Digestion and Absorption
4. Outline mechanisms of secretion and absorption of water and electrolytes in the GIT
Water
Some 9L per day of water are present in the GIT with about 75% from GIS secretions Absorption/reabsorption is by
osmosis that is: the absorption of minerals and organic nutrients creates a concentration gradient
- nearly 80% in the small intestine
- nearly all that enters the large intestine is reabsorbed
-only about 100-150 mL is lost in faeces
Electrolytes
Electrolytes are derived both from diet and GIS secretions (e.g. bile salts)
The bulk of this is absorbed/reabsorbed (e.g. < 0.5% of Na lost in faeces)
• Sodium: transport is principally coupled to that of amino acids and monosaccharides. In turn at the baso-lateral
membrane sodium is exported into the submucosal region in exchange for potassium
• Chloride: Removal of sodium from the chyme makes its more electronegative and drives chloride into the epithelial
cells. Also in the distal ileum chloride/bicarbonate counter-transport occurs
• Potassium: Removal of water from the lumen means that the luminal potassium concentration rises leading to diffusion
of potassium from the lumen into the cells of the mucosa
While the absorption of sodium, potassium and chloride is at a fairly constant rate: calcium and iron absorption vary with
the body’s requirements
• Calcium: Absorption is via active transport (duodenum) but the bulk is via diffusion between cells in the rest of the SI.
Absorption in duodenum is subject to regulation by the hormone partners parathyroid hormone & calcitriol (the most
active form of vitamin D)
• Iron: Absorption of iron varies with its source. Inorganic iron is taken up via a 2+-cation transporter and this requires a
low pH in the local area. Haem-bound iron is taken up via an alternative mechanism. Transport of iron from the cells of
the GIT into the blood stream is inhibited (when the body is replete with iron) by elevated concentrations of the liverderived hormone hepcidin
5. List factors affecting absorption that can lead to malabsorption
-lipolytic phase defects (pancreatic enxyme deficiency):
-micellar phase defects (bile salt deficiency)
-mucosal defects (diseased epithelial lining)
-delivery phase defect (inability to transport fat out of cells to lymphatic’s)
6. Describe the mechanisms of hormonal and local control of GIT motility
•The GIS has it’s own nerve supply:
1) submucosal (Meissner’s) nerve plexuses: regulation of glands and the SMC in the mucosa
2) myenteric (Auerbach’s) nerve plexus: regulation of GIS motility via the muscles of the muscularis
Two levels of control of GIS function:
•
Intrinsic: the enteric nervous system of the GIT and endocrine cells in the stomach and SI
•
Extrinsic: links to CNS – visceral afferent (i.e. sensory) fibres (vagus and splanchnic nerves) – parasympathetic
and sympathetic efferent (i.e. motor) fibres
Parasympathetic
– via vagus and pelvic nerves with little interaction between the ganglia and with little branching: localised excitatory
effects (via the neurotransmitter acetylcholine)
– General increase in enteric function
increased motility (movement of luminal contents), increased secretion, relaxation of sphincters (between sites)
7. Describe the effects of malabsorption on the supply of micronutrients, including minerals, fat-soluble vitamins and
water-soluble vitamins
Vitamins
• Fat soluble vitamins : A, D, E, K and therefore are ferried by micelles in the process of absorption very similar to that of
fats as per described in questions above. Deficiencies in these vitamins will occur in conditions such as bile salt and pancreatic deficiency
as well as blockage of lacteals (lymph vessels).
• Water soluble vitamins: C, B therefore absorbed by diffusion. Deficiency may occur in hypermotility disorders, mucosal
degradation etc
• B12 must be complexed to intrinsic factor thus: receptormediated endocytosis