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| | + | {{frontpage |
| | + | |pagetitle =Stomach and Abomasum - Inflammatory Pathology |
| | + | |pagebody = '''Gastritis''' refers to inflammation of the [[Monogastric Stomach - Anatomy & Physiology|stomach]]. |
| | + | Vesicular gastritis is not seen, as the [[Monogastric Stomach - Anatomy & Physiology|stomach]] has no stratum spinosum. |
| | + | |contenttitle =Content |
| | + | |contentbody =<big><b> |
| | | | |
| − | * '''Gastritis''' refers to inflammation of the [[Forestomach - Anatomy & Physiology|stomach]].
| + | <categorytree mode=pages>Stomach and Abomasum - Inflammatory Pathology</categorytree> |
| | | | |
| | + | </b></big> |
| | + | |logo =path-logo.png |
| | + | }} |
| | | | |
| − | ==[[Gastritis, Catarrhal]]==
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| − |
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| − | ===Oedema Disease In The Pig===
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| − |
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| − | * '''Catarrhal gastritis is an important characterisitic of this condition'''
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| − | * Oedema disease is a sporadic condition that can become important on some farms.
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| − |
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| − | ====Clinical====
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| − |
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| − | * Generally occurs in young pigs, though sometimes in older pigs
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| − | ** 7-10 days after major change in diet e.g. weaning.
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| − | * Signs include
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| − | ** '''No''' [[Intestine Diarrhoea - Pathology|diarrhoea]]
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| − | ** Puffy eyelids
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| − | ** High-pitched voice (oedema of larynx)
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| − | ** Sitting on haunched
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| − | ** "Star-gazing" due to cerebral oedema (hallucinations?).
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| − | * Animals usually die.
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| − | * Disease develops very quickly so pigs do not have time to go off food.
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| − |
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| − | ====Pathogenesis====
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| − |
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| − | * Oedema disease is an enterotoxaemia associated with infection by enterotoxigenic [[Escherichia coli|''E.coli'']].
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| − | * Verotoxin/ shiga toxin- producing ''E. coli'' proliferate in the [[Small Intestine - Anatomy & Physiology|small intestine]]
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| − | ** Especially O138, O139, and O141.
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| − | ** Organisms remain in the gut (are not invasive).
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| − | * Labile shiga-like toxin II is absorbed into body, producing effects everywhere.
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| − | * Blood vessel walls are damaged and become very leaky, producing oedema everywhere.
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| − | ** Histological blood vessel changes are subtle.
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| − | ** Fibrinoid degeneration of media in small arteries.
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| − |
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| − | ====Pathology====
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| − |
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| − | * An important characteristic of oedema disease is the occurrence of catarrhal gastritis and marked oedema in the [[Forestomach - Anatomy & Physiology|stomach]] mucosa and wall.
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| − | * Also oedema of various organs, particularly between coils of spiral [[Colon - Anatomy & Physiology|colon]].
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| − |
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| − | ====Diagnosis====
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| − |
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| − | * Clinical signs are characteristic.
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| − | * Also by culture and typing of ''E. coli'' from gut
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| − |
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| − | ==Erosive and Ulcerative Gastritis ==
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| − |
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| − | * Causes '''gastric ulcers'''
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| − | * Seen
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| − | ** Commonly in the dog and pig.
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| − | ** In young calves weaned onto a coarse diet.
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| − | ** These usually heal as animal gets older.
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| − | ** In the horse, associated with parasites.
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| − | * Once started, gastric ulcers can erode deeply.
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| − | ** May penetrate gastric wall leading to peritonitis.
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| − | ** May erode a blood vessel to cause haemorrhage.
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| − |
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| − | ===Pathology===
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| − |
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| − | ====Gross====
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| − | [[Image:gastric ulcer.jpg|thumb|right|150px|Gastic ulcer- gross (Courtesy of BioMed Image Archive)]]
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| − | * Round or oval lesions from 1-4 cm in diameter.
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| − | * Sharply “punched out” lesions with perpendicular or slightly overhanging walls.
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| − | * Borders are level with, or slightly raised above, the surrounding mucosa.
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| − | * Depth is variable.
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| − | ** Some penetrate the superficial mucosa only.
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| − | ** Some deeply penetrate the muscularis externa.
