Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
264 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
What predisposing factors have been shown to in cats to be associated with more severe periodontal disease or oral inflammation
|
a. Altered immune function with Felv, FIV 2. |
|
|
|
What virus has been implicated as a factor in severe oral inflammation especially in the palatoglossal fold (caudal stomatitis)
|
a. Chronic calicivirus (not bartonella) 3. |
|
|
|
Which bacteria was identified more frequently in cats with caudal stomatitis than healthy cats
|
a. Pasturella multocida 4. |
|
|
|
Cats with chronic caudal stomatitis have lower salivary concentrations of which immunoglobulin
|
Which immune cell is also increased according to immunohistochemistry
|
a. IgA (still have higher IgG, IgM, and IgA concentrations in serum than healthy cats) b. CD8+ predominance over CD4+ which could support a viral cause 5. |
|
|
What are the clinical signs of caudal stomatitis
|
a. Dysphagia, inappetence, anorexia, suspected pain when eating, decreased grooming, headshy 6. |
|
|
|
What treatments have bee shown to be most helpful
|
a. Extraction of premolars and molars to remove plaque which is a source of inflammation, and following with antibiotic therapy for 4-6 weeks after dental surgery (clavamox, clindamycin, and metronidazole are effective). Some cats require methylprednisolone administration every 4-6 weeks 7. |
|
|
|
When extractions, antibiotics, steroids, and pain medications are no longer helpful, what other three treatment options have been shown to be helpful in some cats
|
a. Recombinant feline interferon administered for 90 days; cyclosporine; coQ10 supplementation for 3-4 months 8. |
|
|
|
What 5 cranial nerves are involved in swallowing
|
a. Sensory and motor nerves of the trigeminal, facial, glossopharyngeal, vagus nerve, and motor fibers of the hypoglossal 9. |
|
|
|
What are the four phases of the swallowing reflex
|
a. Oral preparatory phase, oral phase, pharyngeal phase, and esophageal phase 10. |
|
|
|
Which toxins can cause oropharyngeal dysphagia
|
a. Tetanus, botulism, candidiasis, rabies; calicivirus and rhinotracheitis in cats 11. |
|
|
|
What things characterize a normal pharyngeal phase
|
a. Elevation of soft palate in response to food bolus, elevation and forward movement of larynx and hyoid, retroflexion of the epiglottis and closure of the vocal folds to close the larynx, relaxation of the cricopharyngeus muscle that makes up the proximal esophageal sphincter (halted respiration) 12. |
|
|
|
What are the three main categories of oropharyngeal dysphagia
|
a. Oropharyngeal pump failure (pharyngeal weakness) b. Oropharyngeal and pharyngo- proximal esophageal sphincter discoordination c. Pharyngeal outflow obstruction 13. |
|
|
|
Symptoms of retching with meals, nasal regurgitation, swallow related coughing, falling of food from mouth and recurrent pneumonia in a puppy should warrant investigation of what specific diseases
|
a. Cleft palate, cricopharyngeal achalasia, glossal hypertrophy, pharyngeal weakness (golden retriever)(Bovier des frandres and CKCS predisposed to muscular dystrophy) 14. |
|
|
|
If patient has a good gag reflex, does this rule out the pharyngeal dysfunction
|
a. No 15. |
|
|
|
What is cricopharyngeal dysphagia
|
a. Abnormal transport of bolus through the PES (increased incidene in cocker and springer spaniels); 16. |
|
|
|
What is one of the best diagnostics to evaluate real-time swallowing
|
a. Videofluoroscopy 17. |
|
|
|
What are the drawbacks of videofluoroscopy
|
a. Animal positioning is not standardized in veterinary medicine (lateral recumbency slows cervical esophageal transit 18. |
|
|
|
What is crichopharyngeal achalasia
|
a. Inability of the cricopharyngeus muscle to open during cricopharyngeal phase of swallowing (etiology unknown but induced by cutting pharyngeal branch of CN X; seen in miniature dachshunds b. Can have hypertrophy of the crichopharyngeal muscle (cricopharyngeal bar) causing obstruction to propulsion of the bolus through the PES. 19. |
|
|
|
How is cricopharyngeal achalasia treated
|
a. Surgical myotomy or myectomy of the cricopharyngeal muscle b. Alternatives include laser myotomy; use of botulism toxin (lasts 3-4 months) 20. |
|
|
|
What is the most common mechanism for reflux
|
a. Lower esophageal sphincter incompetence 21. |
|
|
|
What effects does esophagitis have on the LES and esophageal motility
|
a. Slows motility and weakens the LES by impairing excitatory cholinergic pathways 22. |
|
|
|
How do upper airway disorders affect GER
|
a. Upper airway obstruction can lead to more negative intrathoracic pressure and increased inspiratory effort which can alter the functional anatomy of the gastroesophageal pressure barrier (lose support of crural diaphragm) 23. |
|
|
|
What changes can occur to the esophagus from chronic esophagitis
|
a. Replacement of normal squamous epithelium with metaplastic columnar epithelium 24. |
|
|
|
Besides aspiration pneumonia, what are some other pulmonary manifestations of GERD
|
a. Chronic bronchitis and interstitial pulmonary fibrosis 25. |
|
|
|
What value does contrast esophagram offer in patients suspected of having esophagitis
|
a. Rule out obvious strictures, see narrowing of the esophagus, may see hiatal hernias, FB; does not diagnosis esophagitis (can sometimes see mucosal irregularities and prolonged retention of contrast media 26. |
|
|
|
What is the most sensitive means for diagnosing esophagitis in dogs and cats
|
a. Endoscopic exam 27. |
|
|
|
What is the gold standard for diagnosing GERD in humans
|
a. Catheter free esophageal pH monitoring (BRAVO system with capsule) 28. |
|
|
|
Studies looking at pre-surgical treatment of dogs to offset GER determined what
|
