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ACVIM Reading List > GI CVT > Flashcards

GI CVT Flashcards

1
Q

Name 2 infectious diseases that are associated with Feline Caudal Stomatitis?

A
  1. Feline Herpes
  2. Feline Calcivirus
    ??Bartonella??
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2
Q

What is the BEST long term outcome for cats with caudal stomatitis?

A

Extractions (potential full mouth)

Up to 60% resolution

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3
Q

Name a non-traditional treatment that can be used for feline caudal stomatitis.

A

Coenzyme Q - Recommended in cats with residual inflammation following extarctions (anecdotal evidence only, used in humans) = Studies are needed

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4
Q

Name the 5 nerves that can involved with swallowing.

A
  1. Sensory and motor of trigeminal n.
  2. Facial n.
  3. Glossopharyngeal n.
  4. Vagus n.
  5. Hypoglossal n.
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5
Q

What are the 3 types of dysphagias?

A
  1. Oropharyngeal dysphagia
  2. Esophageal dysphagia
  3. Gastroesophageal dysphagia
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6
Q

What is cricopharyngeal achalasia?

A

Rare form of dysphagia → Inadequate relaxation of cricopharyngeal muscle § Very young animals, tx with myotomy

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7
Q

What are the 3 stages of oropharyngeal dysphagia?

A
  1. Oral Stage - Prehending, tranporting food to oropharynx
  2. Pharyngeal Stage
  3. Cricopharyngeal Stage - Relaxation of cricopharyngeal muscles (upper esophageal sphincter)
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8
Q

What neuromuscular disease should be consider in a dog with acute onset of dyphagia?

A

Acquired myasthenia gravis (alone or as part of generalized neuromuscular disorder)

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9
Q

What percentage of dogs with acquired MG has focal signs (pharyngeal, esophageal, laryngeal weakness) without limb weakness?

A

About 43% of dogs

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10
Q

What test should be performed to assess for myasthenia gravis?

A

Ach Receptor Antibody Titer

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11
Q

When would myotomy be contraindicated in animals with cricopharyngeal relaxation abnormality?

A

If asynchrony btwn pharyngeal constrictors and relaxation of cricopharyngeal muscle

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12
Q

What are common causes of oropharyngeal dysphagia in dog?

A
  1. Myasthenia Gravis
  2. Myositis
  3. Endocrine myopathies (hypoT4, hypoadrenocorticism)
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13
Q

In which spp is chronic esophagitis well documented?

A

Cats = result of hiatal hernia or lower esophageal sphincter abnormalities

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14
Q

What is a very common cause of esophagitis?

A

Anesthesia - 65% of strictures were attributed to prior anthestic event

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15
Q

What can occur with chronic gastroesophageal reflex?

A

Severe histology changes in distal esophagus (metaplasic changes) = Barrett’s esophagus in humans

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16
Q

What imaging modality can be used to assess for esophageal FB?

A

Fluoro with iodinated contrast

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17
Q

What can be more sensitive way to diagnose hiatal hernia?

A

Could see with fluoroscopy when applying pressure to abdomen

More sensitive to diagnosis with endoscopy

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18
Q

What is the most sensitive and specific way to diagnose esophagitis?

A

Endoscopy - Erythema, friability, erosions, exudative pseudomembranes

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19
Q

Why is the esophagus so easily damaged by gastric acid?

A

The mucosa has NO mucus-bicarbonate pre-epithelial barrier!!! NOT protected

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20
Q

Why is the esophagus so easily damaged by gastric acid?

A

The mucosa has NO mucus-bicarbonate pre-epithelial barrier!!! NOT protected
What are H2 blockers? Competitive inhibitors of gastric acid secretion (famotidine)

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21
Q

What is a proton pump inhibitor?

A

Noncompetitive inhibitor of gastric acid secretion (omeprazole)

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22
Q

How long can it take for a PPI to reach maximum effectiveness?

A

2-5 days

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23
Q

What is benefit of sucralfate?

A

Needs to be administer when high acid production, otherwise neutral esophagus will not allow sucralfate to function
Minimal to no benefit in humans

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24
Q

What are the 2 techniques commonly used to treat esophageal strictures?

A

Ballooning and Bougienage (similar results)

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25
Q

Which technique for esophageal strictures allows you to apply more force?

A

Bougienage

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26
Q

Which method is the best for esophageal strictures to minimize trauma and prevent recurrence?

A

Better to do several less aggressive procedures

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27
Q

What is the reported number of dilations needed for esophageal strictures?

A

2-4 dilations (can be up to 10-15)

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28
Q

If GER is secondary to congenital hiatal hernias what is the treatment?

A

Require sx, but prognosis is good

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29
Q

What is the reported success rate of esophageal strictures?

A

77-88% with stricture dilation

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30
Q

What are 3 classic CS associated with esophageal disease?

A

Regurgitation, dysphagia, ptyalism

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31
Q

What is a common complication of megaesophagus?

A

Aspiration pneumonia

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32
Q

Which nerves controls the upper esophageal sphincter?

A

Glossopharyngeal, pharyngeal , recurrent laryngeal branches of vagus n.

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33
Q

Explain the muscles of the canine esophagus.

A

Two layers of skeletal muscle (innervated by somatic branch of vagus n)

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34
Q

Explain the muscles of the feline esophagus.

A

Smooth muscle in distal 1/3 (different from dog that is all skeletal muscle)

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35
Q

What is different about the LES?

A

Physiological sphincter (rather than anatomical, no distinct muscle mass)

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36
Q

Name 4 factors that increase tone of LES to prevent reflux?

A
  1. Increased intragastric pressure
  2. Acid in Cardia
  3. High protein diet
  4. Hormones (gastrin, histamine, ACh)
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37
Q

What are the 2 types of contractions that occur in the esophagus?

A
  1. Primary peristalsis: In response to swallowing

2. Secondary peristalsis: In response to food in the lunen (afferent receptors)

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38
Q

What are the steps in primary peristalsis in the esophagus?

A

o Afferent vagal receptors (pharynx and proximal esophagus) stimulated by presence of food (solids more effective than liquids in stimulating swallowing reflex) → initiates efferent response via somatic nerve fibers of vagus (ends at myoneural junction) → coordinated contraction of UES and propagation of peristaltic wave aborally along esophagus through LES into stomach

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39
Q

In which breed is congenital megaesophagus inherited?

A

Wirehaired fox terrier, miniature schnauzer

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40
Q

Name 6 breeds that have an increased prevalence of congenital megaesophagus.

A
  1. Great Danes
  2. GSD
  3. Labs
  4. Newfoundlands
  5. Shar Peis
  6. Irish Setter
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41
Q

Up to what age can congenital megaesophagus be seen?

A

Normally CS by 3 months, but can be as long as 1 year

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42
Q

Which 4 breeds are at increased risk of acquired megaesophagus?

A
  1. GSD
  2. Goldens
  3. Irish Setters
  4. Great Danes
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43
Q

What is acquired megaesophagus?

A

· Caused by any disorder that inhibits esophageal peristalsis either by disrupting esophageal neural pathways or by causing esophageal muscular dysfunction

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44
Q

What is the most common cause of acquired megaesophagus in dogs?

