GI Literature Flashcards

1
Q

In dogs with severe pancreatitis what is known about feeding early?

A

• 10 dogs with severe pancreatitis feed either via E -tube or TPN (pilot study) - standard tx (including plasma)
○ Early feeding via E-tube (proximal to pylorus) is well tolerated and has significantly less vomiting and regurg than the TPN group
§ TPN group has more complications (catheter related)
○ No difference in outcome

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2
Q

What is unique about chronic pancreatitis in English Cocker Spaniels?

A

• Chronic Pancreatitis in English Cocker Spaniel (8)
○ Mean age: 7.2 yrs (no difference in CS/presentation)
○ Cockers: Interlobular and periductual fibrosis/inflammation
§ Prominent AntiCd3+ lymphocytic infiltrates around venules and ducts, marked absence of interlobular ducts = Duct destruction!!!
○ Other Breeds: Intralobular dz
§ Mixed cell infiltration, ductular hyperplasia

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3
Q

What had the best overall performance when comparing Spec cPL, cPLI, amylase, and lipase?

A

Spec cPL ○ Spec cPL best overall performance (sen/spec) for diagnosing histopath pancreatitis

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4
Q

What s a method of obtaining FNA of pancreas?

A

• Ultrasound endoscopic FNA of pancreas (12/13 beagles) - Safe and feasible with 19G needle
○ Cellularity adequate 8/12 (transgastric and transduodenal)
○ All recovered within clinical or lab changes (48hrs)

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5
Q

In a population of dogs with clinical acute pancreatitis, what was found about SNAP and Spec cPL?

A

• 84 dogs (27 w/o acute pancreatitis; 57 with CS of acute pancreatitis) - Prospective, retrospectively groups (but blinded)
○ SNAP and Spec cPL = Higher sen/spec for diagnosing clinical AP than amylase/lipase
§ IF + = Good PPV in populations likely to have AP
§ IF - = Good NPV when low prevalence of dz

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6
Q

What was found in Mini Schanuzers in regards to SPINK1?

A

• High prevalence of SPINK1 (serine protease inhibitor Kazal type 1) c.74A>C in Mini (0.77) and Standard Schnauzers (0.55)
○ Allele/genotype freq similar in Mini Schnauzer w/ and w.o hx pancreatitis = NOT an increased risk (Unable to confirm relationship btwn variant and clinical pancreatitis in Mini Schnauzers)

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7
Q

In 35 cats with pancreatitis, what is the sen and spec of AUS?

A

• 35 cats with CS of pancreatitis, AUS, and fPLI
○ Presence of thick left limb of pancreas, severely irregular pancreatic margins, hyperechocic peripancreatic fat (sen 68%) in cats with CS and elevated fPLI = Highly supportive of pancreatitis
§ Ultrasound Sen: 84% Spec: 75%
§ In cats with elevated fPLI

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8
Q

What is another lipase assay that can be considered in cats with pancreatitis instead of Spec fPL?

A

1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6’-methylresorufin) ester (DGGR) lipase assay

• 251 cats suspect to have pancreatitis, 31 cats with histopath
	○ 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6'-methylresorufin) ester (DGGR) lipase assay (26U/l)
		§ Sen: 48%, Spec: 63%
	○ SpecfPL (>5.3ug/l)
		§ Sen: 57%, Spec: 63%

Both lipase assays agreed, DGGR useful and cost-efficient method compared to Spec fPL

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9
Q

When using contrast enhanced ultrasound, what perfusion parameters can help you differentiate acute pancreatitis from a normal pancreas?

A

• 6 Beagle with cerulein-induced AP, Contrast Enhanced Ultrasound (controls: saline)
○ Perfusion parameters: Peak intensity and AUC are useful for differentiating acute pancreatitis from a normal pancreas

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10
Q

Can a sedated CT scan be used to diagnosis pancreatitis in dogs?

A

Yes: • 10 dogs with pancreatitis 3-phase angiographic CT under sedation
○ Enlarged, homogenously to heterogeneously attenutating and contrast-enhancing pancreas with ill-defined borders (all dogs)
○ CT found more features of pancreatitis than US (thrombi 3/10)
○ 3 dogs with heterogeneous contrast enhancement had overall poorer outcome compared to others with homogenous

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11
Q

What is true about contrast enhanced US in natrually occuring pancreatitis in dogs?

A

• 23 dogs with natural pancreatitis (12 controls) - Contrast Enhanced US, perfusion parameters
○ Can detected changes in pancreatitis - Delayed peak with prolonged hyperechoic enhancement of pancreas
○ Duodenal perfusion changes secondary to pancreatitis (peak intensity and AUC) compared to controls

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12
Q

What is known about adipokines in acute pancreatitis in dogs?

A

• 25 dogs with pancreatitis (28 controls, same BCS) - Dysregulation of adipokines might be involved in pathogenesis of pancreatitis
○ Leptin, resistin, visfatin, IL-1B, IL-6, IL_10, IL-18 significantly HIGHER in dogs with AP compared to controls
○ Adiponectin significantly lower in AP compared to controls

Significant differences in leptin (higher) and adiponectin (lower) in nonsurvivors compared to survivors = Leptin and adiponectin are likely associated with mortality rate in AP

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13
Q

How is EPI inherited in GSD?

A

• Test mating (both has EPI) and long term follow-up (12yrs) in 6 GSD puppies
○ Only 2 puppies got pancreatic acinar atrophy
○ NOT congenital dz in GSD - NOT inherited in simple autosomal recessive fashion

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14
Q

What is concerning about the fecal elastase test for EPI in dogs?

A

• 26 decreased fecal elastase = 23% TLI within or above RR (false + elastase) = HIGH
○ Diagnosis of EPI must be confirmed by other means

False positives also had decreased serum cholecystokinin = Suggesting that decreased stimulation of exocrine pancreatic function by other causes may be resulting in this

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15
Q

What was found in cats with traumatic high rise syndrome?

A

• 34 cats with traumatic pancreatitis (high-rise syndrome)
○ Serum fPL >5.4ug/L within 12hrs after fall (decreased slowly 48, 72 hrs after fall)
○ Significant agreement btwn fPLI and AUS (if 3 => traumatic pancreatitic: pancreatic enlargement, hypoechoic or heteroechoic pancreatic parenchyma, hyperechoic mesentery, and peritoneal effusion)

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16
Q

In cats with pancreatitis, what factors are associated with a worse prognosis?

A

○ Dyspnea, hyperkalemia (>5.5) and serum fPLI (>20ug/l) were significant associated with adverse outcome in cats with pancreatitis

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17
Q

In cats with severe pancreatitis that underwent sx, what had the better prognosis?

A

• 10 cats with severe pancreatitis underwent sx (6 EHBO, 3 pancreatic abscess, 1 pancreatic necrosis)
○ 6/8 survived to d/c
○ Better prognosis with EHBO

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18
Q

What was found in SNAP cPL and Spec cPL in dogs that were presenting with an acute abdomen?

A

• 38 dogs presented for acute abdomen (later retrospectively acute pancreatitis vs w/o AP)
○ SNAP cPL and Spec cPL may provide “false positive” diagnosis of pancreatitis in up to 40% dogs with acute abdominal dz
○ Good overall agreement btwn SNAP cPL and Spec cPL = BUT 4/38 dogs + SNAP cPL had “normal” Spec cPL

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19
Q

In cats with pancreatitis how can iCa be used?

