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100 Cards in this Set
- Front
- Back
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_______ stimulation initiates peristalisis
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vagal stimulation
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how can you have peristalsis in a denervated esophagus?
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can occur because of myenteric plexus
vagus doesn't innervate smooth muscle directly - innervates myenteric plexus |
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stress relaxation?
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as the stomach fills it relaxes further
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pacemaker cells of the stomach? frequency? location?
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interstitial cells of Cajal
3-4/min greater curvature body and antrum |
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3 things that trigger spike activity on the BER?
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distention
vagal activity gastrin + ach |
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the stomach homogenizes chyme by ?
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vigorous forward and retrograde movements through narrowed contracted portions of the antrum.
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entero-gastric reflex?
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distention of the duodenum DECREASES stomach emptying
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MMC?
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intense peristalic contractions every 75-90 min that sweep from the stomach to small intestine
stomach and intestinal perisalsis are not normally coupled together |
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__________ is the dominant form of motility in the small bowel; __________ is in the small intestine, if it occurs at all, is local.
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Segmentation type contraction is the dominant form of motility in the small bowel; peristals is in the small intestine, if it occurs at all, is local.
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BER frequency in the duodenum? ileum?
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duodenum = 12/min
ileum = 8/min |
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In general, what agents are inhibitory?
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GIP
VasoIntestinalPeptide (VIP) somatostatin Secretin |
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In general, what agents are excitatory?
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Ach
Gastrin CCK Prostaglandins serotonin |
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endocrine cells of the stomach?
paracrine cells of the stomach? |
endo = G cells
para = enterochromaffin-like cells and D-cells |
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Cells of the Cardiac region
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mucus secreting cells
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Cells Fundus and Corpus = Oxyntic area
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-parietal cells
-chief cells -mucous neck cells -enterochromaffinlike (ECL) cells -D-cells ( somatostatin producing cells) |
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Cells of Pyloric antrum
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-mucus secreting cells
-G-cells (gastrin producing cells) -D-cells |
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Proton pump of the parietal cells?
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H+-K+ ATPase
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pH of venous blood draining the stomach?
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Alkaline tide
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Cl movement out of the parietal cell into the lumen causes?
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depolarization which drives K+ to leak out and keep supplying the H/K ATPase
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R-protein?
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binds B12 in saliva and stomach and is broken down by proteases in small intestine.
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IF?
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binds B12 after R-protein is broken down and enters the enterocytes of the ileum
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Fate of IF+B12 in ileum enterocyte?
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lysosomes degrade IF and B12+transcobalamin is exocytosed into plasma
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Low B12 absorbtion = ?
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pernicious anemia = RBCs dont mature
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Below pH ____ pepsinogens are spontaneously converted to active pepsins by cleavage of acid sensitive peptide bonds. These proteins then activate their precursors by releasing 42 amino acid residues from the N-terminal ends of the polypeptides. The pH optima for pepsins vary from ___ to _____.
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4.0
1.8 to 3.5 |
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PGE2 is released when? effects?
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released after mucosal damage
PGE2 lowers HCl, increases mucus, and dilates blood vessels |
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During the gastric phase, vagal stimulation activates?
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ECL cells
Parietal Cells G-cells |
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During the gastric phase, vagal stimulation inhibits?
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D-cells
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G-cells are activated by? Release? Effects of released product
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Activated by vagal ach and GRP
Release GASTRIN Gastrin activates ECL cells and Parietal cells |
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ECL cells are activated by? Release? Effects of released product?
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Activated by vagal input and gastrin
release histamine histamine activates parietal cells and increases ACH effects |
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Parietal cells are activated by? Release?
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activated by histamine, vagal, and gastrin
release HCl |
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Gastrin release is inhibited by?
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pH < 3 and somatostatin
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D cells are activated by? Release? Effects of released product?
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activated by acid in the antrum or CGRP
release somatostatin somatostatin inhibits G-cells/gastrin release |
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Gastrin and Ach activate parietal cells via?
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increase PLC and Ca2+ = increased K and Cl conductance
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Histamine activates parietal cells via?
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adenylate cyclase and cAMP = increased K and Cl conductance
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Gastric phase distention reflex activates
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gastrin release from pyloric antrum and histamine release from ECL
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Chemical stimulation in the gastric phase is via?
