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Small Animal Medicine Module B > Approach to diarrhoea > Flashcards

Approach to diarrhoea Flashcards

1
Q

What are the main differentials for chronic small intestinal diarrhoea?

A

Dietary - hypersensitivity/ intolerance (intolerances e.g. lactose/ gluten - v rare!)
Parasitic - whipworm/ hookworm/ giardia (coccidia also possible but very rare unless animal is young or immunocompromised)
Bacteria - antibiotic responsive diarrhoea/ others are rarely the primary cause, can incidentally find campylobacter/ can be salmonella carriers. Some that are important are enteropathogenic e.coli/ enterotoxic clostridia
Viral - FIP, FeLV, FIV, distemper
Extraintestinal - hyperthyroidism, addisons, primary lymphangiectasia, dysautonomia, chronic pancreatitis, hepatic dz, EPI
Inflammatory - lymphoplasmacytic/ eosinophilic/ other IBDs/ chronic partial obstruction
Neoplasia - mostly lymphoma, also adenocarcinoma, leimyomas, MCT

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2
Q

What are the main ddx for large intestine diarrhoea?

A

Dietary - hypersensitivity/ fibre responsive
Parasitic - whipworms, giardia (both more SI), Tritrichomonas foetus
Bacterial - more SI, e.coli in boxers causes colitis
Viral - FIP
Perineal - hernia/ tumour/ stricture/ other mass effects
Inflammatory - lymphoplasmacytic enteritis/ colitis/ neutrophilic/ histiocytic/ ulcerative/ granulomatous disease
Infiltrative - same as SI

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3
Q

What initial investigations should be done if there are no concerns in the Hx/ PE?

A

Bloods and UA to assess for more serious disease not clear from PE/ Hx
F+ exam (culture and parasitology) - be aware only 30% of the biome will be assessed, always pool samples
Diet trial

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4
Q

If initial trials and Ix are unrewarding, what bloods should you consider next (based on rest of Hx/ signalment/ PE/ initial bloods?

A 
PLI/ TLI/ folate/ cobalamin
TT4
ACTH stim
FIP profile
Viral testing
Infectious disease testing (if has been out of country)
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5
Q

What are the main tests that can be done once initial tx/ tests was unrewarding?

A 
Bloods
Imaging (US/ rads/ CT/ endoscopy)
Alternative diets
Transabdominal sampling
Biopsies
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6
Q

What is the difference between Addisons, Atypical hypoadrenocorticism and typical hypoadrenocorticism?

A 
Addisons = typical hypoadrenocorticism (both glucocorticoid and mineralocorticoid deficiency)
Atypical = only glucocorticoid deficiency
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7
Q

What is the typical signalment of an animal with hypoadrenocorticism?

A

Young, although can range from 2m-geriatric
Poodles over represented
Conflicting evidence but possibly more in females

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8
Q

What are possible clinical signs of hypoadrenocorticism?

A 
PUPD
V+
D+
bradycardia
could be shocky, with hypoglycaemia possible
Shivering/ stiffness
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9
Q

What are the bloods signs of animal with low glucocorticoid

A 
Haematology:
Regenerative or non regenerative anaemia
Eosinophilia (or at lease not 0 in a sick animal)
Lymphocytosis
No stress leukogram
Neutropaenia

Biochem: (due to effects on liver) mild hypoglycaemia
Mild hypocholesterolaemia
Mild hypoalbuminaemia

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10
Q

What are the bloods signs of low mineralocorticoid (aldosterone)

A 
Haematology - no effects
Biochem - high K+
low Na+
Low Cl-
Pre-renal azotaemia with low USG
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11
Q

When can hypoadrenocorticism cause anaemia?

A

Steroids are needed for gut integrity - can get ulcers that bleed

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12
Q

How can cushings affect the PCV?

A

High end normal

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13
Q

How is looking at the Na:K ratio helpful in hypoadrenocorticism?

