- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
PLAY BUTTON
PLAY BUTTON
16 Cards in this Set
- Front
- Back
|
What are the characteristics of type IIa hyperlipidemia?
|
isolated hypercholesterolemia, high LDL-C only
|
|
What are the characteristics of type I hyperlipidemia?
|
isolated hypertriglyceridemia, high CM
|
|
What are the characteristics of type IV hyperlipidemia?
|
isolated hypertriglyceridemia, high VLDL
|
|
What are the characteristics of type IIb hyperlipidemia?
|
combined hyperlipidemia, high LDL and VLDL
|
|
What are the characteristics of type III hyperlipidemia?
|
combined hyperlipidemia, high CM and IDL
|
|
What are the characteristics of type V hyperlipidemia?
|
combined hyperlipidemia, high CM and VLDL
|
|
What are the normal values of cholesterol, VLDL, LDL, HDL, and TAG?
|
cholesterol: <200 mg/dL
VLDL: 5-40 mg/dL LDL: <100 mg/dL HDL: 40-60 mg/dL |
|
What is the Friedwald equation?
|
LDL-C = total C - TAG/5 - HDL-C
|
|
What is abetalipoproteinemia (CM retention disease)?
|
a los of function mutation in gene encoding microsomal transfer protein (MTP), which transfers lipids to nascent CM and VLDL before they are released from enterocytes and hepatocytes, respectively (low C, TAG, CM, VLDL, LDL)
|
|
What is tangier disease?
|
defect in ATP binding cassette protein A1 (ABC-A1) prevents transfer of cholesterol and phospholipids from peripheral cells to HDL (low levels of HDL)
|
|
What is atherosclerosis?
|
fibrous fatty deposits beneath endothelium of blood vessels,
|
|
What are the risk factors of atherosclerosis?
|
presence of lipoprotein (a) in plasma, high levels of C-RP (these rise with obesity)
|
|
What is the mechanism leading to atherosclerosis?
|
LDL + glycosaminoglycans in intima of vessel → oxidative modification → recruitment of monocytes from blood → monocytes accumulate oxidized lipoproteins → monocytes become foam cells → fatty streak → foam cell necrosis → proliferation of smooth muscle, fibrous tissue, collagen → microlesion → accumulation of clotting factors → formation of fibrous cap and accumulation of calcium → cap rupture → thrombus → occlusion or embolism
|
|
Why is HDL considered "good" cholesterol?
|
because its function in reverse cholesterol transport (removes excess cholesterol from tissues and macrophages/monocytes)
|
|
What are the consequences of cholesterol ester transter protein (CETP) deficiency?
|
decreases transfer of CE from HDL to VLDL, increases HDL-C concentration, increased reverse cholesterol transport, decreased risk of CVD
|
|
How are dyslipidemias treated?
|
exercise!
statins: competetive inhibition of HMG CoA reductase ezetemibe: inhibits cholesterol absorption and increases LDL receptor expression Bile acid sequestrant: bind bile acids and promote excretion of bile in feces (causes the liver to revert to bile acid synthesis) niacin: suppresses lipolysis in adipose and release of hepatic FA into blood fibrates: stimulate (beta) oxidation, stimulate LPL activity and Apo A-I (increased HDL production) |