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Peptides and amino acids bathing the pyloric antrum raise serum gastrin levels by stimulating G-cells directly.
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The hormones responsible for the inhibition of acid secretion are collectively termed
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enterogastrones
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S cells are located in? activated by? Release? Effects of released product?
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-location: duodenal mucosa
-activated by pH < 4.5 -release Secretin -stimulates somatostatin release, inhibits gastrin release, inhibits parietal cells, ACTIVATES chief cells |
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I cells are located in? activated by? Release? Effects of released product?
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-location: duodenal mucosa
-activated by fat, peptides, AAs -release CCK -competes with gastrin but is a weak agonist so: INHIBITS ACID SECRETION |
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K cells are located in? activated by? Release? Effects of released product?
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-location: duodenal mucosa
-activated by fat and carbs -release GIP -decreases gastrin and decreases HCl |
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Other role of GIP secreted from Kcells
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Incretin = promotes insulin secretion from pancreas
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xerostomia
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absence of salivary secretions inflammation of the oral mucosa and tooth disease are common
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How do acinar cells move NaCl into the lumen?
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Na pumped out basolaterally
K leakes out basolaterally Cl enters basolaterally and is excreted into the lumen Na then travels BETWEEN cells into the lumen water follows NaCl |
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Amylase can only cleave? Cant cleave?
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cleaves internal alpha 1,4 linkages
cant cleave terminal A1,4 cant cleave A1,6 |
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Kallikrein release from gland cells cleaves?
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cleaves kininogen to kallidin
kallidin is converted to bradykinin |
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kallidin and bradykinin are __________ and along with _______ act by promoting NO release from endothelial cells
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kallidin and bradykinin are vasodilators and along with VIP act by promoting NO release from endothelial cells
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Which gland has the highest basal volume of salvary gland secretion?
highest stimulated volume? |
basal = submandib
stimulated = parotid |
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_____ and ______ secreted by the pancreas are synthesized and released as inactive precursors called proenzymes
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Proteases and phospholipase A2 secreted by the pancreas are synthesized and released as inactive precursors called proenzymes
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where is enterokinase found
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brush border cells of the duodenum
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Effect of CCK on pancreatic secretion
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CCK = increased digestive enzymes
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Effect of secretin on pancreatic secretion
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secreting = increased HCO3
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acinar cells of the pancreas are stimulated by
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Ach
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duct cells of the pancreas are stimulated by
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Ach and VIP
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CCK stimualtes what cells of the pancreas? what do they secrete?
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stimulates acinar cells to secrete enzyme rich secretion
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Secretin stimualtes what cells of the pancreas? what do they secrete?
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stimulates duct cells to secrete an alkaline secretion
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In duct cells, secretin (and VIP) stimulation is mediated by __________ that activates __________. This enzyme phosphorylates and opens the _______ on the luminal border of the cell.
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In duct cells, secretin (and VIP) stimulation is mediated by cAMP, a second messenger that activates protein kinase A. This enzyme phosphorylates and opens the Cl-channel on the luminal border of the cell.
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What stimulates galbladder contraction
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CCK-PZ
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pancreatic lipase only acts at
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an oil-water interface
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function of colipase?
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cofactor protein = protects lipase from denaturation by bile salts and anchors lipase to the oil-water interface
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_____________ = absorbed mostly in the proximal small intestine, whereas ________ = absorbed mostly in the distal ileum
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Fatty acids and monoglycerides are absorbed mostly in the proximal small intestine, whereas bile acid is absorbed mostly in the distal ileum
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Once enterocytes absorb fatty acids off the micelle/molec phase they are
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-re-synthesize them into triglycerides at the surface of the ER
-assembled into chylomicrons and exocytosed |
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Where are chylomicrons exocytosed to?
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the lymphatics
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Are medium chain fatty acids processed via the chylomicron way?
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no they are absobed directly, pass into portal blood, and are oxidized by the liver
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fate of chylomicrons in the blood
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hydrolyzed by lipoprotein lipase
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where is lipoprotein lipase found?
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high concentration in blood vessels of tissues like muscle and fat
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Effect of heparin on lipoprotein lipase
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activates it and causes it to be released from tissues into the blood
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plasma concentration of bilirubin
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1mg/100ml
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how many molecules of bilirubin can albumin bind?
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1
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kernicterus?
