Flashcards in Intestines are like sponges Deck (20)
Diphenoxylate is a Meperidine (Pethidine, Demerol) analog and a µ-opioid receptor agonist, which slows mouth-to-cecum transit time by decreasing peristalsis. It also has anti-secretory activity against cholera toxin and some forms of E. coli toxin. It is sold as Lomotil where it is combined with a small amount (25 µg) of atropine to prevent substance abuse. Lomotil needs a prescription. Another meperidine analog which has the same action is loperamide, which is sold as Imodium.
symptoms: ulky and frequent diarrhea and weight loss. She experiences recurrent episodes of abdominal distention terminated by passage of stools
cause: gluten-sensitive enteropathy, immunologically mediated inflammatory disorder
dx:microcytic anemia, decreased serum calcium, and decreased serum albumin
fluid movement out of lumen
Sodium-potassium ATPase on the basolateral surface of the enterocyte pumps sodium out creating a gradiet. This results in active transport of sodium from the lumen into the enterocyte coupled with nutrients (glucose, galactose, amino acids, water-soluble vitamins) or via a sodium-hydrogen exchanger. To balance the absorption of Na+, Cl- is absorbed passively paracellularly. Water is also absorbed passively paracellularly.
pancreatic enzymes digest the protein R-binder and releases cobalamin, which binds to intrinsic factor in the duodenum
requires intrinsic factor for absorption
absorbed in distal ileum
Water soluble vitamins
vitamins B1, B2, B3, B5, B6, Biotin and C are also absorbed by sodium-dependent co-transport in the upper small intestine
water soluble, folate-hydroxyl cotransporter in the proximal intestine.
SGLT1: Active transport of sodium coupled with uptake of glucose or galactose via SGLT1 occurs throughout the small intestine. The driving force for apical entry of Na+ is determined by the electrochemical gradient created by Na+ being out of basolateral surface of the cell by the Na-K-ATPase. This is the primary mechanism for sodium absorption after a meal, but it makes little contribution during the inter-digestive period.
Sodium-amino acid transporters: Active transport of sodium coupled with uptake of amino acids occurs throughout the small intestine. There are four such transporters, one each for basic, acidic, neutral and imino amino acids. The driving force for apical entry of Na+ is determined by the electrochemical gradient created by Na+ being out of basolateral surface of the cell by the Na-K-ATPase.
Electroneutral Sodium-hydrogen exchange in the duodenum and jejunum: Luminal HCO3-—the result of pancreatic, biliary and duodenal secretion—increases Na+ absorption in the duodenum and jejunum by stimulating apical membrane Na+-H+ exchange.H+ generated from carbonic acid (H2CO3) is extruded into the intestinal lumen in exchange for sodium uptake. The driving force for apical entry of Na+ is determined by the electrochemical gradient created by Na+ being out of basolateral surface of the cell by the Na-K-ATPase. The diuretic drug amiloride suppresses this process at millimolar concentrations.
Parallel Na+-H+ and Cl- - HCO3- exchange in the ileum and proximal colon: During the inter-digestive period (unfed state), this is the primary mechanism for Na+ absorption. The apical membrane of the ileal enterocyte contains a Na+-H+ exchanger tightly coupled to a Cl- - HCO3- exchanger (anion exchanger) by means of changes in luminal pH. H+ and HCO3- are generated from carbonic acid (H2CO3). H+ is extruded into the intestinal lumen in exchange for sodium uptake, while HCO3- is extruded into the lumen in exchange for chloride
Electrogenic transport- involving the Epithelial Sodium Channel (ENaC) occurs in the distal colon.
cause: presence of non-absorbable solutes in the lumen of the intestine
dx: increased osmotic gap (poorly absorbed substance ->low electrolytes->large osmotic gap)
sypmtoms:increased secretion from intestinal crypts
dx: persists after fasting
cause: overgrowth of enteropathic bacteria (e.g. Vibrio cholera, e.choli)
Luminal transport is via a Trp channel.
Basolateral transport is via (a) Sodium calcium exchanger and (b) plasma membrane Calcium ATPase.
also passive via paracellular route.
packaged in the enterocyte.
found in the lymphatics and blood stream and have a lipid core and apoproteins and phospholipids on the outside
motility of small intestine
parasympathetic activity- Ach SP from vagus nerve
symptoms: progressive fatigue, neurological features (numbness, tingling etc)
cause: antibodies against parietal cells -> IF deficiency -> cobalamin def
dx: hypersegmented neutrophils on blood smear
Water movement in the intestine is primarily passive and paracellular.
Of the 8.5 L of secretions into the GI tract, 8.4 L (98.8%) is reabsorbed in the small and large intestine.
Tight junctions become progressively less leaky from the duodenum to the colon.
post-prandial venous blood
absorbed primarily in the proximal small intestine, particularly the duodenum.
Iron is transported in the blood bound to Transferrin
Antacids decrease iron absorption
ileum net absorption
net absorption of Na+ and Cl- and net secretion of bicarbonate
colon net absorption
net absorption of Na+ and Cl- and net secretion of bicarbonate and K+
Basal electrical rhythm
Basal Electrical Rhythm comprises slow waves representing oscillating depolarizations and repolarizations of the smooth muscle. They are NOT action potentials. The intrinsic frequency of slow waves varies along the GI tract. The stomach is slowest – 3-5/min. It is highest in the duodenum (12/min).
The basal electrical rhythm is NOT influenced by neural and hormonal inputs.
The rate of the BER is set by Interstital cells of Cajal. These are star-shaped mesenchymal cells that lie near the myenteric plexus (between the circular and longitudinal muscle layers) and make electrical synapses with smooth muscle.