A

<23:1 - highly likely has typical hypoadrenocorticism

Atypical will not show abnormality

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14
Q

How many hypoadrenocorticism cases will not have electrolyte changes when bloods are performed?

A

4-24%

Those with atypical can easily go on to get typical

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15
Q

What is the use of basal cortisol for testing for hypoadrenocorticism?

A

If levels are <55nmol, or within the equivocal zone, then need to perform ACTH test.
If higher than equivocal zone, can rule it out
Some very sick animals can have low cortisol so does not provide diagnosis, is just a first step

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16
Q

What is the gold standard test for hypoadrenocorticism?

A

ACTH stimulation test
Do not give IM if any concern animal is dehydrated
All recent steroids except v recent dexamethasone cause interference (within 4 weeks)
Does not differentiate between pituitary/ hypothalamic/ adrenal disease (although most cases have adrenal disease)

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17
Q

What is an endogenous plasma ACTH concentration test for?

A

Differentiating adrenal v pituitary/hypothalamic disease
Needs v careful/ intricate handling!
Can be affected by steroid
ACTH would be high in adrenal disease, low in the others

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18
Q

Outline the aldosterone test

A

Can be run on the ACTH response test (post sample)
If aldosterone is poorly stimulated on a post sample, then the patient is likely to progress to typical disease if not already

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19
Q

What would a normal aldosterone test suggest?

A

Either atypical hypoadrenocorticism or pituitary disease causing glucocorticoid deficiency

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20
Q

What causes hypoadrenocorticism in cats?

N.B just never do IM ACTH in cats

A

Still mostly immune like dogs, however:
Adrenal - haemorrhage, lymphoma, infectious disease
Pituitary/ hypothalamic - neoplasia

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21
Q

What causes granulomatous colitis and who is suscpetible

A

Mostly boxers under 4

has been seen in Frenchies/ a cat

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22
Q

What are the signs of granulomatous colitis?

A

LI signs, but with very severe haematochezia

In some can progress to cachexia, but PE normally fairly unremarkable

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23
Q

How do you investigate granulomatous colitis?

A

Have to follow the normal investigation profile to rue out other causes. If these are unrewarding, proceed to final step of colonic biopsies (minimum 10 samples)

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24
Q

What do you need to assess on colonic biopsies for granulomatous colitis?

A

PAS staining
FISH analysis (fluorescent staining of bacteria in mucosa)
Culture and sensitivity
Can get false positives and negatives, but negative more likely

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25
Q

Why is C and S so important with granulomatous colitis?

A

As up to 50% of cases are now resistant to the standard treatment of 6-8 weeks enrofloxacin with 2 weeks given beyond clinical cure
If you get a negative result but suspect it is a false negative, trial treatment anyway

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26
Q

Describe Tritrichomonas foetus

A

Small single celled protozoa

Likes warm moist O2 deprived areas (cat colon)

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27
Q

Who tends to be infected with tritrichomonas?

A

<1 year old purebreed cats in multicat households
Around 12% co-infected with giardia
often more than one cat infected, they are normally fairly well except for their terribe LI d+

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28
Q

How can you increase your chances of getting a positive sample with tritrichomonas?

A

MUST BE FRESH
No prior treatment
Must be a d+ sample
Cannot be contaminated with cat litter etc

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29
Q

What methods of tritrichomonas diagnosis are there?

A

All faecal analysis:
Light microscopy of direct smear - low sensitivity/ specificity as hard to always see and can be confused with giardia
Protozoal culture - must be done in house, still only approx 55% sensitive
PCR - most sensitive but still relies on it having been present in the faecal sample to being with

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30
Q

If not treated, what happens to tritrichomonas infected cats?

A

Most become tolerant with 6m to 2 yrs

50% may shed still though

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31
Q

How do you treat tritrichomonas?

A 
Ronidazole
Can get neurotoxicity
Can get treatment failure in 1/3
Also need to ensure Tx of co-infections
Need to ensure household management as very contagious
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32
Q

Describe parvovirus

A

Only been around 40 yrs
Small non enveloped DNA virus
Three different types - A, B, C, have emerged with time, seemingly becoming more pathogenic

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33
Q

Who tends to get infected with parvo?

