Approach to diarrhoea Flashcards

(111 cards)

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
Why is C and S so important with granulomatous colitis?
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
26
Describe Tritrichomonas foetus
Small single celled protozoa | Likes warm moist O2 deprived areas (cat colon)
27
Who tends to be infected with tritrichomonas?
<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+
28
How can you increase your chances of getting a positive sample with tritrichomonas?
MUST BE FRESH No prior treatment Must be a d+ sample Cannot be contaminated with cat litter etc
29
What methods of tritrichomonas diagnosis are there?
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
30
If not treated, what happens to tritrichomonas infected cats?
Most become tolerant with 6m to 2 yrs | 50% may shed still though
31
How do you treat tritrichomonas?
``` 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 ```
32
Describe parvovirus
Only been around 40 yrs Small non enveloped DNA virus Three different types - A, B, C, have emerged with time, seemingly becoming more pathogenic
33
Who tends to get infected with parvo?
``` Unvax/ newly vaccinated Black and tan breeds possibly increased risk Normally those 4-12 weeks of age Adult mortality - 1-2% Young mortalitiy - 70% ```
34
How does parvo spread? How does it behave?
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
35
What are possible complications of parvo?
Intussusception Aspiration or parvo pneumonia Sepsis
36
How can you diagnose parvo?
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.
37
What does chronic enteropathy mean?
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
38
What does inflammatory bowel disease mean?
Typically means diet and AB trials have failed Biopsies have been done Immunosuppresant will be needed
39
What are the categories of chronic enteropathy?
Food responsive Antibiotic responsive Immunosuppressive responsive Non responsive
40
Does histology differentiate between the types of chronic enteropathy?
No - this is why in stable patients, definitely worth doing diet and AB trials before endoscopy
41
What are negative prognostic indicators for chronic enteropathies?
Hypoalbuminaemia Hypocobalaminaemia High Canine IBD indexx Hypovitaminosis D
42
How may food responsive and immunosuppresant responsive enteropathies differ?
Food tend to be younger, and more frequently are large intestinal
43
Is there a difference between easily digestible and hydrolysed diet trials?
Yes - hydrolysed much more effective
44
Is there a difference between novel protein and hydrolysed diet responses?
Not proven
45
How long do food responsive patients take to improve?
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
How can food changes affect the intestines?
Within 6 weeks there are ultrasonic improvements
47
What are the main histological changes in dogs with PLEs?
Lymphangiectasia Inflammation Neoplasia Crypt abscess
48
Should you do diet trial alone for dogs with PLE?
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
What antibiotics can be used to assess response and when should you try them?
After diet trial has failed/ only partial response | Metronidazole/ oxytet/ tylosin
50
Which dogs are more likely to respond to ABs for CE? **if there is no response within 2 weeks, re-check and re-evaluate**
young dogs | GSDs/ other large breeds
51
How effecting is AB treatment for CE dogs?
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
What is the most common histological diagnosis for CE dogs?
Lymphoplasmacytic
53
What modality can be used to assess for bacteria in tissue?
FISH - Fluorescence in situ hybridisation
54
Compare treatment styles in PLE dogs cf healthy CE dogs
PLE - step down (immunosuppresant, diet, +/- ABs, drop as response seen) Healthy - step up (diet, then AB, then drugs)
55
How effective is cyclosporin for CE?
Sometimes effective can be useful as a rescue drug is steroids not effective May still see relapses
56
How effective is steroid for CE?
Often effective but can get no response and can get relapses
57
What is the prognosis for PLE dogs with different underlying disease processes?
Large cell lymphoma the worst (<100d) Small cell lymphoma better (<500d) CE or lymphangiectasia had the best (>1000d)
58
Why can it be hard to diagnosis small cell lymphoma in dogs?
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
What is the drug of choice for cats with small cell lymphoma?
Chlorambucil
60
How many dogs with CE are non responsive
Between 15-40%, long term responsive pets tend to be only the food related ones
61
What are possible future areas of treatment
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
What are known risk factors for feline GI lymphoma?
FIV FeLV Smoking household Possibly helicobacter?
63
Compare treatment for lymphocytic lymphoma and lymphoblastic lymphoma
Lymphocytic - pred and chlorambucil, normally live for >2 years Lymphoblastic - Injectable chemotherapy, COP/ CHOP, MST 6-7m
64
When is BM aspiration appropriate?
FeLV associated disease Cytopaenia Circulating malignant lymphocytes
65
How does US appearance differ with lymphcytic lymphoma and lymphoblastic?
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
How useful is FNAing mesenteric LNs that are enlarged for comfirmation of lymphocytic lymphoma?
Questionable - proceed with caution
67
Histologically, where is cellular infiltrate in IBD and lymphoma?
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
What is epitheliotrophic lymphoma?
Subset of lymphocytic lymphoma | Characterised by the infiltration of malignant T cells into the mucosal epithelium
69
How is immunohistochemistry useful?
Lymphoma cases should have a monoclonal population of B or T lymphocytes
70
How can chlorambucil be given?
