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Alimentary > Intestinal pathology > Flashcards

Intestinal pathology Flashcards

1
Q

3 broad categories causing intestinal pathology

A
  • Abdominalpathology (colic in large animals)
  • acute diarrhoea
  • chronic diarrhoea and/or weight loss
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2
Q

Colic can be acute or chronic. Describe causes.

A
  • Torsion (volvulus)
  • Obstruction - internal (Fb, tumour, intussusception) or external (strangulating lipoma)
  • Rupture
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3
Q

Describe the time-dependent mechanism of torsion

A

Intestines twist, veins occluded therefore venous blood cannot leave, arterial blood can continue to enter until the intestine swells so much that arterial blood can no longer enter and blood supply is decreased. Eventually the intestine becomes necrotic and black

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4
Q

Describe intussusception - cause/mechanism

A

Due to increased peristalis,s the proximal SI telescopes into SI,usually at the ileocaecocolic junction (due to strong attachment of colon to abdominal wall but less strong attachment of mesentery/SI).

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5
Q

What is a pedunculated lipoma?

A

benign tumour, on stalk attached to SI mesentery. Usually middle-aged to older horses.
Can wrap around intestine –> external obstruction

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6
Q

Presentation - obstruction of upper intestinal tract

A

Generally acute and severe. Fluid and gas found above obstruction

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7
Q

Clinical signs - obstruction of upper intestinal tract - 4

A
  • Vomiting
  • Metabolic alkalosis (loss of acid in vomitus)
  • Dehydration - causes:
  • reduced renal flow and then uraemia
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8
Q

Clinical signs - obstruction of lower intestinal tract - 3

A
  • Generally less acute (than upper intestinal since vomiting reduced and fluid resorption proximal to the obstruction delays serious distension)
  • pressure (fluid/gas) may lead to ulceration, infarction, haemorrhage and peritonitis
  • Eventual metabolic acidosis (due to dehydration and catabolism of fat and muscle –> ketoacids produced
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9
Q

Causes - acute diarrhoea - 4 - with examples

A

Infectious disease (especially young animals):

  • virus - rotavirus and parvovirus
  • bacteria - campylobacter, salmonella, clostridium
  • endoparasites - cyathostomes
  • protozoa - crytosporidiosis and coccidiosis
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10
Q

5 mechanisms of diarrhoea

A
  • secretory diarrhoea (altered epithelial cell transport)
  • altered structure/permeability (commonest)
  • osmotic effects
  • altered motility
  • damage to colonic mucosa (esp. hindgut fermenters)
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11
Q

How do rotavirus, coronavirus and parvovirus affect the intestinal wall?

A
  • ROTAVIRUS/CORONAVIRUS - infect villus tips causing atrophy. regenerate because crypts not affected
  • PARVOVIRUS (feline panleukopaenia and canine parvo) - infect proliferation cells in villi crypts, little regeneration possible, more severe
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12
Q

Differentiate salmonellosis and clostridial diseases in terms of appearance

A

SALMONELLOSIS (i.e. an aerobic bacteria) - focal or multifocal tissue damage, ulcers
CLOSTRIDIA (anaerobic bacteria) - diffuse damae (all mucosa dark red, necrotic and infected)

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13
Q

Another name for cyathostomin = ?

A

small strongyle infestation (horse)

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14
Q

Where might you see cryptosporidiosis - foals?

A

Like coccidia, they parasitise surface enterocytes, disrupt brush border and cause villus atrophy.

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15
Q

2 broad consequences of acute diarrhoea

A 
WATER LOSS (dehydration, heamoconcentration, hypovolaemic shock)
ION LOSS (principally Na, K, bicarbonate ==> hypokalaemia and metabolic acidosis)
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16
Q

Causes - chronic diarrhoea and/or weight loss - 5

A
  • Chronic enterocolitis (IBD) - lymphoplasmacytic, eosinophilic or granulomatous
  • Lymphagiectasia
  • Endoparasitism
  • Neoplasia
  • Glass sickness
17
Q

Distinguish maldigestion and malabsorption/maladsorption

A
  • MALDIGESTION: liver (decreased bile secretion or obstruction to biliary outflow or pancreas (decreased enzymes - EPI; major cause of intraluminal maldigestion).
  • MALABSORPTION/MALADSORPTION: Intestine (decreased SA for nutrient absorption - villous atrophy or resection of segments)
18
Q

How does bacterial overgrowth lead to malabsorption?

A

Bacterial overgrowth causes bile salt deconjugation, toxin production and nutrient consumption. Either result in bile salt deficiency, intestinal epithelial cell injury. Ultimate result in malabsorption.

19
Q

2 results of changes in protein losing enteropathy

A
  • Increased permeability (to plasma proteins, lost to intestinal lumen)
  • Chronic inflammation (lymphatic blockage)
20
Q

Consequences - protein losing enteropathy

A

Main protein lost is albumin. Loss exceeds ability of liver synthesis and leads to hypoalbuminaemia. Results in decreased plasma osmotic pressure leading to oedema and ascites. eventually wasting and emaciation.

21
Q

How is IBD subdivided? 3

A

According to predominant inflammatory cell (eosinophilic enteritis or lymphoplasmacytic enteritis or granulomatous enteritis - macrophages predominate)

22
Q

Which PRR may be implicated in IBD?

A

TLR (these alleles are restricted in GSDs. 40% of 50 cases had mutation in TLR5 gene versus 8% normal dogs). n.b. TLR 2,4 and 5 are expressed on surface of immune response cells (macrophages, dendritic cells)

23
Q

What wold a finding of granulomatous enteritis suggest?

A

A primary infectious cause - e.g. in cows this may be Johne’s

24
Q

How may endoparasitism cause functional problems?

A
  • Maladsorption - e.g. cyathostominosis
  • Obstruction - ascariasis
  • Vascular compromise - large strongyle disease e.g. Strongylus vulgaris in mesenteric arteries of a horse
25
Q

Which is pretty much the only GIT neoplasia to cause diarrhoea? Why/how?

A

Intestinal lymphoma due to density of nodules causing a malabsorption presentation. In horses this can cause a secondary protein losing enteropathy. Visible on histology/biopsy due to malignant neoplastic lymphoid cell infiltration

26
Q

What is grass sickness?

A

Fatal equine dysautonomia of unknown aetiology. Seen as a marked reduction of GI motility due to widespread destruction of the autonomic nervous system. May be a toxin related to clostridium botulinum.

27
Q

Diagnosis - grass sickness

A

Ileal or rectal biopsy –> look under microscope and you will see ANS cell degeneration (foamy, acidophilic. NORMAL = basophilic)

28
Q

Acute presentation - grass sickness - 2

A
  • Nasogastric reflux and oesophageal ulceration (due to gastric acid damage)
  • Gastric dilation and rupture
29
Q

Subacute to chronic presentation - grass sickness - 7

A
  • Weight loss
  • Muscle tremors
  • Rhinitis sicca (dry mucous membranes, esp nasal mucosa)
  • Dysphagia
  • Patchy sweating
  • Constipation
  • Large colon impaction

Alimentary (37 decks)

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