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| − | * Base may be markedly haemorrhagic.
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| − | ** In advanced chronic cases, scarring may result in a puckered appearance.
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| − |
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| − | ====Histological====
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| − | [[Image:gastric ulcer histopath.jpg|thumb|right|150px|Gastric ulcer- histological (Courtesy of BioMed Image Archive)]]
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| − | * Appearance varies with the degree aggressiveness of the ulcer and the amount of healing which has occurred.
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| − | ** Rapidly excavating ulcers have minimal granulation tissue and collagen deposition.
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| − | ** Others may have a necrotic base with a framework of granulation tissue and collagen.
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| − | * The blood vessels at the base of the ulcer may be thickened and thrombosed.
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| − | * In the bovine, the ulcer may have a superimposed fungal infection.
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| − |
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| − | ===Pathogenesis===
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| − |
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| − | * '''There are differences in pathogenesis between species.'''
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| − |
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| − | ====Cattle====
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| − |
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| − | * Management-related in young calves and dairy cows.
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| − | * May also be caused by infectious agents, e.g. [[Bovine Viral Diarrhoea Virus|mucosal disease/ bovine viral diarrhoea virus]].
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| − | * Ulcers have a tendency to bleed and perforate.
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| − |
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| − | ====Horse====
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| − |
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| − | * Affects the pars oesophagea (margo plicatus) in adults and foals.
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| − | * Due to '''parasites''' - ''Gasterophilus'' (Bots).
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| − | * Bots are not as common as they once were.
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| − | * Look like big pink maggots.
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| − | * Killed by Ivermectin.
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| − | * ''Gasterophilus'' leave large ulcers in glandular regions of the [[Forestomach - Anatomy & Physiology|stomach]].
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| − | ** Ulcers / erosions are quite deep.
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| − | * The parasites are believed to be non-pathogenic, but in large numbers they probably produce some discomfort and poor growth.
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| − | * Carcinoma can also produce ulceration in the [[Forestomach - Anatomy & Physiology|stomach]] of the horse as, in other species.
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| − |
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| − | * In foals, the glandular area may sometimes be affected.
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| − | ** This may be e.g. stress-related, or due to used of NSAIDs.
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| − |
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| − | ====Dog====
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| − |
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| − | * Although ulcers are often secondary to other diseases, primary idiopathic peptic ulcers do occur, due to
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| − | ** Hyperacidity
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| − | ** Gastric carcinoma in older dog
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| − |
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| − |
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| − | * Secondary ulcers are often associated with systemic diseases particularly '''uraemia''' and '''mast cell tumours'''. Gastric ulcer may be the cause of death but is not the primary disease.
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| − | *# '''Mast cell tumours'''
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| − | *#*Boxers and Labradors are predisposed to these.
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| − | *#* Vomit continually together with abdominal pain.
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| − | *#* Ulcers are usually near the duodenum.
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| − | *#** Frequently secondarily infected.
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| − | *#** Often penetrate deeply.
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| − | *#* Actively secreting mast cell tumours produce histame, leasing to gastric hyperacidity and therefore secondary peptic ulcers.
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| − | *# '''Uraemia'''
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| − | *#* Gastric lesions usually occur with chronic renal disease.
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| − | *#** Gastrin is produced by the G cells of the gastric antrum during the gastric phase of digestion .
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| − | *#*** Acts on H2 receptors on parietal cells to increase production of HCl.
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| − | *#*** Increases release of histamine from gastric mucosal mast cells to increase HCl release.
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| − | *#** Serum levels of gastrin are increased in chronic renal disease in dogs and cats.
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| − | *#* In acute renal failure death ensues before gastric ulceration develops.
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| − | *#* '''Pathogenesis'''
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| − | *#** Loss of nephron and medullary concentration gradient in chronic interstitial nephritis mean collecting ducts cannot resorb fluid.
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| − | *#*** A common cause of interstitial nephritis in the dog was leptospirosis.
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| − | *#** Consequently, the animal drinks and urinates in enormous quantities, and urea is washed out with large quantities of fluid ("compensated renal failure").
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| − | *#** If fluid is restricted, urea cannot be washed out and the animal becomes uraemic.
