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29 Cards in this Set

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In what form can carbohydrates be absorbed by intestinal epithelial cells?
monosaccharides (glucose, galactose, fructose)
How is starch digested?
starch is digested by pancreatic and salivary alpha-amylases to oligosaccharides alpha dextrin/maltose/maltotriose, which are hydrolyzed to glucose by brush border enzymes
How are disaccharides trehalose, lactose, and sucrose digested?
trehalose -> glucose (trehalase)
lactose -> glucose and galactose (lactase)
sucrose -> glucose and fructose (sucrase)
How are glucose and galactose transported across the intestinal epithelium?
across apical via SGLT1 (Na dependent cotransport), across basolat via GLUT2 (facilitated diffusion)
How is fructose transported across the intestinal epithelium?
across apical via GLUT5, basolat via GLUT2 (both facilitated diffusion)
What happens in the absences of brush border lactase?
lactose intolerance; causes osmotic diarrhea
What is the difference between endopeptidases and exopeptidases?
endopeptidases hydrolyze interior peptide bonds of proteins, exopeptidases hydrolyze one AA at a time from the C-terminal ends
What are endopeptidases and exopeptidases of the GI tract?
endo: pepsin, trypsin, chymotrypsin, elastase
exo: carboxypeptidases A and B
Where does protein digestion first begin?
in stomach; chief cells s/c pepsinogen -> pepsin in pH 1-3 (becomes denatured in more basic duod environment
Is pepsin essential for protein digestion? How do we know this?
no; ppl whose stomach is removed or who do not s/c gastric H (cannot activate pepsinogen) still have normal protein digest/absorp
What is the activation cascade of pancreatic proteases?
trypsinogen activated to trypsin by enterokinase (brush border enz), and trypsin activates all other enzymes
What are the absorbable forms of peptides?
AAs, dipeptides, tripeptides
Pancreatic proteases yield AAs, dipeptides, tripeptides, and oligopeptides. What happens to the oligos?
oligos get further degraded by brush border proteases into absorbable products
How are AAs absorbed across intestinal epithelial cells?
apical Na-dependent AA cotransport, basolat facilitated diffusion
Do all AAs utilize the same carriers?
no; 4 different carriers for acidic, basic, neutral, and imino AAs
How are dipeptides and tripeptides absorbed across the intestinal epithelium?
apical H-dependent di/tripep cotransport, are hydrolyzed to AAs by cytoplasmic peptidases, then basolat facilitated diffusion
What is the stomach's role in lipid digestion?
1. mixing (breaks into droplets)
2. lingual and gastric lipase digest ~10% TGs to MGs and FAs
3. CCK slows gastric emptying (stimulated when lipids arrive in duod)
What is the small intestine's role in lipid digestion?
1. bile acids emulsify lipids, increasing surf area for digestion
2. panc lipases hydrolyze lipids to FAs, MGs, chol, lysolecithin
3. hydrophopic lipid products solubilized in micelles by bile acide
What are the pancreatic enzymes that digest lipids in the small intestine?
pancreatic lipases, cholesterol ester hydrolase, phopholipase A2
What are the 3 types of dietary lipids?
triglycerides, cholesterol ester, phospholipids
What are the breakdown products of TGs, cholesterol esters, and phospholipids?
TGs -> MG, FA, FA (by panc lipases)
Cholesterol ester -> cholesterol, FA (by chol ester hydrolase)
Phopholipid -> lysolecithin, FA (by phospholipase A2)
How do lipid products get into intestinal epithelial cells?
micelles bring them into contact w/absorptive surface of intest cells and MGs, chol, and FAs diffuse across luminal membrane
How are lipid products transported out of intestinal epithelial cells?
reesterified to TGs, chol E, PLs, and (w/apoproteins) form chylomicrons, which are exocytosed out of cell from Golgi secretory vesicles, enter lymph, to thoracic duct, to blood
What happens if there is a failure to synthesis Apo B?
causes abetalipoproteinemia -> person unable to absorb chylomicorns, and thus dietary lipids -> steatorrhea, or buildup of lipid in intest cells
How might pancreatic disease (e.g. pancreatitis, cystic fibrosis) cause steatorrhea?
panc cannot make sufficient enzymes necessary for lipid digestion
How might hypersecretion of gastrin cause steatorrhea?
increases gastric H s/c, lowers duod pH, inactivates panc lipase (e.g. Zollinger-Ellison synd, or d/o's w/ insufficient panc HCO3 s/c)
How might ileal resection cause steatorrhea?
depletion of bile acid pool b/c bile salts arent r/a'd in ileum and don't recirculate to liver
How might bacterial overgrowth cause steatorrhea?
leads to deconjugation of bile acids -- bact converts bile salts (low pK, ionized form, water soluble) to bile acids (high pK, nonionized form, lipid soluble) -- bile acids are readily absorbed too early
*this could also be accomplished by low intest pH*
How might a decreased number of intestinal cells cause steatorrhea? Example?
reduces microvillar surf area, and lipid absorp occurs by diffusion, which depends on surf area; tropical sprue