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EQUINE > 7.1.1: Intestinal causes of weight loss including diagnosis and treatment > Flashcards

7.1.1: Intestinal causes of weight loss including diagnosis and treatment Flashcards

1
Q

What are some pathophysiological mechanisms of weight loss?

A
  • Decreased dietary intake
  • Increased rate of utilisation
  • Loss of nutrients (malabsorption/maldigestion)
  • Inadequate delivery to tissues
  • Conditions that cause muscle wasting
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2
Q

What are some small intestinal causes of weight loss?

A
  • Chronic inflammatory bowel disease (CIBD)
  • Proliferative enteropathy
  • Alimentary tract neoplasia
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3
Q

What are the 3 types of chronic inflammatory bowel disease?

A
  • Granulomatous enteritis (GE)
  • Eosinophilic enterocolitis (EE)
  • Lymphocytic plasmocytic enterocolitis (LPE)
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4
Q

Cause, pathogenesis, incidence and signalment of granulomatous enteritis (GE)

A
  • Cause: unknown, hypothetical response to intestinal bacteria
  • Pathogenesis: lymphoid and macrophage infiltration into the lamina propria -> ileal villous atrophy
  • Rare
  • Any age, sex, or breed may be affected
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5
Q

Cause and signalment of eosinophilic enterocolitis

A
  • Cause: unknown, speculated to be linked to nematode infestation (parasites inducing hypersensitivity reaction/containing factors that attract eosinophils)
  • Signalment: any age and breed; TBs and standardbreds most commonly affected
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6
Q

Pathogenesis of eosinophilic enterocolitis

A
  • Eosinophil infiltration into the intestinal mucosa
  • Might see Multisystemic eosinophilic epitheliotropic disease (MEED), Diffuse eosinophilic enterocolitis (DEE), or Idiopathic focal eosinophilic enteritis/colitis (IFEE/IFEC)
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7
Q

Cause, pathogenesis and signalment of lymphocytic plasmocytis enterocolitis

A
  • Cause: unknown, speculated to precede development of intestinal lymphoma
  • Pathogenesis: there is lymphocyte and plasma cell infiltration into the lamina propria
  • Signalment: can affect any age, sex and breed
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8
Q

Cause of proliferative enteropathy

A
  • Causative agent: Lawsonia intracellularis
  • Obligate intracellular bacterium
  • Inhabits the cytoplasm of proliferative crypt epithelial cells
  • Found in jejenum and ileum
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9
Q

Signalment and epidemiology of proliferative enteropathy

A
  • Weanling foals 3-8 months old
  • May be seen in individuals or outbreaks
  • Uncommon in yearlings/adult horses
  • Often seen in horses in close proximity to swine
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10
Q

Risk factors for proliferative enteropathy

A
  • Overcrowding
  • Feed changes
  • Antibiotic usage
  • Mixing and transportation
  • Weaning
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11
Q

What are some large intestinal causes of weight loss?

A
  • Parasite infestation
  • Right dorsal colitis (RDC)
  • Sand enteropathy
  • Eosinophilic enterocolitis
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12
Q

Which groups of parasites can affect the large intestine?

A
  • Large strongyles
  • Small strongyles
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13
Q

What is an important and pathogenic large strongyle?

A

Strongylus vulgaris

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14
Q

Pathogenesis of large strongyles

A
  • Migration of (4th stage) larvae through intestinal wall
  • From the lumen through the mucosa and submucosa
  • This affects the myoelectrical activity
  • There is infiltration with inflammatory cells
  • There is oedema and harmorrhage
  • There is increased secretion and decreased absorption of nutrients from the lumen
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15
Q

Pathogenesis of small strongyles

A
  • Migration of L4 through the mucosa of the large intestine
  • The life cycle includes a period of hypobiosis
  • Larvae emerge in response to an unknown stimulus
  • Sudden emergency causes mucosal injury, ulceration, inflammatory reaction
  • This affects motility patterns of the gut
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16
Q

What clinical signs can be caused by both large and small strongyles?

A
  • Diarrhoea (increased secretion secondary to granulomatous inflammation, and disruption of the interstitium). Protein loss is often significant.
  • Weight loss
  • Colic
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17
Q

Cause and pathogenesis of Right Dorsal Colitis

A

Inflammation and ulceration of right dorsal colon is caused by NSAID use which inhibits prostaglandin production
* PGE2 and PGI2 prostaglandins are responsible for maintaining mucosal blood flow, increased secretion of mucus/H₂O, HCO₃⁻, and increased mucosal cell turnover and migration

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18
Q

True/false: right dorsal ulcerative colitis and right dorsal colitis are the same disease.

A

True.

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19
Q

What is a common cause of Right Dorsal Colitis?

A
  • Phenylbutazone is a common cause
  • Seen particularly in horses receiving inappropriately large doses of NSAIDs
  • Some have underlying disorders
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20
Q

Clinical signs of Right Dorsal Colitis

A
  • Intermittent colic
  • Diarrhoea
  • Weight loss
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21
Q

Cause and pathogenesis of sand enteropathy

A
  • Horses live in sandy areas/paddocks and ingest sand over a period of time
  • Intestinal contents and water continue to flow through the lumen but due to its weight sand accumulates in the ventral colon
  • There is damage to the colonic mucosa/inflammation
  • This leads to diarrhoea, weight loss, and in severe cases impaction leading to colic
22
Q

Clinical signs of proliferative enteropathy

A
  • (Seen in foals)
  • Lethargy
  • Anorexia
  • Fever
  • Peripheral oedema
  • Weight loss
  • Colic
  • Diarrhoea

They didn’t teach us this.

23
Q
A

Large strongyle egg

24
Q
A

Small strongyle

25
Q
A

Right dorsal colitis

26
Q
A

Large strongyle larvae

27
Q

What history questions are important in a horse with weight loss of a possible hepatic/intestinal cause?

