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Small Animal Final Year > Chronic Diarrhoea in SA > Flashcards

Chronic Diarrhoea in SA Flashcards

1
Q

What is ARD?

A

Antibiotic responsive Diarrhoea

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2
Q

What is SIBO?

A

Bacterial overgrowth

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3
Q

Discuss quantitive microbiology gut content?

A

Quantitative microbiology-gut content

  • Normal bacterial counts in cats is very wide: 10 2 -10 9 Dogs it is poorly defined
  • Cannot extrapolate from humans (<10 3 normal, 10 5-6 overgrowth)
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4
Q

Secondary bacterial overgrowth is common in many of the conditions outlined?

A
  • Decreased gastric acid production
    • Atrophic gastritis/anti-acid medication
  • Increased small intestinal substrates
    • EPI/malabsorptivedisease
  • Partial obstructions
    • Strictures/neoplasia
  • Anatomic disorders
    • Resection of ileal valve/blind loops
  • Motility disease
  • Hypothyroidism
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5
Q

When might SIBO be seen as primary condition in susceptible breeds?

A
  • Poor tolerance of normal microflora
    • Abnormalities in innate immune system, abnormal flora, mucosal barrier defects
  • GSD in particular
    • possible IgA deficiency, genetic susceptibility, loss of tolerance to endogenous bacteria, multiple underlying reasons why guts cant function in normal state
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6
Q

How should the condition ARD be viewed?

A

The condition of ARD should be viewed as a clinical sign or pathogenetic mechanism

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7
Q

What are the consequences of ARD?

A

Consequences of secondary bacterial overgrowth

  • Utilise nutrients/interfere with absorption
  • Damage epithelium and microvillar enzyme dysfunction
  • Increase mucosal permeability/fluid loss
  • Deconjugate bile acids
  • Hydroxylate fatty acids
  • Stimulate colonocyte secretion
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8
Q

What are signs of ARD/SIBO?

A
  • Chronic d+ -small bowel
  • Weight loss/failure to thrive
  • Vomiting/borborygmus/appetite changes
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9
Q

Diagnosis for ARD/SIBO?

A

Diagnosis:

History to determine underlying cause

  • MDB (faecal biome analysis), UA, Faecal, imaging and endoscopy
  • For idiopathic ARD screening tests -ve

Humans diagnosis by duodenal juice culture

  • Not recommended any longer as interpretation is very difficult
  • Obligate organisms difficult to culture –

RESPONSE TO ANTIBIOTICS –if ruled out other underlying causes –true test is recurrence when withdrawn

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10
Q

Antibiotic responsive diarrhoea/dysbiosisor SIBO how else can we make the diagnosis?

A

Serum folate/B 12 (cobalamin)

  • Localise disease?
  • Folate absorbed in proximal SI
  • B 12 absorbed in distal SI
  • Bacteria synthesis folate and bind B 12
  • BUT poorly sensitive or specific for ARD and so main indication is identifying vitamin malabsorption and requirement for supplementation
  • If we have a low B12 it is important to supplement

Breath hydrogen testing

  • Complex to perform (fasting or with test meal)
  • Research tool at present

Circulating unconjugated bile acids

  • Deconjugated by GI bacteria and reabsorped
  • No longer recommended
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11
Q

Treatment of antibiotic responsive diarrhoea/dysbiosis or SIBO?

A

Treat primary cause

EPI treatment -bacterial numbers fall

Antibiotics

Unclear of true action - possible immunomodulatory effects or acting as prebiotic by selecting for beneficial bacteria

Oxytetracycline

  • Better for primary ARD as rapid resistance develops, bacterial numbers often remain the same
  • However signs resolve and usually remain resolved

Tylosin (not tended to use in the UK a lot as not in suitable preparation)

Metronidazole

Use for 4-6 weeks, review after 2 weeks may need to change type

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12
Q

What are the ancillary approaches to ARD and SIBO?