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| − | *#*** Urea is excreted into [[Forestomach - Anatomy & Physiology|stomach]], giving it a horrible ammoniacal smell and filling it with brown smelly liquid.
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| − | *#*** Urea is also excreted into the [[Colon - Anatomy & Physiology|colon]].
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| − | *#** Urea in the stomach breaks down to ammonia, irritating the mucosa and contributing to gastric ulcer.
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| − | *#** Uraemia also causes arteriolar degeneration in the submucosa, leading to hypoxic damage to the mucosa. This is another contributing factor to gastric ulcer.
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| − | *#** [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] causes dehydration and further raises blood urea.
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| − | *#*** A vicious circle is produced- ends in death by [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]], dehydration and shock.
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| − | *#** '''Note:''' If an animal in compensated renal failure is given anaesthetic, it will not drink much. It then may start to [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomit]] and die due to uraemia.
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| − |
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| − |
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| − | * NSAIDs, Zollinger-Ellison syndrome (due to pancreatic gastrin-secreting tumour), cirrhosis and bile reflux can all also cause gastric ulcers in the dog.
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| − |
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| − | ====Pig====
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| − |
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| − | * Gastic ulceration is quite common in the pig- May be seen in 50-60% of pigs arriving at slaughterhouses.
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| − | * Has serious economic consequences.
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| − |
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| − | *'''Clinical'''
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| − | ** Occasionally a well-grown pig will drop dead.
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| − | *** Deep ulcers have eroded into a blood vessel, causing massive haemorrhage into the [[Forestomach - Anatomy & Physiology|stomach]] from and producing death very rapidly.
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| − | ** If long standing ulcers do not result in death, they do produce pain and discomfort.
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| − | *** Give low growth rate and poor feed conversion.
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| − |
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| − | *'''Pathogenesis'''
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| − | ** Gastric ulceration is associated with modern pig rearing, but the exact cause is unknown.
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| − | ** Causes are associated with gastric hyperacidity, and gastric ulceration is probably a multifactorial disease.
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| − | ** The following are suggested as possible causes:
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| − | *** Infection, e.g. ''Candida albicans'', ''Streptococci'', ''Staphylococci'' and mixes of these.
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| − | *** Copper toxicity- this is probably more significant.
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| − | **** Pigs are fed copper as growth promoter; 50 ppm is know to be toxic, and animals are often fed 250 ppm.
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| − | *** Vitamin E / Selenium deficiency.
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| − | *** Feeding on concrete floors.
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| − | **** Sand is licked up whe pigs eat.
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| − | *** Feeding finely milled cereal.
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| − | *** Stress
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| − | *** Possibly genetic factors.
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| − |
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| − | *'''Pathology'''
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| − | ** Most commonly affects pars oesophagea (squamous or non-glandular portion).
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| − | ** Starts with hyperkeratosis in the stratum corneum
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| − | *** Appears rough and thickened
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| − | *** May stop at this stage.
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| − | ** In approximately 30% of animals, the lesion starts to erode and quite deep ulcers may develop.
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| − | ** In a significant small number ,very deep ulcers develop and may affect virtually all of pars oesophagea.
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| − | ** Histologically, ulcers are large and flask-shaped ulcer with fibrin, necrosis, erosion and fibrosis at base.
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| − |
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| − | ==Fibrinous/ Diptheric Gastritis==
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| − |
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| − | * Not very common, but has severe consequences.
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| − | * Dirty-white, crumbly fibrin is seen on the surface of mucosa.
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| − | *Causes
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| − | ** Toxic
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| − | *** From drinking battery acid or other caustic material.
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| − | **** Also gives with stomatitis and oesophagitis as well.
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| − | ***Poisons such as mercuric chloride and carbolic acid also cause fibrinous/ diptheric gastritis.
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| − | ** Severe systemic disease
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| − | ***e.g. septicaemic Erysipelas and Swine Fever in pigs, or septicaemic Salmonellosis.
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| − | *** Not usually a primary problem but part of more severe generalised disease problem.
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| − |
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| − | ==Haemorrhagic Gastritis==
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| − |
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| − | ===Clinical===
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| − |
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| − | * Usually only seen post mortem.
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| − | * [[Forestomach - Anatomy & Physiology|Stomach]] full of thick tarry clots.