A 
Unvax/ newly vaccinated
Black and tan breeds possibly increased risk
Normally those 4-12 weeks of age
Adult mortality - 1-2%
Young mortalitiy - 70%
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34
Q

How does parvo spread? How does it behave?

A

Oronasal transmission
Incubation 3-7d, no signs during this
Viraemia within 1-5d of infection - fever anorexia, lethargy
Once virus within the mucosa of the SI, causes necrosis of the crypts - V+/D+/Abdo pain
From there can get dehyration, hypovolaemia, bacterial translocation, hypovolaemic or septic shock

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35
Q

What are possible complications of parvo?

A

Intussusception
Aspiration or parvo pneumonia
Sepsis

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36
Q

How can you diagnose parvo?

A

SNAP test - bedside ELISA - detects antigen in the faeces
Can get false negatives if low numbers of antigen in the gut or lots of AB present
Can get false positives if has been vax with a modifeid live vax within 1-3 weeks
PCR - tests for viral DNA
Increased sensitivity and specificity than SNAP
Useful in kennels with d+ outbreaks and you’re checking for low shedding carriers

N.B would need virus characterisation to differentiate field and vaccine strain.

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37
Q

What does chronic enteropathy mean?

A

Animal with chronic GI signs
Can be used for animal where GI inflammation is suspected but not definitely documented
Does not infer the treatment needed

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38
Q

What does inflammatory bowel disease mean?

A

Typically means diet and AB trials have failed
Biopsies have been done
Immunosuppresant will be needed

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39
Q

What are the categories of chronic enteropathy?

A

Food responsive
Antibiotic responsive
Immunosuppressive responsive
Non responsive

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40
Q

Does histology differentiate between the types of chronic enteropathy?

A

No - this is why in stable patients, definitely worth doing diet and AB trials before endoscopy

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41
Q

What are negative prognostic indicators for chronic enteropathies?

A

Hypoalbuminaemia
Hypocobalaminaemia
High Canine IBD indexx
Hypovitaminosis D

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42
Q

How may food responsive and immunosuppresant responsive enteropathies differ?

A

Food tend to be younger, and more frequently are large intestinal

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43
Q

Is there a difference between easily digestible and hydrolysed diet trials?

A

Yes - hydrolysed much more effective

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44
Q

Is there a difference between novel protein and hydrolysed diet responses?

A

Not proven

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45
Q

How long do food responsive patients take to improve?

A

Normally 7 days, up to 14d.

N.B many dogs can have their diet changed again after 12 weeks but this is trial and error.

46
Q

How can food changes affect the intestines?

A

Within 6 weeks there are ultrasonic improvements

47
Q

What are the main histological changes in dogs with PLEs?

A

Lymphangiectasia
Inflammation
Neoplasia
Crypt abscess

48
Q

Should you do diet trial alone for dogs with PLE?

A

Not really recommended
Can trial in happy healthy dogs for up to a week.
If no improvment/ deteriorating during this time then proceed to further Ix/ Tx

49
Q

What antibiotics can be used to assess response and when should you try them?

A

After diet trial has failed/ only partial response

Metronidazole/ oxytet/ tylosin

50
Q

Which dogs are more likely to respond to ABs for CE?

if there is no response within 2 weeks, re-check and re-evaluate

A

young dogs

GSDs/ other large breeds

51
Q

How effecting is AB treatment for CE dogs?

A

For those that respond, there is a very high relapse rate

Often recommend a 6-8 week course initially. Still get relapses extremely frequently within 6-12m

52
Q

What is the most common histological diagnosis for CE dogs?

A

Lymphoplasmacytic

53
Q

What modality can be used to assess for bacteria in tissue?

