GIT, pancreas, liver Flashcards

1
Q

What is the most common viral agent identified in cats with feline gingivostomatitis?

A

Feline calicivirus

Nakanishu JFMS 2019

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2
Q

What is the most common oral bacteria in healthy cats?

In cats with feline gingivostomatitis?

A

Healthy - pasteurella multocida
FGS - Enterococcus faecali and aenaerobic bacteria

Nakanishu JVIM 2019

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3
Q

What concurrent disease is frequently seen with feline gingivostomatitis?
What areas does it affect and in what percentage of cases?

A

Oesophagitis
Proximal - 75%
distal - 90%

Kouki JVIm 2017

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4
Q

Do cats with feline gingivostomatitis and concurrent oesophagitis frequently have GIT clinical signs?

A

No - 0/58

Kouki JVIM 2017

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5
Q

What is the preferred method for assessing dysphagia?

A

videofluoroscopic swallowing study utilizing a normal physiological feeding position.

Harris JVIM 2017

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6
Q

Is gastric reflux always an abnormal finding on physiological feeding position videofluoroscopic swallowing studies?

A

No - can be seen in healthy dogs

Harris JVIM 2017

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7
Q

Is radiation effective for the treatment of sialocele in dogs? If so what is the minimum dose recommended?

A

Yes with 54% achieving complete remission adn 45% achieving partial remission, including 3 dogs with repeat radiation that achieved remission after the second round of radiation.
16 or 20Gy in 4 Gy fractions.

Poirier JVIM 2018

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8
Q

What is the recurrence rate for sialocoels after initial surgery?

A

5-14%

Poirier JVIm 2018

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9
Q

Aside from strategic oral or gastrostomy tube feeding, are there any other options to minimize aspiration pneumonia in dogs with megaoesophagus?
What is the median survival time after implementing this?

A

at home suction of oesophageal contect via either oesophagostomy tube or per os.
median survival - 13.5 months. with none or infrequent aspiration events.

Manning JVIM 2016

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10
Q

What are possible complications of at home oesophageal suctioning in dogs with megaoesophagus?

A
  • obsturction of O-tube
  • skin infection at insertation site
  • oesophagitis

Manning JVIM 2016

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11
Q

What is the frequency of gastro-oesophageal reflux in cats undergoing anaesthesia?

A

33%

Gargia JVIM 2017

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12
Q

Does 2 doses of omeprazole 1,5-2mg/kg PO in 24h increase the gastric and oesophageal pH significantly?
If so, to what pH?
Does this affect serum gastrin concentrations?

A

Yes
Increases pH from 2.8 to 7.2
Does not affect serum gastrin concentrations

garcia JVIm 2017

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13
Q

In regards to canine oesophageal foreign bodies, what is:

  • the most common cause?
  • the most common region of lodgement?
  • the percentage that die in hospital
  • the risk factors associated with death in hospital?
  • percentage that have post removal oesophageal strictures?
A

Cause - bone (81%)
Region - distal oesophagus
% that die - 5% in hospital
Risk factors for death - surgery, declining surgery to try endoscopy again, and increased complications especially oeophgeal perforation, and post procedure oesophageal haemorrhage
Stricutres reportedin 2.1% of survivors.

Burton JVIM 2017

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14
Q

What are the benefits of indwelling oesophageal balloon dilation feeding tube for treatment of benign oesophageal stricture?

A
  • well tolerated
  • significant improvement in modified dysphagia score
  • reduced anaesthetic time.
  • more economical

Tan JVIM 2017

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15
Q

What complications were noted with indwelling oesophageal balloon dilation feeding tube for treatment of benign oesophageal stricture

A
  • swallowing and gagging during insufflation of the balloon
  • regurgitation
  • skin site infection
  • vomiting
  • dislodgement of the tube
  • repeat GA to replace tubes that had moved or been vomited up.

Tan JVIm 2017

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16
Q

How can dogs with lower oesophageal sphincter achalasia-like syndrome be diagnosed?

A

Via the video fluoroscopic swallowing study ising a free-feeding protocol.
Grbman JVIM 2018

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17
Q

What findings and in what percentage of cases with lower oesophageal achalasia-like syndrome in dogs were seen?

A
  • megaoesophagus - 73%
  • baseline oesophageal fluid line - 68%
  • “bird beak” 63%
  • acontractile oesophagus - 8/19
  • hypomotile oesophagus - 8/19
  • hypermotile oesophagus - 3/19

Grobman JVIM 2018

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18
Q

What treatment options may exist for dogs with function obstruction of the lower oesophageal sphincter?

A
  • injecting the LOS with botulinum toxin A
  • pneumatic LOS dilation
  • Surgical LOS myotomy

Grobman JVIm 2018

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19
Q

What proportion of cats with oesophageal feeding tube placement had complications?
what were the most common complications?
In which patients?

A

35% had complications

  • tube dislodgement (14.5%) and stomasite infections (12%) were most common complications
  • Patient on glucocorticoids, chemo or with discharge at the stoma site had an increased odds of stoma site infections

Breheny JVIM 2018

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20
Q

Cats with which diseases and an Otube had an increased odds of death?

A
  • lower weight
  • pancreatic disease
  • neoplastic
  • respiratory
  • urogenital
  • infectious diseases
    had increased odds of death

duration of time in place or discahrge with tube in were not associated with increased odds of death.

Breheny JVIM 2018

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21
Q

Idiopathic oesophageal dysmotility is most common in what type of dogs? of what age?

A
  • brachycephalic dogs
    > 1 year old

Eivers JVIM 2019

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22
Q

What feature of idiopathic oesophageal dysmotility are most commonly seen in brachycephalic dogs?

A
  • prolonged oesophageal transit time
  • decreased propagation of secondary peristaltic waves
  • GER
  • hiatial hernia

Eivers JVIM 2018

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23
Q

What is the oesophagostomy tube complication rate in dogs and cats?

A

44%

Nathanson JVIm 2019

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24
Q

what percentage develop infection and of these, what percentage required surgical debridement of O tube sites in dogs and cats?

A

Cats - 17% infection, 22% surgical debridement
Dogs - 13% infection, 35% surgical debridement

Nathanson JVIM 2019

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25
Q

What percentage of animals are euthanized as a result of complications associated with oesophgeal tube placement?

A

3%

Nathanson JVIM 2019

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26
Q

What treatments can clinically improve outcomes in dogs with lower oesophageal sphincter achalasia-like syndrome in dogs?

A
  • mechanical dialation with botulininum toxin A for 40 days
  • myotomy and fundoplication - effective in the long term

Grobman JVIm 2018

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27
Q

What percentage of dogs that underwent mechanical dilation and botulinum toxin A injection for lower oesophageal sphincter achalasia-like syndrome had improvement in clinical signs?
what improved?

A

100% had improvement

  • body weight increased 20%
  • Body condition score increased
  • regurgitation reduced by 80%

Grobman JVIM 2018

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28
Q

What percentage of dogs and cats undergoing PEG tube placement are likely to have complications?
Is this worse if they are receiving steroids?