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| − | * Occasionally will vomit blood in life.
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| − |
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| − | ===Pathology===
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| − | [[Image:haemorrhagic gastritis.jpg|thumb|200px|right|Haemorrhagic gastritis (Courtesy of BioMed Image Archive)]]
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| − | ====Gross====
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| − |
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| − | * Wall of [[Forestomach - Anatomy & Physiology|stomach]] is blacked and ulcerated.
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| − | ** Red, thickened, necrotic, haemorrhagic mucosa.
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| − |
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| − | ====Histologically====
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| − |
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| − | * Coagulative necrosis with fibrin, oedema, haemorrhage, and sometimes emphysema.
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| − | * May extend deep into submucosa/muscle.
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| − |
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| − | ===Pathogenesis===
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| − |
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| − | * There are several causes of haemorrhagic gastritis
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| − | *# Aspirin and non-steroidal anti inflammatory drug toxicity.
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| − | *# Peracute / acute infections, e.g.
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| − | *#* Swine Fever
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| − | *#* Anthrax
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| − | *#* Leptospirosis in dogs (''Leptospira icterohaemorrhagiae'').
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| − | *#Clostridial disease
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| − | *#* e.g. '''Braxy''' (''Clostridium septicum'')
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| − | *#** Affects older lambs or yearlings producing sudden death.
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| − | *#** Usually seen on sheep grazing on frosted grass so more common in colder areas.
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| − | *#** Bacterial exotoxin causes acute abomasitis.
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| − | *#** '''Pathology'''- At post mortem the [[Forestomach - Anatomy & Physiology|stomach]] is grossly distended with partially clotted blood. The wall of the [[Forestomach - Anatomy & Physiology|stomach]] is thickened,reddened and oedematous.
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| − | *#** Diagnosed by isolation of organism from the [[Forestomach - Anatomy & Physiology|stomach]] wall.
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| − | *#** Is now usually vaccinated against (Heptovac 7 in 1 clostridial vaccine).
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| − | *# [[Stomach and Abomasum Toxicology - Pathology#Warfarin Poisoning| Warfarin poisoning]].
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| − |
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| − | == Vesicular Gastritis==
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| − |
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| − | * Is not seen, as the [[Forestomach - Anatomy & Physiology|stomach]] has no stratum spinosum.
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| − |
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| − |
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| − | ==Chronic gastritis==
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| − |
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| − | * Chronic gastritis is usually proliferative rather any other type of gastric inflammation.
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| − | * Usually a parasitic cause.
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| − | * Occurs mostly in the pig and in cattle.
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| − |
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| − | * '''Pig'''
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| − | ** Redworms (''Hyostrongylus'')
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| − | ** Seen mostly in sows, and are present in up to 30% of pig herds.
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| − | ** Small numbers produce little pathology, but large numbers cause thin sow syndrome.
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| − | *** Animals eat well but slowly lose condition.
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| − |
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| − | * '''Cattle'''
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| − | ** [[Stomach and Abomasum Parasites - Pathology#Ostertagiasis|Ostertagiasis]] produces a condition similar to thin sow syndrome.
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| − |
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| − | ===Chronic Hypertrophic Gastritis In The Dog===
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| − |
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| − | * Clinically see anorexia, weight loss, anaemia and associated hepatic disease.
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| − | * Associated with protein loss into gut.
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| − |
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| − | ====Pathology====
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| − |
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| − | * Hyperplasia of mucosa.
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| − | ** Mucosa thrown up into folds.
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| − | ** Reduced numbers of parietal cells and increased numbers of goblet cells.
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| − |
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| − | === Chronic Atrophic Gastritis In The Dog===
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| − |
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| − | * Aetiology uncertain.
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| − | * '''Grossly:''' (may be difficult to appreciate)
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| − | ** Reduced mucosal thickness.
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| − | ** Loss of rugae.
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| − | * '''Histologically'''
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| − | ** Mucosal thinning.
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| − | ** Loss of gastric glands.
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| − | ** Diffuse inflammatory infiltrate of lymphocytes and plasma cells.
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| − | ** Fewer eosinophils in lamina propria.
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| | [[Category:Stomach and Abomasum - Pathology]] | | [[Category:Stomach and Abomasum - Pathology]] |
