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

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==Vomiting==
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* Has potentially lethal effects in the monogastric animal.
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 +
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===Water Loss===
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* Fluid loss is evident as:
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*# An increased PCV or haematocrit.
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*# An increased total protein concentration.
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*# A prerenal azotaemia.
 +
 +
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===Gastric Electrolyte Loss===
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* The main losses are of H<sup>+</sup> and Cl<sup>-</sup>, and also K<sup>+</sup>
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* Can potentially cause metabolic alkalosis, although this is only likely with disease which stops at the pylorus, e.g.: pyloric outflow obstruction.
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** In cases where mild alkalosis occurs, homeostatic mechanisms produce a more alkaline urine to restore normal body pH.
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** However, in severe metablolic alkalosis with marked dehydration, acidic urine may be produced- this is termed '''paradoxical aciduria'''.
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*** Because [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]] induceses hypokalaemia, there is an overriding stimulus in the kidney for Na<sup>+</sup> (and therefore water) retention.
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*** Na+ can only be resorbed in exchange for H+
 +
**** H<sup>+</sup> is therefore excreted in the urine, causing it to be acidic.
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*** [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] also induces hypochloraemia, meaning bicarbonate rather than chloride is resorbed with the Na+ to maintain electrical neutrality
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**** This perpetuates the alkalosis.
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* [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] does not occur in the ruminant although [[The Abomasum|abomasal]] content may reflux into the [[Stomach and Abomasum - Anatomy & Physiology|forestomachs]].
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** Sequestration of secretions in the [[The Abomasum|abomasum]] will have similar effects to pyloric outflow obstruction with [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]] in the monogastric animal.
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*** e.g. abomasal torsion
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*** Causes dehydration, hypochloraemia, hypokalaemia and metabolic alkalosis.
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 +
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* Lesions in the [[Small Intestine - Anatomy & Physiology|small intestine]] can also lead to [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]]
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** Both gastric acid and pancreatic and intestinal bicarbonate secretions are lost
 +
*** Animal consequently has a normal pH or may even be acidotic.
 +
 +
==Raised Intraluminal pH==
 +
 +
* Associated with some forms of gastritis.
 +
**  e.g. Ostertagiasis
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* Causes failure of digestion.
 +
** Anorexia and weight loss follow.
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* Increases the number of bacteria in the [[Forestomach - Anatomy & Physiology|stomach]].
 +
* Diarrhoea reults
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** Cause is unknwn is unknown but appears to be related to the elevated pH.
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== Hyperacidity==
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* May develop in certain gastric disturbances
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* Thought to be a contributory factor in peptic ulceration.
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==Anaemia==
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* May also develop in certain gastric diseases
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* Is usually haemorrhagic in nature
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** Due to bleeding from gastric ulceration.

Revision as of 23:03, 25 August 2008

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()Map ALIMENTARY SYSTEM (Map)
STOMACH AND ABOMASUM



Vomiting

  • Has potentially lethal effects in the monogastric animal.


Water Loss

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


Gastric Electrolyte Loss

  • 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.

Raised Intraluminal pH

  • 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.

Hyperacidity

  • May develop in certain gastric disturbances
  • Thought to be a contributory factor in peptic ulceration.

Anaemia

  • May also develop in certain gastric diseases
  • Is usually haemorrhagic in nature
    • Due to bleeding from gastric ulceration.
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