Malassimilation
(malabsorption/maldigestion)Introduction: Diarrhea is produced by a variety of different mechanisms, and more than one mechanism is often in operation in a clinical case. There is also some overlap in how these processes produce clinical signs.
The Mechanisms of Diarrhea:
Malassimilation
(malabsorption/maldigestion)
Osmotic
particle accumulation within the GI lumen (osmotic diarrhea)
Hypersecretion
(active secretion of electrolytes into gut lumen)
Intestinal
motility abnormalities (either increased peristalsis
and/or decreased segmentation)
Exudation
(e.g. a "leaky" mucosa due to increased mucosal permeability)
Normal Small Intestine
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Malassimilation (Malabsorption/Maldigestion) Diarrhea
Maldigestion
is an incomplete breakdown of large molecules during digestion.
This can be caused by: indigestible substrates (e.g. poorly digestible milk
replacers), failure to break down ingested macronutrients due to lack of pancreatic
enzymes (Exocrine Pancreatic Insufficiency), failure of the mucosal phase of digestion due
to diminished microvillous enzymes (e.g. lactose intolerance), and failure to form
micelles due to biliary obstruction. These processes produce an osmotic type of diarrhea
as the undigested molecules cannot be absorbed and have an osmotic effect in the
intestinal lumen.
Simple malabsorption can be caused by decreased absorptive surface area (e.g. villous atrophy), mucosal injury, and/or microvillous dysfunction. When retained in the lumen, the unabsorbed nutrients have an osmotic effect, and provide substrate for intestinal bacteria. Some degree of maldigestion may accompany this type of diarrhea since enterocytes, the absorptive cell and one of the primary cells affected, also mediate the mucosal phase of digestion.
Problems
with digestion and absorption lead to accumulation of molecules within the intestinal
lumen. The increased osmotic pressure in the
lumen causes water retention and promotes water moving from the plasma into the intestinal
lumen. The result is diarrhea. Carbohydrate overload, sudden dietary changes,
increased bacterial fermentation, as well as diseases affecting the intestinal mucosa can
all have an important osmotic component.
With
secretory diarrhea, voluminous amounts of feces are produced. This is an active mechanism by which fluids and/or
electrolytes are actively pumped into the intestinal lumen.
One
example is when enterotoxins released by various pathogens (e.g.
enterotoxigenic strains of E.coli or ETEC) cause the hypersecretion. The ETEC enterotoxins stimulate cyclic AMP, which promotes
the enterocytes to secrete chloride, sodium, and other electrolytes. Water follows the electrolytes, thus there is an
increase in the absolute amount of secretion. The
absorptive capacity of the affected intestine may not be significant diminished, at least
for certain molecules.
Intestinal motility abnormalities
Irritation
of the GI tract can cause an increase in peristalsis and/or decrease of segmentation. Primary disorders of motility are not common. Stress, drugs and/or hormones can also lead to
this type of diarrhea. Fecal volume is not
increased greatly with abnormal motility.
The most common examples of
exudative diarrhea are diseases characterized by mucosal
damage and/or mucosal inflammation.
Mucosal damage leads to loss of the normal
membrane barrier, increased mucosal permeability, and passive loss of fluid.
Mucosal inflammation can increase mucosal and
vascular permeability due to the production of vasoactive cytokines and
proinflammatory molecules. The
result is leakage of tissue fluids and, in some cases, serum proteins into the
GI lumen. Clearly these processes
may also be accompanied by some degree of malabsorption.
In addition to diseases that produce overt mucosal injury, congestive heart
failure, blockage of intestinal lymphatics, and/or portal hypertension can be
accompanied by exudative diarrhea due to an increase in mucosal hydrostatic
pressure. The increase in hydrostatic pressure leads to passive
transmucosal leakage, and an overall decrease in absorption of fluid.
The affected mucosa may be leaky but is otherwise intact.
