Difference between revisions of "Consequences of Gastric Disease - Pathology"
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m (Text replace - "[[Forestomach - Anatomy & Physiology|" to "[[Monogastric Stomach - Anatomy & Physiology|") |
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| − | {{ | + | {{toplink |
| + | |backcolour =BCED91 | ||
| + | |linkpage =Alimentary System - Pathology | ||
| + | |linktext =Alimentary System | ||
| + | |maplink = Alimentary System (Content Map) - Pathology | ||
| + | |pagetype =Pathology | ||
| + | |sublink1=Stomach and Abomasum - Pathology | ||
| + | |subtext1=STOMACH AND ABOMASUM | ||
| + | }} | ||
| + | <br> | ||
| + | ==Vomiting== | ||
| − | ==[[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<sup>+</sup> and Cl<sup>-</sup>, and also K<sup>+</sup> | ||
| + | * 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 [[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. | ||
| + | *** Na+ can only be resorbed in exchange for H+ | ||
| + | **** H<sup>+</sup> is therefore excreted in the urine, causing it to be acidic. | ||
| + | *** [[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. | ||
| + | * [[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]]. | ||
| + | ** 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. | ||
| + | *** e.g. abomasal torsion | ||
| + | *** Causes dehydration, hypochloraemia, hypokalaemia and metabolic alkalosis. | ||
| + | |||
| + | |||
| + | * Lesions in the [[Small Intestine - Anatomy & Physiology|small intestine]] can also lead to [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|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== | ==Raised Intraluminal pH== | ||
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* Causes failure of digestion. | * Causes failure of digestion. | ||
** Anorexia and weight loss follow. | ** Anorexia and weight loss follow. | ||
| − | * Increases the number of bacteria in the [[ | + | * Increases the number of bacteria in the [[Forestomach - Anatomy & Physiology|stomach]]. |
* Diarrhoea reults | * Diarrhoea reults | ||
** Cause is unknwn is unknown but appears to be related to the elevated pH. | ** Cause is unknwn is unknown but appears to be related to the elevated pH. | ||
| Line 23: | Line 63: | ||
* Is usually haemorrhagic in nature | * Is usually haemorrhagic in nature | ||
** Due to bleeding from gastric ulceration. | ** Due to bleeding from gastric ulceration. | ||
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Revision as of 23:03, 25 August 2008
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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.