A

Myasthenia Gravis

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45
Q

What is the pathogenesis of myasthesia gravis?

A

§ Acquired auto-immune dz: Interferes with neuromuscular transmission, production of autoantibodies against nicotinic ACh receptors →Decreased receptors = skeletal muscle weakness

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46
Q

What are the 2 forms of myasthenia gravis?

A
  1. Generalized (exercise-related generalized muscle weakness, worsens with exercise)
  2. Focal (muscle weakness affecting esophagus, pharyngeal, facial muscles
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47
Q

What is the diagnostic test for myasthenia gravis?

A

Increased antibody titer to ACh receptors

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48
Q

Can you have seronegative animals that have myasthenia gravis?

A

Yes, estimated to be about 2% of generalized MG are seronegative, unknown in focal MG

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49
Q

How does hypoadrenocorticism result in megaesophagus?

A

Impaired muscle carbohydrate metabolism and depletion of muscle glycogen from glucocoricoid deficiency and decreased catecholamine activity

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50
Q

Is hypothyroidism proven with megaesophagus?

A

NOT proven! 1 case that improved with supplementation of Thyroid meds
Consider that both diseases are immune mediated - association?

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51
Q

What is dysautonomia?

A

Idiopathic condition - Failure of sympathetic and parasympathetic NS = Motility issues
Mydriasis with absent PLRs, decreased tear production, dry mucous membranes

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52
Q

What percentage of dogs with dysautonomia had megaesophagus?

A

In one paper about 60%

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53
Q

What disease affects the vagus n. and is though to be a risk factor for acquired megaesophagus?

A

Laryngeal paralysis

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54
Q

What is the classic signalment for idiopathic megaesophagus?

A

· Spontaneously, large breed dogs (5-12 yrs), no sex or breed predisposition
· Majority of adult dogs are diagnosed with idiopathic megaesophagus

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55
Q

Name 3 types of imaging that can be performed to assess for megaesophagus?

A
  1. Fluoroscopy
  2. Manometric
  3. Scintigraphic
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56
Q

When a dog has megaesophagus why would you want to perform a fecal examination?

A

To assess for Spirocerca lupi

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57
Q

What diagnostic should be performed if ACh receptor antobody test is negative?

A

Submit muscle bx for immunocytocehmical staining (less specific for MG but highly suggestive for seronegative myasthenics)

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58
Q

What test can be performed if you are concerned about dysautonomia?

A

If affected: Miosis in response to ocular pilocarpine, no change in HR with atropine, no flare with intradermal histamine

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59
Q

What is the treatment of choice for MG?

A

Long-acting anticholinesterase drugs (pyridostigmine, neostigmine)
Improves CS and decreased ACh receptor antibody concentratuon

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60
Q

What percentage of MG has clinical and immunological remission with anticholinesterase drugs alone?

A

About 89%

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61
Q

Name 2 other treatments for MG?

A

Immunosuppression (steroids, azathioprine)

Plasmapheresis - filtration of plasma to eliminate circulating antibodies

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62
Q

What is the MOA of prokinetic drugs like metoclopramide and cisapride?

A

Increased motility by bindings to 5-HT4 (serotonin) receptors on enetric cholinergic neurons

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63
Q

What is the estimated recovery rate of congenital megaesophagus and which breed has it been reported in?

A

About 20-46%

Miniature schnauzers acquire improved or normal esophageal function by 6 -12 months of age

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64
Q

Which bone disorder has been seen in humans with achalasia?

A

Hypertrophic osteoarthropathy (seen in 1 GSD)

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65
Q

What is the relationship btwn spiral bacteria and chronic gastritis in dogs/cats?

A

· Direct causal relationship btwn spiral bacteria and chronic gastritis/vomiting has NOT been firmly established (dogs/cats)

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66
Q

What type of bacteria is Helicobacter?

A

Gram Negative

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67
Q

What enzyme does Helicobacter spp have lots of?

A

Urease (production of ammonia and bicarbonate when in contact with urea)
Alters pH surrounding bacteria and helps to colonize in acidic environment

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68
Q

What is different about the Helicobacter in cats/dogs?

A

Larger - Helicobacter heilmannii o Helicobacter felis, Helicobacter bizzozeronii, and Helicobacter salomonis (NOT H. pylori)

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69
Q

Name a diagnostic that can be performed on a sample from gastric brush cytology?

A

Rapid urease test - detects presence of bacteria urease (produced by Helicobacteria spp) - CLOtest (gel with urea and pH indicator (phenol red) - Bacteria will hydrolyze urea to ammonia with change pH of gels leading to a color change from yellow to magenta

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70
Q

What is the treatment of choice for Helicobacter spp?

A

· Triple Therapy: Amoxicillin, metronidazole, bismuth subsalicylate (Pepto Bismol) or dual tx with clarithromycin and amoxicillin = q12hrs for 2 weeks; quadruple therapy (adding on famotidine)

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71
Q

What is the eradication rates with triple therapy for Helicobacter spp?

A

o Eradication rates: 70% and 78.5% 4 wks after triple and quadruple tx; at 6 months 44.4% and 41.7%; 8 dogs were negative at 4 wks and positive at 6 months (Leib, Duncan, and Ward, 2007)

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72
Q

What percentage of dogs/cats with chronic gastritis and Helicobacter spp will improve with treatment?

A

About 50%
What are the 3 main secretagogues to stimulate acid production in parietal cells? acetylcholine (M3), gastrin (CCKB) and/or histamine (H2) receptors on basolateral membrane via secondary messengers

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73
Q

What are the 3 main secretagogues to stimulate acid production in parietal cells?

A

acetylcholine (M3), gastrin (CCKB) and/or histamine (H2) receptors on basolateral membrane via secondary messengers

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74
Q

What are the 3 lines of defense against injury from acid/pepsin?

A
  1. Pre-epithelial - Mucus and bicarbonate barrier
  2. Epithelial - Barrier function of apical plasma membrane, intrinsic cell defense
  3. Subepithelial - Blood flow mediated removal of back diffused H+ and supply of energy
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75
Q

How do prostaglandins play a KEY role in protecting gastric mucosa against injury?

A

§ Inhibition of acid secretion and enhancement of mucosal resistance to injury by mechanisms independent of acid secretion inhibitor called cytoprotection

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76
Q

How do NSAIDs result in mucosal injury?

A

Impairing prostanglandin-dependent mucosal protective mechanisms by nonselective inhibitor of 2 isoforms of cyclooxygenase (COX) = COX-1 and COX-2
Cox-1 inhibitor can lead to reduced bicarbonate levels
Direct topical effect of NSAID on gastric mucosa

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77
Q

What steroid has the most ulcerogenic property?

A

Dexamethasone

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78
Q

What is the diagnostic test of choice for gastric ulcers?

A

Gastroscopy

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79
Q

How does sucralfate work?

A

Suiplhated disaccharide-aluminium hydroxide complex that adheres to ulcerate tissue and provide barrier to acid and pepsin penetration
Effective at acidic to neutral pH

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80
Q

What type of gastric acid suppressor results in suppression from hsitamine, acetylcholine, and gastrin induced gastric acid secretion?

A

PPIs (inhibit that final step in acid secretion = gastric pump)

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81
Q

What is another treatment for gastric ulcerations that is not indicated if an ucler is already present?