A
  • Signalment
  • Length of weight loss
  • Husbandry practices
  • Environmental and pasture managament - type of pasture, size, grass coverage and species, weeds, trees
  • If sharing pasture with other horses (how many?) or other animal species
  • Diet: amount and frequency
  • Worming history
  • Dental care
  • Episodes of diarrhoea/soft manure/inappetance/colic
28
Q

Why might fibrinogen, SAA and globulins be elevated?

A
  • Fibrinogen = marker of inflammation
  • Serum amyloid A = an acute phase protein
  • Acute phase proteins might be elevated esp in cases of parasitism/bacterial infections e.g. Lawsonia, Salmonella and in some neoplasia
29
Q

Intestinal ultrasound: where would you assess the small intestine and what is an abnormal thickness?

A
  • Assessed in the inguinal area and cranioventral abdomen, next to the R kidney
  • Increased intestinal thickness is associated with reduced absorptive capacity
  • Abnormal thickness small intestine >4mm
30
Q

Intestinal ultrasound: where would you assess the large intestine and what is an abnormal thickness?

A
  • Assess the right dorsal colon in the 11-13th ICS; also assess in the left ventral abdomen
  • Increased intestinal thickness is associated with reduced absorptive capacity
  • Abnormal thickness large intestine >6mm
31
Q

True/false: we can image almost the entirety (90+%) of the small and large intestines using ultrasound.

A

False
* We can only image intestinal segments in close contact with the abdominal wall.
* We can see approx. 50% of the large intestine
* We can see approx. 30% of the small intestine

32
Q

Why might we perform abdominocentesis in a horse with a suspected intestinal cause of weight loss?

A
  • Abdominocentesis may not help us find out about inflammatory intestinal diseases but helps rule out other causes of weight loss e.g. peritonitis
  • Assess colour, protein (abnormal >30g/L), lactate (abnormal >2.5 mmol/L)
33
Q

True/false: in horses with intestinal lymphoma, you would expect to see elevated WBC in fluid obtained by abdominocentesis.

A

False
* Intestinal lymphomas/lymphosarcomas remain the most common abdominal neoplasia in the horse
* However these are rarely exfoliative so may not see cytology

34
Q

Diagnosis of proliferative enteropathy

A

PCR
In chronic cases -> biopsy PCR and histo/silver staining

35
Q

Diagnosis of chronic Salmonella

A
  • PCR + enriched culture
  • Don’t rule out if negative; may be intermittent shedding/need several samples
36
Q

Diagnosis of sand enteropathy

A
  • Abdominal radiography = gold standard
  • Can perform abdominal ultrasound
  • Faecal sedimentation test: low sensitivity (may yield false negatives) but is easy and cheap
37
Q

What is the main diagnostic tool for detection of IBD in horses? What does diagnosis rely on?

A

Intestinal biopsies
* Diagnosis relies on samplying the right bit of intestine/disease being diffuse enough to be detected. Horses have 18m of small and 4m of large intestine.

38
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42
Q

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43
Q

Histology reaches diagnosis in what percentage of cases that undergo rectal biopsy?

A

50%
These are mainly cases of GE and MEED

44
Q

Histology reaches diagnosis in what percentage of cases that undergo duodenal biopsies?

A

20%
These are mainly lymphocytic plasmocytic enteritis and eosinophilic enterocolitis

45
Q

Which parts of the intestine can we obtain biopsies from?

A

Proximal part of small intestine (duodenum)
Distal rectum

46
Q

When can we take full thickness biopsies?

A
  • By laparoscopy/laparotomy (probably under GA)
  • Full thickness biopsies are the gold standard
47
Q

Treatment of IBD

A
  • Prolonged corticosteroid therapy: dexamethasone IM for 2 weeks followed by prednisolone/dexamethasone PO for 3 weeks, then dexamethasone tapered for 6 weeks with half dose and every other day dosing
  • Chemotherapeutic agents e.g. azathioprine, vincristine -> recommended for lymphosarcoma/refractory IBD
  • Resection and anastomosis: possible for localised idiopathic eosinopholoc enteritis
    * Diet changes
48
Q

What diet changes would you suggest for a horse with IBD?

A
  • Need a highly digestible and well-balanced feed provided in small amounts throughout the day
  • Add vegetable oils to diet (corn/sunflower/flaxseed)
  • Prioritise a monodiet with fibre; limited/no commercial feeds -> minimise antigen exposure
  • Frequent deworming to avoid parasites triggering inflammation. Even unproblematic parasite levels can be bad for horses with IBD.
49
Q

Treatment of proliferative enteropathy

A

Antibiotics
* IV oxytetracycline for 1 week
* Then doxycycline PO
* OR macrolide + rifampicin (probably this is the less stewardship option)
* Continue antibiotic therapy for 2-3 weeks -> should get a rapid response clinically

Other
* Give NSAIDs (flunixin/phenylbutazone) if pyrexia
* IV fluids and plasma/colloids if profuse diarrhoea and severe hypovolaemia
* Do not give steroids!

50
Q

Treatment of right dorsal colitis

A
  • Withdraw NSAIDs
  • Prostaglandin analogues e.g. misoprostol

Prostaglandin analogues should restore the action of prostaglanding and increase the vascular supply in the affected areas. Should also reduce neutrophilic infiltration of mucosal tissue.

51
Q

Treatment of sand enteropathy

A
  • Psyllium and MgSO4 by NG tube daily
  • NSAIDs: flunixin
  • Surgical emptying if refractory to medical therapy
  • Provide enough roughage: hay/haylage
  • Do not feed on the ground: use haynets, rubber mats, feeders

EQUINE (59 decks)

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