9. Diarrhoea. Causes, pathophysiological forms, consequences

Last updated on June 20, 2019 at 15:23

Introduction

The water content of the stool shouldn’t exceed 200 mL/day – anything above this is regarded as diarrhoea. While the frequency of defecation is commonly increased during diarrhoea is it not decisive for the definition.

The result of the increased water content is that the quantity and consistence of the feces is altered and peristaltic movements are enhanced.

The intestines secrete watery secretion that dissolve and dilute nutrients. They can also reabsorb secretions if the water content of the stool becomes too high. This reabsorption capacity allows up to 8L of digestive juice to be reabsorbed daily.

There are three types of diarrhoea:

  • Osmotic type – where water content increases due to the presence of osmotically active molecules in the feces
  • Secretory type – where there is an increased secretion or decreased absorption of secrete
  • Motor type – where the motility is increased primarily

Clinically do we often not see distinct types but instead combinations of multiple.

Osmotic diarrhoea

In osmotic diarrhoea is there a disorder of digestion and/or absorption. Unabsorbed nutrients may be osmotically active themselves or they can be digested by bacteria which convert them into osmotically active substances. These substances hold on to the water and draws water from the intestinal wall by osmosis, preventing the intestines from reabsorbing water.

The resulting diarrhoea stops when feeding is stopped.

Common causes of osmotic diarrhoea are:

  • Lactose intolerance – lactose isn’t broken down and is instead metabolized by bacteria into osmotically active substances
  • Chronic pancreatitis – undigested nutrients are broken down by bacteria into osmotically active substances
  • Osmotic laxatives
  • Any malabsorption
  • Too much fibre-rich food
Secretory diarrhoea

If the daily secretion exceeds 8 litres will the intestines be unable to reabsorb the surplus secretions. This type of diarrhoea is not related to food intake and will therefore persist despite feeding restriction.

Common causes include:

  • Inflammation of the intestinal wall
  • Poor intestinal perfusion
  • Overproduction of secretory GI hormones like VIP and gastrin due to hormone-producing cancers
  • Carcinoid (neuroendocrine) tumors
  • Infections
    • Enterotoxic pathogens – pathogenic toxins stimulate secretions (cholera, enterotoxic E. coli)
    • Enteropathogenic pathogens – pathogens damage the mucosa
    • Enteroinvasive pathogens – pathogens enter the mucosa
    • Translocation-inducing pathogens
  • Short bowel syndrome – bile acids in the colon stimulate colonic secretions

Secretory diarrhoea should be treated with fluid replacement, and the fluid should contain electrolytes and glucose. Glucose enhances the intestinal absorption capacity, which explains why it’s included.

Motor diarrhoea

When the peristaltic movement of the intestines is increased will the intestines have less time to reabsorb fluid, which reduces the reabsorption capacity.

Primary causes for increased gastrointestinal motility include:

  • Emotional factors (stress)
  • Parasympathetic overactivation – mushroom poisoning, organophosphate poisoning
  • Hyperthyroidism
  • Irritable bowel syndrome
  • Secondarily due to other types of diarrhoea
Consequences of diarrhoea

Diarrhoea is primarily dangerous due to the salt and water loss which can cause hypovolaemia. Metabolic acidosis can occur due to loss of bicarbonate. Significant amounts of potassium are lost, mostly due to secondary hyperaldosteronism due to hypovolaemia but also because GI mucosal cells (which contain potassium of course) detach and are lost with the diarrhoea.

The calorie-loss is only important in chronic cases or in acute cases of patient groups like infants and wasting diseases.


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8. Complex malabsorption syndromes

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10. Bowel obstruction (ileus)

2 thoughts on “9. Diarrhoea. Causes, pathophysiological forms, consequences”

  1. Why would there be potassium loss in kidney compensation of metabolic acidosis? Wouldn’t it rather cause potassium retention (H+ secreted for K+)?

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