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BVetMed - Alimentary > Intestinal pathology > Flashcards

Intestinal pathology Flashcards

1
Q

Give the 3 presentations of intestinal pathology

A
  1. Abdominal pain (colic, obstruction or distension)
  2. Acute diarroea (infections)
  3. Chronic diarrhoea and/or weight loss
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2
Q

What 2 forms of abdominal pain exist? What may cause these?

A

Acute and chronic
-Torsion (Twisting on long axis) or volvulus (twisting around one point)
- Obstruction
> internal (eg. FB, tumour, intussusception)
> external (eg. strangulating lipoma)
- Rupture

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3
Q

What is the general cuase of intussusception? Where does it most commonly occour?

A

^ peristalsis proximal SI -> distal SI
LI more fixed and stable so peristaltic waves “collide” and intessusept.
Usually seen at distal ileum/ileoceacaocolic junction

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4
Q

How do pedunculated lipomas cause abdominal pain?

A

Benign fatty mesentry tumour attached by stalk -> stalk can wrap around intestines

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5
Q

What may occour 2* to intestinal perforation?

A

Fibrinous peritonitis

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6
Q

How do obstructions of the upper interstine present? What are the consequences of an upper GI obstruction?

A

Acute and severe

  • fluid and gas accumulation above obstruction
  • vomiting
  • metabolic alkalosis (loss of H+ in vomitus)
  • dehydration
  • v renal flow -> uraemia
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7
Q

Are proximal or distal gut obstructions more serious?

A

Proximal

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8
Q

How do lower intestinal obstuctions present?

A
  • 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]
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9
Q

What is the usual cause of acute diarrhoea? Give specific examples

A

> Infectious disease (esp in young animals)

  • Viruses (rotavirus, parvo)
  • Bacteria (campylobacter, salmonella, clostridium spp)
  • Endoparasites (cyathostomins)
  • Protozoa (cryptosporidiosis, coccidiosis)
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10
Q

What are the 5 basic mechanisms of diarrhoea pathogenesis? Which is most common in veterinary disease?

A
  1. Altered epithelial cell transport (secretory)
    • Altered structure/permeability * most common
  3. Osmotic effects
  4. Altered motility
  5. Damage to colonic mucosa in similar ways to SI
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11
Q

Give an example of transient diarrhoea caused by altered structure/function

A

Transient rotavirus/coronavirus infection -> villous atrophy. Regenerated by crypt cells as these are not affected so villi regrow.

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12
Q

Give an example of more severe diarrhoea caused by altered structure/function

A

Feline panleukopenia/Canine/Feline parvovirus -> crypts destroyed, villi not repopulated by enterocyttes

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13
Q

What 2 forms of infection of he gut may bacteria cause?

A
  • Diffuse infection (usually anaerobes eg. clostridia)

- Focal/multifocal tissue damage (eg. salmonella)

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14
Q

What is the most common cause of parasitic diarrhoea in the horse? How does this present? Which parasite has similar disease pathology?

A

Cyathostominosis infection. Acute diarrhoea.

- ostertagia has similar disease pathology

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15
Q

Give 2 protozoal causes of diarrhoea. What is their pathophysiology?

A

Coccidiosis and cryptosporidiosis* - ZOONOTIC

- Surface epithelium destroyed -> villous atrophy

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16
Q

What are the 2 main consequences of acute diarrhoea?

A
  1. Loss of water - dehydration, heamoconcentration, ypovolaemic shock
  2. Loss of ions - mainly Na, K, Bicarb -> hypeokalaemia, metabolic acidosis
17
Q

Give 5 causes of chronic D+ and/or weight loss

A
  1. Chronic enterocolitis (IBD) - Lymphoplasmacytic/easinophilic/granulomatous
  2. Lymphangectasia
  3. Endoparisitism
  4. Neoplasia
  5. Grass sickness (functional peristalsis problem)
18
Q

Is maldigestion usually 1* or 2*? What are common causes of maldigestion?

A

2* - Liver: decreased bile secretion or obstruction to biliary outflow
- Pancreas: v enzymes (EPI) - major cuase of intraluminal maldigestion

19
Q

Is malabsorption usually 1* or 2*? What is the most common reason for malabsorption?

A

1* - intestine has decreased surface area for absorption of nutrients eg. due to villous atrophy or resection of segments of bowel

20
Q

For what reasons may ^ bacterial multiplication be seen?

A
  1. ^ entry of bacteria ( v gastric acidity/gastrectomy/colonicjejunal fistula)
  2. Abnormal intestinal loops
  3. v clearance of bacteria (motility, obstruction, immunodeficiency, cachexia)
21
Q

What does bacterial overgrowth in the gut result in? What does this ultimately cause?

A
  1. Bile salt deconjugation and deficiency
  2. Toxins -> intestinal epithelial cell injury
  3. Consumption of nutrients
    - > Malabsorption
22
Q

What occours in end-stage GI disease?

A

Protein losing enteropathy -> ^ plasma protein permeability loss into lumen
- chronic inflammation - lymphatic bloackage

23
Q

What is the main protein lost in PLE?

A

Albumen (smallest protein) - when loss exceeds liver regeneration capibilities hypoalbumenaemia is seen
-> v plasma oncotic pressure -> ascites and oedema, wasting and emaciation

24
Q

Give 2 types of IBD

A

Lymphoplasmacitic enteritis
Eosinophilic enteritis
-Both -> persistent intestinal inflammation

25
Q

Which receptor is involved in the pathogenesis of IBD?

A

TLR 5

26
Q

How are the villi different in IBD?

A

Wider, shorter and thicker due to inflammatory infiltrates

27
Q

What disease causes granulomatous enteritis?

A

Johnes disease

28
Q

What cell predominates in granulomatous enteritis?

A

Macrophages

29
Q

How may lymphangectasia cause PLE?

A

lacteals become distended with lymph -> fat absorption problems and subsequent compromise of gut wall

30
Q

What 3 mays way endoparasites cause GIT problems? Give egs. for each.

A
  1. Maladsorption (eg. cyathostomins)
  2. Obstruction (eg. Ascarids)
  3. Vascualr compromise (eg. large strongyle disease, migration -> thrombus formation)
31
Q

What pathologic change is often seen in associatino with cyathostominosis?

A

Granulomatous

32
Q

How may grass sickness be diagnosed?

A

Ileal or rectal biopsy -> autonomic nerve cells degenerate. (healthy nerve cells are basophilic and defined - become foamy and pale when degenerate)

33
Q

What pathogen is associated with grass sickness?

A

Clostridium botulinum

34
Q

What are the 2 forms of grass sickness? How do they present?

A

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

35
Q

What is the most specific clinical sign assocated with grass sickness?

A

Rhinitis sicca

BVetMed - Alimentary (30 decks)

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