GIT Pathology 4

Question 1

1. What is the epithelium surface layer turnover time?
2. What does the height of the intestinal villi depend on?
3. What is the wall structure of the large intestine and what is the large intestine’s main function?

Answer 1

1. 2-8 days.
2. Coverage with epithelial cells.
3. Deep crypts.
   Some fermentation but mainly absorption of water before excretion.

Question 2

Classifications of intestinal obstructions.

Answer 2

Functional or mechanical/physical.
Congenital or acquired.

Question 3

Functional obstruction of the intestines.

Answer 3

‘Paralytic’ ileus - inhibition of peristalsis secondary to other conditions e.g. peritonitis, abdominal surgery.
Dysautonomia - altered intestinal motility in horses — “grass sickness”.
Colonic inertia:
- idiopathic — middle-aged to older cats.
- secondary to neuro disease.
- secondary to prolonged colonic distension.
Megacolon - from conditions causing colonic hypomotility.

Question 4

Mechanical/physical obstruction of the intestines.

Answer 4

Colorectal or anal obstructions e.g. pelvic fracture malunion, stricture, intrapelvic mass

Question 5

Types of mechanical/physical obstructions of the intestines.

Answer 5

Intraluminal, intramural, extrinsic, extrinsic, displacements and twisting, atresia (developmental problem of the tubular formation of the intestines).

Question 6

Intestinal foreign bodies.

Answer 6

Partial or complete obstruction.
Pressure or traumatic injury from the FB may compromise intestinal wall circulation which can lead to oedema, necrosis, ulceration, perforation.

Linear FBs e.g. string may cause pleating or plication and may cause ulceration and perforation.
Can become embedded within granulation tissue and be nearly impossible to remove.

Question 7

Intestinal impaction.
Intestinal strictures.

Answer 7

Impaction commonly in horses, in small colon or areas of narrowing/flexures etc - especially in cases of extreme dehydration etc.
Strictures - injury > inflammation > fibrosis > tissue contraction > stricture > obstruction.

Question 8

Congenital atresia of the intestines.

Answer 8

Lack of passage formation through intestine or lack of orifice formation
- e.g. atresia coli, atresia ani.
Segment of intestine can drop away e.g. due to blood supply compromise and tissue death, resulting in blind-ending intestine which is not compatible with life.

Question 9

Pedunculated lipoma.

Answer 9

In horses.
Can cause obstruction by strangulation.
- wraps itself around a loop of intestine and compresses the blood supply coming from the mesentery to the intestines — ischaemia and infarction.
Can be non-strangulating obstructors.
- very close to the junction between the mesentery and the intestine and lies over the intestine.
- sometimes stalk loops around the intestine and gets tucked into the mesentery, creating a degree of constriction for the intestine to be able to dilate.

Question 10

Intestinal ischaemia and infarction.

Answer 10

Mucosal epithelial necrosis starts within a few mins and is extensive by 3-4hrs, external muscle layers can remain viable for 6-7hrs.
Necrosis, oedema, haemorrhage and effusion of tissue fluid and blood into the lumen.
Anaerobes proliferate - gas production, toxins.
Septic peritonitis with or without intestinal perforation.

Question 11

Intestinal displacements - hernias.

Answer 11

May be herniation through a natural or acquired foramina or defect in the boundaries of the abdominal cavity.
Can be inguinal, umbilical, diaphragmatic.
Potential complication:
- intestinal obstruction.
- intestinal strangulation.
- intestinal incarceration.
— herniated intestine cannot be returned back through the hernia (non-reducible).

Question 12

Intestinal displacements - entrapment.

Answer 12

E.g. gastrosplenic ligament entrapment in a horse.
- Entrapment of small intestine through a rent (tear) in the gastro-splenic in the gastrosplenic ligament.
- Can cause obstruction and infarction of the segment of entrapped intestine.
E.g. left dorsal displacement of the colon in horses - nephrosplenic entrapment.
— obstructive to intestines and compromised blood supply to the spleen.

Question 13

1. Define intestinal volvulus.
2. Define intestinal torsion.
3. Intussusception.

Answer 13

1. Twisting of the intestine on its mesenteric axis.
2. Twisting of a tubular organ along its long axis.
3. Usually proximal part of intestine (intussusceptum) telescopes into a distal part of intestine (intussuscipiens).
   Cause often not known:
   - intestinal irritability/hypermotility.
   - FB, enteritis, parasites, tumours, handling of intestine in Sx.
   - partial or complete obstruction.
   - ischaemia and infarction.
   - swelling, inflammation, adhesions, may cause intussusception to become irreducible.