a. Conflicting results with reglan, ranitidine did not change outcome, omeprazole did not change outcome when given 4 hours prior to surgery 29. |
|
|
|
What is the mechanism of action of metoclopramide
|
a. Dopamine antagonist 30. |
|
|
|
What is cisapride
|
a. Serotonin receptor agonist that increases acetylcholine release in myenteric plexus 31. |
|
|
|
What is sucralfate
|
a. Aluminum salt of sulfated disaccharide that is a mucosal protectant. Negative charge and binds to positive charged protein. Block diffusion of gastric acid and pepsin across the esophageal mucosa and inhibit erosive action of pepsin and possibly bile. Stimulates growth factors implicated in healing ulcer (PGE2 and epidermal growth factor) 32. |
|
|
|
What are the most effective medications used in humans with esophagitis
|
a. PPI; irreversibly inhibit the H+ K+ ATPase (H2 receptor antagonists are reversible) b. Give before first meal of the day; severe cases may need 2nd dose as not all proton pumps are turned on at same time 33. |
|
|
|
What surgery is used in humans with severe GERD and could be on forefront of canine therapy
|
a. Nissen fundoplication 34. |
|
|
|
How do bougienage and ballooning of strictures compare in efficacy
|
a. Equally effective 35. |
|
|
|
Which cell produces H+ in the stomach
|
a. Parietal cell via H+/K+ ATPase pump 36. |
|
|
|
How is HCL acid secretion stimulated
|
a. Endocrine, neurocrine, and paracrine: Gastrin; acetylcholine, and histamine 37. |
|
|
|
Dogs with what comorbidity are recommended to have a once daily dose of H2receptor antagonists
|
a. Renal disease (avoid cation overload) 38. |
|
|
|
Which H2RA is most potent and which one is least potent
|
a. Famotidine is most potent and cimetidine is least potent 39. |
|
|
|
What is the MOA for misoprostol
|
a. PGE1 analog; cytoprotective as incrases bicarb and mucus production, enhancing gastric mucosal turnover and improved blood supply. Directly decreases proton pump activity of parietal cell. Can cause nausea, vomiting, diarrhea, and abdominal pain 40. |
|
|
|
How do over the counter antacid products like Tums and amphojel work
|
a. Provide aluminum or magnesium which neutralize stomach acid to form water and a neutral salt. 41. |
|
|
|
Experimental infection of dogs and cats with helicobacter spp. Causes what kind of changes
|
a. Lymphoid follicular gastritis 42. |
|
|
|
Is helicobacter a cause of chronic gastritis and vomiting or neoplasia in dogs or cats
|
a. Direct causal relationship not established, believed that in some cases it does given patient response to therapy 43. |
|
|
|
What kind of bacteria are helicobacter
|
a. Curved to spiral gram negative microaerophilic motile bacteria with flagella. Contain urease which results in production of ammonia and bicarb 44. |
|
|
|
Is helicobacter a zoonotic condition
|
a. Not usually but cats and dogs showed increased risk factor for humans with Helicobacter heilmannii 45. |
|
|
|
How is helicobacter diagnosed in dogs and cats
|
a. Endoscopic or surgical gastric biopsy samples (90% sensitivity and 100% specificity); gastric brush cytology (fastest and least expensive modality); rapid urease test (CLOtest)(Increased false neg and false positive results) 46. |
|
|
|
How is helicobacter treated
|
a. Metronidazole, amoxicillin, with famotidine 47. |
|
|
|
What allows for complete emptying of the stomach as synchronized housekeeping contractions
|
a. Migratory motor complexes 48. |
|
|
|
Which chemotherapy drug has been shown to transiently decrease antral motility
|
a. Vincristine 49. |
|
|
|
Name primary disorders of the small or large bowel motility
|
a. Dysautonomia, intestinal pseudobstruction (fibrosing leiomyositis), chronic constipation, megacolon 50. |
|
|
|
What is dysautonomia
|
a. Widespread degeneration of autonomic neurons and ganglions. Clinical signs include vomiting, diarrhea, constipation, tenesmus, and regurgitation, high mortality 51. |
|
|
|
Animals with intestinal inflammation have what changes to their muscle function and contractions
|
a. Decreased nonpropulsive motility and increased GMC resulting in frequent defecation and tenesmus. Nonpropulsive motility might be decreased from inflammation affecting the circular colonic smooth muscle 52. |
|
|
|
How do mu-receptor agonists work
|
a. Increase antral contractions but reduce antral propulsion and also decrease intestinal propulsion, strengthen ileocolic and anal sphincters. Loperamide and diphenoxylate 53. |
|
|
|
Cisapride, a 5HT4 agonist, was removed from the market for what reason
|
a. Reaction in cardiac serotoninergic receptors in myocardium and increased risk of lethal arrhythmias in humans 54. |
|
|
|
Which macrolide antibiotic is a motilin agonist
|
a. Erythromycin, riggers MMC 55. |
|
|
|
Which H2receptor antagonists are acetylcholinesterase inhibitors
|
a. Ranitidine and nizatidine; acotiamide is a novel acetylocholinesterase inhibitor (not H2 blocker) 56. |
|
|
|
What reversal agent of xylazine may have promotility effects especially postoperatively by iducing GMC
|
a. Yohimbine 57. |
|
|
|
What effects does capsaicin have
|
a. Induced release of prokinetic calcitonin gene related peptide, increases antrum contractions and contractions in the intestines and colon 58. |
|
|
|
What functions do intestinal microbiota provide
|
a. Metabolic activities (short chain fatty acids, folate, vitamin K), trophic effects to intestinal epithelia, protection against pathogenic microbes, induced host expression of immunity b. Can contribute to disease by competing for nutrients, metabolism of secretory products contribute to colonic secretions, and injury to the intestinal brush border 59. |
|
|
|
GSD with antibiotic responsive diarrhea have decreased amounts of what secretion at the small intestinal surface
|
a. IgA (incrased IgA producing plasma cells and CD4+ Tcell) 60. |