Either EOD or large dose once every 3 weeks
71
What can be used as a rescue therapy for lymphocytic lymphoma after pred + chlorambucil has failed?
Cyclophosphamide, although many cats do not relapse.
72
What are the most consistent prognostic indicators for lymphoblastic lymphoma?
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
How should you consider diet for GI lymphoma cases?
Highly digestible and palatable hydrolysed if concurrent IBD supplement cobalamin if any concern
74
What may trigger IBD?
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
Which cats are more likely to get IBD
Normally middle aged to older | Breed predispositions - asian breeds
76
What should be considered if there are moderate to large amounts of eosinophils in intestinal biopsies?
Possible parasite involvement or dietary intolerance
77
What is lymphoplasmacytic enteritis?
The most common histological form of feline IBD | HOWEVER can be associated with parasites, dietary sensitivity, hyperthyroidism
78
What is eosinophilic enterocolitis?
Marked mucosal infiltration with eosinophils in lamina propria May be assocaition with hypereosinophilic syndrome in cats
79
What types of neutrophilic enteropathies are there?
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
Where is the most commonly affected GI place for lesions?
Ileum
81
Why are cats at more risk of pancreatitis/ cholangitis?
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
What is the most successful treatment for cats with IBD?
Diet trial (50% response)
83
What are good adjunctive therapies for IBD?
Cobalamin supplementation Soluble fibre if colitis present. e.g. psyllium Probioitcs
84
Why is fibre good in cats with colitis?
Soluble fibre acts as a prebiotic substrate for the production of beneficial short chain fatty acids which promote colonic healing
85
What do prebiotics do in cats with GI disorders?
Stimulate growth of protective bacteria Enhance production of short chain fatty acids Improve intestinal barrier function Decrease pro inflammatory cytokines
86
What do probiotics do in cats with GI disorders?
Alter the intestinal flora to suppress the pathogenic bacteria Improve intestinal barrier function Stimulate production of antimicrobial peptides Decrease pro-inflammatory cytokines
87
What is the meaning of low albumin in a patient with diarrhoea?
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
How is cobalamin absorbed? N.B dogs with low cobalamin have a higher risk of euthanasia, which can be reversed if cobalamin is supplemented
Receptor mediated in the ileum Also involves intrinsic factor, which is mostly produced in the pancreas - therefore pets with EPI normally need cobalamin
89
How is cPLi concentration associated with prognosis for IBD dogs?
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
What is faecal a-1 proteinase inhibitor?
Used as a test for PLE when albumin not yet low, not widely available
91
How can PARR be useful in investigating intestinal disease?
= polymerase chain reaction for antigen receptor rearrangements Used to detect the presence of a clonally expanded population of lymphocytes
92
What are pANCA?
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
What are the most common causes of acute colitis?
Dietary indiscretion Whipworm infestation (trichuris vulpis) Clostridium difficile or perfringens infection
94
What are the two types of chronic idiopathic large bow diarrhoea in dogs?
Fibre responsive | Stress associated
95
What are the diagnostic criteria for chronic idiopathic large bow diarrhoea in dogs?
``` 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
``` What are the following breeds predisposed to for intestinal disease? Irish Setter GSD Basenji Boxer/ Frenchie ```
Irish Setter - gluten sensitive enteropathy GSD - ARD Basenji - immunoproliferative small intestinal disease Boxer/ Frenchie - granulmatous colitis
97
``` What are the following breeds predisposed to for intestinal disease? Lundehund Rotties Soft-coated wheaten terrier Sharpei ```
Lundehund - PLE, lymphangiectasia, crypt lesions, adenocarcinoma, atrophic gastritis Rotties - PLE, lymphangiectasia, crypt lesions Soft-coated wheaten terrier - PLE, PLN Sharpei - cobalamin deficiency
98
How can lymphatic abnormalities look grossly?
small white granules on the intestinal mesentry | This is due to lipogranulomatous infammation
99
Apart from protein, what else is lost with lymphangiectasia?
Malabsorption of long chain fatty acids
100
What is the mainstay of Tx for lymphangiectasia?
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
What are the main things lost with PLE?
Albumin Globulin Fibrinogen Antithrombotics
102
What are the possible causes of PLE?
``` 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
What can cause lymphangiectasia?
infiltration or inflammation of the lymphatic system either by Obstruction of the thoracic duct RHS CHF lymphoma
104
When is it not a panhypoproteinaemia with PLE?
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
How are cholesterol levels different in PLE and PLN
low in PLE, not really in PLN
106
What other biochemical abnormalities are there normally with PLE?
Low Mg | low Ca
107
outline the use of faecal analysis with PLN
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
Outline general treatment for PLE
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
In which animals do you and do you not see ARD?
Do - Young large breeds dogs esp GSD | Don't - cats, doesn't really start in older dogs, small dogs
110
What is the appetite normally like in ARD dogs?
normally polyphagic/ coprophagic
111
Outline treatment regimes for ARD?
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