A

74% developed some level of complication
78% of patients on steroids had a complication compared to 57% of those not on steroids
Severe complications were seen in 43% of patients with steroids vs 18% in those not

Aguiar JVIm 2016

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29
Q

What effects can sucralfate have in the management of stress-related mucosal disease in dogs (ex vivo model)?

A
  • applied at the time of injury or after injruty hastened recovery fo teh barrier function and restroed defects in gastric barrier function.

Hill JVIM 2017

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30
Q

What make sucralfate an attractive potential choice over PPis for stress-related mucosal damage in dogs?

A
  • binds to negatively charged subepithelial proteins exposed during mucosal injury => viscous layer that protects vascular bed
  • absorbs and reduces pepsin
  • stimulates mucus and bicarb synthesis and secretion
  • doesn’t alter pH and thus doesn’t impace bacterial colonization so has lower likelihood of clostridium difficile-associated diarrhoea
  • protective against nosicomal pneumonia in people.
  • doesn’t afffect cytochrom P450 enz

Hill JVIM 2017

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31
Q

What are the odds of that dogs receiving:
- aspirin
- prednisolone 2mg/kg
- both aspirin and prednisolone
will develop endoscopic mucosal lesions > or = 4?

A

Aspirin: no different from placebo

pred: 11.1 x higher
both: 31.5 x higher

Whittemore JVIM 2018

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32
Q

What is the most common type of hiatial hernia seen in cats?

At what age group?

A
Type 1 (85%)
> 3 years old at diagnosis (64%)

Phillips JVIM 2018

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33
Q

What are the survival times of cats with hiatial hernias treated:

  • medically
  • surgically?
A

Medically - 2559 days
Surgically 771 days

Phillips JVIM 2018

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34
Q

What is the % of cats with hiatial hernia that also have concurrent diseases?
What are common concurrent problems?

A

77% have concurrent diseases

  • GIT signs (96%)- vomiting, weight loss and anorexia
  • Respiratory disease (29%) - brachycephalic, chornic infections, aspriation pneumonia

Phillips JVIM 2018

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35
Q

Are ulcers common in dogs receiving clopidogrel? What about clopidogrel and pred?

A

not seen in dogs with clopdiogrel only
7 x higher odds of ulcers in dogs receiveing pred only or clopidogrel and pred.

Whittemore JVIM 2019

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36
Q

Do synbiotic + diet change have a more significant effect on CCECAI scores in dogs with chronic enteropathy, than diet change alone?

A

No.
No difference between treatment groups.

Schmitz JVIm 2015

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37
Q

Is serum Vitamin D (25(OH)D generally lower or higher in dogs with chronic enteropathy? What does this predict? what are the odds of this occurring in these dogs?

A
  • Lower isn dogs with CE
  • significant predictor of death
  • Odds ratio 1.08

Titmarsh JVIM 2015

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38
Q

What bacteria is associated with neutrophilic IBD in cats?
What other infectious agent has it been noted with in cats?
What layer of the intestine is it found in?
What does this suggest about this bacteria?

A
  • Campylobacter coli
  • tritrichomonas foetus
  • mucosa
  • C.coli either produces compound which stimulate neutrophils or induces intestinal cell to produce neutrophil chemoattractants

Maunder JVIM 2016

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39
Q

What is the clinical presentation of intestinal leiomyositis?
what is the median survival?

A

5.4 yr old + signs of intestinal pseudo-obstruction
vomiting
regurg
small bowel diarrhoea

median survival - 19 days post diagnosis

Zacuto JVIM 2016

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40
Q

What are the histopathological changes associated with intestinal leiomyositis?
In what layer?

A
  • mononuclear inflammation
  • myofiber degeneration and necrosis
  • fibrosis within regions of myofiber loss
  • in muscularis propria

Zacuto JVIM 2016

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41
Q

What is the suspected pathogenesis of canine intestinal leiomyositis?

A
  • idiopathic/autoimmune disorer possible associate with autoreactive T-cell response
    => affects contractilityof enteric smooth muscle cells because of infiltration of lymphocytes between functional myocytes => ileus.

Zacuto JVIM 2016

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42
Q

Is oral cobalamin effective at resolving hypocobalaminaemia in dogs with chronic enteropathy?

A

Yes

Toresson JVIM 2016

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43
Q

Does 6 weeks of parenteral cobalamin supplementation resolve the clinical signs of low Vit B12 in the short term?
in the long term?
Does it normalize cellular B12?

A
  • resolves clinical signs while receiving treatment
  • clinical signs returned after discontinuation of therapy
  • Serum and urinary MMA concentrations decreased during treatment (but did not normalize) and then increased with discontination of therapy, suggestive that despite normalization of serum cobalamin, cellular deficiency still persisted.

Kempf JVIM 2017

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44
Q

What can 99m Tc-labeled human serum Albumin Scintigraphy be used for?

A
  • Confirmation and possible localization of gastrointesitnal protien loss in dogs with hypoalbuminaemia.

Englemann JVIM 2017

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45
Q

What are the common causes of chronic diarrhoea in dogs and the percentage they occur in?

A

Primary enteropathy: 90%

  1. Inflammatory - 71%
    - dietary 66%
    - idiopathic -23%
    - antibiotic responsive 11%
  2. Infectious - 13%
  3. Neoplastic 4%
  4. Other - mechanical or systemic vasculitis

Secondary causes: 10%

  • Exocrine pancreas 6%
  • endocrine 2%
  • other: hepatic, renal, cardiac.

Volkmann JVIM 2017

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46
Q

what percentage of dogs with chronic diarrhoea had clinical remission?

A

87% had clinical remission.

Volkmann JVIM 2017

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47
Q

What findings were associated with a lack of recovery in dogs with chronic diarrhoea?

A
  • primary idiopathic or neoplastic disease
  • increased disease severity scores
  • anaemia
  • severe hypoalbuminaemia
  • severe hypocobalaminaemia

Volkmann JVIM 2017

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48
Q

What histopathological differences are noted between dogs with chronic enteropathy and normal albumin and dogs with chronic enteropathy and hypoalbuminaemia?

A

Does with hypoalbuminaremia are more likely to have (and to have higher scores in):

  • villous stunting,
  • epithelial injury,
  • crypt distension
  • lacteal dilation
  • intraepithealial lymphocytes
  • lamina propria neutrophils

Wennogle JVIm 2017

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49
Q

What is the sensitivity and specificity of the granulocyte immunofluorescence assay to detect food responsive disease?
What is this assay measuring?

A

Sensitivyt 0.61
Specificity 1.0

Measures anti-neutrophil cytoplasmic antibodies

Florey JVIM 2017

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50
Q

Dogs with IBD have what changes to the immunphenotype of peripheral blood lymphocytes?

A
  • reduced percentage of TCRyd+ T lymphocytes (also increased in intestinal intraepithelial lymphocytes)
  • reduced percentage CD21+ B cell

Galler JVIm 2017

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51
Q

What associated is seen between FRD, SRD and healthy dogs and:

  • peripheral eosinophilia
  • serum 3-BrY

And CCECAI and serum 3-BrY?