A

• 24 cats with pancreatitis (non-fatal vs fatal groups)
○ Hypocalcemia common with pancreatitis 58.3%
○ iCa may be used as prognosis risk factor for clinical course of dz = Poor prognosis if

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20
Q

What is associated with pancreatitis in Mini Schnauzers?

A

• Association btwn hyperlipdiemia (esp severe >862 mg/dl) and high cPLI in Mini Schnauzers
○ IF severe hyperlipidemia = 4.5X more likely to have serum cPLI consistent with pancreatitis (>200ug/l) than Mini Schnauzers with normal TG
○ 195 Min Schnauzers (normal vs elevated TG)

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21
Q

How has contract enhanced US been used in dogs with pancreatitic tumors?

A

4 dogs: Contrast -enhanced ultrasound was able to establish different enhancement patterns btwn exocrine (adenocarcinoma = hypoechoic, hypovascular lesions) and endocrine (insulinoma = uniform hypervascular lesion) tumors in dogs

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22
Q

With Spirocercosis in dogs what was noted on TEG?

A

• 39 dogs with Spriocerca hypercoagubility based on TEG (increased MA, alpha) and decreased antithrombin activity more severe with neoplastic transformation
○ C-reactive protein and Fibrinogen (acute phase proteins) correlated with MA and may be used as adjunctive test to support suspicion of neoplasic transformation
○ MA: Sen 96%, Spec 73% for differentiation of dz state (neoplastic vs not)

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23
Q

Can C-reactive protein be used to differentiate dogs with neoplastic transformation with Spirocercosis?

A

• 42 dogs with Spirocerca: C-reactive protein CANNOT be used to differentiate btwn benign and malignant transformation
○ C-reactive protein was increased in neoplastic and non-neoplastic compared to controls
○ Decreased in C-reactive protein in dogs with benign lesions once tx started

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24
Q

What hypovitaminosis has been noted in Spirocercosis dogs?

A

• 51 dogs with Spirocerca: Serum 25(OH) D concentrations were significantly different in neoplastic (lowest Vit D levels) vs non-neoplastic vx controls
○ Dogs had similar appetite scores
○ Hypovitaminosis D may place a role in malignant transformation

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25
Q

What is a growth factor that has been noted to be elevated in Spirocercosis in dogs and what is its use?

A

• 18 dogs with Spirocerca: Plasma and serum VEGF can be used to differentiate non-neoplastic and neoplastic lesions
○ Median VEGF HIGHER in neoplastic spirocercosis than BOTH nonneoplastic and controls (about 69 pg/ml higher)

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26
Q

Based on whole mouth radiographs how do cats with chronic gingivostomatitis compared to other cats?

A

101 cats with FCGS compared to 101 cats with other oral dz: More widely distributed and severe periodonitis; higher prevalence of external inflammatory root resorption and retained roots compared to controls = Need full mouth rads in these patients

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27
Q

How does cisapride and metoclopramide affect LES pressures in dogs?

A

• 6 healthy beagles (cisapride, metoclopramide, placebo = 3X each) - LES pressure assessed with high resolution manometry catheter
○ Cisapride increase LES significantly compared to controls
○ Metoclopramide did NOT affect the LES resting pressures in dogs

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28
Q

In dogs with generalized megaesophagus what was assoiciated with a shorter survival time?

A

• 71 dogs with generalized megaesophagus: Radiographic evidence of aspiration pneumonia and age of onset of CS (>13 months) were significantly associated with shorter survival
○ MST: 90 days; 26.7% euthanized prior to d/c

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29
Q

What is recommended to prevent stress induced gastritis in sled dogs?

A

Omeprazole
• 36 sled dogs (famotidine vs no tx, endoscopy after race) - Famotidine reduced prevalence of clinically relevant exercise induced gastric lesions compared to no tx (duh!!)
• 52 sled dogs (famotidine high dose vs omeprazole) - Omeprazole was superior to famotidine in preventing gastritis = Recommended to prevent stress associated gastric disease in exercising/racing sled dogs

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30
Q

What happens in gastrin levels in healthy dogs that are administered famotidine for 14 days?

A

• 11 healthy dogs: After 14 days of famotidine, dogs have normal serum gastrin levels
○ Increased in gastrin on day 3 of administration but it returns to baseline
○ If dogs has clinical signs of gastrinoma, chronic famotidine administeration is unlikely to contribute to serum gastrin concentrations

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31
Q

What has been shown to improve reflux episodes under anesthesia in dogs?

A

• 6 healthy dogs undergoing sx (randomized placebo controlled study: Saline, esomeprazole, esomeprazole + cisapride) Esophageal pH/impedence probe to measure esophageal pH and detected GER
○ 38% placebo, 36% esomeprazole, and 11% esomeprazole+cisapride had >1 episode of GER during anesthesia
§ Esomeprazole significantly reduced gastric and esophageal pH, but no significant decreased in GER
○ Esomeprazole + cisapride = Significant decrease in # reflux events, compared to placebo and esomeprzole alone

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32
Q

What is a sufficient withdrawal time for omeprazole and famotidine if wanting to check gastrin levels?

A

7 days
• 9 healthy dogs: After 7 days omeprazole, there was significant increase in gastrin after first day and returned to baseline within 7 days of withdrawal
○ After 7 days of famotidine, at day 3 there was an increased in gastrin that then returned to baseline
○ 7 day withdrawal from short term famotidine and omeprazole is sufficient for serum gastrin to return to baseline

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33
Q

In patients with GDV, where is the gas dilation from?

A

NOT from areophagia (CO2 too high 13-20%) - 10 dogs

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34
Q

What was a good predictor of gastric necrosis and outcome in dogs with GDV?

A

○ Plasma lactate at admission was a good predictor of gastric necrosis and outcome (78 dogs)
§ Plasma lactate >7.4mmo/L: 82% accurate for predicting gastric necrosis (sen 50%, spec 88%), and 88% accurate for predicting outcome (sen 75%, spec 89%)

Base excess did correlate with lactate, BUT was NOT a good predictor of gastric necrosis or outcome

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35
Q

What does a previous splenectomy put dogs at risk for?

A

○ Increased odds of GDV (5.3X greater) in dogs with hx splenectomy compared to controls
§ Recommended prophylactic gastropexy!

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36
Q

In dogs with GDV, what resulted in decreased cardiac arrhythmias, AKI, and hospital length?

A

Early tx with lidocaine (bolus followed by CRI)

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37
Q

What is the prognosis for cats with gastric lymphoma?

A

○ Feline gastric LSA: 16 cats tx with chemo - 75% remission (mean duration 108 days)
§ Response to tx was prognostic (complete remission survived longer than partial remission)

Prior tx with steroids and stage NOT significant prognostic factors

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38
Q

What has been concluded about MMA and B12 in cats?

A

• Cobalamin def (MMA >1,343 nmol/l) occurred in 42% cats was predictive of cobalamin

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39
Q

In what breeds has Imerslund Grasbeck Syndrome been noted and what is it?

A

• Selective intestinal cobalamin malabsorption and proteinuria (Imerslund-Grasbeck Syndrome) in Juvenile Beagles
○ Failure to thrive, dyshematopoiesis (neutropenia), B12 def, methylmalonic aciduria, hyperammonemia, proteinuria
○ Lacked renal cubilin
○ Homozygous for deletion CUB exon 8 = 8 Autosomal recessive
○ More severe than Border Collies with CUBN defect, but similar to AMN mutations in Giant Schnauzers and Australian Shephards

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40
Q

In which breed of dog had Methylmalonic Aciduria in healthy dogs with normal B12 and others with CS of B12 def?