A

· Misoprostol – Synthetic prostaglandin analog
o Similar to endogenous prostaglandins (stimulation of mucus secretion, increase bicarbonate secretion, gastric mucosal blood flow, reduced acid secretion)

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82
Q

What is soraprazan?

A

K+ competitive acid blocker - Blocks action of H/K ATPase by competing with K+

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83
Q

What are the 2 most common types of inflammation in IBD?

A

Lymphoplasmocytic and eosinophilic

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84
Q

What is a very rare type of inflammation in IBD?

A

Neutrophilic

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85
Q

In what breed is PLE and PLN complex most common?

A

Soft-coated wheaten terriers

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86
Q

In what breed is immunoproliferative enteropathy common?

A

Basenjis

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87
Q

In what breed is IBD common?

A

Norwegian Lundehunds

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88
Q

In what breed is histocytoc ulcerative colitis common?

A

Boxer

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89
Q

Which disease is enrofloxacin responsive and why?

A

Histiocytic ulcerative colitis of Boxer

Selective intramucosal colonization of E. coli strains that are adherent and invasive phenotype

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90
Q

What is the suggested pathogenesis of IBD?

A

• Reportedly has immune-mediated pathogenesis à intestinal mucosa has barrier function (immune exclusion) and controls exposure of antigens à IBD develops when normal decision-making process of what to be tolerant of and what to react to breaks down
• Genetic factors thought to play a role as well
○ End effect of tolerance breakdown is uncontrolled inflammation

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91
Q

What may be a more sensitive marker of early disease in PLE than albumin?

A

Fecal a1-proteinase inhibitor

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92
Q

What does cobalamin deficiency alter the doctor to?

A

Intestinal malabsoprtion (it is not specific for a particualr GI disease)

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93
Q

How useful is measurement of intestinal wall thickness in the diagnosis of IBD?

A

Not useful! In the future we may consider use of doppler to investigate intestinal diseases

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94
Q

What is essential to prove the presence of intestinal inflammation and confirm diagnosis of IBD?

A

Intestinal bx

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95
Q

What is a marker with potential use in IBD and has been suggested to correlate with cases that respond to dietary therapy rather than steroids?

A

Mucosal perinuclear antineutrophilic cytoplasmic antibody (pANCA) - When high pretreatment expression it correlated with cases that responded to dietary therapy rather than steroids

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96
Q

What marker has been shown to correlated with patients that failed to response to steroids?

A

Lamina propria lymphocyte P0glycoprotein expression = transmembrane protein that is drug-efflux pump in intestinal epithelium
High values = poor response to steroids; Low levels = good response to steroids

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97
Q

Name 2 markers for IBD that would require repeat endoscopy in order to monitor case.

A

Mucosal perinuclear antineutrophilic cytoplasmic antibody (pANCA) and lamina propria lymphocyte P-glycoprotein expression

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98
Q

What are the 4 main treatments given if being used a diagnostic for IBD?

A

○ Anthelmintic/Antiparasitic (Fenbendazole, 50 mg/kg PO q3-5 days)
○ Dietary Modification: Antigen-limiting or hydrolyzed protein diet for 3-4 weeks
○ Antibacterial trial: Tylosin 10 mg/kg PO q8hrs OR metronidazole 10 mg/k PO q12hrs for 3-4 weeks
○ Immunosuppressive trial: Prednisolone 1 mg/kg q12hrs PO

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99
Q

What can be used to monitor IBD in dogs?

A

Canine IBD Activity index (CIBDAI)

Increased value when increase in severity of GI signs but does NOT confirm diagnosis of IBD

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100
Q

Which breed is known to have gluten intolerance?

A

Irish Setter

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101
Q

What is a hydrolyzed protein diet?

A

Native chicken or soy protein has undergone chemical or enzymatic treatment - Low molecular weight protein derivatives

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102
Q

Name a low solubility fiber and how it works.

A

Cellulose - Increasing bulk in intestine, binding nonabsorbed fluid, helping regulate intesta

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103
Q

Name a high solubility fiber and how it works.

A

Beet pulp, pectins (carrots/fruit), gumlike fiber: Easily be fermented by intestinal bacteria, SCFA (butyric acid) that can be used by colonic mucosa

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104
Q

Why is budesonide good for IBD?

A

Glucocorticoid that has high first pass metabolism, still suppresses HPA axis and can induce steroid hepatopathy

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105
Q

What is the prognosis with IBD?

A

Only 26% completely resolved, intermittent signs in about 50%, 4% completely uncontrolled, 13% euthanized because of poor response

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106
Q

What is the main negative prognostic sign in IBD patients?

A

Hypoalbuminemia

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107
Q

What type of antibiotic is tylosin?

A

Macrolide, Bacteriostatic

Good for Gram+ and Gram - cocci, gram + rods, Mycoplasma

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108
Q

Which bacteria are intrinsically tylosin resistant?

A

E. coli and Salmonella spp

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109
Q

What the normal amount of time that it takes for an animal to respond to tylosin?

A

Normally animals respond in 3-5 days

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110
Q

How are Trichomonads transmitted?

A

NOT form cysts! Reproduce by binary fission, transmitted directly from host to host in form of trophozoites

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111
Q

Why are antibiotics justified in IBD?

A

Bacterial antigens are thought to drive the pathogenetic pathway

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112
Q

What is a protozoal cause of chronic diarrhea in cats?

A

Tritrichomonas foetus - colonized distal ileum and colon (LP and neutrophilic inflammation)

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113
Q

What are the classic CS of T. foetus in cats?

A

Large bowel diarrhea +/- fresh blood or mucus (semiformed, malodorous,

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114
Q

What disease should cats diagnosed with Giardia spp on fecal smear that fail to respond to antimicrobials be tested for?

A

T. foetus

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115
Q

Name 4 ways that T. foetus can be diagnosed in cats?

A
  1. Direct fecal smear
  2. Selective protozoal culture
  3. PCR
  4. Seen on colonic bx
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116
Q

What is the key microscopic difference btwn trichomonads and Giardia spp?

A

Giardia spp = Falling leaf motility

Trichomonads = Undulating membrane

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117
Q

What is the sensitivity of a direct fecal smear for evaluation of T. foetus?

A

LOW!! 2% in experimentally infected and about 14% in spontaneous disease

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118
Q

Do + In Pouch TF culture preclude the possibility of coinfection with P.hominis or Giardia spp?

A

No! Although these 2 organisms cannot survive in the pouch longer than 24 hours - you could have a co-infection.

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119
Q

Why is it imperative to get multiple bx of colon if you are trying to find T. foetus?

A

They can occur in multiple clusters. Need a minimum of 6 bx to get 95% or > confidence that trichomonads will be identified

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120
Q

Name several coexisting infectious diseases that can occur with T. foetus?

A

Cryptosporidiosis, Giardia spp, parasites

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121
Q

What percentage of cats will have spontaneous resolution of diarrhea within 2 years of T. foetus infection?

A

About 88%, but 57% remained infected when tested 2-5 yrs later!

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122
Q

What is the recommended treatment for T. foetus and what is a potential side effect?

A

Ronidazole - Neurotoxicity (common)

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123
Q

What are several reasons that PLE can develop.

