Difference between revisions of "Vomiting"
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− | + | * Has potentially lethal effects in the monogastric animal. | |
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===Water Loss=== | ===Water Loss=== | ||
− | Fluid loss is evident as | + | * Fluid loss is evident as: |
+ | *# An increased PCV or haematocrit. | ||
+ | *# An increased total protein concentration. | ||
+ | *# A prerenal azotaemia. | ||
+ | |||
===Gastric Electrolyte Loss=== | ===Gastric Electrolyte Loss=== | ||
− | The main losses are of H<sup>+</sup> and Cl<sup>-</sup>, and also K<sup>+</sup> | + | * 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 - Anatomy & Physiology|abomasal]] content may reflux into the [[Stomach and Abomasum - Anatomy & Physiology|forestomachs]]. | ||
+ | ** 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 | ||
+ | *** 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. | ||
− | |||
==The Vomit Reflex== | ==The Vomit Reflex== | ||
− | [[Image:The Vomit Reflex Pathway.jpg|right|thumb| | + | [[Image:The Vomit Reflex Pathway.jpg|right|thumb|150px|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 [[Emetics and Anti-Emetic Drugs|here]] |
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− | === | + | ===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 can be used to treat motion sickness and to treat or prevent vomiting | + | ===Anti-emetic agents=== |
− | *Dopamine (D2) receptor antagonists | + | *Anti-emetic agents can be used to treat motion sickness and to treat or prevent vomiting |
− | *5-hydroxytryptamine antagonists | + | **Dopamine (D2) receptor antagonists |
− | *NK1 receptor antagonists | + | **5-hydroxytryptamine antagonists |
− | *Muscarinic receptor antagonists | + | **NK1 receptor antagonists |
− | *Histamine (H1) receptor antagonists | + | **Muscarinic receptor antagonists |
− | * | + | **Histamine (H1) receptor antagonists |
+ | **Gastroprotective agents | ||
− | |||
[[Category:Feeding Control]] | [[Category:Feeding Control]] | ||
− |
Revision as of 15:58, 2 September 2010
- 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
The Vomit Reflex
- 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