A

• Border collies with Hereditary B12 defs: Stunted growth, lethargy, anemia, proteinuria (normalized with B12 supplementation)
○ Methylmalonic Aciduria in healthy dogs with normal B12 and others with CS of B12 def => considered that dogs may have defect in intracellular processing of B12 or intestinal B12 malabsorption

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41
Q

What was the prevalence of hypoB12 and cellular hypoB12 in dogs with chronic GI dz?

A

• 56 dogs with chronic GI dz: Prevalence of hypoB12 36%, of these only 25% had increased MMA (suggesting that although hypoB12 was common that dogs did not always have B12 def at a cellular level)
○ No correlation btwn canine chronic enteropathy clinical activity indec and serum B12 or MMA!!
○ NOTE: HypoB12 is a risk factor for negative outcome in dogs with chronic GI dz

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42
Q

How does hyperT4 affect B12 levels in cats?

A

6 cats with moderate to severe hyperT4: 40.8% had hypoB12 compared to 25% controls - Suggesting that hypoB12 may directly or indirectly affect B12 uptake, excretion, or utilization
○ Weak negative correlation with B12 and T4 in hyperT4 cats
○ HypoB12 was not associated with an change in neutrophils or RBCs

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43
Q

In cats with GI signs, which disease resulted most commonly in concurrent hypoB12?

A

• 39 cats with GI signs: 28.2% had hypoB12
○ Alimentary LSA and most severe grade of histologic intestinal inflammation were associated most commonly with concurrent hypoB12
§ No significant correlation btwn B12 and histopath score or duration of CS

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44
Q

What disease should you screen for if a Border Collie has ambigous CS and proteinuria?

A

Hereditary juvenile cobalamin def

• Hereditary juvenile cobalamin deficiency in Border Collies:  Intermittent lethargy, poor BCS, odynophagia, glossitis, bradyarrythmia, normocytic non-regenerative anemia, mild proteinuria
	○ Low serum B12, marked methylmalonic aciduria, hyperhomocysteinemia
		§ Full clinical recovery with B12 supplementation, Proteinuria and AST elevation persisted
	○ Need to screen young Border Collies with ambigous CS (mean age 11.5 months)
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45
Q

What is ultrasound thickening of mucularis associated with in cats?

A

• Older cats with muscularis thickening are more likely to have T cell lymphoma than IBD
○ Associated with infiltrate in mucosal and submucosal layers
○ Lymphadenopathy is associated with lymphoma OR IBD

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46
Q

What is ultrasound lymphadenopathy in cats associated with?

A

Lymphoma OR IBD

compared to controls

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47
Q

How helpful is AUS in chronic vomiting dogs?

A

• Diagnostic utility of AUS in dogs with chronic vomiting was HIGH in 27% dogs (vital in 22.5%)
○ 68.5% - Same dx w/o AUS
○ Multivariant analysis: Increasing age, final dx of gastric adenocarcinoma or GI lymphoma associated with increased diagnostic utlity

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48
Q

What is recommended for performing endoscopy in cats with IBD vs LSA?

A

• Population of cats in which dx of Small cell lymphoma can ONLY be made in ileal bx
○ 18/70 cats (26%) had lymphoma
§ 39% Only in duodenum, 44% ONLY in ileum; 17% in both
○ Recommended performing upper and lower (ileal bx) in cats

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49
Q

What are the difference in fecal microflora in lean and obese dogs ?

A

• Obesity and fecal microflora in beagle dogs (7 obese and 7 lean)
○ Leptin higher in obese
○ CSF Adiponectin and 5HT higher in lean
○ Diversity of microbiota decreased in obese
§ Proteobacteria (76%) - Obese = May contribute to chronic inflammatory status
§ Firmicutes (85%) - Lean

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50
Q

What inflammatory prostaglandin is affects in IBD and FRD?

A

• COX-2 (inflammatory prostaglandin) and 5-Lipooxygenase (source of leukotrienes)
○ 15 control dogs, 10 IBD, 10 food responsive diarrhea (before and after tx)
○ COX-2 upregulated in IBD and FRD
§ Consider dual COX/5-LO inhibitors in chronic enteropathies in dogs

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51
Q

What is AST-120 and how can it be used?

A

• Randomized, placebo-controlled, double blind pilot study (10 dogs with chronic idiopathic entropathy) with AST-120 (spherical carbon adsorbent preparation with how adsorptive ability of LW substances)
○ Mean CIBDAI decreased in AST-120 group and in placebo group
○ Compared to baseline, post tx CIBDAI decreased >60% in 4/5 dogs with AST-120 compared to 1/5 dogs in placebo
○ No adverse effects of AST-120
○ AST-120 could be considered in mild to moderate chronic idiopathic enteropathy

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52
Q

What is known about NOD2 and NFkappaB in dogs with LP colitis?

A

• 19 dogs with LP colitis compared to controls (NOD2 triggering host response to bacteria by activating NFkappaB - Proinflammatory cytokine production)
○ NOD2 mRNA (63% higher) and NFkappaB activity (45% higher) significantly higher in inflammed colon in LP dogs compared to controls

No correlation btwn NOD2, NfkappaB and CIBDAV in LP colitis dogs

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53
Q

What is true about D-lactate in cats with GI disease?

A

00 cats with GI signs (31 cats had neurologic signs)
○ D-lactate was higher in cats with GI dz compared to healthy controls (can results in neurologic signs in humans)
§ D-lactate did NOT correlate with fPLI, fTLI, B12, folate, or Neurologic signs
§ More studies need to determine role of microbiota in GI dz in cats
○ L-lactate the same in all groups

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54
Q

What is important about dietary fat in cats with diarrhea?

A

• Randomized, double blind, controlled clinical trial (55 cats with diarrhea feed high fat or low fat diet for 6 wks, daily fecal scores)
○ Fecal scores improved significantly in 78.2% and over 1/3 had normal stool (noted 1wks, max at 3 wks)
○ No difference in response btwn diets = Dietary fat does not appear to affect outcome of diarrhea in cats

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55
Q

What is the difference in hydrolzyed vs intestinal diet in management of canine chronic enteropathy?

A

• Randomized, open-label, positively controlled trial (18 dogs on RC Hypoallergenic/Hydrolyzed and 8 dogs on RC Intestinal diet; compared at baseline, 3 months, 6-12 months, and 3 years)
○ Higher CIBDAI in hydrolyzed diet (even with randomization)
○ No difference at first recheck, significant improvement in hydrolyzed diet at second and third recheck (with a significant decreased in CIBDAI)

Suggested that hydrolyzed diet was high effective for long term management in chronic enteropathy in dogs

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56
Q

Is there a difference btwn prednisone and pred + metronidazole in the induction of dogs with IBD?

A

NO
• 54 dogs with IBD, Randomized study (oral prednsione OR pred + metronidazaole for 21 days; compared CIBDAI scores and serum C-reactive protein)
○ No difference in tx = Pred is just as effective as pred+metro for induction of IBD in dogs
○ CRP may be normal or increased in dogs with IBD (but did decreased with tx) - It could be used to monitor individual dogs response to tx

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57
Q

Can urinary leukotriene 4 be used to differentiate IBD from food responsive diarrhea in dogs?

