Cardiology
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| Fredrickson phenotype I | Serum conc of chylomicrons elevated; trigs are elevated to >99th percentile
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| Fredrickson phenotype IIa | Serum LDL chol elevated; the total chol is >90th percentile. Triglyceride and/or apolipoprotein B may also be ≥ 90th percentile
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| Fredrickson phenotype IIb | Serum LDL & VLDL elevated; TC and/or trigs may be ≥ 90th percentile and apolipoprotein B ≥ 90th percentile
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| Increased Apo A-I prodn has what effect in animals? | Anti-atherogenic (reduced atherosclerosis progression; regression of existing dz)
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| Mechanisms by which oxidized LDL causes atherogenesis | Endothelial damage; changes in vasc tone; Monocyte/ macrophage recruitment; increased LDL uptake by macrophages (foam cell formation); Induction of GF; Increased plt aggregation; Formation of auto-Abs to oxidized LDL
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| HDL antiatherogenic properties include: | Reverse chol transport; antioxidation; protection vs thrombosis; maintenance of endothelial fn; maintenance of low blood viscosity thru permissive action on red cell deformability
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| Process whereby excess cholesterol in cells and in atherosclerotic plaques is removed | Reverse cholesterol transport
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| Fredrickson phenotype III | Serum VLDL remnants & chylomicrons elevated; TC & trigs >90th percentile
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| Fredrickson phenotype IV | Serum VLDL elevated; TC may be >90th percentile & may also see trigs >90th percentile or low HDL
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| Fredrickson phenotype V | Elevated serum chylomicrons & VLDL; triglycerides >99th percentile
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| Hypertriglyceridemia & CHD: Assoc disorders | Accumulation of chylomicron remnants & VLDL remnants; generation of small, dense LDL-C; assoc w/ low HDL-C; increased coagulability (inc plasminogen activator inhibitor (PAI-1); inc factor VIIc; activation of prothrombin to thrombin
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| Lipids carried by LPs for: | energy utilization; lipid deposition; steroid hormone prodn; bile acid formation
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| Lipoprotein consists of: | esterified & unesterified chol, trigs, phospholipids, & protein
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| Protein components of the lipoprotein = | apolipoproteins or apoproteins.
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| Apolipoproteins = | cofactors for enzymes and ligands for receptors
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| Defects in apolipoprotein metabolism lead to: | abnormalities in lipid handling
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| Very large particles that carry dietary lipid = | chylomicrons
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| Chylomicrons are assoc with: | Apolipoproteins (including A-I, A-II, A-IV, B-48, C-I, C-II, C-III, and E)
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| LDL carries: | cholesterol esters
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| LDL assoc with [which protein]: | apolipoprotein B-100.
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| HDL carries: | cholesterol esters
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| HDL is associated with [proteins]: | apolipoproteins A-I, A-II, C-I, C-II, C-III, D, and E
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| One mechanism by which LDL promotes atherosclerosis | oxidative modification
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| VLDL carries: | endogenous trigs (& to a lesser degree chol)
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| Major apolipoproteins assoc with VLDL: | B-100, C-I, C-II, C-III, and E
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| Intermediate density lipoprotein (IDL) carries: | chol esters & triglycerides
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| IDLs are assoc with [proteins]: | apolipoproteins B-100, C-III, and E
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| Function of CETP | transfers oxidized lipids from LDL to HDL
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| The oxidized lipids in HDL are reduced by: | HDL apolipoproteins
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| What does the liver do with reduced lipids? | Liver takes up reduced lipids from HDL more rapidly than from LDL
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| Hypoalphalipoproteinemia = | Low serum HDL; assoc w/ increased risk of overt CHD
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| Strategies for HDL metab as tx target | Increase apo A-I prodn; promote reverse chol transport; delay HDL catabolism
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| Effect of ETOH (wine, beer) on HDL-C | increases HDL-C
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| Theoretical effect of CTEP inhibitors | Lower LDL; increase HDL
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| Familial Dyslipidemias | Fredrickson phenotypes III, IV, & V
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| high levels of trigs may directly promote: | atherothrombosis
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| high levels of trigs assoc w/ increases in: | fibrinogen, clotting factors VII & X, & blood viscosity
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| Framingham focuses on which lipid: | TC (but LDL is primary tx target)
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| Framingham 10-yr CHD risk categories | r >20%, 10-20%, and <10%
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| Low HDL-C is an Independent Predictor of CHD Risk even when: | LDL-C is Low
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| Metab syndrome/girth increases genetic susceptibility to: | dyslipidemia, hypertension, type 2 DM
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| Metabolic syndrome | 3 of 5: abd obesity (waist men >40 in & women >35 in. TG ≥150 or tx for TG. HDL <40 (M) & <50 (F) or tx for low HDL. BP ≥130/85 or tx for HTN. FPG ≥100 or tx
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| 3 levels of prevention | Primary: remove risk factors; secondary: early detection & tx; tertiary: reduce complications
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| A: fat contribute to CV dz; B: fat may be cardioprotective | A: Saturated & trans fat; B: monounsaturated & polyunsaturated fat
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| Lipids carried by LPs for: | energy utilization; lipid deposition; steroid hormone prodn; bile acid formation
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| Lipoprotein consists of: | esterified & unesterified chol, trigs, phospholipids, & protein
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| Protein components of the lipoprotein = | apolipoproteins or apoproteins.
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| Apolipoproteins = | cofactors for enzymes and ligands for receptors
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| Low HDL: risk factors | SMK; sedentary;obese; insulin resistant/ DM; hypertriglyceridemia; chronic inflammatory dz
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| Cardioprotective HDL = | >60 mg/dL (>75 assoc w/ longevity syndrome)
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| Familial Dyslipidemias | Fredrickson phenotypes III, IV, & V
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| high levels of trigs assoc w/ increases in: | fibrinogen, clotting factors VII & X, & blood viscosity
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| HLD primary risk factors | Diet, genetic, obesity, sporadic
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| HLD secondary risk factors | DM, uremia, metabolic & nephrotic syndromes, hypothyroid, PG, acromegaly, Cushing dz, drugs
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| Drugs associated with secondary HLD risk factor: | BB, diuretics, steroids, OCP, progestins, EtOH (for TGs)
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