GIT Pathology 3

Question 1

1. What is the junction between the keratinised and glandular regions of the stomach called in the horse?
2. What is the pars oesophagea in the pig?

Answer 1

1. Margo plicatus.
2. Small keratinised area around the cardiac region of the stomach. Functional difference, as prone to ulceration.

Question 2

Ulceration of the stomach and intestines.

Answer 2

Much more easily ulcerated as only one layer of the epithelium to go through before getting to the basement membrane and supporting tissues (lamina propria) beneath.

Question 3

What cells produce acid in the stomach?
What cells produce pepsin and pepsinogen?

Answer 3

Parietal cells.
Chief cells (released as pepsinogen and converted to pepsin in the acid environment).

Question 4

Causes of gastric dilation in the horse?
What can gastric dilation lead to?
Rupture at post-mortem?

Answer 4

Primary:
- overconsumption of fermentable feeds (e.g. grains), expansile or indigestible foods.
- ingestion of large quantities of water.
Secondary;
- GI obstruction.
- ileus (GI hypomobility).
- dysautonomia (“grass sickness”).
Can lead to rupture, peritonitis, fatal.
PM - build-up of gas – bloat – rupture.
–> differentiate by assessing the level of haemorrhage.

Question 5

Causes of gastric dilation in the dog.

Answer 5

Primary:
- overeating (e.g. young pups).
- component of GDV.
Secondary:
- obstruction.
- gastric ulceration.
- gastric lymphomas.
- uraemia renal failure.

Question 6

GDV.
Causing factors of GDV.

Answer 6

Most common in large and giant dogs, especially with/ deep chests.
Factors:
- gastric distension by gas, fluid, food.
- gas source? (aerophagia?, bacteria?)
- laxity of the gastrohepatic ligament from repeated episodes of gastric dilation.
- dilation, overfeeding, exercise after feeding which may contribute to gastric rotation (usually clockwise and can range from 180 to 360 degrees).
Can get movement of the spleen with the stomach due to gastrosplenic attachments - get torsion of the vessels from the spleen and congestion of the spleen as a result.

Question 7

Potential consequences of GDV?

Answer 7

Gastric infarction (venous first):
- congestion, oedema, necrosis.
– may lead to gastric rupture.
Venous obstruction from volvulus and pressure on surrounding tissues (e.g. VC).
- reduced venous return from the portal vein and CVC – circulatory shock.
Respiratory compromise from increased intra-abdominal pressure on the diaphragm.
Acid-base and electrolyte disturbances:
- can affect cardiac function – arrhythmias.
Death.

Question 8

Displacement and volvulus in other spp.

Answer 8

Pigs - gastric volvulus – may be associated with rapid ingestion of feed, water or air.
Cattle - abomasal displacement/volvulus.

Question 9

Causes of gastric obstruction.

Answer 9

Displacements and volvulus e.g. diaphragmatic hernias.
FBs.
Impaction.
- mainly horses and cattle.
– primary e.g. high roughage feed, low water intake.
– secondary e.g. consequence of GI obstruction or impaired motility.
Pyloric stenosis.

Question 10

Pyloric stenosis as a cause of gastric obstruction.

Answer 10

Benign muscular pyloric hypertrophy (congenital pyloric stenosis).
- uncommon.
- young animals (brachycephalic pups, siamese cats).
- the cause is uncertain.
- may have “projectile” vomiting.
- thickened pyloric smooth muscle.
Pyloric stenosis, secondary to diseases causing pyloric obstruction.
- inflammatory disease.
- neoplasia.
- FB.
- chronic hypertrophic pyloric gastropathy (in middle-aged/older dogs).
– hypertrophy of the pyloric mucosa and/or muscle layer.
– cause not understood.

Question 11

Features of gastric inflammation.

Answer 11

Hyperaemia (reddening).
Thickening or swelling:
- oedema.
- inflammatory cell infiltrate.
- hypertrophy/hyperplasia.
Necrosis, erosion/ulceration.
Haemorrhage.
Fibrosis, atrophy.