A

NO!
• Urinary leukotriene 4 was significantly higher in IBD dogs compared to food responsive diarrhea and controls - Suggests cysteinyl leukotriene pathway activation might be a component of the inflammatory process in IBD
○ No difference btwn food responsive and controls in Urinary LTE4
○ No correlation of urinary LTE4 and CIBDAI

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58
Q

How is fecal, serum, and duodenal IgA affected in dogs with IBD?

A

• 37 dogs with IBD (10 dogs with intestinal LSA + controls; IgA and IgG in serum, feces, and duodenal samples)
○ Dogs with IBD had significantly decreased in IgA in feces and duodenal samples compared to controls; fewer IgA + peripheral blood mononuclear cells
○ Compared to intestinal LSA dogs, the duodenal IgA and IgA + cells were significantly lower in IBD dogs still

Duodenal B cell activating factor (BAFF) and proliferation-inducing ligand (APRIL) mRNA significantly higher in IBD than healthy controls

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59
Q

How did budesonide compared to prednisone for the induction of IBD in dogs?

A

• Double-blind, randomized controlled trial in 40 newly dx IBD dogs (budesonide 6 wks OR pred 2mg/kg 3 weeks then 1 mg/kg 3 wks; compared CIBDAI before and after tx)
○ No difference in remission rate (78% budesonide and 69% prednisone) or adverse events (sadly not less SE…BUT with PU/PD, but it was close to significant for these, lower in budesnoide group) btwn prednisone and budesnoide for induction of IBD in dogs
§ At 6 weeks the ALT was significantly higher in the prednisone dogs; higher albumin in budesonide group

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60
Q

What is known about Vitamin D in cats with IBD and small cell lymphoma?

A

Hypovitaminosis D is a problem (same as dogs and humans)

• 20 cats with IBD or Small Cell Lymphoma compared to 41 ill cats and 23 healthy cats = Lower serum 25 hydroxyvitamin D in cats with IBD/LSA than in healthy or hospitalized ill cats (BUT there was overlap)
	○ Moderate positive correlation btwn albumin and Vit D concentrations (SAME as dogs and humans)
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61
Q

Can endoscopic bx be used in dogs for flow (lymphocyte analysis)?

A

YES! Same as full thickness bx

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62
Q

What was noted about the intraepithelial lymphocytes in dogs with IBD compared to controls?

A

• 10 dogs with IBD that had endoscopic and full thickness bx - NO difference in intestinal intraepithelial lymphocytes btwn sample types
○ Endoscopy bx are fine for flow!
○ IBD dogs had higher CIBDAI and WSAVA score than controls (GOOD!)

Increased % of TCR-gamma delta+ T cells in IBD dogs - Intraepithelial lymphocytes from IBD dogs express significantly different immunophenotype compared to control dogs

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63
Q

In dogs with PLE that are tx, what happens to their TEG results?

A

REMAIN hypercoagulable!
• 15 dogs with PLE assess with recalcified unactivated TEG) = ALL dogs were hypercoagulable on TEG (decreased R, decreased K, increased alpha, increased MA)
○ Did not appear to be related to severity of hypoalbuminemia
○ Antithombin borderline low - NOT solely attributed to hypercoag state
○ 9 dogs tx (improved CIBDAI scores and albumin) - STILL hypercoagulable!!

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64
Q

Can endoscopic appearance be used to make dx of intestinal lymphangectasia instead of histopath?

A

NO!! • 25 dogs with endoscopy (confirmed on histopath): Endoscopic duodenal mucosal appearance ALONE lacked spec (sen 68%, spec 42%) - White foci
○ If endoscopic images combined with biomarkers (lymphopenia, hypocholesterolemia, and hypoalbuminemia = Sen increased to 80%)
○ BUT with poor spec still NEED histopath

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65
Q

In Yorkies with PLE, what factors were associated with survival

A

VOMITING (esp if with monocytosis, severity of hypolabuminemia, low BUN, villous blunting)

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66
Q

In dogs with intestinal lymphangectasia that was NOT responding to pred or get hypoalbuminemia when pred taper, what has been shown to help?

A

Feeding fat restricted diet

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67
Q

What was associated with a worse outcome in boxers with granulomatous colitis?

A

• 14 Boxers: Antimicrobial resistance common in GC-associated E. coli = Need to culture BEFORE (do not use empirical wisdom)
○ Enrofloxacin tx before dx was associated with antimicrobial resistance in boxers and a WORSE OUTCOME
○ E. coli phylogroups similar with controls
○ GC had higher resistance (ampicillin, clavamox, cefoxitin, tetracycline, TMS, cipro, chloramphenicol) - (21-64% compared to 0-24%)

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68
Q

Which dog breed has a similar disease to Boxer granulomatous colitis?

A

• 6 French Bulldogs: Invasive E. coli with multifocal accumulations of PAS+ macrophages = Similar to boxer granulomatous colitis
○ All dos

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69
Q

What enteropathogens were noted in racing sled dogs?

A

• 135 racing sled dogs (before and after race) - High prevalence of diarrhea +hematochezia (36-57.5%), BUT not significantly associated with common enteropathogens (C. perfringens enterotoxin, C. difficile toxin A/B, Campylobacter, Salmonella (found in 71-78% before race), E.coli. Giardia, and Crytospordium spp)
○ Dogs more likely to be + for C. perfringens enterotoxin during race than before

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70
Q

In nospetic dogs with HGE did what did not help with clinical outcome?

A

• 53 dogs with HE (NOT septic): Blinded placebo controlled study (Clavamox for 7 days or placebo) = No significant difference in mortality rate, dropout rate (? Power analysis), duration of hospitalization, severity of CS (based on HE activity index - appetite, vomiting, stool consistency, freq, dehydration) btwn tx groups

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71
Q

What biomarked is severely decreased in parvo puppies but has no prognostic value?

A

• 61 puppies with parvoviral enteritis associated with severe decreased in plasma citrulline (marker of global enterocyte mass in humans) compared to age matched controls
○ BUT is NOT of any prognostic value

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72
Q

In dogs with PLE what may be more efficacious than azathioprine and prednisolone?

A

7 dogs with PLE (tx with azathioprine-prednisolone vs chlorambucil-prednislone - retrospective!! But groups were similar)
○ Albumin and weight grain significantly greater in chlormabucil group
○ MST in azathioprine: 30 days compared to the MST could not be determined for chlormabucil (they live so long!)
○ Suggests that chlorambucil-pred may be more efficacious in PLE compared to azath - pred

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73
Q

In cats that presented to the shelter which enteropathogen was associated with diarrhea?

A

• 100 cats at a shelter (50 w/ diarrhea and 50 w/o diarrhea) - Feline coronavirus significantly more prevalent in cats with diarrhea (58%) compared to controls (36%)
○ All others no associated with anything (C. perfringens enterotoxin A, Crytospordium, Giardia, Cystoisosopra, Hookworms, Ascardis, Salmonella, Atrovirus, Feline Panleukopenia virus, Calicivirus, Spirometra)

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74
Q

In dogs that presented to the shelter which enteropathogen was associated with diarrhea?

