Diarrhoea - Lecture 152
1. Knowledge of normal structure and function and key features of various organs/tissues and how abnormal structure/function (pathology) can lead to the specific signs of clinical disease relating to that organ.
Structure/function of intestinal villi:
- Villus tip
- cells die and are shed in lumen after 3-5d
- cells migrate to the villous tip and develop absorptive and surface digestive capabilities (brush boarders and carrier proteins)
- Villi become shorter, but more numerous in ileum (compared to duodenum) - surfaces areas are equivalent (see picture below)
- Crypt
- cells are formed by division
- stem cells to regenerate villous tip are made here
Any disease that increases the space between epithelium and vessels will result in problems with digestion/absorption

Carbs and Proteins:

Absorption:
Carbs and Proteins:
- brush border enzymes on mature enterocytes (epithelium) are involved in final digestion or monosaccharides, amino acids and peptides
- anything that destroys enterocytes hampers this
- lymph lacteals take up monoglycerides and free fatty acids via diffusion
- increase width of villi, fats cannot make it through to lacteals
Water:
- ~ 98% of fluid reabsorbed in intestines therefore faecal fluid content is very low
2. To appreciate that the intestinal tract is well adapted to its function of digestion and absorption of the products of digestion – and water, that the intestine has evolved a specialised anatomy to serve that function and that diarrhoea is a sign of loss of that structure/function
Villous tip:
- mature enterocytes absorb sodium, glucose and amino acids across brush border on apical surface
- Sodium pumped out of cell at basolateral aspect
- results in net absorption of fluid (water follows sodium)
Crypt base:
- stem cells ( with leaky intercellular junctions allow sodium to leak back into lumen
- results in net secretion of fluid
Glucose and amino acid transport - major forces for absorption in duodenum
Sodium pump - more important in ileum and colon
Net absorption at villous tip > net secretion in crypts
Diarrhoea when decreased absorption and/or increased secretion
- increased volume/fluidity of faeces
- sign of disease affecting intestinal tract
- not a disease, a sign of disease
3. To be able to name, describe and give examples for each of the four underlying mechanisms to diarrhoea, some cases of diarrhoea have more than one mechanism acting at once
Pathogens of diarrhoea:
1) altered epithelial cell transport (secretory diarrhoea)
2) altered structure of permeability of mucosa (largest group)
- a) Cytotoxins (eg salmonellosis)
- b) Infiltration of cells into villi (eg, lymphoma, inflammation, Johnes disease)
- c) Lytic infection of villous epithelial cells by viruses (coronavirus and rotavirus)
- d) Lytic infection of stem cells in crypts by viruses (parvoviruses)
3) osmotic effects
4) altered motility
1) Altered epithelial cell transport (secretory diarrhoea)
- some types of bacteria attach to villus epithelial cell and inject a toxin into cell
- toxin prevents sodium pump at apical surface
- promotes excretion of sodium from mature villus epithelial cells
- Water follows sodium and massive fluid loss into lumen
- produces profuse, watery diarrhoea
- no destruction of cells; histology and gross appearance of intestinal tissue are normal
- self-limiting as cells shed every 3-5d so new cells replaced 'blocked' cells
E Coli in calf:
2) Altered structure of permeability of mucosa
a) Cytotoxins: (eg salmonellosis)
- Bacterial infection of enterocytes
- bacteria (eg Salmonellae) produce toxins that damage and kill cells
- death of enterocytes - allow blood, fluid and other contents to leak into the lumen
- villus isn't absorptive as enterocytes have been lost
- altered structure and permeability ---> loss of function
- blood and shreds of intestine tissue in diarrhoea = dysentery
Haemorrhagic enteritis - calf
b) Infiltration of cells into villi: (eg, lymphoma, inflammation, Johnes disease)
- Massive increase of cells of villus core will cause width of villus to increase and height to decrease. Therefore surface area decreases
- epithelial have to stretch to cover - flatten and lose brush border. Loss of SA and enzymes for digestion
- cannot absorb nutrients. Nutrients stay in lumen, bacteria grow to eat it - can make condition even worse
Intestinal lymphoma - dog
Lymphocytic/plasmacytic enteropathy - dog
- Inflammatory bowel disease
- infiltrate is mixed with population of lymphocytes and plasma cells (cellular infiltrators)
-Cobblestone gut due to massive infiltration by macrophages
c) Lytic infection of villous epithelial cells by viruses (coronavirus and rotavirus)
- shaded area indicates the cell areas attacked by the virus
- virus in villus
- crypts are fine
- new cells will replace the villus cells
- fluid support during acute phase
Coronavirus: piglet
Brown cells have the virus
d) Lytic infection of stem cells in crypts by viruses (parvoviruses)
- virus replicates in crypts
- mucosal collapse
- lose blood and fluid into lumen
- haemorrhagic diarrhoea
- susceptible to secondary infections - no mucosal protection
Feline parvo:
3) Osmotic effects
- lack of certain brush border enzymes
- accumulation of small osmotic solutes in lumen results
- draws water from blood into intestine
- milk intolerance in cats (no lactase enzymes)
- laxatives are designed to induce mild osmotic diarrhoea
4) Altered motility
- Altered function of intestine - may not have alterations to structure
- disruption/disorganisation/reduced co-ordination of peristalsis
- hypermobility of intestinal tract
- hypomobility of intestinal tract
- risk of increases microbe over development due to static intestine
- increased bacteria load can lead to diarrhoea
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