|
|
|
What mutations in immune genes do GSD have
|
a. TLR2, TLR5, NOD2- loss of host tolerance to microbiota 61. |
|
|
|
What two bacteria are best diagnosed through fecal culture
|
a. Clostridium jenjuni and salmonella 62. |
|
|
|
How long should dogs with antibiotic responsive enteropathies be treated with abx
|
a. 4-6 weeks (metronidazole or tylosin) 63. |
|
|
|
What are probiotics
|
a. Live microorganisms which when administered in adequate amounts confer a health benefit to the host 64. |
|
|
|
What is the type of bacteria used most frequently
|
a. Lactic acid bacteria: Lactobacillus, enterococcus, streptococcus, and bifidobacterium 65. |
|
|
|
What are proposed benefits of probiotics
|
a. Enhanced IgA secretion, pathogen phagocytosis, anti-inflammatory cytokines, reduced intestinal permeability, production of bacteriocins (antimicrobial substance), competitive inhibition of pathogenic bacteria 66. |
|
|
|
What is the only antimicrobial showed to be effective in treating tritrichomonas foetus
|
a. Ronidazole; narrow margin safety as causes neurotoxicity at high dosages, not available in US 67. |
|
|
|
How is tritrichomonas diagnosed
|
a. Fecal PCR (can give lactulose to cause loose stool and perform saline flush to get feces) 68. |
|
|
|
What antibiotic are most tritrichomonas resistant to
|
a. Metronidazole 69. |
|
|
|
Which assemblage of giardia infects dogs mostly
|
Cats
|
a. C and D; F 70. |
|
|
Canine parvovirus is what kind of virus
|
a. Single stranded, nonenveloped DNA virus; replicates lymphoid tissues, fecal shedding 3 days after infection, resides in infecting intestinal crypts and bone marrow 5-7 days after infection 71. |
|
|
|
Which assay can distinguish vaccinated dogs vs. infected dogs with parvo
|
a. Quantitative PCR not qualitative 72. |
|
|
|
When should enteral nutrition be started in dogs with parvo
|
a. As soon as possible, no need to wait until vomiting has stopped 73. |
|
|
|
Antivirals such as Tamiflu (Oseltamivir) improved what in dogs with parvo
|
a. Weight gain and WBC counts but no change in survival or clinical signs 74. |
|
|
|
What component of the immune system helps to regulate immune reaction has been shown to be decreased in inflamed mucosa and may explain exaggerated inflammation
|
a. Dendritic cells 75. |
|
|
|
Which toll like receptors are upregulated in the duodenum of dogs with IBD
|
a. TLR2 (specifically correlated with disease), TLR4, and 9 76. |
|
|
|
What is perinuclear antineutrophilic cytoplasmic antibodies (pANCAs)
|
a. Serum antibodies result in a perinuclear staining pattern seen in neutrophils can be used as a marker for ulcerative colitis in people. Has had poor sensitivity in dogs but potentially good specificity 77. |
|
|
|
What is calprotectin
|
a. Calcium binding protein that is abundant in neutrophils and can be increased in feces of humans with IBD 78. |
|
|
|
Poor prognostic indicators for IBD are what
|
a. Hypoalbuminemia, increased cpli 79. |
|
|
|
What is crypt disease
|
a. Can occur without lymphangiectasia and causes PLE. Lesions can be patchy/isolated, seen more commonly in yorkies and rotties; surgical biopsies may be more helpful in patchy cases 80. |
|
|
|
Lesions found on endoscopy or surgery are most often found in what segment of the intestinal tract
|
a. Ileum 81. |
|
|
|
What amino acids should be added to diet to maintain gut health
|
a. Glutamine and arginine (found in vivonex) 82. |
|
|
|
In PLE, where is the inflammation normally found
|
a. Around the lacteals in the villous spaces 83. |
|
|
|
Cats with GI lymphoma most commonly have what phenotype
|
a. T cell 84. |
|
|
|
What is the remission response and MST for cats treated with prednisolone and chlorambucil
|
a. 69-96% with MST of 23-30 months 85. |
|
|
|
Which chemotherapy drug is used as a rescue for feline GI lymphoma
|
a. Cyclosphosphamide 86. |
|
|
|
What factors have NOT shown to be prognostic
|
a. Immunophenotype, AgNOr, PCNA, Felv status 87. |
|
|
|
What are the most common types of infectious causes for canine colitis
|
a. Camylobacter, salmonella, clostridium, invasive E. Coli, trichuris vulpis, giardia, histoplasma, prototheca 88. |
|
|
|
What is a limitation of the WSAVA guidelines as it pertains to colitis
|
a. Does not include evaluation of goblet cells, which correlate with granulomatous colitis and severity of LPS colitis; poor agreement between pathologists 89. |
|
|
|
With LPS, what cells are upregulated
|
a. CD3 T cells, IgA, IgG, plasma cells, IL-2, and TNFa; considered worse severity if there are decreased goblet cells 90. |
|
|
|
What non boxer breeds are predisposed to granulomatous colitis
|
a. Mastiff, Alaskan malamute, Doberman, English bulldog, French bulldog 91. |
|
|
|
Where are serum amylase and lipase produced in the pancreas
|
a. Acinar cells and released when damaged , must be 3-5 x normal to suggest pancreatitis 92. |
|
|
|
What is trypsin-like immunoreactivity
|
a. Measures trypsinogen, trypsin; not specific for pancreatitis but is very sensitive and specific for exocrine pancreatic insufficiency 93. |
|
|
|
What is the most sensitive test for pancreatitis
|
a. Serum pancreatic lipase immunoreactivity- measures lipase only from pancreas (exocrine) 94. |
|
|
|
What factors influence the results of cPli
|
a. Single measurement has poor correlation with histopathologic severity of pancreatitis, not affected by CKD or administration of steroids but can be higher in dogs with Cushing’s 95. |
|
|
|
Once hypocobalaminemia has resulted, what portion of the pancreas is nonfunctional
|
a. Over 80% (pancreas makes intrinsic factor) 96. |
|
|
|
What is fecal pancreatic elastase-1
|
a. Protease made only by pancreas and secreted as a zymogen; found undegraded in the feces; has good sensitivity and specificity for pancreatic function but there is a lot of variation on daily basis; high false positive rate when no clinical signs 97. |