A

Loss of mucosal barrier function = increased permeability

Malfunction or abnormalities of intestinal lymphatic drainage

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124
Q

In which spp is PLE more common in?

A

Dogs

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125
Q

Name several diseases that can result in PLE.

A

Tons of things cause PLE: intestinal lymphangiectasia, inflammatory disorders, GI ulceration, GI neoplasia, intestinal fungal or parasitic infection (histoplasmosis, pytiosis, trichuriasis, ancyclostomiasis), foreign bodies, chronic intussusceptions, acute or chronic viral or bacterial infections, immune-mediated and allergic diseases (SLE), constrictive pericarditis, right-sided heart failure, hypoadrenocorticism

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126
Q

What is considered to be the most common disorder associated with PLE?

A

Intestinal Lymphangiectasia

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127
Q

Name the 2 forms of intestinal lymphangiectasia.

A

○ Primary – congenital disease where lymphatic vessels are insufficient or malformed
§ Poor lymphatic flow and drainage, may also have systemic lymphatic abnormalities
§ Rare in dog and cat
○ Secondary – obstruction to lymphatic flow in lymphatic system or due to venous hypertension
§ Increased pressure in lymphatic vessels = dilation of lacteals = leakage of lymph into the intestine
§ Leakage of chylomicrons, proteins and lymphocytes
§ Underlying disease may also limit resorptive capacity for the injured GI
§ May see lipogranulomas around lymphatics in inflammatory disorders

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128
Q

What is the most common form of IBD (diffuce infiltration of cells into lamina propria of intestinal mucosa?

A

Lymphoplasmocytic

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129
Q

Which breed has PLE that is associated with hypoalbuminemia and hyperglobulinemia?

A

Basenjis

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130
Q

Which breeds have PLE that are predisposed to LP enteritis?

A

Basenjis, SCWT, Lundehunds

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131
Q

What is the hallmark chem changes with PLE?

A

Low albumin and globulins (PLE is non-selective)

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132
Q

Although PLE normally results in low albumin and globulins, which two diseases are the exception?

A
  1. Intestinal histoplasmosis
  2. PLE of Baenjis
    = HYPERglobulinemia
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133
Q

What is the purpose of Sudan staining of feces?

A

Detect steatorrhea = malassimilation of fat

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134
Q

What is the purpose of oral D-xylose?

A

Assess carbohydrate malabsorption

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135
Q

What test can be performed to quantify protein loss in feces? Why can it be used?

A

○ Fecal alpha-1 proteinase inhibitor – used to quantify protein loss in feces
§ Has molecular weight similar to albumin but unlike albumin is not broken down in the feces after it’s leaked out
§ Valuable for diagnosis and treatment
§ Needs to be performed on 3 samples, freshly voided (NOT with loops)

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136
Q

What is important to consider in a diet for intestinal lymphangiectasia?

A

○ Diet low in TGs and LCFAs (require lymphatics for transport into circulation)
§ SCTGs transported directly into portal system
§ Medium chain triglycerides (MCT) - Does not provide essential fatty acids, may not be absorbed directly, may need normal lymphatic flow = CONTROVERSIAL!

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137
Q

How does the colon play a role in digestion and metabolism?

A

Colonic bacteria ferment undigested carbs from dietary fibers

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138
Q

What is the most common form of colitis in dogs and cats?

A

Lymphoplasmocytic

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139
Q

What is different about granulomatous colitis compared to histiocytic colitis?

A

Macrophages are NOT periodic acid-Schiff + in granulomatous colitis

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140
Q

In which 2 breeds should T. foetus be considered if large bowel diarrhea is present?

A

Abyssinians and Bengals

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141
Q

What are the two main components of sulfasalazine?

A

○ Good large intestinal absorption, metabolized by colonic and cecal bacteria
§ Mesalamine acts locally to reduce inflammation
§ Sulfapyridine is systemically absorbed and blamed for side effects of the drug
○ Side-effects – vomiting, KCS

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142
Q

Why is sulfasalazine not used in cats?

A

Not use in cats – very long T ½ due to reliance on glucuronyl transferase for liver metabolism

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143
Q

What are the 3 things that are recommended for treatment of chronic colitis in cats?

A

Steroids, metronidazole, and dietary change

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144
Q

Why is tylosin good for colitis?

A

macrolide antibiotic that interferes with bacterial adhesion to mucosa and has immune-modulating effects

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145
Q

What does PAS stand for?

A

Periodic acid-Schiff

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146
Q

What is the thought about macrophages in ulcerative colitis being PAS +?

A

PAS+ may be due to defective phagocytosis and accumulation of bacterial cell wall glycoprotein

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147
Q

What is an uncommon type of IBD that is found in Boxer dogs < 4 yrs old?

A

Granulomatous colitis (also seen in French bulldogs)

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148
Q

What is a unique and pathognomonic feature of granulomatous colitis in dogs?

A

Marcophages are PAS +

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149
Q

What is FISH and how is it used?

A

Fluorescence in situ hybridization (FISH) - Fluorescent molecules attaches to oligonucleotide probes that hybridize to bacterial 16S ribosomal DNA (rDNA) - Enables clear visualization of bacterial morphology and spatial localization

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150
Q

What is thought to be the causative agent of granulomatous colitis?

A

Adherent and invasive E. coli

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151
Q

What is a candidate gene that has been identifies in granulomatous colitis in boxers?

A

NCF2 (gene associated with CGD in humans) - related to neutrophil function (respiratory burst)

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152
Q

What is the suspected enrofloxacin resistance that is seen in granulomatous colitis cases?

A

About 43% - Need to culture all colonic bx that are being submitted for FISH

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153
Q

What other antibiotics can be considered for granulomatous colitis if resistant to enrofloxacin?

A

Need to penetrate macrophages - Chloramphenicol, TMS, tetracyclines, clarithromycin

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154
Q

What is a major concern about treating with enrofloxacin for granulomatous colitis empirically?

A

Has been associated with isolation of resistance E. coli esp if inadequate duration of treatment - Need to treat for at least 6 wks

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155
Q

Name several diseases that have been associated with flatulence.

A

EPI, IBD, SIBO, wheat-sensitive entropathy, food sensitivity, lymphangiectasia

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156
Q

Which carbohydrate is thought to reduce flatuence?

A

Rice

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157
Q

What are the major gases in the intestine?

A

Nitrogen, oxygen, hydrogen, carbon dioxide, methane

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158
Q

What is a carminitive?

A

Used to relieve flatulence

activated charcoal, bismuth subsalicylate, alpha-galactosidase, pancreatic enzyme supplements, probiotic

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159
Q

What are the 4 primary sources of gas in the intestines?

A

○ Aerophagia (O2 and N2)
§ This contributes the most!
○ Gastric acid interacting with food, saliva or pancreatic HCO3- (CO2)
○ Diffusion from blood (CO2, O2, N2)
○ Large amount of gas comes from bacterial fermentation in the colon
§ Foods with large amounts of oligosaccharides produce gas
§ High fiber and fructose diets also create gas
§ Foods with sulfates are converted by sulfate reducing bacteria to H2S and others
§ High protein foods may also contribute

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160
Q

What are the 3 components of innervation to the anus?