A

• 100 dogs at shelter (50 w/ diarrhea and 50 w/o diarrhea) - Clostridium perfringens enterotoxin A significantly more common in dogs with diarrhea (64%) compared to normal (40%) - also more likely to have >1 enteropathogen
○ All others no association with anything (Hookworms, Giardia, Crytospordium, whipworms, ascarids, Salmonella, Cystoisosopra, canine distemper virus, Dipyldium caninum, canine parvovirus, rotavirus

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75
Q

What could be considered a cheaper alternative in HGE dogs than IVF?

A

• 20 dogs with HE - 65% (13) voluntarily consumed oral electrolyte solution, 35% (7) refused it and needed IVF
○ PCV, total protein, and BUN significantly lower than hospital admin in OES group = Rehydration with OES was effective and safe (also LOTS cheaper for owner)

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76
Q

When parvo puppies were administered CPV immune plasma, what was the outcome?

A

• Randomized, double blinded placebo controlled clinical trial (14 dogs, 12 ml CPV immune plasma IV or saline IV)
○ No significant difference in CS, reducing viremia, neutrophil/monocyte counts, or days in hospital

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77
Q

Is there a difference btwn CPV-2b and CPV-2c in dogs?

A

NO! • 72 dogs with parvo: Fecal testing for antigen: 73.5% CPV-2c and 26.5% CPV-2b = No association btwn CPV strain and dz severity or clinical outcome

Diagnostics used could detect CPV type2c

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78
Q

What is true regarding pANCA and IBD vs GI LSA dogs?

A

04 dogs with IBD and 23 dogs with intestinal lymphoma - Circulating pANCA (perinuclear antineutrophilic cystoplasmic antibodies) present in some dogs with IBD (36.5%) and intestinal LSA (27.4%)
pANCA detection could NOT be used to distinguish dogs with IBD vs LSA

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79
Q

Which tight junction or apical junction protein is different btwn IBD dogs and controls?

A

○ In 12 IBD dogs: Claudin-1, -2, -3, -4, -5, -7, and -8 and β-catenin was not significantly different between duodonal mucosa samples from IBD vs controls

E-cadherin expression significantly LOWER in villus epithelium in duodenal mucosa from IBD vs controls = Suggested that decreased expression of E-cadherin has a role in the pathogenesis of IBD in dogs

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80
Q

In dogs that have cutaneous food hypersensitivity, what was seen in their intestine?

A

11 dogs with cutaneous food hypersensitivity: No change in T-cell phenotypes or a distinct Th1, Th2, or Treg profile was detected in duodenum of dogs with cutaneous CS of food hypersensitivity = Suggested that intestinal mucosa is not primary site of T-cell activation that eventually leads to cutaneous food hypersensitivity

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81
Q

What were the findings of using oseltamivir in dogs with parvo?

A

• Randomized, blinded, placebo controlled trial with oseltamivir: 35 dogs with parvo
○ Significant gain in weight and no drop in WBCs (as seen in controls) in tx group

No major adverse effects

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82
Q

Of the acute phase proteins, which has the potential to predict prognosis in dogs with parvo?

A

• 43 dogs with parvo (23 that died!) - Serum acute phase proteins (C-reactive protein, haptoglobin, ceruloplasmin and albumin)
○ Serum C-reactive protein, ceruloplasmin and haptoglobin levels HIGHER; Albumin LOWER in parvo dogs compared to controls
○ In non-survivors: C reative protein and ceruloplasma HIGHER than survivors
§ C-reactive protein >92.4 mg/l could predict mortality (sen 91%)

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83
Q

How do vitamin D. PTH, and iCa compared in PLE vs IBD vs normal dogs?

A

• 12 PLE, 21 IBD, 49 hospitalized, 36 healthy dogs = Hypovitaminosis D state!
○ PLE dogs (IBD + hypoalbuminemia) frequently had ionized hypoCa, HIGH PTH, and low serum 25 hydroxyvitamin D concentrations
§ Lower Vit D in PLE than all other groups
§ Higher PTH and lower iCa compared to hospitalized dogs
○ IBD dogs had positive correlation of serum 25 hydroxyvitamin D and albumin

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84
Q

Which spp is more likely to have neoplasia with an intussuscpetion?

A

• Intussusceptions: Cats are older and more likely to have neoplasia compared to dogs that are more likely to have inflammatory disease

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85
Q

Can LSA be ruled out with a normal GIT AUS?

A

NO! • AUS findings in dogs with intestinal lymphoma are non-specific! 26.7% has no abnormalities (LSA should still be considered in normal GIT on AUS)

Intestinal wall thickness and wall layering = HIGHLY variable

86
Q

Where animals that has a pyloric perforation more likely to die?

A

NO! • 44 dogs and 11 cats: Animals that had anti-inflammatory drugs were significantly more likely to have perforation at pylorus (but NOT worse outcome compared to non-pylorus)
○ Overall survival: 63.3%

87
Q

How effective if quadruple tx in cats with Helicobacter?

A

• Use of quadruple tx (omeprazole, amoxicillin, metronidazole, and clarithromycin) lead to transient suppression of Helicobacter in cats BUT is ineffective in eradicating it

88
Q

What are considered the biomarkers for eosinophilic enteritis in cats?

A

Prominent muscularis layer, palpably thickened GI loops, and peripheral eosinohilia are biomarkers in cats with chronic GI signs

89
Q

What are risk factors for GI perforation during endoscopy?

A

• Perforation secondary to Endoscopy (1.6% cats and 0.1% dogs over 17 yr study) = RISK IS LOW
○ Increased risk with intestinal infiltration in cats; GI ulcers in dogs and cats

90
Q

Which toxin has milk thistle been evaluated and successfully in treating?

A

• Milk Thistle (silibinin)

○ Esp for Amanita phalloides intoxication (experimental dogs)

91
Q

In dogs with cycad intoxication, what was associated with longer survival = Protective effect?

A

Administeration of charcoal at presentation

92
Q

In dogs with cycad intoxication, what parameters did non-survivors have?

A

• Cycad Intoxication in 34 dogs (cycasin metabolized my gut microbes to methylazoxymethanol, MAM; esp in seeds but found in all parts)
○ 50% die!!!
○ Many had severe hypoglycemia (but not significant)
○ Centrilobular necrosis with midzonal coagulation
○ Non-survivors: Higher ALT, higher bilirubin, lower albumin at presentation; lower albumin nadir, more had prolongation in coags
○ Administration of charcoal at presentation was associated with longer survival
○ Higher AST negative prognostic factor

93
Q

What was the prognosis of dogs with cycad intoxication?

A

POOR, 50% dead from severe liver failure

94
Q

What was unique about the histopath from Cocker Spaniels from Japan with chronic hepatitis?

A

Severe hepatic fibrosis leading to cirrhosis, extensive ductular/putative hepatic progenitor cell proliferation, portal hypertension, and acquired portosystemic collateral shunting, but relatively long survival times. Lobular dissecting hepatitis was COMMON (not noted previously)

95
Q

If you see renal glucosuria and increased ALT in lab, you should think….

A

Copper Hepatopathy!!!!

§ Unknown effect on prognosis, but it tx can have good prognosis

96
Q

What was seen in labs with renal glucosuria and copper hepatopathy?