|
|
|
When might fecal pancreatic elastase-1 be superior to TLI
|
a. If there was obstruction of pancreatic duct b/c TLI would be normal in this instance 98. |
|
|
|
What can falsely elevate TLI
|
a. Renal disease 99. |
|
|
|
What are the most common tumors of the exocrine pancreas
|
a. LSA and pancreatic adenocarcinoma 100. |
|
|
|
What is exocrine pancreatic insufficiency and which breeds are predisposed
|
a. Acinar atrophy and found in german shepherds, rough coated collies, Eurasians (atrophic lymphocytic pancreatitis leads to astrophy) 101. |
|
|
|
What is the most common cause of EPI in cats and people
|
a. Chronic pancreatitis, see fibrosis in pancreas vs. in dogs, find that can be increased lymphocytes 102. |
|
|
|
What are the clinical signs of EPI
|
a. Weight loss; increased fecal volume and defecation frequency, yellow to gray feces, weight loss and flatulence, polyphagia, skin disorders 103. |
|
|
|
What are the ways EPI can be diagnosed
|
a. TLI (normal does not rule it out), fecal pancreatic elastase 1 (sensitive but not specific) 104. |
|
|
|
How is EPI treated
|
a. Non enteric coated suppelemental enzyme or pancreas (no pork pancreas); antibiotics as needed for secondary infections , cobalamin 105. |
|
|
|
What is the long term prognosis
|
a. Generally good but 20% will not respond well and be euthanized within a year 106. |
|
|
|
What is the mechanism of action for ondansetron and dolasetron
|
a. 5HT3 antagonists 107. |
|
|
|
How long can a cpli remain elevated after initial incident of pancreatitis
|
a. For at least 2 weeks 108. |
|
|
|
What therapy may be beneficial in dogs with diabetes that have long term chronic pancreatitis
|
a. Cyclosporine SID 109. |
|
|
|
Which large breed dogs are predisposed to congenital portovascular anomalies
|
a. Australian cattle dog, golden retriever, irish wolfhound, labs, 110. |
|
|
|
Which breeds are predisposed to idiopathic inflammatory liver disease
|
a. American and English Cocker spaniels, English springer spaniels, Dobermans, labs, standard poodle 111. |
|
|
|
What red blood cell changes can occur in liver disease due to altered lipoprotein content
|
a. Target cells and poikilocytes 112. |
|
|
|
What is the half life for ALT in dogs and cats
|
a. 2.5 days in dogs; 6 hours in cats 113. |
|
|
|
””” of AST
|
a. 22 hours in dog, 77 minutes in cat 114. |
|
|
|
“”ALP
|
a. 70 hours in dog, 6 hours in cat 115. |
|
|
|
What are the isoenzymes for ALP
|
a. T (serum), B (bone), L (liver), C(Corticosteroid) 116. |
|
|
|
How long does it take liver enzymes to normalize after stopping steroids
|
a. 2-3 months 117. |
|
|
|
What is the pathophysiology of cholestasis of sepsis
|
a. Cytokines from sepsis inhibit expression of hepatocyte transporters necessary for bilirubin transport 118. |
|
|
|
What percentage of the liver is nonfunctional when hypoglycemia is present
|
a. 75% (Hypoglcyemia in PVSA is secondary to reduced glycogen stores and decreased responsiveness to glucagon) 119. |
|
|
|
What is seen as a % of synthetic failure with hypoalbuminemia
|
a. 70% 120. |
|
|
|
Which amino acids are bile acids conjugated to in order to be secreted into bile
|
a. Glycine or taurine 121. |
|
|
|
Ultrasound is more sensitive for the detection of portosystemic shunts when they are located where
|
a. Intrahepatic 122. |
|
|
|
What portal vein/aorta and portal vein/caudal vena cava value was able to completely rule out extrahepatic PSS
|
a. Greater to or equal to 0.8 and 0.75 respectively 123. |
|
|
|
What is the sensitivity and specificity of scintrigraphic imaging of the biliary tract for an obstruction
|
a. Cutoff of 180 minutes for the dye to enter small intestines, 83 to100% sensitive 124. |
|
|
|
When does transplenic portal scintigraphy miss cases of PSVA
|
a. When the shunt originates distal to the splenic vein 125. |
|
|
|
What is the discordance rate between wedge and trucut biopsies
|
Between biopsy and FNA
|
a. 48%; 70% 126. |
|
|
What kind of toxicity is phenobarbital
|
a. Most likely dose dependent, causes bridging portal fibrosis, bile duct hyperplasia, and nodular regeneration; acts as p450 inducer 127. |
|
|
|
Azathioprine liver injury is associated with what
|
a. Generation of oxidative metabolites and depletion of hepatic antioxidants; can be prevented with N-acetylcysteine 128. |
|
|
|
What is the means of ketoconazole hepatoxicity
|
a. Formation of oxidative metabolite that leads to covalent binding to liver proteins and glutathione depletion 129. |
|
|
|
How does acetaminophen induce toxicity to the liver
|
a. Dose dependent and causes acute centrilobular hepatic necrosis 130. |
|
|
|
How is Amiodarone toxic to the liver
|
a. Creation of reactive oxygen species that uncouple oxidative phosphorylation and lead to mitochondrial damage 131. |
|
|
|
Describe CCNU mediated liver toxicity
|
a. Greatest risk to boxers and younger dogs; liver histopath shows hemosiderin laden kuppfer cells, hepatocyte vacuolization, enlargement of nuclei. Recommended to give with SAMe and silybin (Denamarin) 132. |
|
|
|
Which antibiotic is commonly associated with idiosyncratic reactions affecting the liver
|
a. Potentiated sulfonamides (hepatic necrosis; will develop SLE like signs) b. They ar oxidized to form nitroso metabolites that act as haptens c. Treat like Tylenol toxicity 133. |
|
|
|
What drug causes an idiosyncratic liver toxicity in cats
|
a. Diazepam –jaundiced and hepatic failure b. Marked centrilobular hepatic necrosis 134. |
|
|
|
Which drug in cats represents a dose dependent centrilobular hepatic necrosis manifested in presence of glutathione depletion
|
a. Methimazole (not prevented by transdermal version) 135. |
|
|
|
Zone 3 necrosis tends to result in what enzyme elevation
|
a. ALT 136. |
|
|
|