Question 14

1. Define diarrhoea.
2. Basic mechanisms of diarrhoea.

Answer 14

1. Excess water relative to the proportion of dry matter within the faeces. FA = “scour “.
2. Malabsorptive - e.g. due to decrease in SA for absorption of nutrients and solutes so osmotic retention of water in the intestine lumen e.g. due to villus atrophy.
   Hypersecretory - Increase in secretions into intestines — enterotoxogenic e. Coli can secrete toxins that increase fluid secretion into SI.
   — endogenous histamine e.g. MCT can increase secretion.
   Increased permeability/effusion
   - Increase amount of fluid passively flowing across mucosa e.g. due to damage to mucosal integrity.
   — damage to the mucosal integrity by injury to cells causing altered tight junction permeability or increased cell turnover, or loss of epithelium/ulceration.
   — vascular damage causing leakage of plasma components or haemorrhage.
   — inflammation.
   — increased hydrostatic pressure e.g. due to portal hypertension.
   — impaired lymphatic drainage e.g. due to lymphangiectasia.
   — hypoproteinaemia.
   — get increased effusion of fluid and proteins into intestinal lumen which may cause a PLE.
   Altered motility - hypermotility > decreased gut transit time > decrease mucosal contact time > reduce efficiency of digestion and absorption of nutrients and water.
   — hypermotility probably secondary rather than primary mechanism in diarrhoea in domestic animals.

Question 15

Parvoviral enteritis in cats and dogs.

Answer 15

Parvovirus infects proliferating enterocytes in crypts
Get early regenerative response with hyperplasia of surviving epithelium.
Necrosis of crypt enterocytes and loss of enterocytes proliferation to renew surface epithelial layer as the cells are shed.
Villus atrophy with short, blunted and denuded villi and collapse of villus lamina priori and villus atrophy.
Diarrhoea results from reduced absorptive surface area causing malabsorption and effusion of tissue fluids and blood from denuded mucosa also contributes.

Question 16

Lymphangiectasia.

Answer 16

Most common in the dog.
Malabsorption and PLE.
Obstruction of lymphatics with increased lymphatic pressure.
Dilation if lacteals (villi) and intestinal mesenteric lymphatics.
Lymphatics may also be dilated.
Can get leakage of chyme from distended lymphatics which can cause lipogranulomatous lymphangitis which show as cream/white modular foci.
Causes of lymphangiectasia can include mucosal inflammatory cell infiltrates, intestinal neoplasia, mesenteric LN disease.

Question 17

1. Define enteritis.
2. Define colitis.
3. Define proctitis.
4. Classification for intestinal inflammation.

Answer 17

1. Inflammation of SI.
2. Inflammation of LI.
3. Inflammation of the rectal mucosa.
4. Based on pathological features.
   - Acute or chronic.
   - Ulcerative, necrotising, fibrinous, haemorrhagic.
   - Inflammatory cell population e.g. lymphoplasmacytic, eosinophilic, granulomatous (macrophages), neutrophilic.
   - the causative agent.

Question 18

Causes of intestinal inflammation.

Answer 18

Infectious agents e.g. bacteria, viruses, Protozoa, helminths.
Toxins, drugs e.g. NSAIDs.
Hypersensitivity responses, intolerance to foods.
Trauma.
Ischaemia.
Idiopathic.

Question 19

Idiopathic inflammatory bowel disease.

Answer 19

Most commonly in digs and cats.
Clinical signs consistent w/ malabsorption and/or plasma loss (effusion) from gut wall.
Microscopic mucosal features of inflammation, often lymphoplasmacytic, may be eosinophilic.
Villi may variable appear normal, blunted, strophic or sometimes fused.
May also have inflammation of stomach and/or LI.
Cause I known (dx of exclusion).
Lymphocytic infiltrate can sometime be difficult to differentiate from lymphoma.

Question 20

1. General features of neoplasia in the stomach.
2. Most common intestinal tumours.
3. Epithelial intestinal tumours.
4. Mesenchymal intestinal tumours.
5. Round cell intestinal tumours.

Answer 20

1. Uncommon or rare, except cats where it is more common.
   Malignant more common than benign.
2. Adenocarcinoma (more in dogs), lymphoma (more in cats).
3. Adenocarcinoma, adenoma.
4. Leiomyoma, leiomyosarcoma, GI stroma tumours.
5. Lumphoma (other sites often involved), extramedullary plasma cell tumours, MCT.

Question 21

Intestinal Adenocarcinoma in the dog.

Answer 21

May appear as an annular thickening of the wall or an intraluminal mass protruding from the wall.
May be associated with fibrosis and stenosis.
Metastatic spread common - local LNs, peritoneum, distant sites.

Question 22

Rectal hyperplastic polyps in dogs
- adenoma and Adenocarcinoma.

Answer 22

Adenoma benign.
Adenocarcinoma malignant.
Difficult to distinguish between the 2.
- need histology.

Question 23

Intestinal lymphoma.

Answer 23

Localised or diffuse.
May appear nodular, circumferential or plaque-like.
Advanced diffuse tumours may give mucosa a cobblestones or granular appearance.
May have involvement of LNs or other organs.