A

Peripheral eosinophilic: no difference
serum 3-BrY - higher in dogs with steroid responsive disease
CCECAI and serum 3-BrY - no correlation.

Sattasathuchana JVIM 2017

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52
Q

do cats with chronic intestinal disease have alterations to their whole blood taurine levels?
What is the proposed mechanism of this?

A
  • taurine was wnl but cats with large intestinal signs and chronic inflammatory enteropathy had significantly lower concentrations than those with small or mixed bowel signs.

2 proposed mechanism of decreased taurine:

  • reduced absorption of taurine conjugated bile acids due to ileal disease
  • increased production of taurine-conj bile acides due to increase cholecystokinin => increased elivery to the colon => inflam from alterations to the microbiota.

Kathrani JVIm 2017

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53
Q

What impact does using an animal protein-free diet have on the faecal microbiota of:

  • healthy dogs
  • dogs with food responsive enteropathy
A

Healthy dogs - no impact
Dogs with FRE - increased microbial richness but not return to normal (initially lower bacterial alpha diversity)

Bresciani JVIM 2018

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54
Q

what changes in faecal bile acids are noted in dogs with CE?

A

incresed % of primary bile acids in faeces compared to controls

Giaretta JVIM 2018

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55
Q

What changes in intestinal expression of apical sodium-dependent bile acid transporters are noted in dogs with CE?
What are the proposed mechanisms of this?

A
  • decreased expression in the ileum => negatively correlated with histopath score
    => down regulation of apical sodium-dependent bile acid transporter in ileium may be secondary to inflam, dysbiosis or faecal bile acid dysmetabolism.

Giaretta JVIM 2018

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56
Q

regarding eosinophils, what is the limitation of H&E staining on histopath samples?

A
  • doesn’t detect degranulated eosinophils.

Bastan JVIM 2018

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57
Q

What staining technique can improve detection of intact and degranulated eosinophils?
When is this useful?

A

use of monoclonal antiboides against the eosinophile granule protein (eosinophile peroxidase) then stained with H&E.

Useful for the detection of eosinophilic GIT disease and detecting degranulated eosinophils.

Bastan JVIM 2018

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58
Q

In dogs with eosiniphilic GIT disease, what area and layer of the gut has the highest number of eosinophils compared to the control group?

A
  • duodenum
  • lamina propria

Bastan JVIm 2018

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59
Q

In dogs with PLE, is serum tryptophan usually increased or decreased? What else does this correlate with?

A
  • decreased
  • correlates with serium albumin in dogs with PLE.

Kathrani JVIIM 2017

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60
Q

What are the limitations generally to consider regarding biomarkers?

A
  • Quantitative - can have grey zones
  • performance criteria including analytical performance (eg bedside tests) and preanalytical validation
  • Biological variability and evalation of the critical change value to ensure alterations are relevant and nor a relfecion of biological or analytical variability
  • diagnostic accuracy (sensitivity, specificity)
  • diagnostic performance - PPV/NPV

Helimann JVIM review 2018

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61
Q

What are the goals of an ideal biomarker?

A
  • assessment of the risk for disease development
  • diagnosis of disease
  • evaluation of organ function
  • determination of organ origin
  • assessment of disease severity
  • assessment of response to treatment
  • prediction of individual outcomes
  • monitoring
  • detection of disease flares

Helimann JVIM review 2018

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62
Q

What biomarkers are currently used for chronic enteropathies in dogs?

A

Functional biomarker:

  • serum cobalamin
  • serum Folate
  • Faecal a1PI

Inflammatory marker

  • serum CRP +/- faecal calprotectin
  • rest not widely available
  • likely useful for predicting response to treatment

Genomic marker
- not widely available

Helimann JVIM review 2018

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63
Q

Serum and faecal alpha-1PI:

  1. what is it?
  2. when to use?
  3. limitations?
A

Serum and faecal alpha-1PI:

  1. what is it:
    - protease inhibitor produced by the liver.
    - similar size to albumin thus lost in GI disease at similar rate but resists proteolysis
  2. when to use:
    - early detection of GI protein loss before hypoalbuminaemia/clinical signs
    - differentiate GI protein loss from hepatic hypoalbuminaemia
    - imporved accuracy in hypoalbuminaemic dogs
  3. limitations:
    - not very specific
    - day to day variation => average over 3 days.
    - <12m old
    - corticosteroids

Helimann JVIM review 2018

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64
Q
Serum cobalamin:
1. what is it?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy
A

Serum cobalamin:

  1. what is it:
    - water sol vitamien absorbed in ileum wiht intrinsic factor (from pancreas)
  2. when to use?
    - reflects distal SI malabsoprion, dysbiosis or both
    - hypoalbuminaemia => low B12 is a negative prognositic indicator
  3. limitations?
    - not specific for chronic inflammatory enteropathy (EPI)
    - normal doesn’t rule out CE

heilimann JVIM review 2018

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65
Q
Methylmalonic acid:
1. what is it?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy
A

Methylmalonic acid:

  1. what is it?
    - metabolite that increases with reduced intracellular Vit B12 => marker of cobalamin deficiency at a cellular level.
  2. when to use?
    - superior (urine and serum) to cobalamin concentrations
  3. limitations?
    - cost
    - techinical difficulty

Heilmann JVIm review 2018
- increased in serum with renal insufficiency

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66
Q
Folate:
1. what is it?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy
A

Folate:

  1. what is it:
    - absorbed by duodenum and jejunum
    - chronic malabsorption in prox SI -> reduced levels
  2. when to use?
    - monitoring supplementation
  3. limitations?
    - falsely increased with dysbiosis

Heilmann JVIm review 2018

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67
Q
Faecal IgA
1. what is it?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy
A

Faecal IgA:

  1. what is it?
    - reflects IgA synthesis and scretion by intestinal mucosa
  2. when to use?
    - insufficient data
    - may be decreased in German shepherds with chorinc GIT disease.
  3. limitations?
    - insufficient data

Heilmann jVIM 2018

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68
Q

Faecal and mucosal intestinal microbiome + FDI:
1. what changes?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy

A

Faecal and mucosal intestinal microbiome:

  1. what changes?
    - reduced faecalbacterium and fusobacteria
    - reduced abundance of spercific bacteria
    - increased FDI, especially dogs with immunosuppressent responsive enteropathys (sens 74%, spec 95%)
  2. when to use?
    - assessment for IRE
  3. limitations?
    - expense
    - not widely available

Heilmann JVIm review 2018

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69
Q
Metabolomic markers - serum:
1. what is it?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy
A
Metabolomic markers - serum:
1. what is it?
increased:
- 3-hydroxybuturate
- hexuronic acid
- ribose
- gluconic acid lactone
=> indicated oxidative stress and functional changes to the microbome 
  1. when to use?
    - monitor treatment and repsonse
  2. limitations?
    - exprnse
    - not widely available.