A

• 9 labs with renal glucosuria and bx confirmed Copper Associated Hepatitis (centrilobular hepatitis with copper accumulation, rhodanine staining) - All elevated bilirubin
○ Renal tubular dysfunction (hyperchloremic metabolic acidosis (type II), acidemia with paradoxical alkalinuria) = All kidneys had copper (tubular vaculozation, degeneration, and regeneration)
§ 2 dogs: urine metabolic profiles (amino aciduria, cystinuria, glucosuria, and lactic aciduria) - Consistent with Fanconi’s syndrome
§ Glucosuria, low phos, low bicarbonate
§ Possible that distal tubular function also abnormal (Hyperchloremic metabolic acidosis)
○ Dogs that underwent copper chelation - Resolved renal tubular dysfunction (BUT many died, 4/9; 4 dogs >1 yr)
○ If you see renal glucosuria and increased ALT in lab = THINK Copper Hepatopathy!!!!

Unknown effect on prognosis, but it tx can have good

97
Q

In healthy lab, what dietary factors lead to higher hepatic copper levels?

A

Higher copper and low zinc levels (found in current commercial diets!!!!)

98
Q

What neurotoxic element has been shown to be increased in congenital PSS dogs?

A

• Dogs with Congenital PSS significantly HIGHER whole blood Manganese (Mn) than non-hepatic illness or healthy dogs
○ Liver important in clearance of Mn (Mn = neurotoxic; could be related to HE??)

99
Q

How quickly does the liver growth after surgical attenuation of PSS?

A

FAST!! • After surgical attenuation of PSS, liver volume (hepatic growth, measured by CT or MRI) was rapid!!! Betwn 0-8 days (stayed the same 1 and 2 months)
○ No significant difference in dogs with partial closure, dogs with CS, or persistent shunting at 2 months

CT is preferred method dt speed

100
Q

Can Keppra be given to prevent post-op seizures with EHPSS attenuation?

A

YES!
• Levetiracetam (Keppra) was protective (reduced relative risk) in dogs undergoing surgical attenuation of EHPSS (ameroid ring constrictor) compared to giving NO anti-convulsant
○ 20 mg/kg POq8hrs (min of 24 hrs prior to sx)
○ No post-op seizures in keppra dogs and 5% in untreated (all seizure dogs died!!)

101
Q

In congenital PSS dogs, some were hypercoaguable based on TEG, did this have an association with hepatic encephalopathy?

A

YES!!!
• Some dogs with congenital PSS were hypercoaguble based on kaolin-activated TEG (9/21: higher platelet count, shorter K, alpha angle and MA higher)
○ Plasma: CPSS had significantly prolonged PT, lower platelet counts, lower antithrombin and protein C, increased d-dimers, increased factor VIII)
○ Dogs that were hypercoagulable were more likely to have hepatic encephalopathy (40X more likely!!! Compared to PSS dogs not hypercoag)

102
Q

Was hepatic hepcidin related to microcytosis with PSS?

A

NO! • cPSS significant increase in RBC and MCV (not mirocytoic after sx attenuation of shunt) - BUT NOT related to hepcidin (hepatic mRNA) which did not changes after sx

103
Q

In Scottish Terriers with progressive vacuolar hepatopathy would other factors needs to be considered?

A

• 34% Scottish Terriers with progressive vacuolar hepatopathy had hepatocellular carcinoma noted - Preceded by dysplastic hepatocellular foci
○ No significant difference in clinpath or age at death w/ or w/o HCC
○ 58% had high hepatic copper - copper associated hepatopathy
○ 40% has CS of AHC but inconsistent testing
○ Adrenal panels after ACTH: High progsterone (88%) and androstenedione (80%) - Vacuolar hepatopathy linked to adrenal steroidogenesis and predisposition for HCC
§ Also saw increased mucoceles in this population (related??)
○ Need to check Scotties with AUS to monitor for HCC even if vacuolar hepatopathy noted

104
Q

Was there a difference in labs with chronic hepatitis and labs without hepatitis in hepatic copper over two different time periods, and what does this suggest?

A

• 36 Labs with chronic hepatitis compared to 36 age/sex matched controls (2 time periods, 80-97 and 98-2010)
○ Mean hepatic copper was significantly higher in dogs with chronic hepatitis than controls (increased significantly OVER TIME)
§ More with copper >400 ug/g dry weight in 2010 group (may be the results on increased environmental copper exposure (like in diet, higher bioavailability in diets now))
○ Qualitative copper score did NOT accurately predict quantitative hepatic copper in 33% dogs

105
Q

What can be concluded from a cohort of dogs managed medically and surgically for PSS?

A

• Surgical tx of PSS dogs (97) significantly improved survival rates and had lower freq of ongoing CS compared to dogs managed medically (27), follow-up 1936 days
○ Medical: 89% died or euthanized during study (MST: 836 days, longest 2,948 days)
○ Surgery: 22% died or euthanized during study (MST: unknown, too many alive, follow up 3,415 days) = Hazard ratio was 8X that in dogs medically managed
○ Age and shunt type did NOT affect survival

106
Q

Which type of PSS in dogs can result in more clinical abnormalities than other shunts?

A

• Splenocaval shunts in dogs have more clinical abnormalities than other shunt morphologies = Suggests that dogs with shunt insertion in caudal vena cava (esp caudal to liver) more likely to have CS

107
Q

What is something that is rare in CPSS but is more common in acquired PSS?

A

ASCITES

108
Q

For AUS of hepatic lesions, what can help to predict malignancy?

A

Greater lesion size and peritoneal fluid had a positive associated with malignant liver histopath

109
Q

How did hydrocortisone affect the bile in dogs?

A

• Hydrocortisone in dogs (84 days) results in reversible shifts to higher concentrations of hydrophobic unconjugated bile acids (chenodeoxycholic and deoxycholic acids) and lower amphipathic taurine conjugated bile acids

No effect on glycine conjugated bile acids

110
Q

On MRI, what did dogs with HE have different than controls?

A

• In vivo MRI spectroscopy could be used in dogs to diagnose HE
○ HE dogs: Significantly HIGHER glutamine-glutamate complex, significantly LOWER myoinositol; slightly lower choline and N-acetyl asparate compared to controls
○ Suggested that this could be used in subclinical HE dogs, or monitoring medical management

111
Q

Which two liver conditions are likely inherited in Maltese dogs?

A

• Strong support (based on test matings) that EHPSS and elevated post Bile acids (likely portal vein hypoplasia) are both inherited in Maltese

112
Q

What are potential markers of dz severity in pancreatitis?

A
Serum paraoxonase (LOWER with panc)
CRP (HIGHER with panc)
113
Q

When pancreatitis bx taken in dogs and cats, which spp was it more useful in?

A

CATS - chronic pancreatitis

Dogs more likely to have no path seen

114
Q

What is true about nutrition in pancreatitis?

A

Early and enteral is BEST

115
Q

In regards to SNAP cPL and Spec cPL in dogs with acute abdomens, what is concerning?

A

False positive dx of panc in 40% dogs with acute abdominal dz (NOT panc)

116
Q

What adipokines may be associated with mortality in AP?

A

Leptin (higher)
Aponectin (lower)
in nonsuvivors!

117
Q

How did CT compared to US in AP?

A

CT found more features of AP (esp thrombi)

Heterogenous contrast = Worse prognosis

118
Q

Was hyperlipdemia asscoaited with high cPLI in Mini Schanuzers?

A

YES, esp with severe HyperTG >862 = 4.5X more likely to have cPLI consistent with panc (>200) than Mini Schnauzers with normal TG

119
Q

Which cut off for cPLI is recommended to dx panc?