A

○ PSNS – controls defecation (contraction of rectum, relaxation of internal anal sphincter)
○ SNS – control storage of feces (relaxation of rectum, contraction of internal anal sphincter)
○ Pudendal n. – striated muscle of external anal sphincter

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161
Q

What is atresia ani?

A

congenital anal agenesis - grave prognosis ○ May develop recto-vaginal, recto-urethral or recto-vestibular fistulae

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162
Q

What neoplasia is malignant, locally aggressive, and can result in PU/PD in patients (hypercalcemia)?

A

Adenocarcinoma of Apocrine Gland of Anal Sac

Most have mets at diagnosis (sublumbar LNs)

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163
Q

What chemo options are available for adenocarcinoma of Apocrine Gland of the Anal Sac?

A

Melphalan and mitoxantrone - Need to also be sx and radiation

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164
Q

What is the most common perianal tumor?

A

Perianal adenoma - Most commonly seen in intact males (growth is hormone mediated) - Sx and castration = excellent prognosis

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165
Q

What is anal furunculosis?

A

perianal fistula disease ○ Progressive inflammatory condition with perianal ulceration and sinus tract formation
○ GSD predisposed, also described in Labs, Irish setters, OESD and collies
○ Etiology not known – contributing factors include breed specific anatomy, infectious agents and endocrine or hormonal influences

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166
Q

What is the recommended treatment for perianal fistula disease and what is the rate of recurrence in these patients?

A

Cyclosporine

Recurrence 30-50%

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167
Q

What is the classic signalment for perineal hernia?

A

Older, intact male dogs, esp brachycpehalics (though to be related to relaxin secreted by prostate that results in weakening of pelvic diaphragm

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168
Q

Which cat breed is predisposed to rectal prolapse?

A

Manx cats

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169
Q

What portion of the exocrine pancreas must be lost to get EPI CS?

A

Need to have lost about 90%

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170
Q

Name 4 causes of EPI in dogs.

A

pancreatic acinar atrophy, chronic pancreatitis, pancreatic hypoplasia, pancreatic neoplasia

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171
Q

What is the most common disease that results in EPI in dogs?

A

Pancreatic acinar atrophy - thought to be immune mediated destruction - leading to total loss = Progressive disease

172
Q

What 2 breeds are predisposed to pancreatic acinar atropy and EPI?

A

GSD and Rough Coated Collies

173
Q

What is the most common disease that results in EPI in cats?

A

Chronic pancreatitis (humans too) - Progressive destruction of exocrine AND endocrine pancreas = FIBROSIS

174
Q

What should be considered if EPI is suspected in a young puppy?

A

Consider that EPI and exocrine/endocrine pancreatic hypoplasia

175
Q

How common is EPI from pancreatic neoplasia?

A

RARE

176
Q

Discuss the use of amylase and lipase in EPI?

A

NOT useful!

177
Q

What is the most common pancreatic function test in dogs?

A

Serum trypsin-like immunoreactivity

This test is species and pancreas specific

178
Q

Which test can be used to test for EPI?

A

Serum TLI = high sensitivity and specificity
EPI dogs = Very low cTLI (<2.5 mcg/l) = Severe loss of digestive enzyme producing acinar tissue
Gray zone 2.5-5 mcg/l (consider subclinical EPI - partial atrophy)

179
Q

What are fecal enzyme measurements that can be used to diagnose EPI in dogs?

A
  1. Fecal proteolytic Activity (can be low in normal dogs)
  2. Canine Fecal Elastase § New species and pancreas specific test
    § High sensitivity but LOW specificity
    § Fecal elastase >20 mcg/g = excluding EPI in dogs with chronic diarrhea
    § If < 20 mcg/g and CS of EPI = Suggestive of severe pancreatic dysfunction (Spillmann et al., 2000; Battersby et al., 2005)
180
Q

What is the treatment of choice for EPI in dogs?

A

Enzyme Replacement Therapy (Viokas, raw frozen pancreas)

181
Q

Why is SIBO though tot be associated with EPI in dogs?

A

· Increased substrates for bacteria in SI: Lack bacteriostatic factors of pancreatic juice, changes in intestinal motility, immune factors = Accumulation of bacteria in SI in EPI dogs

182
Q

What vitamin needs to be supplemented in EPI?

A

Vitamin B12 (cobalamin) - Needs intrinsic factor from pancreas in cats and dogs (little from parietal cells in stomach)

183
Q

Since pancreatic acinar atrophy is thought to be immune mediated, should immunsuppression be used to slow progression of IM tissue destruction?

A

NOT recommended

184
Q

What is the prognosis of EPI in dogs?

A

· If CS of EPI = Loss of pancreatic tissue is almost TOTAL loss
· Irreversible changes → Lifetime enzyme tx required
· Response to tx in a few wks (wt gain, cessation of diarrhea, decreased fecal volume)
· Some dogs will have short relapses with CS

185
Q

What percentage of dogs with EPI has a poor response to treatment?

A

o Poor response to tx in 20% of dogs

o 20% of dogs with EPI were euthanized within 1st year of diagnosis (poor response to tx, expense, and life-long tx)

186
Q

What is a reported complication of EPI in dogs?

A

Mesenteric torsion (Rare)

187
Q

What is the suspected pathogenesis of pancreatitis?

A

· Exocrine pancreas respond to noxious stimuli by decrease in secretion of pancreatic enzymes, followed by formation of giant cytoplasmic vacuoles within pancreatic acinar cells (seen with EM)
o Vacuoles: Colocalization of zymogens of digestive enzymes and lysosomal enzymes (which are normally strictly segregated)
o Decreased pH and/or presence of lysosomal enzymes (cathepsinB) lead to premature activation of trypsinogen
o Trypsin activates other zymogens = Local effects (inflammation, pancreatic edema, hemorrhage, pancreatic necrosis, parapancreatic fat necrosis) = CS of abdominal pain and vomiting
o Systemic CS are thought to be related to circulating pancreatic enzymes

188
Q

Dogs that are showing neurologic signs with pancreas may have….

A

Pancreatic encephalopathy

189
Q

What is the use of amylase and lipase in diagnosis of pancreatitis. What is sensitivity and specificity?

A

§ Serum amylase and lipase = Limited clinical use
□ Specificity of these only about 50%
□ Sensitivity < 35%
□ Only used for prelim diagnosis of pancreatitis

190
Q

What is the use of AUS in diagnosis of pancreatitis. What is sensitivity and specificity?

A

Useful § Sensitivity of AUS in dogs: 68% (operator dependent)
§ Pancreatic swelling, changes in echogenicity of pancreas (hypoechogenicity – pancreatic necrosis, hyperechogenicity – pancreatic fibrosis), peripancreatic fat (hyperechogenicity if fat necrosis), fluid accumulation around pancreas, mass effect (less common), dilated pancreatic duct/enlarged duodenal papilla

191
Q

What is the use of TLI in diagnosis of pancreatitis. What is sensitivity and specificity?

A

· Trypsin-like immunoreactivity (TLI): Specific exocrine pancreatic function
§ Sensitivity of cTLI: 30-60% (suboptimal for pancreatitis in dogs)
§ Sensitivity below 35%

192
Q

What is the use of PLI in diagnosis of pancreatitis. What is sensitivity and specificity?