Heilmann JVIM review 2018

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70
Q
CRP
1. what is it?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy
A

CRP

  1. what is it?
    - positive, tye II acute phase protein expressed int he liver.
    - nonspecific
  2. when to use?
    - assess disease progression and response to treatment
    - must increase or decrease by at least 2.7 fold be consider clinically relevant
    - ditinguish anti-inflammatory or immunosuppressive treatment from those dogs responding to elimination diet or antibiotitic trial
    =» or = 9.1mg/L = IRE. sens 72%, spec 100%
    - high PPV
  3. limitations?
    - non specific marker on inflammation
    - high biological variability

HeilmannJVIM review 2018

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71
Q

Perinuclear anti-neutrophilic cytoplasmic antibodies:
1. what is it?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy

A

pANCA

  1. what is it:
    - serum autoantibodies again neutrophil granule components and suspected cross reactivity with GI bacterial antigen
  2. when to use?
    - higher in dogs with food responsive enteropathy (61-62%) vs IRE/NRE (0-37%) so may be useful to differentiate FRE from IRE/NRE.
    - PLE, PLN and soft coated wheaten terrier priot to the onset of hypoalbuminaemia
  3. limitations?
    - not specific for CE

Heilmann JVIM review 2018

72
Q
Serum 3 Bromotyrosine:
1. what is it?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy
A

Serum 3 bromotyrosine:

  1. what is it:
    - stabel metabolite of eosinophine peroxidase (released during activation and degranulation) => marker of eosinophilic inflam
  2. when to use?
    - higher in dogs req anti-inflamm or immunosuppressant treatment than FRE.
  3. limitations?
    no sensitivitiy and specificity yet so can’t be used as yet as a biomarker.

Heilmann JVIM review 2018

73
Q
N-methylhistamine
1. what is it?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy
A

N-methylhistamine:

  1. what is it
    - stable product of histamine metabolism => marker of MC activation and degranulation.
  2. when to use
    - correlates with severity of histological lesions but not number of MC or clinical signs
  3. limitations?
    no sens or spec data yet

Heilmann JVIM review 2018

74
Q

Faecal and serum calprotectin (S100A8/A9) protein complex.
1. what is it?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy

A

Faecal adn serum calproteictin (S100A8/A9) protein complex

  1. what is it:
    - part of calgranulin DAMP molecules from sites of inflammation.
    - release by macrophages and neutrophils + epith cells.
  2. when to use?
    faecal: good surrogate for disease severity in dogs with CE
    50ug/g = severe clinical disease
    - predict treatment response
    > or = 15.2 ug/g = partial or NRE
    < 15.2 ug/g + IRE with complete clinical remission
    sens 80%
    spec 75%
    PPV 77%
    NPV 82%
  3. limitations?
    - serum : not specific for GIT + corticosteroid interferance
    - faecal: can be increased in acute GIT inflam disease.
    not sure of the effect of GIT neoplasia.

Heilmann JVIM 2018

75
Q
Faecal and serum calgrnulin C (S100A12)
1. what is it?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy
A

Faecal and serum calgranulin C (S100A12)

  1. what is it:
    - DAMP molecule - target protein pattern recognition receptor RAGE
    - role in innate and acquired immune response
    - sensitive and specific marker of localized inflmmaotyr processes.
  2. when to use?
    - faecal - corticosteroids don’t affect
    - correlate with severity of clinical signs and endoscopic lesion but no histo.
    >490ng/g can distinguish IRE/NRE from FRE/ARE with sen of 64% and spec of 77%
    >2700ng/g distinguish NRE from partial response with sen of 100% and spec 76%
  3. limitations?
    Serum - increased with various inflammaotry disorders
    Faecal - increased wiht acute GI inflam conditions.
    - unsure of effect of GI neoplasia.

Heilmann JVIm review 2018

76
Q
sRAGE:
1. what is it?
2. when to use?
3. limitations?
in relation to chronic inflammatory enteropathy
A

sRAGE:

  1. what is it?
    - anti-inflam decoy receptor sequestering ligands of RAGE => non-specific
  2. when to use?
    - marker to assess response to treatment as sRAGe concentratiosn increase/normalize only in dogs achieving complete clinical remission.
  3. limitations?
    - decreased in dogs with CE but not correlated with clinical signs, histo or outcomes.
    - further studies needed

Heilmann JVIM review 2018

77
Q

What cytokines have been shown to commonly increase in dogs with chronic inflam enteropathy?

A

increased

  • IL-2
  • IL-6
  • TNF-alpha

Heilmann JVIM review 2018

78
Q

what genomic biomarkers have been identified in dogs with CE?

A
  1. Genetic polymorphisms:
    Genes encoding:
    - TLR4
    - TLR5 => hyperresponsive to flagellin
    - NOD2 - PRR fr peptioglycan gram + and gram -bacteria
    - NCF2 - found in boxers with granulomatous colitis

Altered gene expression:

  • increased mucosal expression of TLR2, TLR4 and TLR 9
  • Decreased expression of TLR5

Cellular biomarkers:
Decreased T-reg in duodenal biopsies and peripheral blood.

Heilmann JVIM review 2018

79
Q

Faecal calprotein + what test/s increased the ability to differentiate between SRE/IRE and FRE or ARE?

A

Faecal calprotectin and CCECAI or CRP.

Heilmann JVIM 2017

80
Q

what alterations in IL-1beta would be expected in the duodenal and colinc mucosa of dogs with IBD?

A
  • increased ratio of IL-1beta to IL-1 receptro antagonist in the colonic mucosa
  • IL-1 beta suppresses ocln expression in the colonc but not duodenal mucosa => intestinal barrier dysfuntion and increased inflammation

Ogawa JVIm 2017

81
Q

Is serum citrulline useful to predict optimal therapy for dogs with CE?

A

No.
not associated with efficacy of treatment or outcome in dogs with CE

Gerou-Ferriani JVIm 2017

82
Q

What factors are associated with an increased risk of death in dogs with PLE?

A
  • CCECAI: increased hazard of death by 22.9%
    CCECAI <8 + 256d longer survival than >8
  • Urea <7mmol/L = 279 day more survival than >7mmol/L

Kathrani JVIM 2018

83
Q

What are the suspected mechanisms of thromboembolism in dogs with PLE?

A
  • systemic inflam
  • altered Vit K absorption
  • loss of antithrombin III
  • hyperaggregation of platelets
  • hyperfibrinogenemia
  • vascular compromise

Crave JVIM review 2018

84
Q

What immunlogical defecits are potentially expected in dogs with PLE?

A
  • impared antibody function
  • B-cell depletion
  • diminished IgG, IgA and IgM
  • T-cell depletion, espeically CD4 T-cells

Craven JVIM 2018

85
Q

In what breeds in PLE most prevalent in?

A
  • Yorkshire terrier
  • Boerder Collie
  • German Shepherd
  • Rottie.

Craven JVIM 2018

86
Q

What are teh most common causes of PLE and their percentage of reported cases?

A
  • lymphoplasmacytic enteritis - 68%
  • lymphangectasia - 58%
  • inflammatory lymphatic disease (lymphangitis, lipogranuloma) - 8%
    Crypt disease 7%
    other types of IBD - granulomaouts, eosinophlic - rare.