Which toxins tend to affect Zone 3
|
a. Aflatoxcin, sago palm, acute severe copper hepatotoxicosis 137. |
|
|
|
Zone 1 necrosis tends to result in what enzyme elevation
|
a. ALP and GGT 138. |
|
|
|
Thiamine deficiency has what effect in patients with liver disease
|
a. Resemble neurologic signs, promote lactic acidosis, and hypoglycemia 139. |
|
|
|
Why are H2 blockers and PPI not recommended routinely in acute liver failure
|
a. Hepatic splanchnic hypertension causes gastric mucosal edema and reduced gastric acid production 140. |
|
|
|
What is the definition of chronic heptatitis
|
a. Hepatocellular apoptosis or necrosis, variable mononuclear or mixed inflammatory cell infiltrate and regeneration and fibrosis 141. |
|
|
|
What infectious organisms have been reported in a few cases to have been associated with hepatitis
|
a. Bartonella spp., ehrlichia, and leptospirosis 142. |
|
|
|
What should be suspected as a cause for hepatitis if there is a neutrophilic inflammation in the periportal region
|
a. Chronic hepatic or biliary tract infection, consideration given to culture bile or liver 143. |
|
|
|
What test should be performed if there is a granulomatous inflammatory response seen on histopathology
|
a. PCR for bartonella or FISH for bacterial etiology 144. |
|
|
|
Which two drugs are not strongly advocated for their use in dogs with chronic hepatitis and especially in dogs that do not have a biopsy
|
a. NEVER use NSAIDS and should not use steroids in dogs without a biopsy demonstrating inflammation without other underlying causes 145. |
|
|
|
What is the source for hepatic fibrosis in the liver
|
a. Hepatic stellate cell or Ito cell, transforms from quiescent vitamin A storing cell to a collagen-secreting myofibroblast 146. |
|
|
|
What benefit is colchicine
|
a. Use early in hepatic fibrosis in dogs may be beneficial (can cause anorexia and gastrointestinal signs). NEVER USE IN CATS 147. |
|
|
|
What does CVT recommend as the treatment for ascites
|
a. Spironolactone, +/- loop diuretics, as it may help reduce fibrosis and portal hypertension in addition to just being a diuretic 148. |
|
|
|
How is copper transported in the blood
|
a. Ceruloplasmin (transport protein) 149. |
|
|
|
How is copper stored in the cells
|
a. Metallothionein (protect the cell from effects of copper) 150. |
|
|
|
How is copper excreted
|
a. 80% excreted in bile 151. |
|
|
|
How does copper become toxic
|
a. Overwhelms the metallothioneins 152. |
|
|
|
How do copper chelators work
|
a. Bind copper for purpose of removing it and renally excrete it 153. |
|
|
|
Copper associated with copper storage disease will be present in what zone if it is a primary copper disorder
|
a. Zone 3 (zone 1 is if it is secondary to something else) 154. |
|
|
|
When is a copper chelator recommended
|
a. If copper levels are over 1,5000 ug/g regardless of cause b. If a breed predisposed to copper storage disease and has levels over 750 in zone 3, recommend chelation therapy if already on other therapies such as diet or zinc 155. |
|
|
|
What is the chelator most often used
|
a. Penicillamine- has a thiol group and that allows it to chelate metal . high affinity for copper and forms stable water soluble complex 156. |
|
|
|
What is trientine
|
a. Another chelator but uknown mechanism of action. Works faster and good if patient is having hemolysis from copper 157. |
|
|
|
What is the recommended means of administering copper chelators
|
a. Must be given on empty stomach 158. |
|
|
|
Which chelator allows copper to be excreted in bile (may be defective in copper hepatic disease)
|
a. Tetrathiomolybdate 159. |
|
|
|
How long do dogs need to be treated with chelators
|
a. Some dogs like bedlington terrier, need life long therapy b. Others like labs and Dobermans can probably have chelation therapy for 3-6 months and then maintenance with zinc and diet 160. |
|
|
|
How does zinc prevent copper absorption
|
a. Competes for uptake and induces enterocyte metallothionein synthesis and binds copper and sequesters in feces (DON’t GIVE ZINC AND CHELATORS TOGETHER) 161. |
|
|
|
What are the systemic effects of ascites
|
a. Lymphatics overwhelmed as cannot increase capacity from increased intrahepatic resistance of the from the fibrosis so fluid leaks into abdomen (splanchnic vasodilation)-> causes hypotension which activates RAAS. Vasoconstriction systemically which worsens PH 162. |
|
|
|
Why is spironolactone the diuretic of choice
|
a. Because it inhibits aldosterone which has been activated by the RAAS; help mitigate some of the already significant sodium retention 163. |
|
|
|
Why do cats get HE more quickly than other species
|
a. They cannot make arginine which is part of the metabolism of ammonia 164. |
|
|
|
What other substances besides ammonia can cause HE
|
a. Short chain FA, aromatic AA, neurotransmitters, tryptophan, methionine, phenols, bile acids 165. |
|
|
|
What electrolyte can exacerbate HE
|
a. Potassium, when low will make HE worse 166. |
|
|
|
How does ammonia directly affect brain function
|
a. It is an inhibitory substance: glutamate depletion, altered glutamate receptors, blockade of GABA receptors, altered amino acid membrane transport, inhibition of Na-K ATPase, impaired cerebral energy metabolism 167. |
|
|
|
How does lactulose work
|
a. Disaccharide that passes into the colon, degraded by bacteria into short chain FA (acetic and lactic acid) and this acidifies the colon and traps Ammonia into ammonium (NH4+) 168. |
|
|
|
What breeds are predisposed to portal vein hypoplasia
|
a. Cairn terriers, Tibetan spaniels, maltese, havanese, yorkie, Norfolk terrier, miniature schnauzer 169. |
|
|
|
Why might someone suspect portal vein hypoplasia in a dog
|
a. Normal dog with elevated bile acids; may have an elevated ALT 170. |
|
|
|