A

FISH - Fluorescence in situ hybridisation

54
Q

Compare treatment styles in PLE dogs cf healthy CE dogs

A

PLE - step down (immunosuppresant, diet, +/- ABs, drop as response seen)
Healthy - step up (diet, then AB, then drugs)

55
Q

How effective is cyclosporin for CE?

A

Sometimes effective
can be useful as a rescue drug is steroids not effective
May still see relapses

56
Q

How effective is steroid for CE?

A

Often effective but can get no response and can get relapses

57
Q

What is the prognosis for PLE dogs with different underlying disease processes?

A

Large cell lymphoma the worst (<100d)
Small cell lymphoma better (<500d)
CE or lymphangiectasia had the best (>1000d)

58
Q

Why can it be hard to diagnosis small cell lymphoma in dogs?

A

A positive test for clonality (PARR +ve) is suggestive of neoplasia
However, clonality can sometimes just be present in inflammatory disease
Some cases very suggestive will be PARR -ve
PARR sensitivity depends on the methodology used

59
Q

What is the drug of choice for cats with small cell lymphoma?

A

Chlorambucil

60
Q

How many dogs with CE are non responsive

A

Between 15-40%, long term responsive pets tend to be only the food related ones

61
Q

What are possible future areas of treatment

A

motility issues are likely under diagnosed
Some promise with the use of pre and probiotics and
Faecal transplants
mesenchymal stem cells
Vitamin D deficiency treatment

62
Q

What are known risk factors for feline GI lymphoma?

A

FIV FeLV
Smoking household
Possibly helicobacter?

63
Q

Compare treatment for lymphocytic lymphoma and lymphoblastic lymphoma

A

Lymphocytic - pred and chlorambucil, normally live for >2 years
Lymphoblastic - Injectable chemotherapy, COP/ CHOP, MST 6-7m

64
Q

When is BM aspiration appropriate?

A

FeLV associated disease
Cytopaenia
Circulating malignant lymphocytes

65
Q

How does US appearance differ with lymphcytic lymphoma and lymphoblastic?

A

Lymphocytic - same as IBD - normal or increased intestinal walk thickening with preservation of wall layers, although more likely to be lymphoma than IBD if the muscularis layer is thickened
Lymphoblastic - disrption of normal wall layering, reduced wall echogenicity, localised hypomotility, abdominal lymphadenomegaly, mass lesions

66
Q

How useful is FNAing mesenteric LNs that are enlarged for comfirmation of lymphocytic lymphoma?

A

Questionable - proceed with caution

67
Q

Histologically, where is cellular infiltrate in IBD and lymphoma?

A

IBD - mucosa
Lymphoma - starts in mucosa, often irregularly distributed, freqent progression to submucosal and transmural infiltration

N.B lyphoma is not associated with the oedema and mucosal inflammation associated with IBD

68
Q

What is epitheliotrophic lymphoma?

A

Subset of lymphocytic lymphoma

Characterised by the infiltration of malignant T cells into the mucosal epithelium

69
Q

How is immunohistochemistry useful?

A

Lymphoma cases should have a monoclonal population of B or T lymphocytes

70
Q

How can chlorambucil be given?

A

Either EOD or large dose once every 3 weeks

71
Q

What can be used as a rescue therapy for lymphocytic lymphoma after pred + chlorambucil has failed?

A

Cyclophosphamide, although many cats do not relapse.

72
Q

What are the most consistent prognostic indicators for lymphoblastic lymphoma?

A
  1. Those with complete remission have much longer survival times
    Others: stage 1 (single lymph site) or 2 (regional lymphadenopathy or resectable GI mass) better than other stages
    FeLV = poorer prognosis
73
Q

How should you consider diet for GI lymphoma cases?

A

Highly digestible and palatable
hydrolysed if concurrent IBD
supplement cobalamin if any concern

74
Q

What may trigger IBD?

A

Overly aggressive T cell responses
Genetic defects in regulating microbial killing, mucosal barrier function, or immune responses
Environmental factors
Disbalances in expression of innate immunity receptors (toll-like receptors)

75
Q

Which cats are more likely to get IBD

A

Normally middle aged to older

Breed predispositions - asian breeds

76
Q

What should be considered if there are moderate to large amounts of eosinophils in intestinal biopsies?

