Difference between revisions of "Consequences of Gastric Disease - Pathology"
Jump to navigation
Jump to search
m |
|||
Line 33: | Line 33: | ||
*** [[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 | *** [[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 | ||
**** This perpetuates the alkalosis. | **** This perpetuates the alkalosis. | ||
− | * [[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]]. | + | * [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] does not occur in the ruminant although [[The Abomasum - Anatomy & Physiology|abomasal]] content may reflux into the [[Stomach and Abomasum - Anatomy & Physiology|forestomachs]]. |
− | ** 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. | + | ** Sequestration of secretions in the [[The Abomasum - Anatomy & Physiology|abomasum]] will have similar effects to pyloric outflow obstruction with [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]] in the monogastric animal. |
*** e.g. abomasal torsion | *** e.g. abomasal torsion | ||
*** Causes dehydration, hypochloraemia, hypokalaemia and metabolic alkalosis. | *** Causes dehydration, hypochloraemia, hypokalaemia and metabolic alkalosis. |
Revision as of 23:28, 25 August 2008
|
Vomiting
- Has potentially lethal effects in the monogastric animal.
Water Loss
- Fluid loss is evident as:
- An increased PCV or haematocrit.
- An increased total protein concentration.
- 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.
- 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.
- Both gastric acid and pancreatic and intestinal bicarbonate secretions are lost
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.