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33 Cards in this Set

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What are the primary classes of lipids?
1. Triglycerides (TG)
2. Phospholipids
3. Cholesterol
4. Non-esterified fatty acids
5. Cholesterol esters (CE)
Lipoproteins

What are Chylomicrons composed of?
Major lipids: Dietary TG
Apolipoproteins: B-48, C-I, C-II, C-III, E
Lipoproteins

What is VLDL composed of?
Major lipids: Endogenous TG
Apolipoproteins: B-100, C-I, C-II, C-III, E
Lipoproteins

What is IDL composed of?
Major lipids: CE, TG
Apolipoproteins: B-100, E, C-II, C-III
Lipoproteins

What is LDL composed of?
Major lipids: CE
Apolipoproteins: B-100
Lipoproteins

What is HDL composed of?
Major lipids: CE, Phospholipids
Apolipoproteins: A-I, A-II
Lipoproteins

What is Lp(a) composed of?
Major lipids: CE
Apolipoproteins: B-100, a
What are the steps of exogenous derivation of lipids?
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
What are the steps of endogenous derivation of lipids?
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.
What is the function of HDL?
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
How is cholesterol excreted?
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
What are the possible causes of secondary dyslipidemias?
Diabetes, hypothyroidism, kidney disease, obstructive liver disease, drugs
What is familial combined hyperlipidemia?
Increased secretion of VLDL from liver
What is hyperapobetalipoproteinemia?
Increased levels of small, dense LDL
What is familial hypertriglyceridemia?
VLDL more enriched with TG
What is dysbetalipoproteinemia?
Apo E deficiency or defect
What is homozygous familial hypercholesterolemia?
No functional LDL receptors
What are the risk factors for elevated TG levels?
Excess alcohol, kidney disease, corticosteroids, protease inhibitors, and estrogens
What are the drug risk factors for low HDL levels?
Anabolic steroids, progestins
What are risk factors for elevated TG and low HDL?
obesity, inactive lifestyle, smoking, high carbohydrate diet, Type II diabetes, genetics, B-blockers
What are the traditional risk factors of atherosclerosis/thrombosis?
hypertension
smoking
diabetes
obesity
physical inactivity
diet
age
male sex
family history
low HDL
What are the newly emerging risk factors for atherosclerosis/thrombosis?
Small dense or oxidized LDL
Lp(a)
small VLDL
IDL
homocysteine
CRP
Low level of endothelial progenitor cells
Apo B, Apo A-I
What is the function of normal endothelium?
maintains blood flow
barrier to monocytes and macrophages
regulates smooth cell function
What are the characteristics of endothelial dysfunction?
Increased permeability
Decreased NO synthesis and release
Chemoattractants overproduced
Increased adherance of molecules to cell surfaces
What are the possible causes of endothelial dysfunction?
Elevated/modified LDL
Free radical formation
Genetic mutations
Elevated Homocysteine, Lp(a), and fibrinogen
Infectious organism
Mechanical injury
Vasoconstrictors
What is the role of LDL in atherosclerosis/thrombosis?
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
What is the mechanism of thrombosis formation in atherosclerosis?
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.
What is the function of HDL in atherosclerosis/thrombosis?
HDL removes LDL from vessel wall, counteracts LDL oxidization, and has a protective effect on endothelium.
What is the function of Homocysteine in atherosclerosis/thrombosis?
High levels of homocystein are caused by genetic disposition and vitamin deficiency.
May induce platelet aggregation, endothelial dysfunction, hypercoagulability, vascular cell proliferation.
What infections may play a role in atherosclerosis/thrombosis?
C. pheumoniae
Herpesviruses
H. pylori
Cytomegalovirus
What role do C-reactive proteins play in atherosclerosis/thrombosis?
Markers of inflammation
Direct effects
What role does fibrinogin play in atherosclerosis/thrombosis?
Thrombosis
Vascular cell adhesion/proliferation
Vasoconstriction
Platelet aggregation
What role do EPCs play in aterosclerosis/thrombosis?
Bone marrow derived cells
Likely involved in neovascularization (protective)