What are the histopathologic changes seen with this disease
|
a. Juvenile or underdeveloped portal triads, hepatic arteriolar reduplication, small/absent portal veins, prominent ventral venous musculature, lobular atrophy (identical to PSS) 171. |
|
|
|
How is noncirrhotic portal hypertension different from portal vein hypoplasia
|
a. Typically in young large breed dogs and they have clinical signs of liver disease such as ascites, HE, and GI signs; multiple acquired shunts; portal hypertension 172. |
|
|
|
What breeds are predisposed to noncirrhotic portal vein hypoplasia
|
a. Rottweilers, cocker spaniels, Dobermans 173. |
|
|
|
What are the extrahepatic biliary tracts
|
a. Hepatic ducts; common bile duct; gallbladder, cystic duct, and duodenal papillae 174. |
|
|
|
Where is the gallbladder located
|
a. Between right medial and quadrate lobes 175. |
|
|
|
What is the blood supply for the gallbladder
|
a. Cystic artery 176. |
|
|
|
How is the anatomy for the duodenal papilla different for dogs vs. cats
|
a. Cats have the pancreatic duct join the common bile duct prior to reaching the duodenal papilla 177. |
|
|
|
What cells synthesize cholecystokinin and what does cholecystokinin do
|
a. I cells; CCK causes gallbladder contraction 178. |
|
|
|
What is the definition of idiopathic vacuolar hepatopathy
|
a. Reversible parenchymal change characterized by swollen hepatocytes with clear cytoplasm resulting from glycogen without displacement of the nucleus from the center 179. |
|
|
|
What are the most common causes for vacuolar hepatopathy
|
a. Most often from Cushing’s disease or steroid use; can also be from glycogen storage diseases b. Glucocorticoids inhibit nonhepatic glucose use and increase hepatic gluconeogenesis and glycogen formation 180. |
|
|
|
What kind of stain can be performed to determine if the patient has vacuolar hepatopathy
|
a. PAS stain 181. |
|
|
|
What treatments have been successful in some dogs with idiopathic vacuolar hepatopathy
|
a. Low dose mitotane, trilostane, melatonin, and flaxseed products (improved ALP and clinical signs) 182. |
|
|
|
Anorexia causes release of what hormone
|
a. Hormone sensitive lipase to cause fat breakdown and release of fatty acids 183. |
|
|
|
Deficiencies of what macronutrients may contribute to development of fatty liver disease
|
a. L-carnitine and apolipoprotein 184. |
|
|
|
What is seen on labwork panels in cats with fatty liver
|
a. Possible Heinz body anemia, hyperbilirubinemia, ALP > ALT, hypokalemia, hypercholesterolemia 185. |
|
|
|
What are the negative prognostic indicators in cats with HL
|
a. Hypokalemia, anemia, advanced age 186. |
|
|
|
What percentage of cats will have coagulopathies
|
a. 45% 187. |
|
|
|
Which intravenous fluid is considered not ideal to give to cats with HL
|
a. LRS 188. |
|
|
|
What is the most common electrolyte abnormality in cats with HL
|
a. Hypokalemia 189. |
|
|
|
How does L-carinitine help in cats with HL
|
a. Necessary for long chain fatty acid transport into mitochondria and helps protect against loss of lean body tissue during weight loss, may improve FA oxidation, decrease ketosis, and protect against further lipid accumulation 190. |
|
|
|
How does taurine help
|
a. Obligatory AA for bile acid conjugation and increases water solubility , reduces cellular toxicity and facilitates circulation and renal elimination 191. |
|
|
|
How are canine and feline esophagus different
|
a. Feline has smooth muscle in the distal portion whereas the dog has skeletal muscle the entire esophagus 192. |
|
|
|
How has bethanecol been shown to be helpful in dogs with megaesophagus
|
a. May help bind to muscarinic receptors 193. |
|
|
|
What is the pathogenesis of gallbladder mucoceles
|
a. Accumulation of mucous component of bile within the gallbladder (lamellar striations); likely impaired gallbladder motility and accumulation of bile salts which stimulate mucous production from endothelial lining 194. |
|
|
|
What diseases can cause delayed GB emptying
|
a. Steroids, diabetes, hypothyroidism 195. |
|
|
|
Dogs with cushing’s are how many more times likely to develop a mucocele
|
a. 29x 196. |
|
|
|
What mutation in transporter gene in shelties predisposes them to mucoceles
|
a. ABCB4 (normally facilitates phosphatidylcholine across canalicular membrane) 197. |
|
|
|
What breeds are predisposed to mucoceles
|
a. Dachshunds, cocker spaniels, miniature schnauzers 198. |
|
|
|
How does ursodial help in patients with gallbladder mucoceles
|
a. Upregulate canalicular transport 199. |
|
|
|
What is the perioperative mortality rate
|
a. 20-25%, intervention early is associated with best results 200. |
|
|
|
What is the mechanism of action for colchicine
|
a. Antifibrotic that binds selectively and reversibly to microtubules and inhibits polymerization as to prevent collagen secretion 201. |
|
|
|
How is Losartan used in hepatic disease
|
a. ACE inhibitor and can attenuate liver fibrosis during injury and may reduce portal hypertension 202. |
|
|
|
What kind of antibiotic is tylosin
|
a. Macrolide, bacteriostatic antibiotic with activity against most gram + and gram – cocci, gram + rods, and mycoplasma (poor spectrum against E. coli and salmonella). Believed to produce transient changes in the composition of the small intestinal microflora (promotes commensal bacteria while suppressing deleterious bacteria); may also have anti-inflammatory properties as well 203. |
|
|
|
What are the characteristics of tylosin responsive diarrhea
|
a. Watery, mucoid, diarrhea with increased flatulence and borborygmus, usually large breed younger dogs that are affected 204. |
|
|
|
Dogs that present with diarrhea that have normal bloodwork should be screened for what
|
a. Endoparasites, adverse food reactions 205. |
|
|
|
