Download Weak peristaltic contractions move food slowly toward the jejunum

Digestion & Absorption Part II
Outline mechanisms of secretion and absorption of water and electrolytes in the GIT:
Cells cannot actively absorb or secrete water, and passive flow down osmotic gradients is used.
These movements are rapid, so interstitial fluid and lumen fluid always have the same osmolarity
Approx 2L of water is ingested each day. Salivary, gastric, intestinal, pancreatic & bile
secretions add another 7L. Only approx 150mL is lost in faeces. In the jejunum, ileum water is
reabsorbed as part of ion absorption. In the large intestine, the majority (up to 80%) of water is
reabsorbed.
Intestinal epithelial cells absorb water & electrolytes continuously, reducing the [lumen]. As the
lumn [solute] drops, water then also moves into epithelial cell, causing hydrostatic pressure that
drives it through the basement membrane into capillaries, thereby maintaining equilibrium.
Movement is through transcellular and paracellular pathways, regulated by tight junctions or
zonulae occludens.
Ions are treated individually by intestinal cells, and may enter by various means:
- Na2+: diffusion, cotransport with another nutrient, or active transport
- Ca2+: active transport, accelerated by parathyroid hormone
- K+: diffusion
Other ions (eg Mg2+, Fe2+) require specific carrier proteins. Anions:
- chloride, iodide, bicarbonate, nitrate: diffusion or carrier-mediated transport
- phosphate & sulfate enter by active transport.
The rate of uptake is directly proportional to the [ion] in the lumen (electrochemical gradient) &
Starling forces (hydrostatic pressures across membrane walls).
Both the LI & SI secrete water and electrolytes, via the crypt cells. Transcellular secretion of Clis the most common, where an osmotic gradient is created that draws water into the lumen.
List factors affecting absorption that can lead to malabsorption:
Malabsorption involves pathological interference with the normal physiological sequence of
digestion (intraluminal process), absorption (mucosal process) and transport (postmucosal
events) of nutrients. Intestinal malabsorption can be due to:
- Mucosal damage (celiac disease, milk intolerance)
- Infection: bacterial or parasitic (travelers diarrhea, Giardia)
- Congenital or acquired reduction in absorptive surface area
- Defects of hydrolysis (adding of water to nutrients to access them)
- Defects of ion transport
- Pancreatic malfunction (eg cystic fibrosis, pancreatitis, carcinoma)
- Impaired circulation of bile from the liver to SI
Describe the mechanisms for local and hormonal control of GIT motility:
An outer & inner layer of smooth muscle controls small intestine (SI) contractions: These weak
peristaltic contractions move food slowly toward the ileum, with muscle thickness decreasing
distally from the duodenum. The contractions are controlled by either intrinsic or extrinsic
systems.
Intrinsic: the enteric nervous system (autonomic) involves control by motor neurons in the
submucosal and myenteric nerve plexuses’, which lie in between the muscle layers. Additionally
some stomach smooth muscle cells contract periodically establishing a contractile rhythm that
spreads.
Extrinsic: links to the CNS via vagus and pelvic nerves. Stimulation of the parasympathetic
nervous system increases the myenteric reflexes to accelerate peristalsis and segmentation
(movement between local bowel ‘segments’), and relaxes sphincters. Two reflexes are stimulated
by stretch receptors in the stomach as it fills:
- Gastroenteric reflex: stimulates motility and secretion along the entire SI
- Gastroileal reflex: triggers relaxation of the ileocecal valve, resulting in material
passing from SI to LI.
Nb. Stimulation of the sympathetic nervous system inhibits GI motility.
Once material inters the large intestine (LI) it is subject to a variety of contractions. Most in the
ascending colon are segmental in nature (12-60secs) increasing the level of mixing. By the time
material enters the descending colon it has changed from liquid to semi-solid state. Segmentation
here actually resists flow so that excess water can be absorbed.
Intestinal Hormones relating to GIT motility:
Part of the intrinsic control, a variety of peptide hormones released by the endocrine cells are
scattered along the epithelia of the GIT. They enhance or suppress motility reflexes:
Gastrin: increases the degree of ileocecal valve relaxation, mostly in antrum, duodenum
Motilin: stimulates upper GI motility, released cyclically during fasting, under neural
stimulation. Mostly in duodenum, jejunum.
GIP: Gastric inhibitory protein, reduces gastric sectretion, located in duodenum
Villikinin: helps to move villi, promoting digestion
Somastatin: inhibits gastrin release and acid secretion from parietal cells
Describe the effects of malabsorption on the supply of micronutrients (including minerals,
fat & water-soluble vitamins):
Some amino acids & fatty acids, as well as vitamins and minerals are considered as ‘essential’ as
they are derived from the diet. Any process that slows or prevents absorption of an essential
nutrient will also induce a state of deficiency. In the case of vitamins, which are not readily
stored by the body, this is particularily true.
Water-soluble vitamins (C, B’s) are easily absorbed by diffusion across epithelia. Luminal
bacterial overgrowth can cause a decrease in the availability of substrates (including
carbohydrates, proteins, and vitamins eg B-12, folate). Vitamin B-12 deficiency due to
pernicious anemia is caused by a lack of intrinsic factor and by pancreatic enzyme deficiency.
Water-soluble vitamin malabsorption can cause generalised motor weakness (pantothenic acid B5, vitamin D) or peripheral neuropathy (thiamine B-1), a sense of loss for vibration and position
(cobalamin B-12) and night blindness (vitamin A).
Fat-soluble vitamins (A, D, E, K) require solubilisation within bile salt micelles for absorption,
and hence ingestion of dietary lipids. Fat malabsorption is known as Steatorrhea. If bile salt
uptake is impaired (either via obstruction, liver dysfunction or Ileal dysfyunction [decreased bile
salt uptake]) then these vitamins are prone to malabsorption. Vitamin D deficiency can cause
bone disorders, such as osteopenia or osteomalacia
Vitamin deficiencies can also cause mucositis, rendering the GIT epithelia to infection and
damage. Crohn's disease is an autoimmune disease, caused by the immune system attacking the
gastrointestinal tract and producing inflammation – affecting any part of the gastrointestinal tract
and contributing to a variety of associated pathology including micronutrient malabsorption.
The levels of major and trace minerals are tightly controlled in plasma, as they play a role in
fluid balance, membrane potential, and their limited solubility. The most common minerals
include Ca2+ & Fe2+. Ca2+ is responsible for bone & teeth formation, synaptic transmission &
glandular secretion. Excess absorption can lead to kidney/gall stones, whilst deficiency leads to
rickets in children & osteoporosis in adults. Low Vit-D can be a causative factor. Fe2+ forms
insoluble complexes that are slowly absorbed and carried by transferring to bloodstream.
Deficiency results in anaemia, a condition where haemoglobin synthesis is defective.