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free bilirubin can cross the blood/brain barrier and enter the brain in infants = seizures and brain damage
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Causes of unconjugated hyperbilirubinemia
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-ABO incompatability
-Hemolytic anemia -carrier molecule defect -glucornyl transferase defect |
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Causes of conjugated hyperbilirubinemia
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Dubain Johnson disease = ABC2 defect
Biliary obstruction |
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Bile salts in the liver cytoplasm are transported to the canaliculus and ultimately the intestine by?
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BTEP aka ABC B-11
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In the Ileum bile salts are translocated into the enterocyte via ______ and is then picked up by
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IBAT then picked up by ILBP
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The bile salt exits the enterocyte through another carrier. It moves into the portal system bound to _________ and is taken up by a carrier __________that transports it across the sinusoidal membrane of the hepatocyte.
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albumin
taken up by a carrier Na+Taurocholate-Cotransport Protein (NTCP) |
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The cycle of bile is called?
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enterohepatic circulation
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Bile salts that dont make it across the intestine pass to colon and care converted to
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deocycholic acid = recycled to liver
lithocholic acid = excreted |
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ABC B-4 location? function? Disease?
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location = hepatocyte canaliculus
function = transports phosphatdlcholine/lecithin into bile disease = PFIC-type 3 |
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ABC G5/8 A heterodimer location? function? Disease?
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location = hepatocyte canaliculus and enterocyte apical membrane
function = transports sterols into bile transports sterols out of enterocytes into lumen disease = Sitosterolemia |
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Sitosterolemia symptoms?
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poor biliary excretion of sterols, increased absorption of plant and dietary sterols, hypercholesterolemia, hypersitosterolemia, and early coronary artherosclerosis
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in carbohydrate digestion only _______ can be absorbed the intestines
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monosaccharides
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metabolism of cellulose?
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bacteria in the large intestine metabolize it into short chain fatty acids
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Glucose and Galactose are transported into the small intestine via?
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SGLT1 = Na cotransport across the apical membrane
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basolateral exit of monosaccharides in the intestine?
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downhill = fructose, glucose, galactose all go out thru GLUT2
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Apical uptake of fructose is via?
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GLUT 5 = not dependent on Na
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signs of sugar intolerance?
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sugar in feces
Excess Hydrogen in expired air |
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Protein absorption is optimal at what length amino acid chain?
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2-4 amino acids
one amino acid = slowest |
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apical membran protein necessary for oligopeptide uptake?
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PROTON DEPENDENT PepT1
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Hartnups disease?
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neutral amino acid transporter doesn't work
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Normally chyme is ________ and water movement is from the _____ into the ______
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Normally chyme is hypertonic and water movement is from the blood into the lumen
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Highest rate of Na+ absorption occurs?
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in the jejunum
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Entry of Na+ across the luminal membrane of colonic cells is mainly via a ____________
Na+ absorption by the colon is stimulated by ________ |
Na+-selective channel (Epithelial Na+ Channel, ENaC.
stimulated by aldosterone |
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the exit of Na+ through the basolateral membrane is ____________ in all cells of the intestine, since it is against its electrochemical potential difference.
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via the Na+-K+ ATPase
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In the jejunum there is large __________ absorption of Cl- driven by the electrical potential difference set up by the _______
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paracellular
Na+ absorption |
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The colon absorbs Cl- ______________ as well as by a ______________ route through a luminal ________
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The colon absorbs Cl- paracellularly as well as by a transcellular route through a luminal Cl- / HCO3- exchanger
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In the small intestine the net movement of K+ is from _______ to _______.
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lumen to blood.
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In the Colon the net movement of K+ is from _______ to ______.
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blood to lumen = high K in feces
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_______ stimulates K+ secretion
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Aldosterone
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_______ is the most potent agonist for the parietal cell.
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Histamine
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________ binds to the basolateral iron transporter _________ inducing its internalization and degradation. Then what happens?
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Hepcidin binds to the basolateral iron transporter ferroportin (Ireg1) inducing its internalization and degradation.
Iron cannot leave the enterocytes and is lost in the feces when the cells desquamate. |
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Vit D3 upregulates ?
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Vit D3 upregulates the synthesis of calbindin and Ca2+-ATPases that leads to an increase in transcellular Ca2+ absorption.
Paracellular Ca2+ transport is passive and unaffected by vitamin D action. |
