Difference between revisions of "Vomiting"

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(Created page with '==The Vomit Reflex== right|thumb|150px|The Vomit Reflex - Copyright nabrown RVC *Emesis is the process of vomiting *Persistent vomiting ca…')
 
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* Has potentially lethal effects in the monogastric animal.
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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+
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**** 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 - Anatomy & Physiology|abomasal]] content may reflux into the [[Stomach and Abomasum - Anatomy & Physiology|forestomachs]].
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** 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.
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*** e.g. abomasal torsion
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*** Causes dehydration, hypochloraemia, hypokalaemia and metabolic alkalosis.
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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
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*** Animal consequently has a normal pH or may even be acidotic.
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==The Vomit Reflex==
 
==The Vomit Reflex==
 
[[Image:The Vomit Reflex Pathway.jpg|right|thumb|150px|The Vomit Reflex - Copyright nabrown RVC]]
 
[[Image:The Vomit Reflex Pathway.jpg|right|thumb|150px|The Vomit Reflex - Copyright nabrown RVC]]

Revision as of 12:10, 26 July 2010

  • 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.


The Vomit Reflex

The Vomit Reflex - Copyright nabrown RVC
  • Emesis is the process of vomiting
  • Persistent vomiting can be exhausting and can lead to metabolic alkalosis, dehydration and electrolyte inbalances which may require fluid therapy
  • Extreme cases of persistent vomiting can lead to shock
  • Retching involves the abdominal and chest walls contracting
  • Vomiting includes retching and the action of the diaphragm
  • Diaphragm moves caudal to open the cardia
  • Gastrointestinal tract have protective stimuli to recognise harmful products ingested. The mechanoreceptors and chemoreceptors respond using viscerent afferent pathways.
  • Medulla co-ordinates process
  • Chemoreceptive trigger zone in the 4th ventricle responds to blood and CSF
  • Inputs also from inner ear and higher centres
  • Emetic agents can be used in cases of gastric obstruction and to remove non-corrosive poisons from the stomach (for corrosive poisons charcoal can be used which will help adsorb the substance and decrease its absorbtion into the GIT)
  • For more information on emetic and anti-emetic drugs click here

Emetic agents

  • Drugs cause emesis by irritating the gastric mucosa
    • Histamine
    • ACh
    • Dopamine
    • Catecholamines
    • 5-hydroxytryptamine
    • Substance P
    • Enkephalins
    • NK1 receptor agonists

Anti-emetic agents

  • Anti-emetic agents can be used to treat motion sickness and to treat or prevent vomiting
    • Dopamine (D2) receptor antagonists
    • 5-hydroxytryptamine antagonists
    • NK1 receptor antagonists
    • Muscarinic receptor antagonists
    • Histamine (H1) receptor antagonists
    • Gastroprotective agents