A

Possible parasite involvement or dietary intolerance

77
Q

What is lymphoplasmacytic enteritis?

A

The most common histological form of feline IBD

HOWEVER can be associated with parasites, dietary sensitivity, hyperthyroidism

78
Q

What is eosinophilic enterocolitis?

A

Marked mucosal infiltration with eosinophils in lamina propria
May be assocaition with hypereosinophilic syndrome in cats

79
Q

What types of neutrophilic enteropathies are there?

A

Primarily seen with erosive mucosal lesions
Suppurative IBD can occur in young cats but very rare - normally LI signs
May be associated with enteropathogenic bacteria incl clostridium and campy

80
Q

Where is the most commonly affected GI place for lesions?

A

Ileum

81
Q

Why are cats at more risk of pancreatitis/ cholangitis?

A

Pancreatic duct enters the common bile duct before it opens into the proximal duodenum
This allows for reflux of GI bacteria (mostly e.coli) or intestinal contents into the pancreatic and biliary system
Small intestinal inflammation (i.e. IBD) may also ascend in the same way

82
Q

What is the most successful treatment for cats with IBD?

A

Diet trial (50% response)

83
Q

What are good adjunctive therapies for IBD?

A

Cobalamin supplementation
Soluble fibre if colitis present. e.g. psyllium
Probioitcs

84
Q

Why is fibre good in cats with colitis?

A

Soluble fibre acts as a prebiotic substrate for the production of beneficial short chain fatty acids which promote colonic healing

85
Q

What do prebiotics do in cats with GI disorders?

A

Stimulate growth of protective bacteria
Enhance production of short chain fatty acids
Improve intestinal barrier function
Decrease pro inflammatory cytokines

86
Q

What do probiotics do in cats with GI disorders?

A

Alter the intestinal flora to suppress the pathogenic bacteria
Improve intestinal barrier function
Stimulate production of antimicrobial peptides
Decrease pro-inflammatory cytokines

87
Q

What is the meaning of low albumin in a patient with diarrhoea?

A

negative prognostic indicator
Agressive early treatment is important as this may potentially decrease mortality rates in severely ill animals.
Increases in albumin can show treatment success, even when d+ still happening - measure every 2-3 weeks
PLE is not really a syndrome seen in cats, but there is some evidence to show cats with IBD and low albumin likely also have pancreatitis

88
Q

How is cobalamin absorbed?

N.B dogs with low cobalamin have a higher risk of euthanasia, which can be reversed if cobalamin is supplemented

A

Receptor mediated in the ileum
Also involves intrinsic factor, which is mostly produced in the pancreas - therefore pets with EPI normally need cobalamin

89
Q

How is cPLi concentration associated with prognosis for IBD dogs?

A

IBD dogs with high cPLi were often older and had a worse prognosis. There is a suggestion that there is a subset of patients with IBD may also have immune mediated pancreatitis, and treatment should be aimed in a way that can target both (e.g. cyclosporine)

90
Q

What is faecal a-1 proteinase inhibitor?

A

Used as a test for PLE when albumin not yet low, not widely available

91
Q

How can PARR be useful in investigating intestinal disease?

A

= polymerase chain reaction for antigen receptor rearrangements
Used to detect the presence of a clonally expanded population of lymphocytes

92
Q

What are pANCA?

A

Perinuclear antineutrophilic cytoplasmic antibodies
Serum autoantibodies, similar to ANA, but more specific for intestinal disease.
Can also be high in pets with other auto-immune diseases

93
Q

What are the most common causes of acute colitis?

A

Dietary indiscretion
Whipworm infestation (trichuris vulpis)
Clostridium difficile or perfringens infection

94
Q

What are the two types of chronic idiopathic large bow diarrhoea in dogs?

