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BVetMed3 Alimentary > Intestinal Pathology > Flashcards

Intestinal Pathology Flashcards

1
Q

How long does it take for the cell population of the gut to turn over?

A

3–5 days

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2
Q

How does inflammatory infiltrate of the lamina propria affect the level of absorption?

A

Decreased SA, reduced absorption

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3
Q

What are the clinical signs associated with intestinal dysfunction?

A

Abdominal pain
V+
Diarrhoea - acute and chronic
Constipation

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4
Q

What types of displacement of the intestine can cause abdominal pain?

A

Volvulus

Torsion

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5
Q

What is the difference between torsion and volvulus?

A

Torsion - twisting on long axis

Volvulus - twisting on mesenteric axis

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6
Q

What types of obstruction are there?

A

Internal and external

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7
Q

Give examples of an internal obstruction

A

FB
Parasites
Tumour
Intussusception

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8
Q

Give an example of an external obstruction

A

Strangulating lipoma

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9
Q

What is the most common type of intestinal displacement?

A

Volvulus

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10
Q

Where in horses is torsion common?

A

Free end of the left colon

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11
Q

What vessels get compressed first in volvulus/torsion/intussuception?

A

Thin walled veins

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12
Q

How does a volvulus/torsion/intussuception result in peritonitis?

A 
Veins get compressed
Venous congestion
Ischaemic infarction 
Necrosis 
Reduced gut barrier function - bacteria in and endotoxaemia (if G-)
Proximal obstruction 
Perforation - gut contents into abdo
PERITONITIS
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13
Q

What clinical presentation would you associate with an upper intestinal tract obstruction?

A

ACUTE AND SEVERE

Vomiting
Metabolic alkalosis
Dehydration
Reduced renal flow and uraemia

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14
Q

What clinical presentation would you associate with lower GI tract obstruction?

A

LESS ACUTE THAN UGIT
- increased fluid resorption proximal to the obstruction - less vomiting

  • pressure - ulceration and infarction +/- perforation
  • eventually haemorrage and peritonitis

Eventual metabolic acidosis due to dehydration + catabolism of fat+muscle - ketones

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15
Q

What is the difference between fibrin and fibrinous tissue?

A

Fibrin - soft, yellow, stringy

Fibrinous tissue - scar tissue - firm, white

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16
Q

What are the four mechanisms of diarrhoeal pathogenesis?

A
  1. Altered structure/permeability (malabsorption)
  2. Altered epithelial cell transport (secretory diarrhoea)
  3. Osmotic effects (e.g. maldigestion)
  4. Altered motility
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17
Q

How can osmotic effects result in diarrhoea ?

Give an example

A

Lactose Intolerance

Increased solutes in gut lumen therefore water moves out

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18
Q

What bacteria causes a secretory diarrhoea?

A

E.Coli

Chloride ions into gut lumen

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19
Q

What are the broad consequences of acute diarrhoea?

A

Loss of water

Loss of ions

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20
Q

How does acute loss of water affect the patient?

A

Dehydration
Haemoconcentration
Hypovolaemic shock

21
Q

How does acute loss of ions affect the patient?

What ions are typically lost?

A

Sodium, Potassium, Bicarbonate

Hypokalaemia
Metabolic acidosis

22
Q

What viruses can cause acute diarrhoea?

A

Rotavirus
Coronavirus
Parvovirus

23
Q

What bacteria can cause acute diarrhoea?

A

C. Diff
Campylobacter
Salmonella

24
Q

What Protozoa can cause acute diarrhoea?

A

Coccidia

Cryptosporidium

25
Q

What endoparasites can cause acute diarrhoea?

A

CYATHOSTOMES (horses principally)

26
Q

What pathogens target the tips of villi?

A

CRYPTOSPORIDIUM

E.COLI

27
Q

How could you identify cryposporidium on histology?

A

Oocysts (dots) seen on tips of villi - adhering to brush border

28
Q

What pathogen attacks intestinal crypt cells?

Why?

What other cell type does it attack?

A

PARVO

Needs DNA polymerase therefore needs rapidly dividing cells

Immune cells

29
Q

How does rotavirus affect villi?

A

Attacks enterocytes towards the tips of villi

Villi become blunted, stunted and fused

Loss of epithelium

30
Q

What appearance of the intestine is pathognomonic of Parvo?

A

Payer’s patches ‘punched out’

+crypts with necrotic cells on histology

31
Q

What types of lesions are associated with salmonellosis?

A

Necrotising + Ulcerative lesions - fibrino-necrotising

severe focal or multi focal mucosal damage

ILIOTIFLOCOLITIS

32
Q

What causes ‘colitis X’?

A

Clostridial colitis

Toxins released into gut lumen cause diffuse reddening

33
Q

What is seen in the colon of horses with cyathostominosis?

A

Red dots within mucosa (encysted L3/4 larvae)

34
Q

What can cause chronic diarrhoea +/- weight loss?

A

Chronic enterocolitis (IBD)

  • lymphoplasmacytic
  • eosinophilic
  • granulomatous

Lymphangiectasia
Endoparasites
Neoplasia
Grass sickness

35
Q

How can IBD be subdivided histologically?

A
  • Lymphoplasmocytic

- eosinophilic

36
Q

What can cause protein losing enteropathy?

A
  • increased permeability to plasma proteins - lost to intestinal lumen
  • chronic inflammation - lymphatic blockage
37
Q

How can PLE result in oedema and ascites?

What other clinical sign might be associated with this?

A 
Albumin lost 
Loss exceeds liver synthesis 
Hypoalbuminaemia 
Decreased plasma osmotic pressure 
Oedema and ascites

Wasting and emaciation

38
Q

How can bacterial overgrowth result in malabsorption?

A

Toxins - intestinal epithelial cell injury
Consumption of nutrients
Bile salt deconjigation and subsequent deficiency.

39
Q

What neoplastic condition can cause a secondary PLE?

A

Intestinal lymphoma

40
Q

What does fibrin education of a granulomatous lesion indicate?

A

Chronic active lesion

41
Q

How could you describe exaggerated folding of the intestinal mucosa (granulomatous enteritis)?

A

Cerebroform

42
Q

When might you expect to see a giant, multinucleated cell in the intestines in a cow with diarrhoea ?

A

Johnes

43
Q

What endoparasite is associated with malabsorption?

A

Cyathostomins

44
Q

What endoparasite is associated with obstruction?

A

Ascarids

45
Q

What endoparasite is associated with vascular compromise?

A

large strongyles

E.g. strongylus vulgaris in horses

46
Q

What endoparasite can cause mesenteric arteritis in horses?

How does this affect the gut?

A

Strongylus vulgaris

necrosis

47
Q

What can be seen histologically in horses with acute grass sickness?

A

Dark (pyknotic) small, marginalised nucleus of neurones in e.g. submucosa plexus
Decreased number, hypereosinophilic

48
Q

What is the acute presentation of grass sickness?

A

Nasogastric reflux and oesophageal ulceration

Gastric dilation and rupture

49
Q

What is the subacute/chronic presentation of grass sickness?

A 
Weight loss
Muscle tremors 
Rhinitis Sicca (dry nose)
Dysphagia 
Patchy sweating 
Constipation 
Large colon impaction

BVetMed3 Alimentary (16 decks)

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