A

· Pancreatic lipase immunoreactivity (cPLI)
§ Measures as Spec cPL
□ Many cell types synthesize and secrete lipases, immunoassay allows for specific measurement of lipase from exocrine pancreas
§ Sensitivity above 80%

193
Q

What is the gold standard for diagnosing pancreatitis in dogs?

A

Pancreatic bx (in one study 50^ of dogs had pancreatitic inflammaiton when pancreas secreted every 2 cm)

194
Q

Can steroids cause pancreatitis in dogs?

A

Steroids do NOT appear to cause pancreatitis = But can increase serum lipase activity in some dogs without causing pancreatitis

195
Q

Name several risk factors for pancreatitis in dogs.

A
  1. Nutrtion - Little evidence for fatty meals, check for hypertriglyceridemia
  2. Toxins/Drugs: Calcium, KBr, L-asparaginase, azathioprine, estrogen organophosphates
  3. Trauma/Hypoperfusion
  4. Hypercalcemia
  5. Neoplasia (pancreatic adenocarcinoma)
196
Q

Which antiemetic is controversial in dogs with pancreatitis?

A

Metoclopramide (dopamine antagonist)

Pancreatic blood flow regulared via dopaminergic receptors = AVOID IT!!

197
Q

What is the rational for using plasma in dogs with pancreatitis?

A

· α2-Macroglobulin (scavenger proteins for activated proteases in plasma): Depleted rapidly in severe pancreatitis → uninhibited protease activity leading to acute DIC, hypotensive shock, and death
§ Fresh frozen plasma replenishes α2-Macroglobulin, supplies albumin and coag factors = beneficial effects (maintaining oncotic pressure, preventing DIC)
□ NO scientific evidence that plasma has beneficial effects in humans or dogs

198
Q

What is aprotinin?

A

Protease Inhibitor
Not very good = new pathogenesis of severe pancreatitis (once premature activation of pancreatic zymogens = massive inflammatory response mediated by inflammatory cytokines) § Premature activation of zymogens = Very minor role in progression of dz – thus inhibiting pancreatic enzymes may not have benefit

199
Q

What is an antioxidant that has been used in pancreatitis?

A

Selenium, no clear benefit but in one study did significantly decrease mortality rate

200
Q

How does dried pancreatic extract (Viokase/Pancrezyme) reduce discomfort associated with pancreatitis?

A

§ Although these case do NOT have EPI and do NOT require pancreatic replacement for digestive purposes, feedback effect of digestive proteases within gut lumen appear to reduce the drive for pancreatic secretion and may reduce pancreatitis associated discomfort
Noted in humans too

201
Q

What form of pancreatitis is more common in cats?

A

Chronic pancreatitis = Most cases are idiopathic!

202
Q

What is the pathogenesis of pancreatitis?

A

· Hypothesis: pancreatic acinar cells ultimately respond in common fashion to variety of differing harmful stimuli
○ Initial decrease in secretion of pancreatic enzymes is followed by formation of abnormal cytoplasmic vacuoles → contents of lysosomes and zymogen granules colocalize = inappropriate intracellular activation of trypsin and subsequently other digestive zymogens
o Local effects: inflammation, hemorrhage, acinar cell necrosis, and peripancreatic fat necrosis
o Systemic effects: Inflammatory changes, systemic vasodilation (hypotension), pulmonary edema, DIC, central neurologic deficits, resp failure, multiorgan failure

203
Q

What are potential risk factors in feline pancreatitis?

A

o Traumatic pancreatitis (HBC, falling) – secondary to pancreatic ischemia
o Infectious agents: Caudal relationship of Toxoplasma gondii, Amphimerus pseudofelineus fluke infestation (rare), feline parvovirus in kittens (weak), feline herpesvirus-1, FIP
o Topical use of fenthion (organophosphate cholinesterase inhibitor)
o Drugs in dogs/humans: azathioprine, chlorothiazide, hydrochlorothiazide, estrogens, furosemide, tetracycline, sulfonamides, L-asparaginase, 6-mercaptopurine, methyldopa, pentamidine, nitrofurantoin, dideoxyinosine, valproic acid, and procainamide = NO cases in cats

204
Q

What are several concurrent conditions with feline pancreatitis?

A

hepatic lipidosis, IBD, interstitial nephritis, diabetes mellitus, and cholangiohepatitis (Akol et al.,1993)

205
Q

What is a better clinical diagnostic test for acute and chronic pancreatitis in cats?

A

· Serum feline pancreatic lipase immunoreactivity (fPLI)

Increased fPLI - more prolonged lasting 7-10 days

206
Q

Why should antibiotics be considered in a cat with neutrophilic cholangitis from ascending bacterial infection of biliary system?

A

Concurrent infection in pancreatic duct system (Direct communication of common bile duct and pancreatic ducts in cats) o Ensure Abx that cover enteric aerobes

207
Q

What has been given experimental in acute feline pancreatitis to increase blood flow to pancreas?

A

Dopamine - No benefit after 12 hrs

208
Q

What infectious disease can result in pancreatitis in cats?

A

Fluke - Eurytrema procyonis (rare)

209
Q

What is a reliable test for EPI in cats?

A

Serum fTLI (radioimmunoassay)

210
Q

What can be low that would result in an EPI cat not responding to pancreatic enzyme supplementation?

A

Cobalamin - Will require life long treatment!

211
Q

What should be consider if an EPI cat is not responding to enzyme and vitamine supplemenation?

A

MANY have concurrent SI disease - Need to treat IBD too

212
Q

What is the most common malignant neoplasia in pancreas of cats?

A

Pancreatic adenocarcinoma

Mets in >80% cats at time of diagnosis

213
Q

What is a pancreatic bladder?

A

· Abnormal extension of pancreatic duct that forms a sac (only few feline cases reported)

214
Q

What is a pancreatic psuedocyst?

A

· Collection of sterile pancreatic juice enclosed in fibrous or granulation tissue
Complication of pancreatitis in human, seen in 1 cat

215
Q

What is the pancreatic fluke of cats?

A

Eurytrema procyonis - within pancreatic ducts (foxes, raccoons)
Eggs noted in feces
Fenbendazole

216
Q

What is the hepatic fluke of cats?

A

Amphimerus pseudofelineus
Also invased pancreas
Eggs in feces
Praziquantel

217
Q

What is a clinical signs of hepatic encephalopathy in cats?

A

Ptyalism

218
Q

What can result from impaired iron transport in dogs and cats with hepatobiliary disease?

A

Microcytosis without anemia

219
Q

Why can you see mild thrombocytopenia in heptobliary disease?

A

systemic infectious disorder or synthetic failure from decreased hepatic thrombopoietin production

220
Q

What is ALT (location, half life)?

A 
Alanine aminotransferase (ALT)
LEAKAGE
Liver-specific cytosolic enzyme
 · ↑ with severe muscle necrosis (dog)
Half Life: 2.5 days (dog); Cats?  - 6hrs
Large ↑:  Acute hepatocellular necrosis/ inflammation
Mild-to-moderate ↑:  Hepatic neoplasia
221
Q

What is AST (location, half life)?