If bloodwork changes are present including hypoalbuminemia, presence of melena or abnormal exam findings, what additional diagnostics should be considered
|
a. Radiographs, ultrasound, endoscopy, and biopsy 206. |
|
|
|
What is haptocorrin
|
a. Cobalamin binding protein that originates in salivary glands and stomach (has high affinity for cobalamin in an acidic pH so much of the binding occurs in the stomach) 207. |
|
|
|
Where is cobalamin transferred to intrinsic factor
|
a. In the duodenum. Haptocorrin is degraded by pancreatic proteases and cobalamin is transferred to intrinsic factor (facilated by neutral pH) 208. |
|
|
|
How is the cobalamin-IF absorbed in cats
|
a. Bind to specific receptors (previously called intrinsic factor cobalamin receptor recently dubbed cubulin) located in microvillus pits of the apical brush-border membrane of ileal enterocytes 209. |
|
|
|
Once absorbed, how does cobalamin get to target cells
|
a. Transcytosed to portal bloodstream bound to transcobalamin 2 (TCII) which mediates cobalamin absorption by target cells; portion of cobalamin is taken up by hepatocytes and though to be re-excreted rapidly in bile bound to haptocorrin (undergoes enterohepatic recirculation which means they can deplete their supply of cobalamin more rapidly) 210. |
|
|
|
What diseases are known to decrease cobalamin in cats
|
a. Dietary deficiency, iBD, alimentary LSA, EPI, pancreatitis, cholangitis, hyperthyroidism, intestinal bacterial utilization 211. |
|
|
|
Cobalamin is an essential cofactor for what two enzymes
|
a. the activity of methylmalonyl-CoA mutase and methionine synthase 212. |
|
|
|
Cats with low cobalamin were found to have increased serum concentrations of what
|
a. Methylmalonicacid 213. |
|
|
|
Are there clear guidelines that predict cobalamin deficiency based on serum cobalamin concentrations
|
a. No 214. |
|
|
|
What are the two most common clinical signs of pancreatitis in cats
|
a. Lethargy and anorexia 215. |
|
|
|
What bloodwork abnormalities would indicate that a cat with pancreatitis requires more aggressive treatment
|
a. Hypoglcyemia and ionized hypocalcemia 216. |
|
|
|
What are the sensitivity and specificity of fPli and ultrasound for diagnosing pancreatitis in cats
|
a. fPli is 79% sensitive and 79% specific b. ultrasound is 73% sensitive but 24-67% specific c. Combined, positive predictive value of 68-80% 217. |
|
|
|
What risk factors are not associated with pancreatitis in cats but are associated with pancreatitis in dogs
|
a. Dietary fat intake, obesity, or drugs 218. |
|
|
|
What infections and toxins have been linked to pancreatitis in cats
|
a. FIP, FIV, calicivirus, toxoplasma, amphimerus pseudofelineus, organophosphates 219. |
|
|
|
What opioid causes spasm of the pancreatic duct and should be avoided
|
a. Morphine 220. |
|
|
|
For refractory pain, what treatment may help provide pain relief secondary to reducing pancreatic secretions
|
a. Addition of pancreatic enzymes 221. |
|
|
|
Which bacteria have been shown to hematogenously spread to the feline pancreas following colonic transmigration and by reflux into the pancreatic duct
|
a. E.coli; other are gram negative and anaerobic bacteria from the GI tract 222. |
|
|
|
Reduced hepatic blood flow that occurs as a result of portosystemic shunts leads to what derrangements
|
a. Decreased protein synsthesis, decreased glycogen storage, reticuloendothelial function, and altered metabolism of ammonia and other toxins 223. |
|
|
|
What are predisposing factors of severe neurologic signs in dogs with PSS
|
a. Protein overload, hypokalemia, alkalosis, hypovolemia, hypoxia, gastrointestinal hemorrhage, infection, azotemia, constipation, drugs, and transfusion 224. |
|
|
|
What protein sources are recommended for dogs with liver disease
|
a. Soybean and dairy sources of protein because highly digestible 225. |
|
|
|
What is the difference between midazolam and diazepam in patients with liver disease
|
a. Diazepam contains propylene glycol and this requires liver metabolism so clinicians prefer midazolam IV 226. |
|
|
|
What factors were associated with decreased MST in dogs that were medically managed with CPSS
|
a. Intrahepatic shunt location, younger age at onset, greater severity of clinical signs, lower BUN (52% vs. 88% surgically treated dogs survival rate) 227. |
|
|
|
What factors are associated with poorer response for surgical shunt occlusion
|
a. Preoperative hypoalbuminemia, hypoproteinemia, anemia, or leukocytosis 228. |
|
|
|
Why is the term cholangitis used in cats now and it is not recommended to describe inflammatory liver disease as cholangiohepatitis
|
a. Unlike dogs, cats have inflammatory changes around their bile ducts and ductules and not the hepatic parenchyma. Descriptions of inflammatory liver disease are based on cellular infiltrate, degree of periportal fibrosis, presence of destructive lesions in bile ducts, and evidence of fluke infestation 229. |
|
|
|
What is lymphocytic portal hepatitis
|
a. No longer classified as a primary inflammatory liver condition in cats but rather a secondary disorder b. Lacks bile duct involvement, inflammatory cells into hepatic parenchyma, and periportal necrosis, uncommon occurrence of icterus and most cats do well calling into question use of steroids. Laboratory changes differ between this and neutrophilic form only with neutrophilic form commonly having a neutrophilia peripherally 230. |
|
|
|
Describe neutrophilic cholangitis
|
a. Suppurative cholangitis and is the most common type of biliary tract disease in cats in NA. Subdivided between acute and chronic forms (despite overlap). Affects middle-aged cats and clinical signs include anorexia, weight loss, lethargy, vomiting, fever, dehydration, icterus, abdominal pain, hepatomegaly 231. |
|
|
|
What is the difference between the acute and chronic form of neutrophilic cholangitis
|
