatives
Examples
Use
MOA

Back 13

Ex: Clofibrate, Gemfibrozil, and Fenofibrate
Use:
Pts with severe hypertriglyceridemia and type III hyperlipoproteinemia

MOA:
AGONIST
Unknown
Peroxisome Proliferator Activated Receptors (PPAR-α)
Nuclear Transcription Receptor
Increase fatty acid oxidation
Increase LPL synthesis
Reduce of hepatic ApoC-III
ApoC-III is an inhibitor of LDL receptor-mediated clearance
Increase ApoA-I, II expression = Increase HDL
Increase LDL receptor expression

ADR:
Hair loss, myalgias, impotence

DDI:
-Potentiate the action of oral anticoagulats (plasma bound)
-Statins (myopathy)
-Not recommended to pts with hepatic and/or renal failure

Front 14

Fish Oil (Omega-3 Fatty Acids)
-Ex
-MOA

Back 14

Ex:
Eicosapentaenoic acid (EPA)
Docosahexaenoic acid (DHA)
prescription-strength (Omecor)

MOA:
-Reduce TG biosynthesis
-Increase fatty acids oxidation in the liver
-Direct effects on vascular endothelium and smooth muscle cell function
-Protective effects against local vascular injury