Craven JVIM 2018

87
Q

What are the most common breeds affected by lymphangectasia?

A
  • soft coated wheaten terrier
  • Norwegian Lundhund
  • Yorkshire terrier
  • Maltese terrier
  • Shar Pei

Craven JVIM 2018

88
Q

What are the negative prognostic factors associated with PLE in dogs?

A
  • medium body weight
  • normal calprotectin and calgranulin
  • ascites
  • mild lacteal dilation
  • higher CIBDAI score and >5 at 1 month post diagnosis
  • increased Urea
  • lower albumin, TP an dcholesterol
  • treatment with immunosuppressants and low serum 25(OH)D conc at diagnosis.
  • intestinal vilus blunting
  • vomiting
  • monocytosis

Craven JVIM 2018

** however Salavati Schmitz JVIM 2019 found that no routine diagnostic test was predictive of clinical response, treatment group or outcome…

89
Q

what dietary components are recommended for dogs with PLEd?

A
  • Carbs 55-60%
  • fat 10-15%
    protein 25-30% with a highly digestible protein (>87%), but can increase to 35% if severely hypoaluminaemic patients don’t increase albumin within 3 day.
  • supplemntation with medium chain triglycerides (absorbed straight into portal circulation)
  • low chain fatty acids
  • fat sol vitamine - A, D E K
    +/- hypoallergenic/hydrolysed

Craven JVIM 2018

90
Q

What correlations are noted in patient with CE and low serum 25(OH)D concentations?

A
  • higher CECAI score
  • lower alpha tocopherol
  • lower cholestrol and albumin
  • higher CRP
  • negatively correlates with duodenal morphology and inflam histopath scores.

Wennogle JVIM 2019

91
Q

What is the median tim for serium albumin to reach >20g/L in dogs with PLE and hypoalbuminaemia?

A

13 days

Salavati Schmitz JVIM 2019

92
Q

what is the median survival times after starting treatment for dogs with PLE receving:

  • glucocorticoids
  • glucocorticoids and a second line immunosppressant
A

CS: 85 days
CS + second line - 166d

Salavati Schmitz JVIM 2019

93
Q

what results from contrast enhanced ultrasonography can be useful in the diagnosis of CE?

A
  • peak intensity and area under the curve are higher in the symptomatic CE group
  • peak intesnisty and clinical score were positively correlated in the CE group
  • no difference in perfusion parameters were detected between the lyphoma and CE groups or the lymphoma and control groups.

=> PI and AUC can detect duodenal inflammation and may potentially be useful for EXCLUDING a diagnosis of CE

Nisa JVIM 2018

94
Q

What changes in faecal short chain fatty acids may be seen with dogs with CE?

A
  • lower acetate
  • lower propionate
  • lower total short chain fatty acids

Minamoto JVIM 2019

95
Q

Based on endoscopic biopsies of clinically healthy cats, what abnormalities were detected?
What percentage of these cats actually developed clinical signs?

A
  • Small cell lymphoma (12/20)
    Emercing small cell lymphma (1/20)
    lymphocytic enteritis (6/20)
  • pseudoclonality (1/20)

Of which 3 developd signs, but the remaining 17/20 did not show signs after a median of >700 days.

Marsilio JVIm 2018

96
Q

Changes wot which IL are noted in german shepherds with CE?

A

IL-13 and IL-33 mRNA are underexpressed in the duodenal mucosa

Kathrani JVIM 2019

97
Q

What does the addition of lympatic endothelial cell immunohistochemical marker add to the diagnosis of chronic enteropathy?

A
  • identified presumptive proprial mucosal lymphangetasia in some dogs that were not recognosed with routine H&E staining - especially the ileum of hypoalbuminaemic dogs.

Wennogle JVIM 2019

98
Q

What changes with the microbiome and metabolome are expected in dogs with IRE?

A
  • DI increased and does not change over time (suggestive that subclinical disease ie dysboisis persists even with clinical improvement)
  • secondary faecal unconj bile acids were low and increased with treatment

Guard JVIM 2019

99
Q

What changes are expected to be seen in plasma amino acid profiles of dogs with CE?
what do these correlate with?

A

reduced:

  • methinone
  • proline
  • serine
  • tryptophan

Negative correlation between plasma seine and CCECAI

Tamura JVIM 2018

100
Q

What is the prevalence of clostridium perfringes netE and netF toxin genes in the faeces of dogs with :

  • AHDS
  • Parvo
  • healthy
A
  • AHDS - 48%
  • Parvo - 0%
  • healthy - 12%

Sindern JVIM 2018

101
Q

Regarding the treatment of CE, what is there grade 1 evidence to support the use of?

A
  1. therapeutic elimnation/hydroled GI diets in dogs and cat
  2. Tylosin for dogs with ARD (Weak)
  3. Pred for short term remission in dogs with IBD
  4. Budesonide for short term remission in dogs with IBD
  5. Combination probiotic + pred for short term remission in dogs with IBD.

Makielski JVIM review 2017

102
Q

What are the PPV and NPV of ultrasound in the SI of cats for predicting histological lesions.

A

duodenum PPV 82%, NPV 27%
Jejunum PPV 91%, NPV 27%
Ileum PPV 88%, NPV 40%

High PPV for mucosal lesions (72-100%) but low PPV for submucosal or muscularis lesions (18-57%)

Thus in a population with high disease prevalence, most cat with SI mucsal US lesion will have mucosal histological lesions, however submucosal or muscularis ultrasound lesion are not predictive of histological disease in these layers.

Guttin JVIM 2018

103
Q

Regarding EPI in cats, what are the:

  • median age
  • clinical signs
  • changes in B12 and folate
  • Treatment response
A

EPI in cats:

  • median age: 7 yes (>5y)
  • clinical signs:
  • weight loss
  • unformed faeces
  • poor coat
  • anorexia
  • increased appetite
  • lethargy
  • watery diarrhoea
  • vomiting
  • changes in B12 and folate
    B12 - low (77%)
    Folate - increased in ~50%, low in ~5%
  • Treatment response
    Good in 60%
    Poor in 13%
    Better with cobalamin supplementation and TLI <4 ug/L

Xenoulis JVIM 2016

104
Q

What changes to lipid soluble vitamins would be expected in dogs treated for EPI?

A

reduced:

  • retinol
  • alpha tocopherol
  • 25OHD in dogs with weight loss.

Barko JVIm 2018

105
Q

What is the agreement between SNAP and SPEC fPL?

A

<3.5 ug/l (negative) = 97% agreement
>5.4 ug/l (positive) = 90% agreement

Schnaub JFMS 2019

106
Q

What can contrast-enhanced ultrsound assessment of pancreatitis detect?

A
  • pancreatic perfusion changes characterized by a delayed peak with prolonged hyperechoic enhancement of the pancreas
  • duodenal perfusion chagnes secondary to pancreatitis (prolonged peak and AUC).

LIm JVIm 2015

107
Q

What changes may be seen with pancreatitis in dogs on CT?