A

400 ug/l - Higher spec

120
Q

Did feeding AP via E-tube vs TPN affect outcome?

A

NO!! But E-tube dogs had less regurg and vomiting than TPN dogs

121
Q

What changes in the liver are associated with chronic pancreatitis?

A

Reactive hepatitis

NOT chronic hepatitis

122
Q

What % of cats have triaditis?

A

50% cats with panc

50% cats with cholangitis/IBD

123
Q

In cats what is associated with a poor prognosis for AP?

A

iCa 5.5)

fPLI >20!!!! (dx >5.4)

124
Q

Which high rise syndrome what is a potential complication?

A

AP!!! Serum fPL>5.4 within 12 hrs after fall (decreased over 48-72hrs)
Agreement with AUS

125
Q

In cats with CS and elevated fPL, how did US perform?

A

GREAT, Sen 84%, Spec 75% esp if thick left limb, severely irregular margins, hyperechoic peripancreatitic fat

126
Q

In cats with IBD what was more frequently seen when fPL>12 (panc)?

A

Hypoalbuminemia

Hypocobalaminemia

127
Q

Was periodontal dz associated with systemic health?

A

Increased attachment loss associated with lower plt and changes in creatinine
Decreased CRP when tx!! (interesting increase in BUN after tx)

128
Q

In dogs with esophageal FBs, what reduced esophagitis and hospitalized time?

A

Early intervention

129
Q

What % of cases of Spirocercosis undergo neoplastic transformation?

A

About 25%

130
Q

What TEG parameter has been used to differentiate dz state (neoplasia or NOT) in Spirocerca cases?

A

All cases hypercoag but neoplasia cases WORSE
MA used to differentiate!
MA correlated with CRP and fibrinogen (maybe could be used instead)

131
Q

Can VEGF be used to differentiate non-neoplastic from neoplastic lesions in Spirocerca cases?

A

YES, high WEGF with neoplastic lesions

132
Q

Can Serm Vit D be used to differentiate non-neoplastic from neoplastic lesions in Spirocerca cases?

A

YES, lowest Vit D in neoplasia cases (Hypo Vit D may play a role in malignant transformation)

133
Q

Can CRP be used to differentiate non-neoplastic from neoplastic lesions in Spirocerca cases?

A

NO, no difference

But CRP decreased with tx in benign lesions

134
Q

What was the effect of metoclopramide and cisapride on LES in dogs?

A

Cisapride increased LES significantly

Metoclopramide did NOT affect LES resting pressuresin dogs

135
Q

Did owner noted CS accurate document GERD in dogs?

A

Based on using Bravo pH system - CS reflux association was POOR only 12.5% in 10 dogs

136
Q

What reduced # reflux events in dogs undergoing anesthesia?

A

Esomeprazole + cisapride

137
Q

When comparing omeprazole and famotidine, which is superior?

A

Omeprazole tablet AND paste superior

138
Q

What is recommended in sled dogs to prevent race induced gastritis?

A

Omeprazole is superior to high dose famotidine BUT famotidine is better than no tx at all

139
Q

With omeprazole and famotidine what effect is seen with gastrin levels?

A

They increased initially and then return to baseline after withdrawal
Recommend 7 days withdrawal prior to checking gastrin

140
Q

In dogs on chronic famotidine, what was the effect on gastrin?

A

Initially increased in gastrin but this returned to baseline - Determined that it is unlikely that chronic famotidine (14d) will interfere with gastrin readings in cases that may have gastrinoma

141
Q

In cats with gastric LSA what was prognostic?

A

Response to tx (chemo) - Longer survival with complete remission
NOT related to prior steroids or stage

142
Q

What are risk factors for GDV in dogs?

A
Dry diet
Anxiety
Fmaily pet
5hrs with owner/day
FI at highest risk
Less likely if playing with other dogs, running fence line
143
Q

In dogs with chronic GI disease, there a correlation bwtn CCECAI and serum B12 and MMA?

A

NO!!!
Also B12 was low in 36% but only 25% had low MAA (suggestive of cellular def of B12)
NOTE: Low Vit B12 is NEGATIVE OUTCOME in dogs with GI dz!!

144
Q

Which breeds are predisposed to HypoB12?

A

Shar Peis
Staffordshire bull terriers
GSD
Mixed breeds

145
Q

Which breeds are predisposed to low folate?

A

Goldens

Boxer

146
Q

What is the association of hyperT4 and hypoB12 in cats?

A

41% cats with moderate to sever hyperT4 had low Vit B12 = Weak negative correlation with B12 and T4 in hyperT4 cats

147
Q

In cats with GI dz was there a correlation of B12 with histopath score?

A

NO! Or with duration of CS

But cats with GI LSA or more severe intestinal inflammation (histopath) had lower Vit B12

148
Q

If AUS is normal in dog, can you exclude GI LSA?

A

NO!! 27% has no changes on AUS

149
Q

Is there a difference in wall thickness in intestines on AUS in dogs of different sizes?

A

NO!!

150
Q

How help is AUS with chronic vomiting and diarrhea?

A

Chronic vomiting: HIGH use 27% (vital in 23%) - More so with increasing age, final dx adenocarcinoma and LSA

Chronic diarrhea: LOW value in 66% (vital in 15%) - 30X more utility if there was a mass palated or rectal mass

151
Q

Is there a relationship btwn BW and GI transit times?

A

NO!! But smaller dogs had longer Gastric and SI transit than larger dogs

152
Q

What is known about the fecal microbiota in obese dogs?

A

Decreased diversity noted

153
Q

Which probiotic resulted in significantly firmer stool and 72% owners noted improved diarrhea in cats?

A

Proviable DC

154
Q

Did Enterococcus faecium SF68 help in shelter dogs and cats?

A

If did in cats (fewer episodes of diarrhea >2 days)
No change in dogs
But diarrhea was uncommon in dogs/cats

155
Q

What is more likely in dogs and cats with intussceptions?

A
Cats = Older with neoplasia
Dogs = Inflammatory dz
156
Q

Can pANCA be used to distinguish IBD vs LSA dogs?

A

NO, perinuclear antineutrophilic cytoplasmic antibodies found in both groups

157
Q

Was there a difference in endoscopic vs full thickness bx in dogs?

A

NO, no change in lymphocytes btwn samples

158
Q

Can you perform flow on endoscopic intestinal bx?

A

YES, revealed that IBD dogs had more intraepithelial lymphocytes with different immunophenotypes than controls

159
Q

What happens to COX-2 in dogs with IBD and food responsive diarrhea?

A

Increase in COX-2 (inflammatory prostaglandins)

160
Q

What happens to fecal calprotectin in dogs with diarrhea and IBD?

A

Fecal calprotectin HIGHER in dogs with diarrhea and CIBDAI >12, and dogs with histopath lesions
Cut off: 48.9 ug/g

NOTE: Serum calprotectin was NOT correlated with CIBDAI or histopath

161
Q

How did IgA and IgG compared in IBD, LSA, and control dogs?

A

IgA lower in feces and duodenum of IBD dogs compared to controls and LSA dogs
NOTE: Duodenal BAFF and APRIL were higher in IBD dogs

162
Q

In LP colitis dogs, was NOD2 correlated with CIBDAI?

A

NO! But NOD2 and NFkappaB were higher in LP colitis dogs compared to controls

163
Q

What happened to urinary leukotriene 4 in IBD and FRD dogs?

