Difference between revisions of "Consequences of Gastric Disease - Pathology"

Revision as of 14:00, 26 September 2008

Fluid loss is evident as:
1. An increased PCV or haematocrit.
2. An increased total protein concentration.
3. A prerenal azotaemia.

The main losses are of H⁺ and Cl^-, and also K⁺
Can potentially cause metabolic alkalosis, although this is only likely with disease which stops at the pylorus, e.g.: pyloric outflow obstruction.
- In cases where mild alkalosis occurs, homeostatic mechanisms produce a more alkaline urine to restore normal body pH.
- However, in severe metablolic alkalosis with marked dehydration, acidic urine may be produced- this is termed paradoxical aciduria.
  - Because vomiting induceses hypokalaemia, there is an overriding stimulus in the kidney for Na⁺ (and therefore water) retention.
  - Na+ can only be resorbed in exchange for H+
    - H⁺ is therefore excreted in the urine, causing it to be acidic.
  - Vomiting also induces hypochloraemia, meaning bicarbonate rather than chloride is resorbed with the Na+ to maintain electrical neutrality
    - This perpetuates the alkalosis.
Vomiting does not occur in the ruminant although abomasal content may reflux into the forestomachs.
- Sequestration of secretions in the abomasum will have similar effects to pyloric outflow obstruction with vomiting in the monogastric animal.
  - e.g. abomasal torsion
  - Causes dehydration, hypochloraemia, hypokalaemia and metabolic alkalosis.

Lesions in the small intestine can also lead to vomiting
- Both gastric acid and pancreatic and intestinal bicarbonate secretions are lost
  - Animal consequently has a normal pH or may even be acidotic.

Associated with some forms of gastritis.
- e.g. Ostertagiasis
Causes failure of digestion.
- Anorexia and weight loss follow.
Increases the number of bacteria in the stomach.
Diarrhoea reults
- Cause is unknwn is unknown but appears to be related to the elevated pH.

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