A
  • enlarged
  • homogenous to heterogenous attenuating
  • contrast enhancing
  • ill defined borders
  • thrombi

Poorer outcomes with heterogenously enhancing pancreas.

Adrian JVIM 2015

French JVIM 2018:
- heterogenous contrast enhancement had increased portal vein thrombosis, high spec cPL, longer hospitalization and more relapses.

108
Q

Overall, what percentage of newly diagnosed DM cats have subclinical pancreatitis at the time of diagnosis?
Does this have any prognostic value?

A

60%
Cats achieving remission had a lower fPL at 2 months, but otherwise there was no significant difference.

Zini JVIM 2015

109
Q

Can BOHB be increased in dogs without DM?

A

Yes
Acute pancreatitis without DM>sick dogs with out pancreatitis > healthy fasted dogs

Hurrell JVIM 2016

110
Q

What is the sensitivity and specificity of FUJI DRI-Chem lipase for diagnosingacute pancreatitis?

A

Sens - 100%
Spec 89%

Yuki JVIM 2016

111
Q

What is the sensiticity and specificity of Spec fPL with histological pancreatitis?

A

Sens: 42%
Spec: 100%

Oppliger JVIM 2016

112
Q

What are the 4 factors associated with increased risk of short term death in the canine acute pancreatitis severity score?

A
  1. SIRS
  2. Coag disorders
  3. Increased creatinine
  4. ionised hypocalcaemia

Fabres JVIM 2018

113
Q

Using what optimal cut off for CAPS, what was the sensitivity and specificity?

A

CAPS cut off - 11
Sens: 895
Spec: 90%

Fabres JVIm 2018

114
Q

What is considered an abnormal feline gall bladder wall thickness on ultrasound?
and an abnormal common bile duct diameter suggestive of obstruction?

A

GB wall > 1mm
CBD >5mm

Griffin JFMS review 2019

115
Q

What is the sensitvity and specificity of an abnormal gall bladder ultrasound for bacterial cholangitis in cats and dogs?
what is the icidence of complications after cholecystocentesis?

A

Cats:
sens- 96%
Spec 49%
NPV 96% (normal GB = unlikely to have potive bile culture)

Dogs:
Sens: 81%
Spec: 31%
PPV 20%
NPV 88%

Complications - 3.4%

Policelli Smith, JVIM 2017

116
Q

How can contrast enhanced ultrasonography differentiate between inflam and non-inflamm hepatic disorders in dogs?

A

Washout ratio < or = 37.1% had a sens of 100% and spec of 85% for teh prediction of hepatitis compared to other non-inflam conditions.
- may reflect impaired Kupffer cell phagocytosis of perflubutane microbubbles.

Morishita JVIM 2017

117
Q

What changes in liver haemodynamic indices and liver enz are noted in obese and overweight dogs?

A
Haemodynamic:
Obese
- lower mean portal velocity
- higher % of abnormal hepatic vein spectral wave
- lower portal blood flow volume

Liver enz:
Obese- higher ALP
Overweight - higher GGT.

Belotta JVIM 2018

118
Q

Regarding the liver, what can non-invasive shear wave elastography be useful for predicting the presence of?

A
  • hepatic fibrosis

Tamura JVIM 2019

119
Q

what are the characteristics of a normal liver and GB/billary ducts on MRI?

A
  • uniformly hypointense relative to the spleen on T1 weighted and T2 weighted sequence
  • homogenous contrast enhancement of the parenchyma

GB and biliary duct:
- homogenously hyperintense on T2 weighted and hypointense on T1 weighted.

Marolf VCNA 2017

120
Q

what proportion of cats undergoing percutaneous ultrasound guided liver biopsy have:
- minor bleeding
- major bleeding
What disease is major bleeding likely to occur in?
Do standard Coag tests help predict bleeding risk?

A

Minor bloeeding - 42%
major bleeding - 56%
Hepatic lipidosis => more likely to have major bleeding

Standard coags do no predict complication ot eh magnitude of PCV drop.

Pavlick JFMS 2019

121
Q

What is the minimum recommended number of portal tried required for histopatholigcal interpretation of a liver sample?
What proportion of needle, cup and punch samples correspond with larger necropsy samples?

A

3-12 portal triads, however accuracy compared to large samples (30+) is low

no difference between minimally invasive sampling options:
needle - 66%
cup - 60%
punch - 69%

Kemp JVIm 2015

122
Q

By biopsying at least 2 liver lobes, what % of cases is the predominant abnormality detected?
What percentage of dogs have < or = to 3 lobes with the same diagnosis?

A

biopsy of at least 2 lobes identified primary histo abnormality in 98% of cases

14% of dogs had < or = to 3 lobes in agreement, thus could be misclassified or unable to be classified with less biopsies.

Kemp JVIm 2015

123
Q

What changes in serum microRNAs are expected in

  • mucocoel
  • hepatocellular carcinoma
  • chronic hepatitis
A
  • mucocoel: increased miRNA-122, miR-21, miR-222
  • hepatocelluar carcinoma: increased miR-200c
  • chronic hepatitis: increased miR-126

Dirksen JVIm 2016

124
Q

Are 5mm cup laparoscopic liver biopsies superior to 3mm cups?

A

3mm - significantly smaller surgace area snd less portal triads, but histopath diagnostic accuracy was similar between the 2.

Kimbrell JVIm 2017

125
Q

What is the sensitivity and specificity of miR-122 in diagnosing liver disease in dogs, using what cut off?

A

miR-122 - cut off for healthy < 3312
Sens: 77%
Spec: 97%
for identifying liver disease

Oosthuyzen JVIM 2018

126
Q

Does erythrocyte or plasma glutathionine indicate liver glutathionine concentrations?

A

no

Barry-Heffernan JVIM 2018

127
Q

What is the sensitivity and specificity of:
- ALP
- ALT
- Bile acids
For detecting acute and chronic hepatitis in clinically well labradors?

A

ALP
Sens (Acute): 15%
Sens (Chronic): 35%
Spec:>90%

ALT:
Sens (Acute): 45%
Sens (Chronic): 71%
Spec:>90%

Bile acids:
Sens (Acute): 15%
Sens (Chronic): 13%
Spec:>90%

Dirksen JVIM 2017

128
Q

What breeds are associated with congenital intrahepatic PSS?

A
  • Irish Wolfhound
  • deerhound
  • australian cattle dog
  • golden retriever
  • labrador
  • old english sheepdog

Watson VCNA 2017

129
Q

What breeds are associated with congenital extrahepatic PSS?

A
  • Cairn
  • yorkshire
  • Maltese
  • JRT
  • Dachshund
  • Havanese
  • Dandy dinmont
  • Mini Schnauzer
  • Westie
  • Shih tzu
  • pug

Watson VCNA 2017

130
Q

What breeds are associated with congenital microvascular dysplasia?

A
  • Cairn
  • Yorkshire
  • Papillion
  • Toy poodle

Watson VCNA 2017

131
Q

What is the ductal plate?

What are ductal plate abnormalities?