A

Ancillary approaches

  • Dietary manipulation
    • Highly digestible diet
    • Low fat (unclear of efficacy for primary ARD and tylosin responsive disease)
      • Secondary overgrowth leads to hydroxylation of fats and diarrhoea
      • Caution as calorie restriction will reduce weight recovery
  • Prebiotics
    • Alter colonic flora in cats but no current evidence that alter small intestinal numbers in dogs
  • Probiotics
    • Unclear if this improves the outcome in primary or secondary overgrowth (don’t give antibiotic at same time as cancels out any effect)
  • Cobalamin (B12) supplementation
    • Essential to improve recovery rate
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13
Q

What is this appearance indicative of?

A

Chicken korma D+

Skinny ribs

Eating well

=EPI

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14
Q

Define and adverse food reaction?

A

Adverse food reactions refer to any clinically abnormal response attributed to the ingestion of a food or food additive. Adverse food reactions are categorized as either food allergy or food intolerance reactions.

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15
Q

Define a food allergy reaction?

A

Food allergy reactions refer to an immunologically mediated adverse reaction to food unrelated to any physiological effect of the food or food additive. Relapse when specific antigens from previous diet are reintroduced (distinguishes from intolerance)

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16
Q

Define a food intolerance reaction?

A

Food intolerance reactions refer to any abnormal physiologic response to a food that is not believed to be immunologic in nature and may include food poisoning, food idiosyncrasy, pharmacologic reaction, toxicological reaction or metabolic reaction.

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17
Q

Discuss some adverse food reactions?

A

Food intolerance (no primary immunologic response)

  • Food additives and all other causes

Food toxicity (poisoning)

  • Aflatoxins, deoxynivalenol

Disturbed microflora

  • Rapid changes in diet

Dysmotility

  • Types and frequency of feeding

Pharmacologic reactions

  • Methylxanthines(methylxanthine A group of naturally occurring agents present in caffeine, theophylline, and theobromine.), histamine (raw fish)

Maldigestion/malabsorption

  • Undigested components –fermentation and osmotic diarrhoea

Physical

  • Home prepared carcass diet –bone/wool etcirritant effect

Non-specific sensitivity

  • Response to certain formulations of diet –high moisture diets in giant breeds

Food hypersensitivity/allergy

  • Type I and Type IV
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18
Q

What is the aetiology of food responsice D+?

A

Aetiology

  • Adverse reaction to food catergory
  • Inflammatory bowel disease (sub-category of)

Usually chronic small bowel diarrhoea

Vomiting can be seen

Maybe skin signs in some cases

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19
Q

Name diet responsive conditions?

A
  • V+
  • D+
  • Pruritis
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20
Q

Discuss food trials?

A
  • Needs to be accepted by patient and owner
  • Offending antigen excluded
  • For GI disease should be no longer than 3 weeks
  • In cats with ARF most resolved within 7 days
  • Reintroduction of diet should lead to relapse
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21
Q

What should be in a diet trial diet?

A
  • Home-cooked or commercial
  • Novel intact (novel protein source so one kind) or hydrolysed proteins (care with osmolarity)
  • Single or limited source
  • High digestibility
  • Reduced fat
  • Avoid high protein
  • Moderate amount of fermentable fibre
22
Q

What is diagnosis of food responsive D+?

A
  • Diagnosis –by response to food trial

Specific approaches:

  • Food specific serum-immunoglobulin
  • Commercially available
  • GI disease of various causes can increase serum IgG
  • No current evidence that food-specific antibody production contributes to clinical disease
  • No evidence that measuring antibodies aids with diagnosis of food hypersensitivity or identifying offending antigens

Endoscopic food-sensitivity testing

  • Direct application of antigen to mucosa
  • Can also inject into the mucosa –Thought more sensitive
  • Identifies IgE mediated hypersensitivity
  • Biopsies taken from reacting sites
  • Greater sensitivity of ileocolic valve injection than gastroscopic testing
  • Difficult to justify in place of oral challenge testing
23
Q

Discuss inflammatory bowel disease?

A

Inflammatory bowel disease

Idiopathic Protein loosing enteropathy loosing albumin and globulins

  • Persistent/recurrent GI signs with histopathological evidence for inflammation
    • Mucosal infiltration with inflammatory cells
    • Variable severity/length of SI affected
      • If severe -PLE
  • Characterised by cellular infiltrate
    • Eosinophilic
    • Lymphocytic-plasmacytic(breed variants e.g. Basenji enteropathy)
    • Granulomatous
    • Neutrophilic
    • Regional
  • Gastroenteritis
  • Enterocolitis
  • Gastroenterocolitis
  • Triaditis in cats
24
Q

What is the IBD pathogenesis?

