Pathology of the stomach Flashcards
Clinical signs of displacement of the stomach into the thorax
Produces respiatory distress over several days
Pathogenesis of displacement of the stomach into the thorax
Relatively common in smaller dogs and cats following road traffic accidents.
Can also result from kick or any severe blow to abdomen, diaphragm splits and stomach forced into thorax.
Pathology of displacement of the stomach into the thorax
Abdominal viscera in thoracic cavity.
Disturbs flow of ingesta.
Thorax distended and lungs collapse.
If caught reasonably early (before adhesions begin to form) can be repaired and there is a good chance of recovery.
Gastric dilation
Occurs in dogs, cats, horses, rabbits, and primates.
Cause unclear but may be associated with overeating – excess fermentable carbohydrate.
Can be caused by overeating in puppies
Acute or chronic
Clinical signs of displacement of stomach within abdomen and volvulus
Mainly in giant dogs - Great Dane, St. Bernard’s occasionally German Shepherd dogs (laxity of hepatogastric ligament?).
Animal collapses suddenly and must be operated on rapidly.
It is a true emergency.
Pathogenesis of displacement of stomach within abdomen and volvulus
Usually 1/2 hour after meal.
Stomach distends and when animal runs around and rolls over stomach may twist on its mesentery through 180 degrees clockwise (viewed from ventral axis).
Volvulus impairs blood supply.
Arterial supply maintained but venous drainage blocked.
Stomach wall becomes severely congested and infarction of gastric mucosa may occur.
Spleen also affected, becomes very congested and moves from left to right side of abdomen.
Stomach blows up with gas and fluid and venous return to heart blocked and compression of diaphragm interferes with respiration.
Cause of displacement of stomach within abdomen and volvulus
Actual cause of the problem and the reason for accumulation of gas unclear- may be Cl. Perfringens, fluid, or feed.
Obstruction of the pylorus, aerophagia, no eructation.
Better to feed big dogs, small amounts regularly.
Rupture/perforation of the stomach
Can be seen in dogs that develop dilation and torsion of stomach, but usually die first.
Acutely fatal as bacteria can invade abdomen and produce peritonitis, but usually die first from shock.
Perforation of the stomach can follow a severe gastric ulcer, a sharp foreign body.
Impaction of the stomach
Rare in companion animals.
Several associated causes: roughage, foreign bodies (hairballs – trichobezoares in cats), inadequate water intake, damage to vagal nerves (pneumonia, pleuritis, infiltrative lymphoma).
Signs of gastritis
Vomit
Dehydration
Hypovolaemia
Abdominal pain
Discomfort
Low grade rate/poor feed conversion
Anorexia
Anaemia
Types of gastritis
Catarrhal
Erosive and ulcerative
Fibrinous
Haemorrhagic
Necrotic
Hypertrophic
lymphoplasmacytic
Clinical signs of catarrhal gastritis
Can be fatal as makes animal vomit and can produce rapid dehydration and electrolytes loss.
May die in day or two if vomiting persistent and untreated.
Losing extracellular fluid, isotonic, so blood very quickly becomes viscous.
Die from hypovolaemic shock - particularly in young animals (can be very quick).
Pathology of catarrhal gastritis
Appearance of stomach - swollen hyperaemic mucosa, with thickening of ruggae.
Surface of mucosa covered by sticky mucous which lines stomach.
Mild inflammation, hyperaemia, oedema and infiltration with inflammatory cells in stomach wall but no fibrin or haemorrhage.
Pathogenesis of catarrhal gastritis
Ingestion of mild irritant
Systemic bacterial diseases
- Infectious enteric diseases e.g. colibacillosis, salmonellosis, helicobacteriosis (more common in cats), etc.
Ulcer development
Local disturbances or trauma.
High gastric acidity.
Local disturbances in blood flow leading to ischaemia.
Steroids and nonsteroidal anti-inflammatory drugs (NSAIDs) (depress prostaglandin formation or concentration, leading to decrease phospholipids secretions which are protective) – chemical gastritis.
Pathology of erosive and ulcerative gastritis
Once start can erode deeply and may penetrate gastric wall (perforating ulcer) leading to peritonitis or erode a blood vessel and cause haemorrhage.
Small ulcers relatively common, do not necessary result in death.
Seen commonly in dog.
Pathogenesis of erosive and ulcerative gastritis in dogs
Primary idiopathic peptic ulcers associated with hyperacidity do occur but ulcers often secondary to other diseases.
Also consider gastric carcinoma in older dog.
Secondary ulcers often associated with systemic diseases particularly uraemia and mast cell tumours.
In both cases gastric ulcer may be cause of death but is not the primary disease.
Gastric ulcers caused by mast cell tumours in dogs
Boxers and Labradors have predisposition towards mast cell tumour.
Seem to vomit continually together with abdominal pain.
Usually ulcer near duodenum, frequently secondarily infected and often penetrate deeply.
Physiologically these lesions are associated with actively secreting mast cell tumours with production of histamine leading to gastric hyperacidity (“secondary” peptic ulcers).
Pathogenesis of gastric ulcers caused by uraemia in dogs
In chronic interstitial nephritis collecting ducts cannot reabsorb fluid due to nephron loss and loss of medullary concentration gradient.
Animal drinks a lot, and urinates a lot (enormous quantities).
Urea is washed out with large quantities of fluid (compensated renal failure) otherwise often clinically seem normal.
If fluid is restricted, cannot washout urea and becomes uraemic.
Urea is excreted into stomach and colon.
Stomach has horrible ammoniacal smell and is filled with brown smelly liquid.
Urea in stomach, breaks down to ammonia, which irritates mucosa and contributes towards gastric ulcer (also seen in mouth).
Other contributing factor is arteriolar degeneration in the submucosa, which occurs in uraemia and leads to hypoxic damage to mucosa.
Vomiting causes dehydration and raises urea in blood still further –produces vicious circle that gets worse and ends in death (vomiting, dehydration, shock, results in death).
Clinical signs of haemorrhagic gastritis
Can be very severe, usually only seen post mortem.
Stomach full of thick tarry clots.
Occasionally will vomit blood.
Wall of stomach is blacked and ulcerated.
Pathogenesis of haemorrhagic gastritis
Seen with aspirin and non-steroidal anti-inflammatory drug toxicity.
Peracute / acute infections.
E.g. leptospirosis (Leptospira icterohaemorrhagiae) in dogs.
Clinical signs of chronic hypertrophic gastritis in dogs
Anorexia
Weight loss
Anaemia
Associated heptatic disease
Protein loss into gut
Pathology of chronic hypertrophic gastritis in dog
Hyperplasia of mucosa that is thrown up into folds with reduced numbers of parietal cells and increased goblet cells.