A

Ductal plate: a double layer of embryonic epithelium that surrounds teh portal veins and is the precursor of interlobular and intralobular bile ducts

Abnormal development => persistence of embryonic bile ducts + varying degrees of fibrosis

  • depends on what bile ducts are affected:
    1. Maturation arrest of small interlobular bile ducts => congential hepatic fibrosis
    2. Maturation arrest of medium intrahepatic bile ducts => caroli disease

Watson VCNA 2017

132
Q

How are ductal plate abnormalities diagnosed?

What breeds has it been seen in?

A
  • negative immunohisto stain using Ki67 to show lack of proliferation of the embryonic bile ducts + billary hyperplasia and fibrosis

seen in boxers, skye terrie, golden retrievers

Watson VCNA 2017

133
Q

What is caroli disease?

A

congenital dilation of the large and segmenatl bile ducts secondary to maturation arrest of the medium intrahepatic bile ducts.
- a form of ductal plate anomaly.

Watson VCNA 2017

134
Q

in dogs with cPSS, what vessels are usually affected in:

  • Irish Wolfhound
  • Australian cattle dogs
A
  • Irish Wolfhound: patent ductus venosus on the left (left dividsional cPSS)
  • Australian cattle dogs: right divisional shunt

Watson VCNA 2017

135
Q

What breeds are predisposed to chronic hepatitis?

What are the suspected underlying causes?

A
  1. Labrador
    - copper but more associated with high copper diets?
  2. Dalmatian
    - primary copper
  3. Bedlington terrier:
    - primary copper storage: genetic abnormalities (COMMD1 + others)
  4. doberman:
    - autoimmune (DLA class II alleles and haplotypes)
    - copper storage disease
  5. Westie:
    - classic copper storage
    - idiopathic
  6. American and english cocker spaniels:
    - multiorgan duct centered autoimmune disease (IgG4)
  7. English springer spaniels:
    - infectious or autoimmune (suspected DLA class II haplotype)

Watson VCNA 2017

136
Q

Waht are the difference in primary copper storage disease and copper dopisiton secondary to cholestasis:

A

Primary: Copper

  • accumulates around central vein (zone 3)
  • accumlates before inflam
  • colocates with inflam
  • high degree liver disease
  • hepatic copper < 400ug/g dry weight

secondary to cholestasis: Copper

  • accumulates around portal triad (zone 1)
  • accumulates after inflam
  • doesn’t colocate with inflam
  • accumulation is less that the severity of the liver disease
  • hepatic copper conc >1800ug/g dry weight.

Watson VCNA 2017

137
Q

What bacteria are commonly found in dogs with bacterial cholangitis and cholecystitis?

A
  • Ecoli (frequently resistant)
  • Enterococcus
  • Clostridium

Tamborini JVIM 2016

138
Q

What antbody test may be a screening test for dobermanns with increased ALT and suspicion of doberman hepatitis?

A
  • Antihistone antibodies
    increased in 92% of dogs in the subclinical stange and 84% in the clinical stage.

Dyggve JVIm 2017

139
Q

Are there consistent TEG findings in dogs with chronic hepatitis?

A

No - variable.
portal hypertension had lower G, MA and angle + prolonged K, R and PT.

Fry JVIM 2017

140
Q

What portal vein pressure is consistent with portal hypertension?

A

> 10mmHg
anaesthestiz normal = 6-9mmHg

VCNA 2018

141
Q

Apart from H&E what additional stains should be used on histopathology of suspected fibrotic liver and what do they stain?

A
  • Masson’s trichrome (tyoe 1 collagen)
  • picrosirius red (type I and III collagen)
  • reticulin (type III collagen)

VCNA 2018

142
Q

What is the prognostic importance of senescence marker p21 in histopath samples in dogs with chronic hepatitis?

A

increased immunopositive for was negatively associated with survival time
those >91.8% of hepatocytes displaying immunopositiveity for p21 had significantly shorter survival than those with <88.9%

Fortum JVIM 2018

143
Q

what type of inflammation is seen with:

  1. Lobular dissecting hepatitis:
  2. Chronic hepatitis:
  3. Cirrhosis:
  4. Non-specific reactive hepatopathy:
A

all have but chronic hepatitis have:

  • mild to moderate
  • lymphocytic,
  • neutrophilic
  • plasmocytic
  • granulomatous

CH has moderate to severe + eosinophilic.

  1. Lobular dissecting hepatitis:
    *mild to moderate
    - lymphocytic,
    - neutrophilic
    - plasmocytic
    - granulomatous
    + necrosis/apoptosis
  2. Chronic hepatitis:
    * moderate to marked
    - lymphocytic,
    - neutrophilic
    - plasmocytic
    - granulomatous
    - eosinophilic
    + necrosis/apoptosis
  3. Cirrhosis:
    *mild to moderate
    - lymphoplasmacytic
    - neutrophilic
    - plasmocytic
    - granulomatous
    + Necrosis/Apoptosis
  4. Non-specific reactive hepatopathy:
    *mild to moderate
    - lymphocytic,
    - neutrophilic
    - plasmocytic
    - granulomatous
    NO necrosis/apoptosis

Webster consensus JVIM 2019

144
Q

what type of fibrosis and regeneration is seen with:

  1. Lobular dissecting hepatitis:
  2. Chronic hepatitis:
  3. Cirrhosis:
  4. Non-specific reactive hepatopathy:
A
  1. Lobular dissecting hepatitis:
    - disruption of normal lobular architecture with fibrosis dissecting around single or groups of hepatocytes
    +/- ductal reaction
  2. Chronic hepatitis:
    +/- ductal prolif
    +/- fibrosis
    +/- Regen nodules
  3. Cirrhosis:
    - portal-portal or portal-central fibrosis with lobular architectural distortion
    - regen nodules
  4. Non-specific reactive hepatopathy:
    - no fibrosis
    - no architecture remodelling.

Webster consensus JVIM 2019

145
Q

What infectious causes are associated with chronic hepatitis?

A

bacterial:

  • lepto
  • bacillus piliformis
  • helicobacter canis
  • bartonella

Protozoal

  • Ehrlichia canis
  • babesia
  • leishmania

Viral - no strong evidence… (canine adenovirus type I??)

Those that could cause CH but generally cause acute +/- necrotizing/multisystemic disease

  • anaplasma
  • neospora
  • toxoplasma
  • sarcocystis
  • histoplasmaosis
  • mycobacteriaum
  • shistosoma
  • viceral larval migrans

Webster consensus JVIM 2019

146
Q

What copper dietary restriction level is recommended fro dogs with copper concentration >600ug/g dw?

A

<0.12 mg/100kcal

147
Q

What is the median dose of cyclosporine needed to induce biocheical remission of chronic hepatitis?
How long did this take to occur?
and in what percentage of dogs with CH was it effective?

A
  • 7.9mg/kg/day
  • time to remission 2.5m
  • remission in 79% of dogs

Ullal JVIm 2018

148
Q

What are miR-122 and miR29a correlated with?

