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21 Cards in this Set
- Front
- Back
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What is trypsinogen? How is it activated?
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Protease excreted from pancreas into small intestine and activated to Trypsin by enteropeptidase from GI epith cells. Also Trypsin can then form more active proteases.
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What is pepsinogen? How is it activated?
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Stomach protease activated by low pH.
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What activates the following: chymotrypsinogen, proelastase, procarboxypeptidases?
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Trypsin
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How are peptides taken up by intestinal cells?
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Via Na co-transport. Dipeptides through H co-transport.
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What is Hartnup dz? How is it treated?
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Def. in uptake of neutral AAs (including Trp). If pt is also def. in B3 = dec. NAD+ production = photosens., tremors, ataxia, nystagmus. Tx: Niacin rich diet, high protein diet.
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What AAs are elevated in the urine of patients with cystinuria.
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Cystine, Ornithine, Arginine, Lysine. ("Can Only ARGue LYS")
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What is the cause and tx of cystinuria?
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Def. uptake of COAL at the brush border leading to cystine stones and hyperaminoaciduria. High fluid intake and meds that elevate urine pH.
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What is lysinuric protein intolerance? Tx?
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Defect in basal transport of basic AAs. (OAL). Patients get secondary hyperammonemia after meals (n/v). Tx with arginine and lys scavengers to reduce blood ammonia. Also protein restr. diet
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What are cathepsins?
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Major lysosomal proteases.
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What is ubiquitin?
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A small protein that "marks" other intracellular proteins for degradation by proteasomes.
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What does a proteasome need to function?
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CAP proteins (ATPases) to feed the protein into protease for degradation
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Why is Bortezomib (Velcade) effective in tx MM and certain lymphomas?
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It is a protease inhibitor. It is thought to stop the degradation of pro-apoptotic factors leading to cancer cell death.
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What is the result of the chromosomal deletion that occurs in Angelman syndrome?
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Codes for E3 subunit of ubiquitin ligase.
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What is Von Hippel-Landau syndrome?
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Def. in E3 ubiquitin subunit (VHL) prevents destruction of hypoxia inducible factor (factor that promotes angiogenesis). Inc. incidence of tumors.
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What is the fate of the vast majority of AAs in the fed state?
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AAs are shuttled to liver and broken down. C core is used in the synthesis of glycogen and TGs. N is excreted in the urine as urea or NH4.
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How are AAs utilized during fasting?
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Skeletal muscle (esp. myosin) is broken down into AAs and sent to the liver to produce glucose through gluconeogenesis.
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What is the major glucogenic AA?
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Alanine
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Which organs provide what AAs to the AA pool?
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Kidney and intestine - alanine. Sk. muscle - All, but mainly alanine and glutamine. Brain - glutamine.
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How is glutamine used as an energy source in fast dividing cells?
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Glutamine is converted to glutamate and then to alpha-ketoglutarate (by transaminases) and fed into the TCA.
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How does usage of the AA pool shift during metabolic acidosis?
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Most glutamine is shuttled to kidney to produce NH4, facilitating excretion of H+ ions.
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How does usage of the AA pool shift during sepsis?
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AAs are preferentially used by the liver to produce proteins used in acute phase reactions and to immune cells for energy (glutamine is especially used here).
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