A

Currently suspected that this a syndrome comprising a group of disorders with similar characteristics –

  • Important that not the same disease as in humans
    • Crohns and Ulcerative colitis
  • Idiopathic only applicable if no underlying cause found (e.g no response to food elminationor antibiotic)
  • Mucosa controls exposure of luminal antigens to GALT
    • GALT must be immunocompetent but also tolerant of non-pathogenic resident flora and food
    • Loss of tolerance is critical to development of disease
      • Via breakdown of mucosal barrier -excessive exposure of antigens
      • Dysregulation of immune response –
        • Altered TLR expression
        • Altered lymphocyte populations
        • Acute phase protein increase is variable
  • Consequence is uncontrolled inflammation and products thereof
    • Altered architecture
    • Signs dependent on the region of GI tract involved
  • Lymphoplasmacytic inflammation –pre-lymphoma particularly cats
    • Difficult to make clear diagnosis in this species in particular
25
Q

IBD pathogenesis diagram?

A
26
Q

IBD clinical signs?

A

Milddle aged animals mainly

  • Uncommon in dogs <12months
  • Cats of any age are reported but mostly middle aged
  • Suspected to be largely the result of small intestinal IBD though no epidemiological data for this

Chronic diarrhoea common

  • SI in character but if prolonged or involving colon can be mixed

Vomiting more common in cats

  • Can be haemorrhagic (esp cats)
  • May not notice diarrhoea as passed outside

Weight loss with more severe mucosal disruption Appetite very variable –increased, decreased, no change

Abdominal discomfort –variable and concomitant signs

27
Q

How is IBD diagnosed?

A

History and clinical signs

  • Typical breeds, non-specific signs

Physical examination

  • Thin, thick gut loops, abd LN palpable? [CAT] Ascites/oedema

R/O other differentials

  • MDB should include specPLI and TLI, folate, cobalamin, UPC, full faecal analysis

Diagnostic imaging

  • Radiographs and Ultrasound
    • Rule out other disease e.g. chronic FB/intussusception
    • Evaluate wall layering with ultrasound –mucosal speckling/striations

Biopsies –Endoscopic vs. full thickness

28
Q

What are the benefits of biopsies?

A

Endoscopic vs. full thickness? In full thickness you get an idea of what is going on in all the layers whereas endoscopic you only get the mucosa but they are less invasive and it can be an outpatient procedure.

Full thickness –get all the layers

Endoscopic –only tells you about the mucosa

Don’t do full thickness biopsy on dogs on steroids as it compromises healing

Duodenum AND ileum? Pathology isn’t always the same in both it can be present in one and not the other When doing endoscopy –do duodenum AND ileum, as if you don’t, can miss a lot of the IBD dogs

29
Q

What can be seen here?

A

IBD mucosal changes

30
Q

Discuss IBD Eosinophillic enteritis?

DDx?

A

IBD -Eosinophilic enteritis

  • Second most common form (after LPE)
  • Can present with more severe signs
    • GI haemorrhage
    • Bowel perforation
  • This form can be more difficult to control

DDx

  • Endoparasitism
  • Hypersensivitiy disorders
  • Mast cell tumours/paraneoplastic disease
  • Hypoadrenocorticism
  • Hypereosinophilic syndrome
    • Rottweilers
    • Cats
31
Q

Discuss feline triaditis?

A

Three conditions at once and these are usually an ascending disease:

  • IBD
  • Pancreatitis
  • Cholangiohepatitis
    • No gender, age, or breed predisposition (may see more in Siamese)
    • Middle to old-aged cats (some young)
    • SI or LI signs
    • Lethargy, anorexia or ravenous appetite.
    • Jaundice/palpable hepatomegaly
  • Severity NOT linked to severity of the infiltrate or site involved.
32
Q

How is feline triaditis complex diagnosed?

