Pathology of the stomach

Question 1

Clinical signs of displacement of the stomach into the thorax

Answer 1

Produces respiatory distress over several days

Question 2

Pathogenesis of displacement of the stomach into the thorax

Answer 2

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.

Question 3

Pathology of displacement of the stomach into the thorax

Answer 3

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.

Question 4

Gastric dilation

Answer 4

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

Question 5

Clinical signs of displacement of stomach within abdomen and volvulus

Answer 5

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.

Question 6

Pathogenesis of displacement of stomach within abdomen and volvulus

Answer 6

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.

Question 7

Cause of displacement of stomach within abdomen and volvulus

Answer 7

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.

Question 8

Rupture/perforation of the stomach

Answer 8

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.

Question 9

Impaction of the stomach

Answer 9

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).

Question 10

Signs of gastritis

Answer 10

Vomit

Dehydration

Hypovolaemia

Abdominal pain

Discomfort

Low grade rate/poor feed conversion

Anorexia

Anaemia

Question 11

Types of gastritis

Answer 11

Catarrhal

Erosive and ulcerative

Fibrinous

Haemorrhagic

Necrotic

Hypertrophic

lymphoplasmacytic

Question 12

Clinical signs of catarrhal gastritis

Answer 12

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).

Question 13

Pathology of catarrhal gastritis

Answer 13

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.

Question 14

Pathogenesis of catarrhal gastritis

Answer 14

Ingestion of mild irritant

Systemic bacterial diseases
- Infectious enteric diseases e.g. colibacillosis, salmonellosis, helicobacteriosis (more common in cats), etc.

Question 15

Ulcer development

Answer 15

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.

Question 16

Pathology of erosive and ulcerative gastritis

Answer 16

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.

Question 17

Pathogenesis of erosive and ulcerative gastritis in dogs

Answer 17

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.

Question 18

Gastric ulcers caused by mast cell tumours in dogs

Answer 18

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).

Question 19

Pathogenesis of gastric ulcers caused by uraemia in dogs

Answer 19

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).

Question 20

Clinical signs of haemorrhagic gastritis

Answer 20

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.

Question 21

Pathogenesis of haemorrhagic gastritis

Answer 21

Seen with aspirin and non-steroidal anti-inflammatory drug toxicity.

Peracute / acute infections.

E.g. leptospirosis (Leptospira icterohaemorrhagiae) in dogs.

Question 22

Clinical signs of chronic hypertrophic gastritis in dogs

Answer 22

Anorexia

Weight loss
Anaemia

Associated heptatic disease

Protein loss into gut

Question 23

Pathology of chronic hypertrophic gastritis in dog

Answer 23

Hyperplasia of mucosa that is thrown up into folds with reduced numbers of parietal cells and increased goblet cells.