Flashcards in Intestinal pathology Deck (35):
Give the 3 presentations of intestinal pathology
1. Abdominal pain (colic, obstruction or distension)
2. Acute diarroea (infections)
3. Chronic diarrhoea and/or weight loss
What 2 forms of abdominal pain exist? What may cause these?
Acute and chronic
-Torsion (Twisting on long axis) or volvulus (twisting around one point)
> internal (eg. FB, tumour, intussusception)
> external (eg. strangulating lipoma)
What is the general cuase of intussusception? Where does it most commonly occour?
^ peristalsis proximal SI -> distal SI
LI more fixed and stable so peristaltic waves "collide" and intessusept.
Usually seen at distal ileum/ileoceacaocolic junction
How do pedunculated lipomas cause abdominal pain?
Benign fatty mesentry tumour attached by stalk -> stalk can wrap around intestines
What may occour 2* to intestinal perforation?
How do obstructions of the upper interstine present? What are the consequences of an upper GI obstruction?
Acute and severe
- fluid and gas accumulation above obstruction
- metabolic alkalosis (loss of H+ in vomitus)
- v renal flow -> uraemia
Are proximal or distal gut obstructions more serious?
How do lower intestinal obstuctions present?
- less acute than upper GI (vomiting reduced, fluid resorption proximal to obstruction delays serious distension)
- fluid and gas pressure build up gradually -> ulceration and infarction (due to circulatory compromise), eventually haemorrhage and peritonitis
- eventual metabolic acidoisis due to dehydration and catabolism of fat and muscle -> ketoacidosis production [only occours with long term pathology]
What is the usual cause of acute diarrhoea? Give specific examples
> Infectious disease (esp in young animals)
- Viruses (rotavirus, parvo)
- Bacteria (campylobacter, salmonella, clostridium spp)
- Endoparasites (cyathostomins)
- Protozoa (cryptosporidiosis, coccidiosis)
What are the 5 basic mechanisms of diarrhoea pathogenesis? Which is most common in veterinary disease?
1. Altered epithelial cell transport (secretory)
2. * Altered structure/permeability * most common
3. Osmotic effects
4. Altered motility
5. Damage to colonic mucosa in similar ways to SI
Give an example of transient diarrhoea caused by altered structure/function
Transient rotavirus/coronavirus infection -> villous atrophy. Regenerated by crypt cells as these are not affected so villi regrow.
Give an example of more severe diarrhoea caused by altered structure/function
Feline panleukopenia/Canine/Feline parvovirus -> crypts destroyed, villi not repopulated by enterocyttes
What 2 forms of infection of he gut may bacteria cause?
- Diffuse infection (usually anaerobes eg. clostridia)
- Focal/multifocal tissue damage (eg. salmonella)
What is the most common cause of parasitic diarrhoea in the horse? How does this present? Which parasite has similar disease pathology?
Cyathostominosis infection. Acute diarrhoea.
- ostertagia has similar disease pathology
Give 2 protozoal causes of diarrhoea. What is their pathophysiology?
Coccidiosis and cryptosporidiosis* - ZOONOTIC
- Surface epithelium destroyed -> villous atrophy
What are the 2 main consequences of acute diarrhoea?
1. Loss of water - dehydration, heamoconcentration, ypovolaemic shock
2. Loss of ions - mainly Na, K, Bicarb -> hypeokalaemia, metabolic acidosis
Give 5 causes of chronic D+ and/or weight loss
1. Chronic enterocolitis (IBD) - Lymphoplasmacytic/easinophilic/granulomatous
5. Grass sickness (functional peristalsis problem)
Is maldigestion usually 1* or 2*? What are common causes of maldigestion?
2* - Liver: decreased bile secretion or obstruction to biliary outflow
- Pancreas: v enzymes (EPI) - major cuase of intraluminal maldigestion
Is malabsorption usually 1* or 2*? What is the most common reason for malabsorption?
1* - intestine has decreased surface area for absorption of nutrients eg. due to villous atrophy or resection of segments of bowel
For what reasons may ^ bacterial multiplication be seen?
1. ^ entry of bacteria ( v gastric acidity/gastrectomy/colonicjejunal fistula)
2. Abnormal intestinal loops
3. v clearance of bacteria (motility, obstruction, immunodeficiency, cachexia)
What does bacterial overgrowth in the gut result in? What does this ultimately cause?
1. Bile salt deconjugation and deficiency
2. Toxins -> intestinal epithelial cell injury
3. Consumption of nutrients
What occours in end-stage GI disease?
Protein losing enteropathy -> ^ plasma protein permeability loss into lumen
- chronic inflammation - lymphatic bloackage
What is the main protein lost in PLE?
Albumen (smallest protein) - when loss exceeds liver regeneration capibilities hypoalbumenaemia is seen
-> v plasma oncotic pressure -> ascites and oedema, wasting and emaciation
Give 2 types of IBD
-Both -> persistent intestinal inflammation
Which receptor is involved in the pathogenesis of IBD?
How are the villi different in IBD?
Wider, shorter and thicker due to inflammatory infiltrates
What disease causes granulomatous enteritis?
What cell predominates in granulomatous enteritis?
How may lymphangectasia cause PLE?
lacteals become distended with lymph -> fat absorption problems and subsequent compromise of gut wall
What 3 mays way endoparasites cause GIT problems? Give egs. for each.
1. Maladsorption (eg. cyathostomins)
2. Obstruction (eg. Ascarids)
3. Vascualr compromise (eg. large strongyle disease, migration -> thrombus formation)
What pathologic change is often seen in associatino with cyathostominosis?
How may grass sickness be diagnosed?
Ileal or rectal biopsy -> autonomic nerve cells degenerate. (healthy nerve cells are basophilic and defined - become foamy and pale when degenerate)
What pathogen is associated with grass sickness?
What are the 2 forms of grass sickness? How do they present?
Acute - nasogastric reflux and oesophageal ulceration OR gastric dilation and rupture
Subacute/chronic - weight loss, muscle tremors, rhinitis sicca, dysphagia, patchy sweating, constipation due to v peristalsis, LI impaction