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22 Cards in this Set
- Front
- Back
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classification of lipoproteins
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chylomicrons: from intestine to deliver dietary TG and cholesterol, B-48
VLDL: from liver to tissue carrying cholesterol and TG, B-100 LDL: from VLDL, carrying cholesterol to tissue and liver HDL: from intestine, liver and VLDL, apo A-1, storing of apo E and C-II for maturation of chylomicron and VLDL, it carries excess cholesterol back to liver |
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protective nature of HDL
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it competes with VLDL to be taken up by tissue
remove cholesterol and slow down the cholesterol deposit receive surface components from chylomicrons as an indicator of the efficiency of handling ingested fat |
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different apoprotein
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apoprotein on the surface of lipoprotein to increase the water affinity
special functions apo A-II and apo C-III : inhibit LPL lipoprotein lipase Apo C-II stimulate LPL ligands for receptor: apo B-100 and apo E VLDL: B-100 chylomicron: B-48 |
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lipoprotein lipase
site action requirements |
site: endothelial wall in muscles and adipose tissue
action: break down the TG and chylomicrons to glycerol and FA promote uptake of chylomicron remnants, and chol.-rich lipoprotein & FFA need cofactor C-II |
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hepatic lipase
site substrate actions 3 |
site: liver
substrate: TG and phospholipid of small VLDL, IDL and large HDL 1. HDL2 to HDL 3 2. IDL to LDL final metabolism of chylomicrons remnants |
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Cholesterylester transfer protein
actions 2 |
transfer TG from VLDL/LDL to HDL
transfer cholestrylester from HLD to VLDL/LDL exchange: TG and cholesterylester |
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Familial Hypercholesterolemia
genetic inheritance trend disease predisposed presentation |
autosomal dominant
MI early age (heterozygotes also has higher risk) xanthoma in tendon |
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hyperlipidemia
can include three diseases |
hyperlipoproteinemia
hypercholesterolemia Hypertriglyceridemia |
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Hypertriglyceridemia
diagnosis requirement two types which two? and their causes |
TG > 250 mg/dl
familial combined hyperlipidemia - overproduction of apo B -> high level of VLDL familial hypertriglyceridemia - overporduction of VLDL / defective lipolysis of VLDL |
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Abetalipoproteinemia
disease pathology presentation treatment |
defect in apo B production
low lvl of lipid, chol, TG symptoms Psychomotor retardation - multiple nutrional deficiencies - multiple neuromuscular consequences - abnormal RBC - Treatment: massive dose of vit. E |
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familial hypercholesterolemia
pathophysiology |
pathophysiology of familial hypercholesterolemia
NOT in the control of HMG-coA regulation of synthesis of cholesterol/break down of LDL defect in the transporting regulatory signal decrease in LDL receptor -> decrease in breakdown of LDL -> increase of cholesterol in blood |
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cholesterol synthesis steps
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acetyl coA to acetoacetyl coA (thiolase)
to HMG coA ... lanosterol cholesterol |
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cholesterol regulation 4
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1. embed into the cell mem
2. stimulate ACAT for turning cholesterol to chol. ester 3. decrease the synthesis of LDL 4. decrease the action of HMG coA -> decrease synthesis of cholesterol |
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how cholesterol is taken up from LDL
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LDL receptor (need apo B-100) on the cell membrane
lysome -> lysoendosome digested and release of free cholesterol |
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LDL receptor structures 4 domains
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from outer to inner
N-oligosarrcharide domain O-oligosarrcharide domain transmembrane domain Cytoplamsic domain = receptors prior to clathrin-coated vesicle |
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molecular defects in synthesis of LDL receptors 4
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receptor -ve : few or no receptor
receptor +ve : receptor cant bind to LDL deficient receptor : receptor is unable to travel from synthesize site to the membrane cytoplasmic carboxyl terminus (domain) defect: unable to internalize LDL-LDL receptor complex |
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name the lipid lowering drugs
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1. BIle acid binding resins
2. HMG CoA reductase inhibitor 3. intestinal sterol absorption inhibitor 4. fibric acid derivatives 5. nicotinic acid |
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HMG CoA reductase inhibitor
name the example functions adverse side effects |
statin: atorvastatin, fluvastatin
fx: 1. decrease the syn of chol, 2. increase LDL receptors in liver result in decrease in chol, LDL, TG and increase in HDL adverse side effects 1. liver damage 2. myopathy 3. rhabdomyolysis |
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fibric acid derivatives
name examples functions adverse side effects |
fenofibrate, bezafibrate
fx: 1. increase the syn of FA oxidation in liver 2. increase PPAR-alpha, increase LPL transcription 3. increase prod. of HDL decrease in VLDL, decrease in TG, increase in HDL, rise or lower LDL level adverse side effects: myopathy and liver damage cannot be used with statin |
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bile acid binding resin
examples functions adverse side effects |
cholestyramine, colestipol
fx: bind to the bile acid increase chol usage for bile acid production decrease reabsorption of bile acid adverse side effects: dyspepsia, constipation, bile acid malabsorption diarrhoea, poor compliance not used with ezetimibe |
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intestinal sterol absorption inhibitors
examples functions adverse side effects |
ezetimibe
fx decrease the absorption of sterol: chol and phytosterol usu, used with statin, not used with bile acid binding resin low toxicity |
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nicotinic acid
vit B3 functions adverse side effects |
increase the activity of LPL
decrease TG production in liver decrease act. of hormone-sensitive lipase -> decrease clearance of apo A-1 -> increase HDL result favor all hyperlipidemia adverse side effects: liver damage nausea flushing |