A

Aspartate aminotransferase (AST)
LEAKAGE
Cytosol and mitochondria
· More sensitive, LESS liver specific
Half Life: 22 hours (dog); 77 mins (cat)
↑ Parallel ALT (smaller magnitude)
· If opposite consider muscle source or release of mitochondrial AST(severe irreversible hepatocellular injury)

222
Q

What is ALP (location, half life)?

A

Alkaline phosphatase
(ALP)
Membrane-bound enzyme
· Dogs: high sensitivity (80%) but low specificity (51%) for liver dz

L-ALP: Luminal surface of biliary epithelial cells and hepatocyte canalicular membrane
C-ALP: Hepatocyte canalicular membrane
Half Life L-ALP: 70 hrs (dog); 6 hrs (cat)
Isoenzymes (dog)
· Bone (B-ALP): 1/3
· Osteoblastic activity (bone growth, osteomyelitis, osteosarcoma, and secondary renal hyperparathyroidism)
· Liver (L-ALP)
· Largest ↑: Focal or diffuse cholestatic disorders and primary hepatic neoplasms
· Less ↑: chronic hepatitis, hepatic necrosis, and canine nodular hyperplasia
· Corticosteroid (C-ALP)
· ↑ exogenous or endogenous steroids (dog ONLY)
· Chronic illness (endogenous steroids)
Drug induction
Feline hepatocytes have less ALP
Cats lack C-ALP: T-ALP less sensitive (50%) but more specific (93%) for liver dz

223
Q

What is GGT (location, half life)?

A

γ-glutamyl transferase (GGT)
Hepatocyte canalicular membrane
· Dogs: lower sensitivity (50%) but higher specificity (87%) for hepatobiliary dz
· If concurrent ↑ ALP: specificity for liver dz ↑ to 94%
· Cats: Higher sensitivity (86%) but lower specificity (67%) for hepatobiliary dz than T-ALP

Largest ↑: Dz of biliary epithelium → bile duct obstruction, cholangiohepatitis, and cholecystitis

Moderate ↑: Primary hepatic neoplasia

Mild ↑: Hepatic necrosis

Cats: GGT>ALP: cirrhosis, extrahepatic bile duct obstruction (EHBDO), or cholangitis

Feline Idiopathic Hepatic Lipidosis: GGT only MILDLY elevated

224
Q

What is only mildly elevated in feline idopathic hepatic lipidosis?

A

GGT

225
Q

Name 2 enzymes that result from leakage from damage hepatobiliar cells?

A

ALT and AST

226
Q

Name 2 enzymes that results from elution from damage membranes

A

ALP and GGT

227
Q

Name 1 enzymes that can have increased synthesis in hepatobiliary disease?

A

ALP

228
Q

What enzymes can be elevated with steriod use? How long does this take to get to normal after stopping the steroids?

A

Steroids: ↑ L-ALP, C-ALP, ALT (less) and GGT secondary to induction
◊ Stopping them results in gradual normalization of values (2-3 months)

229
Q

Which drug can result in induced ALP synthesis BUT also idiosyncratic hepatotoxic reactions?

A

Phenobarbital (dogs)

230
Q

Do the magnitude of liver enzyme elevation correspond to prognosis?

A

NO, lots of regenerative capacity of liver, NOT predictive of liver function

231
Q

How much of the liver needs to be lost in order to result in synthetic failure?

A

□ Synthetic failure occurs only when 70% of hepatic functional mass has been lost

232
Q

What is cholestasis of sepsis?

A

Cholestasis of sepsis: Cytokines that inhibit expression of hepatocyte transported necessary for bilirubin transport (+/- liver dz)
– Esp common in cats

233
Q

When would you expect to see hypoglycemia with hepatobiliary disease?

A

ONLY if 75% of hepatic mass is nonfunctional

Decreased gluconeogenesis and clearance of insulin

234
Q

What is the difference of bilirubin in dog vs cat urine?

A

§ Dogs: Renal threshold for bilirubin is low, capable of tubular secretion of bilirubin → bilirubinuria may be present in absence of bilirubinemia
§ Cats: High threshold for bilirubin and are not bilirubinuric unless also bilirubinemic

235
Q

Name several infectious diseases that should be consider with hepatobiliary disease is present.

A

§ Leptospirosis, ehrlichiosis, RMSF, toxoplasmosis, neosporosis, dirofilariasis, systemic mycosis

236
Q

What diseases should be considered if secondary hepatobiliary disease is suspected?

A

§ Pancreatitis: Lipase, PLI
§ Endocrinopathies: hypothyroidism, hyperthyroidism, hyperadrenocorticism, and adrenal hyperplasia syndromes
§ GIT: IBD

237
Q

What is the basis behind using total serum bile acids for hepatobiliary disease?

A

§ Bile acids are synthesized from cholesterol exclusively in the liver
§ Conjugated to glycine or taurine → secreted into bile → stored/concentrated within gallbladder
§ Meal = cholecystokinin (CCK) release → GB contraction
§ Bile acids transported in intestines = Aid in emulsification and digestion of fats
§ Terminal ileum bile acids resorbed and return to liver (enterohepatic circulation) – Re-extracted by hepatocytes
□ Normally enterohepatic circulation of bile acids = 95-98% efficiency
□ Disruption of circulation = ↑ TSBAs (acquired or congenital PSVA or cholestatic hepatobiliary disease)

238
Q

What is the sensitvity and specificity of using total serum bile acids in dogs and cats with hepatobiliary disease?

A

§ High specificity for hepatobiliary dz in dogs (95-100% with cut-offs of >15 μmol/L and 25 μmol/L) in cats (96-100%)
§ Sensitivity 54-74% = NOT great, expect for congenital PSVA (dogs/cats), cirrhosis (dogs) = 100%

239
Q

What has likley occurs if you have a higher fasting bile caids than postpranial?

A

Secondary to interdigestive gallbladder contraction, variations in gastric emptying, intestinal transit, or response to CCK release

240
Q

What can result in a decreased postpraial bile acids?

A

severe ileal dz or resection can decreased bile acid resorption

241
Q

What is another test that can be performed to assess bile acids?

A

· Urine BAs
§ Urinary excretion of water-soluble bile acids reflects the TSBA concentration during period of urine formation → persistently elevated TSBAs = elevated urine bile acid levels
□ DOGS: Normalized urine nonsulfated bile acids (UNSBAs): urine creatinine combined with normalized urine sulfated (USBAs) and UNSBAs: urine creatinine = higher specificity (100% vs 67%) but lower sensitivity (62% vs 78%) than TSBAs (Balkman et al., 2003)
□ CATS: Equivalent to TSBAs; sensitivity (87%) and specificity (88%) for hepatobiliary dz (Trainor et al., 2003)

242
Q

Name 3 possibilities when increased blood ammonia levels are noted.

A

portosystemic shunting, < 70% reduction in liver parenchyma, inborn errors of metabolism in urea cycle

243
Q

Which breed can have a transient hyperammonemia?

A

Young Irish Wolfhounds

244
Q

What deficiencies can lead to transient hyperammonemia in dogs and cats?

A

deficiencies of cobalamin (dog) and arginine (cat)

245
Q

What is the sensitivity and specificty of ammonia for hepatobiliary disease?