Question 12

Potential causes of gastritis or abomasitis.

Answer 12

Traumatic (mechanical) injury e.g. FB.
Chemical and toxic injury:
- irritant/corrosive/toxic chemicals or plants.
- bile reflux from the duodenum.
- NSAIDs.
Hypersensitivity reaction.
Secondary to systemic infections/diseases.
- uraemia (renal failure).
- septicaemia e.g. salmonellosis (pigs).
Idiopathic.
Infectious agents:
- viruses e.g. BVD.
- bacteria e.g. clostridium septicum.
- fungi (often secondary rather than primary).
- parasites e.g. Ostertagia.
Ulceration due to:
- stress, diet, NSAIDs/glucocorticoids, hypoxia/ischaemia, paraneoplastic effects, gastric neoplasia.

Question 13

The general cause of gastric ulceration.

Answer 13

Increase acid/pepsin.
Decreased mucosal integrity and protection.
A balance.

Question 13

Classification of gastritis.

Answer 13

Based on gross and microscopic features.
Acute or chronic.
Inflammatory cell infiltrate:
- lymphoplasmacytic.
- eosinophilic.
- neutrophilic.
- granulomatous.
Mucosal hypertrophy/hyperplasia.
Erosion/ulceration.
Fibrosis.
Atrophy.

Question 14

Factors causing increased secretion of acid.

Answer 14

Paraneoplastic effect - histamine released from mast cell tumours e.g. skin/subcutis
– histamine binds to receptor on gastric parietal cells which stimulates acid secretion.
- excess gastrin production by gastrinomas – gastrin stimulates acid production by parietal cells (Zollinger-Ellison-like syndrome).

Question 15

Formation of gastric ulcer.

Answer 15

Causative factors&raquo_space; acute superficial ulcer&raquo_space; progressive increase in depth in the mucosa (may be rapid)&raquo_space; submucosal involvement (increased haemorrhage risk as larger blood vessels here)&raquo_space; progression into and through the muscularis externa and serosa layers will result in a perforating ulcer w/ potential to leak gastric content into the peritoneal cavity.
Common in the gastro-duodenal junction.

Question 16

Factors causing decreased mucosal protection.

Answer 16

NSAIDs - Prostaglanin that is involved in the stimulation of bicarbonate inhibited by NSAIDs, less bicarbonate produced, acidic on gastric mucosa, ulceration.
Glucocorticoids?
Mucosal trauma.
Bile salts (damage to surface cell membrane).
Reduced mucosal perfusion or ischaemia.
Stress (incl. strenuous activity e.g. performance animals).
Neurosurgery, spinal trauma (may be stress related).
Diet.

Question 17

Gastric neoplasia.

Answer 17

Uncommon/rare.
Frequently malignant.
Can originate from epithelium:
- adenocarcinoma.
- SCC.
Can originate from mesenchymal cells:
- Leiomyoma and leiomyosarcoma.
- GI stroma tumours (GIST) (from the interstitial cells of Cajal).
Can originate from round cells:
- lymphoma. (often involving other sites).
- MCT.

Question 18

Gastric adenocarcinoma in dogs.

Answer 18

Distal parts of the stomach more commonly.
Often appear as ulcerated craterous masses.
Occasionally may present as diffuse thickening of the gastric wall with no mass.
They occasionally appear as an exophytic (outward-growing) mass on the mucosal surface.
Infiltrate the gastric wall.
Mets to local LNs (70% cases at dx) or distant sites e.g. lung, liver, spleen, adrenal glands (15-70% cases at dx).
Fibrous thickening of the gastric wall.

Question 19

Gastric SCC in horses.

Answer 19

Exophytic, vegetative, roughened and ulcerative mass.
Can appear as diffuse thickening and ulceration without a detectable mass.
Infiltrate the stomach wall and frequently metastasize - often within the abdomen (transcoloemic spread).

Question 20

Gastric lymphoma.

Answer 20

Diffuse.
Localised.
Ulcerated.
Can be difficult to differentiate from other neoplasia.