A

Diagnosis

  • exclude other causes of diarrhoea/weight loss
  • Biopsy –NB MULTIPLE SITES! Ex lap appropriate as need biopsies from multiple sites that an endoscope could not reach

Baseline tests:

  • complete blood count
    • Inflammatory/eosinophilia, anaemia
  • serum biochemistry panel
    • Liver disease, pancreatic serology
    • Note different sensitivity and specificity of liver parameters in cats vs. dogs Liver enzymes have a much shorter half life in cats
  • urinalysis
  • Serum T4 concentration
  • FeLV/FIV test

Radiography

  • rule out other conditions/confirm liver enlargement.

Ultrasound

  • GI tract anatomy
  • Liver/pancreas involvement
  • Involvement of biliary system –ascending cholangitis/cholangiohepatitis
33
Q
A
34
Q

Discuss IBD histopathology?

A

Previously very subjective

  • Problems with endoscopic vs. full thickness biopsies
  • Widely variable reports on same biopsy sections
  • Difficult to determine IBD from lymphoma

Increased inflammatory cells in lamina propria – mild/moderate/severe

Often multiple cell lines, diagnosis based on predominant cell type.

  • Lymphoplasmacytic IBD (LPE)
  • Eosinophilic IBD
  • Neutrophilic component would suggest superimposed infection
  • Regional granulomatous form rare
    • Thickened, stenotic segment of bowel
    • DDx granulomatous inflammation/neoplasia
35
Q

Discuss IBD histopathology further?

A

Historically scoring was as below:

  • Mild: Inflammation without architectural distortion
  • Moderate: Inflammation with separation and distortion of glands or crypts and mild villous blunting
  • Severe: Inflammation with multifocal epithelial necrosis, marked separation of glands or crypts, fibrosis, and marked villous blunting and fusion
36
Q

What is the morphological criteria to define small intestinal muscosal inflammation?

A

Morphologic criteria to define small intestinal mucosal inflammation

  • Increased intraepithelial lymphocytes

Altered mucosal architecture

  • Villous fusion or stunting/atrophy
  • Epithelial injury
  • Crypt dilation (common in yorkshireterriers), distension or abscessation
  • Oedema
  • Fibrosis
  • Dilation of lacteals

Submucosa often not commonly affected unless severe

37
Q

Draw a diagram for pathogenesis of IBD?

A
38
Q

What is the treatment approach to IBD?

A

Treatment depends on severity of clinical signs

  • Most patients have chronic disease and are managed on out- patent basis
    • Exception would be severe PLE (protein loosing enteropathy) cases
  • Valuable to have owners keep a diary once start treatment
    • Activity indices can be also used
  • It is important to have a standard approach to management
    • Dietary manipulation
    • Significant proportion of IBD cases will have food responsive disease
  • Antiparasitidesand vitamin (B12 requirments?) supplementation
  • Antibiotics
  • Immunosuppressive therapies
39
Q

Discuss diet treament for IBD?

A

Commercial vs home cooked

  • Restricted constituent
    • Rarely used protein and CH sources (squash and sweet potato)
    • Gluten free
    • Highly digestible preferable
  • Pre and probiotics
  • Hydrolysed diets based on soya or chicken increasingly used
  • Introduce increasing amounts over the first 4-7 days
40
Q

Restricted constituent options for GI disease?

A
  • Obesity Management
  • Obesity Management Wet
  • Satiety Support
  • Weight Control
  • Hypoallergenic Dry Dog Food
  • Hypoallergenic Small Dog Food
  • Hypoallergenic Moderate Energy
  • Sensitivity Control Dry
  • Sensitivity Control Wet
  • Skin Support Dry
  • Intestinal Dry
  • Intestinal Wet
  • Digestive Low Fat Dry
  • Digestive Low Fat Wet
41
Q

Discuss antiparasitics and vitamins in IBD treatment?

A

Antiparasitic agents

  • Fenbendazole 50mg/kg PO for 3-5 days
  • Care if suspect giardia/tritrichomonas as these are not treated effectively

Vitamins

  • Cobalamin malabsorption frequent in IBD
    • Negative prognostic indicator
    • Often associated with severity of disease
    • Reduces efficacy of therapy, leads to poor thrift and poor appetite
  • Parenteral supplementation necessary
  • Usually weekly for 4 weeks then monthly
  • Serology to assess response 1-4 weeks after last injection
  • Rarely need to supplement folate
    • Unclear benefit
42
Q

Discuss antibitoics in IBD treatment?