A
  • grade of hepatitis
  • stage of fibrosis

Sakai JVIM 2018

149
Q
regarding triaditis: What proproption of symptomatic and asymptomatic cats showed evidence of inflammation in:
> 1 organ
IBD + cholangitis
IBD + pancreatitis
Triaditis
A

> 1 organ: 57%
IBD + cholangitis 34%
IBD + pancreatitis 6%
Triaditis 17%

Triaditis should be considered in symptomatic cats with severe IBD.

Fragkou JVIM 2016

150
Q

In cats with hepatic lipidosis, what changes would be expected to be seen in their lipoprotein profiles compared to healthy cats?
What is the sensitivity and sepcficity of the specific fraction within nominal LDL to differentiate cats with HL from normal?

A
  • similar serum cholesterol and triglycerides
  • higher low density lipoprotein
  • lower high density lipoproteins

Specfic fraction 1.037-1.043 g/ml
Sens:87%
spec 90%

Minamoto JFMS 2019

151
Q

Dogs with acute liver disease have variable TEG changes. What is most common?

A
  • hypocoagulable
  • hyperfibrinolytic

Kelley JVIm 2015

152
Q

What is the interobserver agreement using histological scoring of the canine liver for fibrosis and necroinflammatory activity?

A

Fibrosis - 0.35 =Fair
necroinflam - 0.16 = poor

Lidbury JVIM 2017

153
Q

What are the most common causes of acute liver failure?

A
  • toxin
  • neoplaisa
  • leptospirosis

Thawley VCNA 2017

154
Q

What is the reported survival to discharge in patient with acute liver failure?

A

14%

Thawley VCNA 2017

155
Q

What are the 3 categories of hepatic encephalopathy and their subcatgory/subdivision?

A

A - Acute liver failure
B- PSS with no intrinsice hepatocellular disease
C - Chriosis + portal hyperension or PSS including intrinsic hepatocellular disease => portal hypertension and PSS
Subcategory:
Episodic: pricipitated, spontaneous, recurrent
Persistent: mild, severe
Minimal

Gow VCNA 2017

156
Q

What are the veterinary modified west haven grading scale for HE?

A

0 - asymptomatic
I mild decreased in mobility, pathy or both
II severe apathy, mild ataxia
III combined hypersalivation, severe ataxia, head pressing, blindness, circling
IV stupor/coma, seizures

Gow VCNA 2017

157
Q

Is acute or chronic hepatopathy a more common presentation of HE?

A

chronic

Gow VCNA 2017

158
Q

What are the two mechanisms of ammonia detoxification in the liver?

A
  1. Periportal hepatocytes convert ammonia to urea via the urea cycle + enterohepatic recirc, in degraded by urease bacteria in the GID
  2. Perivenous hepatocytes conversion of glutamate to glutamine via glutamine sythetase, consuming ammonia. (also present in kidney, skeletal muscle and astrocytes => acstrocyte dysfunction due to increased inhibitory neurotransmitter glutamine)

Gow VCNA 2017

159
Q

What are the 5 types of extrahepatic PSS seen in cats?

A
  • left gastrophenic
  • left gastrocaval
  • splenocaval (left gastric to prehepatic CVC)
  • left gastroazygous
  • those arising from the left colic vein.

first 3 = 92% of shunts

Griffin JFMS 2019

160
Q

What percentage of canine and feline bile aspirates in patients with hepatobilliary disease have:

  • bacteria
  • inflammation
A

Dog:

  • bacteria - 30%
  • inflam - 5%

Cat:

  • Bacteria - 22%
  • inflam 19%

Peters JVIM 2016

161
Q
liver fluke (platynosomum) can be diagnosed based on eggs found where?
Which area has a higher egg count?
A
  • faeces
  • bile - higher egg count.

Koster JVIM 2016

162
Q

What imidocloprid use in shetland sheepdogs is associated with an increased risk of what condition?

A
  • 9.3 x higher risk of gall bladder mucocoel.

Goodkin JVIM 2015

163
Q

What proportion of dogs with billary sludge had changes when monitored over a year?

A
2% resolved
19% decreased
40% Static 
29% increased
10% recurrent

De Monaco JVIM 2016

164
Q

What breeds are predisposed to GB mucocoels?

A
  • Shetland sheepdog
  • American cocker spaniel
  • Chihuahua
  • Pomeranian
  • Mini Schnauzer
  • Border terrier

Allerton JVIM 2017

165
Q

What is the liklihood that a dog with a GB rupture and bile peritonitis at the time of surgery will die compared to those without rupture and peritonitis?

A

2.7 x higher risk of death

Jaffey JVIM 2018

166
Q
What is the :
- sensitivity
- specificity
- PPV
- NPV
for detecting gall bladder rupture with ultrasound?
A
  • sensitivity: 56.1%
  • specificity 91.7%
  • PPV 6.74
  • NPV 0.44

Jaffey JVIm 2018

167
Q

What is the difference in survival times between dogs with GB mucocoels that undergo surgery and survive 14 days vs medical management?

A

1802 days
1340 days.

Parkanzky JVIM 2019

168
Q

What breed is gall bladder agenesis most often seen in?
What concurrent histopathological change is noted in these animals?
what is the best imaging modality to see CBD dilation without evidence of obstruction?

A
  • Chihuahua
  • Ductal plate malformation
  • CT

Sato JVIM 2018

169
Q

What does the addition of a synbiotic after clindamycin do in cats?

A
  • reduced vomiting and hyporexia but didnt change antibiotic diarrhoea

Stoke JVIm 2017

170
Q

What does the use of Prokolin advanced do in dogs with acute diarrhoea?

A
  • shorter duration
  • faster resoltuion (1.6 x)
  • reduced requirement for additional medication

Nixon JVIm 2018

171
Q

What changes are seen with the use of tylosin on the faecal microbiota?

A
  • reduced bacterial diversity
  • reduced Fusobacteriacea and Veillonellacea
  • increased unconj faecal bile acids
  • variable recovery after discontiniation

Manchester JVIM 2019

172
Q

What is the recommended new categorization of effusions?

A
  1. Categorize based TNCC
    TNCC <3000/uL = transudate
    TNCC >3000/uL = exudate
  2. split transudated based on protein levels
    - <2.5 g/dL = low protien
    - > 2.5 g/dL = high protein

Bohn VCNA

173
Q

what testing confirms the presence of uroabdomen:

A
  1. Fluid creat > 2 x serum creat
  2. Fluid K+ > 1.4 x serium K+

Bohn VCNA

174
Q

what testing confirms the presence of bile peritonitis?

A
  1. Fluid bilirubin > serum bilirubin
  2. if equivocal, Fluid bile acids > serum bile acids

Bohn VCNA

175
Q

what testing confirms the presence of chylous effusion?

A
  1. fluid cholesterol to triglyceride ratio <1
  2. Fluid triglyceride > 100mg/dL

Bohn VCNA

176
Q

what testing confirms the presence of Septic peritonitis?

A
  1. Blood to fluid glucose difference of > 20mg/dL
  2. Blood to fluid lactate difference of <2 mmol/L
    * useful if bacteris not seen.