A

High in IBD dogs, no difference in FRD vs controls

Also NOT correlated with CIBDAI

164
Q

Which tight junction/apical protein is LOW in IBD dogs?

A

E-cadherin

165
Q

Did AST-120 result in improvement in chronic enteropathy dogs?

A

Yes!

166
Q

Was there a difference with budesonide vs pred induction of IBD dogs?

A

NO! Similar remission rates

Sadly also no difference in SE!!! Pu/PD was slightly lower in budesonide group BUT not significant

167
Q

Which diet resulted in lower CIBDAI over 3 year study in chronic enteropathy dogs? RC Hypoallergenic Hydrolyzed vs RC Intestinal

A

RC Hypoallergenic Hydrolyzed did better starting at 2nd (6-12 months) and third (3 years) rechecks
No difference at 3 months btwn diets

168
Q

Was there a difference in induction of IBD with pred or pred+ metro?

A

No difference, just as effective!

169
Q

In dogs with PLE, what was their Vit D status?

A

Hypovitaminosis D = Low iCa, HIGH PTH, low Vit D

170
Q

In IBD dogs, vit D was correlated with?

A

Albumin (low Albumin = Low vit D)

171
Q

In PLE in Yorkies, what was the difference in MST btwn responders to pred and nonresponders?

A

44 months vs 12 months

172
Q

In PLE Yorkies what were predictive of

A
******Vomiting!
Monocytosis
Severity of hypoAlb
Low BUN
Villous blunting
173
Q

In PLE dogs which is better, pred-azathioprine or pred-chlorambucil?

A

Pred-Chlorambucil
Higher albumin and weight
Longer MST (could not be determined vs 30 days in azathioprine group)

174
Q

In lymphangiectasia, what is recommended in dogs unresponsive to pred or recurrent CS when pred tapered?

A

Ultra LOW fat diet (lower clinical score, higher albumin, total protein, BUN!!)

Much better than ultra low fat combined with low fat

175
Q

Can you use endoscopic appearance to dx lymphangiectasia?

A

NO!! Lacks sens and spec
Even when combination with biomarkers (lymphopenia, low cholesterol, and low albumin) - Sen 80% BUT low spec
NEED HISTOPATH

176
Q

Is antithrombin the reason that PLE are hypercoaguble?

A

NOT sole contributed, AT is borderline LOW

also NOT related ot severity of hypoAlb

177
Q

Does hypercoagubility improve with tx in PLE dogs?

A

NO!!! Even with improved CIBDAI and albumin

178
Q

What is the Vit D status in IBD/LSA cats?

A

Hypovitaminosis D - Some overlap with ill cats

Correlation btwn albumin and VIt D (same as dogs)

179
Q

Was d-lactate correlated with neurologic signs in cats with GI dz?

A

NO, D-lactate was higher in cats with GI dz but not correlated with neurologic signs
L-lactate the same in all groups

180
Q

Does dietary fat effect outcome of diarrhea in cats?

A

NO, same response with high fat or low fat diets

181
Q

In cats what % of LSA cases would have been missed if only upper had been performed?

A

44% LSA only in ileum!!! Need upper and lower in cats

182
Q

Is lymphadenopathy seen in LSA or IBD cats?

A

Sadly it can be seen in both

183
Q

Is the high prevalance of diarrhea and hematochezia in sled dogs related to enteropathogens?

A

NO! Dogs more likely to be + for C. perfringens enterotoxin during race than before

184
Q

In dogs and cats in the shelter with diarrhea what is found?

A

Most have > enteropathogen
Association with
Dog: C. perfringens enterotoxin A
Cat: Feline coronavirus

185
Q

Should you sequence parvo dogs?

A

NO, there is no difference in dz severity or CS with 2c vs 2b

186
Q

Was there a benefit of using CPV immune plasma in dogs?

A

NO!
• Randomized, double blinded placebo controlled clinical trial (14 dogs, 12 ml CPV immune plasma IV or saline IV)
○ No significant difference in CS, reducing viremia, neutrophil/monocyte counts, or days in hospital

187
Q

What effects did oseltamivir have on parvo dogs?

A

Significant wt gain and NO drop in WBC (that was seen in control group)

188
Q

What were acute phase proteins in dogs with parvo?

A

HIGH: CRP, ceruloplasmin, and haptoglobin
LOW: Albumin

189
Q

In parvo dogs which APP were higher in nonsurivors?

A

CRP (>92.4 mg/dl) and ceruloplasmin

190
Q

Did plasma citrulline predict outcome in parvo dogs?

A

NO! But it was severely decreased (marker of global enterocyte mass in humans)

191
Q

What was the response to ronidazole in cats with T. foetus?

A

104 cats
64%: Good clinical response
36%: Partial or no response!

192
Q

Where intrahepatic bacteria found in cats with inflammatory liver disease?

A

Yes, 41% based on FISH

193
Q

Did cats with primary copper hepatopathy have hepatocellular neoplasia?

A

Yes, there were some cats that did have centrilobular copper that also had neoplasia (similar to Wilson/s dz in humans)

194
Q

Does renal tubular dysfunction copper hepatitis labs improve with chelation?

A

YES

195
Q

What is the prognosis for dogs with renal tubular dysfunction and copper hepatopathy?

A

Unknown, but can be good with tx

196
Q

If you see renal glucosuria and elevated ALT in lab….

A

Copper Hepatopathy

197
Q

Regenerative nodules in liver have ____copper.

A

LESS

198
Q

What % of Scotties had hepatocellular carcinoma from progressive vaculoar hepatopathy?

A

34%

199
Q

What did adrenal panels of Scotties with vacuolar hepatopathy reveal?

A
High progsterone (88%) and androstenedione (80%)
More mucoceles see too ?!? (link?)
200
Q

Can you get heaptopathies with Vit B12 def?

A

YES, noted in 2 beagles (def in cubilin)

201
Q

Is hyperinsulinemia the cause of hypoglycemia in dogs with CPSS?

A

NO, there was no difference btwn controls (some dogs did have increased insulin but not sign)

202
Q

CPSS dogs that were hypercoaguable, were more likley to be?

A

Hepatic encephalopathic (40X)

203
Q

Which mature dog breed was more likely to be diagnosed wiht cPSS?

A

Mini Schnauzer

204
Q

Can hypercoagaubility be seen in patients with EHBO?

A

YES, opposite from the dogma that they have Vit K def and should be hypocoag

205
Q

Can AUS differentiate btwn types of feline cholangitis?

A

NO!

206
Q

What effect did pred have on feline lymphocytic cholangitis?

A

Inflammation was decreased but no change in # cholangiocytes and no difference in fibrosis

207
Q

What % of AUS normal livers had histopath disease?

A

64% - AUS has limitations to predict underlying disease

208
Q

What makes up the CIBDAI?

A
  1. Activity
  2. Appetite
  3. Vomiting
  4. Stool Quality
  5. Stool Freq
  6. Weight Loss
209
Q

What makes up the CCEAI?

A

All CIBDAI + albumin, ascites/edema. pruritis

(1. Activity
2. Appetite
3. Vomiting
4. Stool Quality
5. Stool Freq
6. Weight Loss)

210
Q

What risk factors are associated with negative outcome in K9 IBD?

A
62X higher
CCEAI > 12
Low B12
Hypoalb
High endoscopic score in duodenum