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27 Cards in this Set
- Front
- Back
Hemolytic anemia can cause what type of hyperbilirubinemia?
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Unconjugated (indirect) hyperbilirubinemia
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Why phototherapy in unconjugated hyperbilirubinemia?
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UV light produces more hydrophilic (soluble) conformational species -> excretoin in urine and bile
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Dubin Johnson Syndrome
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MRP2 transporter mutation leads to accumulation of conjugated bilirubin in the serum
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rotor Syndrome
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Can't excrete bilirubin, benign, idiopathic origin
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What energy source does ethanol generate in the liver? What are the impications of this?
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NADH; increases NADH/NAD+ ratio; NAD+ needed to drive gluconeogenesis (via lactate/malate); results in alcohol induces hypoglycemia
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What effect can alcohol have on blood sugar levels?
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Lowers them by disturbing NADH/NAD+ ratio; creates NADH; need NAD+ to drive gluconeogenesis
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Describe acetaldehyde toxicity
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Since acetaldehyde levels can be increased by ethanol, excess acetaldehyde can impair protein and lipid secretion, causing accumulation in the liver
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Disulfiram (antabuse)
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Blocks aldehyde dehydrogenase activity and causes accumulatoin of acetaldehyde, which causes unpleasant affects by decreasing the synthesis of glucose
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What are the two phases of drug metabolism in the liver?
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Phase 1: Addition of polar group by oxidation
Phase 2: Conjugation with bigger molecules These all serve to increase their solubility/polarity to prevent their absorption |
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How can excess iron (hemochromatosis) or copper (wilson's disease) affect the liver?
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Excess free radicals damage tissue
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Where is the genetic defect in WIlson's disease?
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Mutation in ATP-dependent copper transporter (ATP7B)
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Classic clinical triad for hereditary hemochromatosis?
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Skin pigmentation, cirrhosis, diabetes
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HFE related hemochromatosis
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HFE regulates the release of hepcidin from the liver, which binds to ferroportin transporters on the base of enterocytes and macrophages preventing the secretion of iron into the portal system; if HFE is mutated, there is uncontrolled absorption/release of iron into the system
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What are the lab findings for pre-hepatic hyperbilirubinemia?
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Normal direct (conjugated), INCREASED INDIRECT (unconjugated), normal urine/stool
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What are the lab findings for hepatic hyperbilirubinemia?
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Normal to elevated direct/indirect bilirubin, dark urine color
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What are the lab findings for post hepatic hyperbilirubinemia?
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INCREASED direct (conjugated), normal indirect, dark urine, light stools
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Pyruvate Carboxylase (irreversible enzymes)
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In mitochondria
Pyruvate -> Oaxaloacetate Requires biotin, ATP, activated by acetyl-CoA |
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PEP carboxykinase
(irreversible enzymes) |
In cytosol
Oxaloacetate -> Phosphoenolpyruvate Requires GTP |
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Fructose 1,6 biphosphatase
(irreversible enzymes) |
In cytosol
Fructose 1,6 biphosphate -> fructose 6 phosphate |
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Glucose 6 phosphatase (irreversible enzymes)
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In ER
Glucose 6-P -> glucose |
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What does a deficiency of a key gluconeogenic enzyme cause?
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Hypolycemia
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Why can't muscle participate in gluconeogenesis?
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Because it lacks glucose-6-phosphatase
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Significance of Pathway Produces Fresh Glucose?
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P = pyruvate carboxylase
P = PEP carboxykinase F = fructose 1,6 biphosphtase G = glucose |
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What are the four glucogenic amino acids?
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Met, Val, Arg, His
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What liver metabolic molecule is depleted in hyperammonemia?
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Alpha ketglutarate; depletion of AKG leads to inhibition of TCA cycle
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Symptoms of ammonia intoxication
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Tremor, slurring of speech, somnolence (drowsiness), vomiting, cerebral edema, blurring of vision
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Describe the metabolism of bilirubin
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