A

Antibiotics as described for ARD earlier

  • Oxytetracycline, Tylosin, metronidazole
  • Metronidazole is usually first choice
  • Immunomodulatory properties in addition
  • Also reported for tylosin and OTC
  • Alteration of microbiome
    • Probiotics
    • Faecal microbiota transplantation in humans
      • Resolution of poorly responsive IBD
43
Q

Discuss immunosuppressives in IBD treatment?

A

Immunosuppression

Mainstay of treatment in non-food responsive disease

  • Prednisolone 1-2mg/kg PO SID
    • Used at this dose for 2-4 weeks before tapering
    • Care with large dogs as tolerance of prednisolone is poor and suffer muscle weakness and behavioural changes –Should dose on BSA not mg/kg (40mg/m2)
  • Budesonide –locally acting high potency steroid
  • Cats may need higher doses –up to 2mg/kg PO BID

Adjunctive therapies

  • Azathioprine –delayed onset TOXIC IN CATS
  • Cyclosporine –longer onset than prednisolone EXPENSIVE
  • Chlorambucil–very good adjunct but now also EXPENSIVE
  • Methotrexate, cyclophosphamide and mycophenolate often discussed but no clear evidence of efficacy
44
Q

Discuss monitoring in IBD treatment?

A

Monitoring

  • Important to review how effective the treatment is being

Various methods

  • Owners keeping diary
  • Images of faecal character
  • Activity indices –Canine inflammatory bowel disease activity index
45
Q

What is Lymphangiectasia?

A

Abnormalities of the lymphatics

Extensive Lymphatic dilation

  • Here ‘balloon’ dilated lymphatics with LP oedema and loss of lymph into the gut lumen (leads to PLE)

Can be secondary to inflammation or neoplasia or primary

  • Generalised primary condition of lymphatics
    • Breed association
    • Lipogranulomatous changes (microscopic granulomas) –Centred on lymphatics
  • Can also see secondary to blocked C. chyli/thoracic duct
    • R heart failure
    • Liver tumour
  • Outcome is lipid malabsorption
    • chronic small bowel d+ –PLE –Weight loss+++
    • Protein-rich ascites (anasarca/pleural effusion)
46
Q
A
47
Q

What is the diagnostic approach to lymphangiectasia?

A

Diagnostic approach

  • PLE
    • Low albumin and globulin (c.f. liver dz/PLN)
  • Low cholesterol
  • Lymphopaenia
  • Low Ca/Mg (exacerbates the effect of hypocalcaemia)
  • Ultrasound –mucosal striations
  • Endoscopy –white spots on villus tips, white nodules or plaques
  • Biopsy -endoscopy preferable but problems with depth of samples
48
Q

What is the treatment for lymphangiectasia?

A

Treat any primary cause

  • Neoplasia, IBD, anatomic disease

Primary lymphangiectasia

  • Ultra-low fat diet
    • Previously MCTG –as diets had poor calorific value
    • MCTG not absorbed via lymphatics
  • Fluid therapy particularly if ascitic as dehydrated
  • Albumin/Colloid for hypoproteinaemia
    • Plasma requires large volume to alter COP and protein concentration
    • Albumin improves integrity of vascular endothelium
  • Diuretic for effusions
    • Caution as this can worsen hypovolaemia
  • Fluid withdrawal –not indicated unless causing morbidity
  • Short term single centesis may be beneficial –Immunosuppress if inflammatory component or if lipogranulomas are present
49
Q

Name intestinal tumours?

A
50
Q

What is intestinal tumour management?

A

Lymphoma

  • CHOP based protocols
  • COP chemotherapy
  • Prednisolone and chlorambucil
  • Lomustine
  • Prednisolone alone
    • Caution with perforation of bowel when starting any chemotherapy
  • Others –surgical resection and adjunctive chemotherapy

Small Animal Final Year (317 decks)

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