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27 Cards in this Set
- Front
- Back
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which of the following is the most abundant component of Chylomicrons?
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triglycerides
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Pancreatic Diseases
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The pancreas makes enzymes up to 3 months in advance. so when there is a problem by the time you find out, its too late and the person is in serious trouble
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Orlistat
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The anti obesity drug Orlistat inhibits lipases → undigested lipids → fat malabsorption → weight loss
Orlistat does not inhibit absorption |
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Lipid Malabsorption
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Individuals suffering from lipid malabsorption should consider the intake of short and medium length FAs only. Long chain FA need Micelles to enter cells but short and medium chains dont.
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Cystic Fibrosis
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Lipid malabsorption results from this. From blocked mucus secreting cells in pancreas, or malfunction of exocrine cells of the liver, pancreas or gallbladder. Things the body needs for digestion won't be secreted.
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Shortened Bowel
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Lipid malabsorption results from this. Born or developed chrome's disease.
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Steatorrhea
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Lipid malabsorption causes this. Dietary lipids and fat soluble vitamins will be eliminated when there is lipid malabsorption. Chronic diarrhea results with weight loss and sometimes neuropathy.
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Why are TGs exchanged for cholesterol esters between VLDL and HDL?
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In order to esterify cholesterol collected by HDL. FA degradation is in mitochondria and there is no HDL in the mitochondria. Storage is of TG. HDL's job is to collect cholesterol from tissues. As vldl it gets cholesterol esters from HDL which increases the concentration of VLDL.
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Abetaliproteinemia
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Chylomicron deficiency in plasma
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The oxidation of LDL particles leads to their uptake by microphages an therefore the formation of foam cells. This process results in --------------.
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Atherosclerosis
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Diabetes mellitus
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low or absent insulin → low LPL and high concentration of hormone-sensitive lipase → hypertriacylglycerolemia
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Familial lipoprotein lipase deficiency or type I hyperlipoproteinemia
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is an autosomal recessive disorder resulting in massive chylomicronemia
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Two Insulin potential problems
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Low sensitivity or low synthesis of insulin resulting in the accumulation of lipotprotines(chylomicrons or others)
2)Presence of insulin leads to the inhibition of hormone sensitve lipase in adipose--causes lack of release of FA |
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Type III hyperlipoproteinemia/ dysbetalipoproteinemia
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Compromised removal of chylomicron remnants by the liver results in their accumulation in plasma. ApoE on a chylomicron remnant is recognized by the membrane receptors on hepatocytes, LRP → endocytosis → degradation by lysosomal enzymes → products reused by the cell:
Fatty acids Amino acids Glycerol Cholesterol |
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Fatty liver/Hepatic Steatosis
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Occurs when TG in the liver are higher than those secreted as VLDL=fatty liver.
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Difference between TG in chylomicrons and TG in VLDL...
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Chylomicron TGs--> come from diet
VLDL TGs--> from synthesis in the liver |
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Hepatic Triglyceride Lipase (HTGL) deficiency
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lack of LDL production bc it converts IDL into LDL in the break down of VLDL.
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A deficiency in functional LDL results in
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Type II hyperlipidemia or familial hypercholesterolemia which results in
Premature atherosclerosis |
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Hypothyroidism causes
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hypercholesterolemia, or
Hypercholesterolemia secondary to hypothyroidism The thyroid hormone, T3, stimulates the binding of LDL to its receptor |
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Wolman disease
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Deficiency in enzymes for cholesteryl esters hydrolysis
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Niemann-Pick disease, type C
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Deficiency in releasing cholesterol from lysosomes
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Tangier disease
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Familial deficiency of HDL results in Tangier disease aka familial high-density lipoprotein disease
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dyslipidemias
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arise from genetic defects of lipoprotein metabolism
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dyslipidemias--> homozygote
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[Cholesterol] 800 to 1000 mg/dL
First heart attack in teenage years |
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Dyslipidemias-->Heterozygote
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[Cholesterol] 300 to 600 mg/dL
Heart attack between 20s and 50s |
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Familial Hypercholesterolemia (FH):
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Homozygote (1:1000,000)
[Cholesterol] 800 to 1000 mg/dL First heart attack in teenage years Heterozygote (more frequent, 1:500) [Cholesterol] 300 to 600 mg/dL Heart attack between 20s and 50s FH→ tuberous xanthomas under the skin and in vessels of the eye Only heterozygotes can be helped with statins Homozygotes can benefit from LDL pheresis |
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CVD Risk Factors
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Positive risk factors
Age (years) Male ≥ 45 Female ≥ 55 or premature menopause without estrogen replacement therapy Family history of premature CHD Current cigarette smoking Hypertension Diabetes mellitus Low HDL Cholesterol, < 350 mg/L Negative risk factors High HDL cholesterol, ≥ 600 mg/L |