a. The acute form is characterized by a neutrophilic infiltration (thought to be triggered by enteric bacteria) and the chronic form has mixed cellular infiltrate with neutrophils, lymphocytes, and plasma cells and degree of biliary hyperplasia; infiltration is associated with walls and lumen of biliary duts and surrounding portal areas 232. |
|
|
|
What percentage of cats had intrahepatic bacteria with neutrophilic cholangitis with FISH
|
a. 33% 233. |
|
|
|
Cats with neutrophilic cholangitis are more likely to have sonographic evidence of what disease compared to cats with lymphocytic cholangitis
|
a. Pancreatitis 234. |
|
|
|
What is the recommended treatment for neutrophilic cholangitis
|
a. Cephalosporins, amoxicillin, clavamox and sometimes addition of fluoroquinolone 235. |
|
|
|
When is prednisone recommended
|
a. When biopsy shows relatively few neutrophils and increased lympolasmacytic cells 236. |
|
|
|
What is lymphocytic cholangitis
|
a. Lymphocytic inflammation directed at bile ducts with some cases having ductopenia, peribiliary fibrosis, portal Beta cell aggregates or portal lipogranulomas; predominant T cell population (supportive of immune component) 237. |
|
|
|
How are cats with lymphocytic cholangitis different from those that get neutrophilic
|
a. Cats with lymphocytic cholangitis are older and have similar clinical signs as in neutrophilic and they generally need steroids to help resolve clinical signs 238. |
|
|
|
What is CTR1
|
a. Copper transporter 1 that facilitates copper uptake in the small intestines as well as hepatocellular uptake of copper 239. |
|
|
|
How does copper get from the basal side of the enterocyte into portal circulation
|
a. ATP7A (ATPase) 240. |
|
|
|
What does COMMD1 do
|
a. Interacts with ATPase (ATP7B) to promote copper excretion in bile, may also help activate superoxide dismutase (SOD1) and help prevent oxidative damage b. Loss of COMMD1 in bedlington terrier results in decreased excretion of copper into the bile 241. |
|
|
|
What breeds are predisposd to primary copper associated hepatitis
|
a. GSD, Anatolian shepherd, keeshond, boxer, Airedale, Norfolk terrier, beagle, cocker spaniel, CKCS 242. |
|
|
|
Females of what breeds are more likely to get copper associated hepatitis
|
a. Dobermans and labs 243. |
|
|
|
In a subclinical state, what might someone see on bloodwork to be the preliminary indication of copper storage disorder
|
a. Elevated ALT 244. |
|
|
|
What concurrent comorbidities might be seen in dogs with copper hepatitis
|
a. Fanconi’s syndrome 245. |
|
|
|
What stain will stain copper
|
a. Rubeanic acid or rhodanine (grading scheme exists and anything over 2 is considered abnormal) 246. |
|
|
|
Why is esophageal mucosa more easily damaged than gastric mucosa
|
a. Does not have mucus-bicarbonate preepithelial barrier and does not heal by epithelial restitution; endogenous prostaglandins are not as effective in protecting the esophageal epithelial surface, esophagus does not produce a mucus cap after epithelial injury 247. |
|
|
|
What parenteral promotility drug similar to cisapride will soon be available in the US
|
a. Mosapride 248. |
|
|
|
How high of a pH do most H2 blockers raise gastric pH
|
a. Raise to 4 and 5 249. |
|
|
|
What is lafutidine
|
a. H2 receptor antagonist that has been reported to have enhanced efficacy against treating esophagitis as it stimulates the capsaicin pathway increasing hyperemia and raising pH 250. |
|
|
|
What therapy is recommended by CVT for patients with severe esophagitis and or inflamed strictures
|
a. Cisapride, omeprazole and gastrotomy feeding tube 251. |
|
|
|
How does cholestasis induce ALP production
|
a. Accumulation of bile salts from impaired bile flow induces production of L-ALP; ALP accumulates on hepatocyte membranes and are solubilized by glycosylphosphatidylinositrol phospholipase 252. |
|
|
|
Which gene is responsible for corticosteroid alkaline phosphatase
|
a. I-ALP gene 253. |
|
|
|
Is C-ALP specific
|
a. No, diseases other than HAC and exogenous steroids can cause it to be elevated such as stress, diabetes mellitus, and even primary liver disease; possibly induced by progresterones 254. |
|
|
|
What are common causes for ALP elevation in asymptomatic patients
|
a. Neoplasia, benign nodular hyperplasia, chronic hepatitis, idiopathic vacuolar hepatopathy, breed-related conditions 255. |
|
|
|
Which layer of the stomach is involved in ulcer formation
|
a. Muscular layer 256. |
|
|
|
What new hormone in addition to histamine, gastrin, and acetylcholine is known to stimulate gastric acid secretion
|
a. Enterooxyntin 257. |
|
|
|
Where is histamine secreted
|
a. Enterochromaffin like cells in the lamina propria of the gastric glands 258. |
|
|
|
What two receptors are on enterochromaffin cells
|
a. Acetylcholine and gastrin 259. |
|
|
|
Where is pepsinogen produced
|
a. By chief cells in the gastric mucosa; converted to pepsin when pH is below 5.0 260. |
|
|
|
What triggers pepsinogen secretion
|
a. Vagal stimulation (acetylcholine); gastrin in dogs; acid triggered local effects; Secretin by the secretin cells in the duodenum 261. |
|
|
|
What is gastrin-releasing peptide
|
a. Also called bombesin and stimulates the gastrin cell 262. |
|
|
|
What four main factors protect the stomach from the effects of proteases and acid
|
a. Blood flow, bicarbonate production, cellular renewal, and chemical factors such as prostaglandins, gastrin, and epidermal growth factor 263. |
|
|
|
What two ways do prostaglandins protect the gastric mucosa
|
a. Inhibition of acid secretion and enhancement of mucosal resistance to injury by mechanisms independent of acid secretory inhibition (cytoprotection) 264. |
|
|
|
Large ulcers in the pyloric antral region near the incisura are likely from what in dogs
|
a. Gastric tumors |
|