A

Fibre responsive

Stress associated

95
Q

What are the diagnostic criteria for chronic idiopathic large bow diarrhoea in dogs?

A 
Chronic or chronic recurring d+ more than 3-4 weeks
LI d+
No abnormal findings on PE or bloods
No or minimal changes on colonoscopy
Unremarkable histopathology
(no identifiable cause)
96
Q 
What are the following breeds predisposed to for intestinal disease?
Irish Setter
GSD
Basenji
Boxer/ Frenchie
A

Irish Setter - gluten sensitive enteropathy
GSD - ARD
Basenji - immunoproliferative small intestinal disease
Boxer/ Frenchie - granulmatous colitis

97
Q 
What are the following breeds predisposed to for intestinal disease?
Lundehund
Rotties
Soft-coated wheaten terrier
Sharpei
A

Lundehund - PLE, lymphangiectasia, crypt lesions, adenocarcinoma, atrophic gastritis
Rotties - PLE, lymphangiectasia, crypt lesions
Soft-coated wheaten terrier - PLE, PLN
Sharpei - cobalamin deficiency

98
Q

How can lymphatic abnormalities look grossly?

A

small white granules on the intestinal mesentry

This is due to lipogranulomatous infammation

99
Q

Apart from protein, what else is lost with lymphangiectasia?

A

Malabsorption of long chain fatty acids

100
Q

What is the mainstay of Tx for lymphangiectasia?

A

Supplement medium chain tryglycerides (e.g. coconut oil)
Pred - try to avoid immunosuppression as there is a higher risk of sepsis in these patients, therefore 1mg/kg
Consider AB trial at the same imes to prevent bacterial translocation
Can consider antithrombotic

101
Q

What are the main things lost with PLE?

A

Albumin
Globulin
Fibrinogen
Antithrombotics

102
Q

What are the possible causes of PLE?

A 
Inflammation (IBD)
---lymphocytic. plasmacytic/ eosinophilic/ granulomatous enteritis
Neoplasia
---lymphosarcoma, adenocarcinoma
Infection
---Parvo, salmonella, pythium, histoplasma
Lymphangiectasia
---Primary or secondary
Endoparasites
---Giardia, ancyclostoma, uncinaria (pups!)
Anatomical
---intussuscpetion, chronic obstruction
103
Q

What can cause lymphangiectasia?

A

infiltration or inflammation of the lymphatic system either by
Obstruction of the thoracic duct
RHS CHF
lymphoma

104
Q

When is it not a panhypoproteinaemia with PLE?

A

Basenjis - have a proliferative disease that leads to excess immunoglobulin production
Can be a rise in globulin with lymphoma (would have a monoclonal spike if protein electrophoresis is performed

105
Q

How are cholesterol levels different in PLE and PLN

A

low in PLE, not really in PLN

106
Q

What other biochemical abnormalities are there normally with PLE?

A

Low Mg

low Ca

107
Q

outline the use of faecal analysis with PLN

A

if campylobacter found, not always pathogenic/ the cause, but should be treated as it may be, and it may be zoonotic
Really important with pups to do faecal analysis as uncinaria can cause gut damage which leads to PLE

108
Q

Outline general treatment for PLE

A

Consider the use of colloids
Use of prophylactic antithrombotic medication
Movement of recumbent patients
use of a diurectic -spironolactone drug of choice as it is K+ sparing and slower acting reducing the chance of dehydration
Ensure nutrition - and consider Vit D and E supplementation

109
Q

In which animals do you and do you not see ARD?

A

Do - Young large breeds dogs esp GSD

Don’t - cats, doesn’t really start in older dogs, small dogs

110
Q

What is the appetite normally like in ARD dogs?

A

normally polyphagic/ coprophagic

111
Q

Outline treatment regimes for ARD?

A

Normally a 4-6 week course of ABs, should see a response within 2 weeks
many relapse days to months after treatment, many can be maintained long term on a much lower dose than the original

Small Animal Medicine Module B (13 decks)

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