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33 Cards in this Set
- Front
- Back
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What are the primary classes of lipids?
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1. Triglycerides (TG)
2. Phospholipids 3. Cholesterol 4. Non-esterified fatty acids 5. Cholesterol esters (CE) |
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Lipoproteins
What are Chylomicrons composed of? |
Major lipids: Dietary TG
Apolipoproteins: B-48, C-I, C-II, C-III, E |
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Lipoproteins
What is VLDL composed of? |
Major lipids: Endogenous TG
Apolipoproteins: B-100, C-I, C-II, C-III, E |
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Lipoproteins
What is IDL composed of? |
Major lipids: CE, TG
Apolipoproteins: B-100, E, C-II, C-III |
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Lipoproteins
What is LDL composed of? |
Major lipids: CE
Apolipoproteins: B-100 |
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Lipoproteins
What is HDL composed of? |
Major lipids: CE, Phospholipids
Apolipoproteins: A-I, A-II |
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Lipoproteins
What is Lp(a) composed of? |
Major lipids: CE
Apolipoproteins: B-100, a |
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What are the steps of exogenous derivation of lipids?
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1. TG and cholesterol absorbed in SI as FFA and free cholesterol
2. Re-esterified to TG (and CE) - incorporated into chylomicrons with apo B-48, A-I and A-IV 3. Enter plasma via lymph system 4. Acquire apo C-II and C-III 5. Broken down by lipoprotein lipase (LPL), leftover is chylomicron remnant 6. Taken up by liver via apo-E ligands at the LDLR and LRP |
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What are the steps of endogenous derivation of lipids?
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1. Liver synthesizes TG and FFA and cholesterol (HMG-Co-Reductase is rate-limiting step)
2. Liver packages TG, CE, and apo B-100 into VLDL - released into plasma 3. VLDL hydrolyzed by LPL - remaining particle called IDL 4. IDL metabolized to LDL or taken up by liver at LDLR or LRP by apo E ligand 5. LDL take up by liver at LDLR by apo B ligand. |
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What is the function of HDL?
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1. synthesized in liver and intestine
2. Accepts excess surface proteins from chylomicrons and VLDL 3. Accepts phospholipids and free cholesterol from VLDL and peripheral cells 4. Esterifies cholesterol into CE 5. Back to liver via direct uptake of entire HDL lipoprotein, uptake of CE component only, or by transfer to other lipoproteins |
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How is cholesterol excreted?
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1. Liver can convert cholesterol into bile
2. Bile acids secreted into bile along with free cholesterol 3. 95% of bile acids reabsorbed into enterohepatic circulation |
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What are the possible causes of secondary dyslipidemias?
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Diabetes, hypothyroidism, kidney disease, obstructive liver disease, drugs
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What is familial combined hyperlipidemia?
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Increased secretion of VLDL from liver
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What is hyperapobetalipoproteinemia?
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Increased levels of small, dense LDL
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What is familial hypertriglyceridemia?
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VLDL more enriched with TG
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What is dysbetalipoproteinemia?
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Apo E deficiency or defect
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What is homozygous familial hypercholesterolemia?
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No functional LDL receptors
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What are the risk factors for elevated TG levels?
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Excess alcohol, kidney disease, corticosteroids, protease inhibitors, and estrogens
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What are the drug risk factors for low HDL levels?
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Anabolic steroids, progestins
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What are risk factors for elevated TG and low HDL?
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obesity, inactive lifestyle, smoking, high carbohydrate diet, Type II diabetes, genetics, B-blockers
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What are the traditional risk factors of atherosclerosis/thrombosis?
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hypertension
smoking diabetes obesity physical inactivity diet age male sex family history low HDL |
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What are the newly emerging risk factors for atherosclerosis/thrombosis?
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Small dense or oxidized LDL
Lp(a) small VLDL IDL homocysteine CRP Low level of endothelial progenitor cells Apo B, Apo A-I |
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What is the function of normal endothelium?
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maintains blood flow
barrier to monocytes and macrophages regulates smooth cell function |
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What are the characteristics of endothelial dysfunction?
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Increased permeability
Decreased NO synthesis and release Chemoattractants overproduced Increased adherance of molecules to cell surfaces |
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What are the possible causes of endothelial dysfunction?
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Elevated/modified LDL
Free radical formation Genetic mutations Elevated Homocysteine, Lp(a), and fibrinogen Infectious organism Mechanical injury Vasoconstrictors |
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What is the role of LDL in atherosclerosis/thrombosis?
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LDL deposits, accumulates, and oxidizes on the smooth muscle lining blood vessels
Oxidized LDL recruits monocytes Oxidized LDL is directly toxic to smooth muscle cells Oxidized LDL inhibits secretion of fibronolytic molecules |
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What is the mechanism of thrombosis formation in atherosclerosis?
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Accumulated, oxidized LDL attracts macrophages. Monocytes and T-lymphocytes are then attracted by VCAM-1 and ICAM-1. After incorporation into cell wall, scavenger receptors bind oxidized LDL. Foam cells form and are accumulated as fatty streaks. Plaques evolve due to dynamic smooth muscle cell proliferation and removal. Plaque is held together by a fibrous cap, which weakens and causes plaque rupture. Rupture leads to further thrombosis, remodeling, etc.
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What is the function of HDL in atherosclerosis/thrombosis?
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HDL removes LDL from vessel wall, counteracts LDL oxidization, and has a protective effect on endothelium.
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What is the function of Homocysteine in atherosclerosis/thrombosis?
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High levels of homocystein are caused by genetic disposition and vitamin deficiency.
May induce platelet aggregation, endothelial dysfunction, hypercoagulability, vascular cell proliferation. |
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What infections may play a role in atherosclerosis/thrombosis?
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C. pheumoniae
Herpesviruses H. pylori Cytomegalovirus |
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What role do C-reactive proteins play in atherosclerosis/thrombosis?
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Markers of inflammation
Direct effects |
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What role does fibrinogin play in atherosclerosis/thrombosis?
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Thrombosis
Vascular cell adhesion/proliferation Vasoconstriction Platelet aggregation |
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What role do EPCs play in aterosclerosis/thrombosis?
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Bone marrow derived cells
Likely involved in neovascularization (protective) |