A

§ >46 μmol/L: Sensitive (98%) and specific (89%) test →congenital or acquired PSVA in dogs (Gerritzen-Bruning, van den Ingh, and Rothuizen, 2006)

246
Q

True or False. Normal AUS does NOT preclude hepatobiliary dz.

A

TRUE

247
Q

What is EHBO?

A

EHBO: dilation of cystic duct, common bile duct (>3 mm dogs; >4 mm cats)

248
Q

What are 2 nuclear methods that can be used to diagnosis liver shunts?

A

· Transcolonic pertechnate scintigraphy (TCPS) = Detection of PSVA
o Absorbed by portal venous system = Detected in liver PRIOR to heart (normal)
o PSAV = heart BEFORE liver
o Dogs: High PPV for PSVA: Discriminates macroscopic PSVA (abnormal) from primary hypoplasia of portal vein (normal)
· Transplenic portal scintigraphy (TSPS) = Detect PSVA
o US guided, reduced radiation exposure (smaller dose)
o NOTE: misses cases when shunt originates distal to splenic vein

249
Q

What is the estimated discordance btwn wedge and Tru-cut liver bx?

A

About 48%!! Need to bx multiple times (3-5X) in different areas of liver

250
Q

What is the estimated discordance btwn FNA and liver bx?

A

As high as 70%

251
Q

What breeds are predisposed to hepatic amyloidosis?

A

Shar Pei

Abyssinian and Siamese

252
Q

What breeds are predisposed to copper associated hepatopathy?

A 
Bedlington Terrier
Dalmatian
Skye Terrier
WHWT
Siamese
253
Q

What breeds are predisposed to idiopathic inflammatory hepatopathy?

A

American and English Cockers
Doberman
Labs
Standard Poodle

254
Q

What breeds are predisposed to congenital portosystemic vascular anomalies?

A 
Australian cattle dog
Cairn terrier
Dachshund
Goldens
Irish Wolfhound
Lab
Maltese
Mini Schnauzer
Yorkie
Hiamalyan
Persian
255
Q

What is the sensitivity and specificity of ALP in detecting liver disease?

A

· High sensitivity (86%) for detecting liver disease BUT poor specificity (49%) due to lots of disease outside the liver, drugs, steroids = induced production of enzyme

256
Q

Name 5 tissues that membrane bound ALP is found.

A

Kidney, liver, bone, placenta, intestine

257
Q

What are the two genes for ALP synthesis?

A

Tissue nonspecific and intestinal → two isoenzyme proteins with different polypeptide sequences but similar enzymatic function o Tissue Nonspecific: ALP in kidney, liver, bone, placenta (differ only in degree of glycosylation)
o Intestinal: ALP in intestine and corticosteroid ALP (C-ALP)

Corticosteroid ALP (C-ALP): UNIQUE, only found in dogs

258
Q

Which form of ALP is unique to dogs?

A

Corticosteroid ALP (intestinal gene)

259
Q

What are the 3 isoenzymes of ALP that are measured in the blood?

A 
o Liver (L-ALP)
   § Predominant isoenzyme in dogs > 1 yrs
  o Bone (B-ALP)
   § Dogs < 1 yrs = 96% of total ALP, declines to 25% in dogs >8yrs
  o Corticosteroid (C-ALP)
   § 0-30% in normal dogs (higher in older dogs)
260
Q

Why are intestinal ALP, kidney, and placenta not measured in the blood?

A

T1/2 = minutes (other 3 isoenzymes have longer T1/2)

261
Q

What isoenzyme of ALP is predominant in dogs > 1 yrs?

A

Liver ALP

262
Q

What isoenzyme of ALP is predominant in dogs <1 yrs?

A

Bone ALP (96% of total ALP)

263
Q

Name 2 situations that liver ALP can be induced.

A

§ Cholestasis: Accumulation of bile from impaired bile flow = Induced L-ALP production
□ Accumulate on hepatic membranes and solubilization of membrane-bound enzymes occurs by glycosylphosphatidylinositol (GPI) phospholipase (found in plasma and on cell membranes)
® Bile salts also increase activity of GPI phospholipase → release L-ALP into circulation
§ Drugs: Phenobarbital, endogenous/exogenous glucocorticoids
□ Poorly understood

264
Q

What is bone ALP related to?

A

· Attached to external cellular membrane of osteoblasts
· Function of enzyme unknown (plays role in bone formation)

Increased levels related to increased osteoblastic activity = Bone growth in young animals, fracture healing, osteosarcoma (mild, <4x normal, but correlated with POOR survival, found in tumors with increased osteoblastic acitvity), nutritional osteopathies (less common), renal secondary hyperparathyroidism

265
Q

What is correlated with poor survival if increased with osteosarcoma?

A

Bone ALP

266
Q

Which breed has a benign familial hyperphosphatasemia that is from increased B-ALP?

A

Siberian Huskies

267
Q

What results in increased ALP in HAC animals?

A

dramatic increase in ALP; due to increased cortisol, intrahepatic cholestasis caused by hepatocyte swelling from glycogen accumulation – 90-95% dogs

268
Q

What results in increased ALP in diabetes mellitus?

A

mild-moderate, 2-5x normal with concurrent changes in ALT from intrahepatic cholestasis secondary to hepatocellular swelling from metabolic derangement, hepatic lipidosis

269
Q

Name 3 conditions where only ALP is increased?

A

Benign nodular hyperplasia, idiopathic vacuolar hepatopathy, and breed-related conditions

270
Q

Which breed has a higher incidence of increased ALP?

A

Scottish Terriers

Benign familial hyperphosphatasemia (increased C-ALP but no elevation in others??)

271
Q

What are the 7 general principles of treating hepatic disease?

A

· Address the underlying cause, if known (withdrawal of hepatotoxic drug).
· Reduce and prevent inflammation.
· Reduce and prevent copper accumulation, if applicable.
· Reduce and prevent oxidative damage.
· Reduce and prevent fibrosis.
· Provide adequate nutrition.
· Treat complications as needed (e.g., hepatic encephalopathy, coagulopathy, gastric ulceration, fluid/electrolyte disturbances, ascites, and infection/endotoxemia)

272
Q

What can result with obstructive biliary or inflammatory hepatic disorders?

A

Reduced glutahione concentrations

§ Predisposes them to oxidative hepatic injury (since glutathione detoxifies reactive oxygen spp)

273
Q

What is the most biologically active form of Vitamin E?

A

α-Tocopherol

274
Q

Which antioxidant should not be use in patients with liver disease if there is evidence of vitamin K deficiency?

A

Vitamin E

275
Q

What is milk thistle?

A

· 4 flavonolignan isomers (silybin, isosilybin, silydianin, silychristine) → herb milk thistle (Silybum marianum)
§ Silybin = 50-70% of milk thistle
· Antioxidant and free radical scavenger (MAIN effects) but also antifibrotic, antiinflammatory, and immunomodulatory actions

276
Q

Which antioxidant is effective are reducing Amanita phalloides toxicosis by preventing hepatocyte uptake of mushroom toxins?

A

Milk thistle = Silymarin (IV formation in dogs and humans)

277
Q

What is SAME?

A

S-Adenosylmethionine
SAMe plays crucial role in transmethylation, transsulfuration, and aminopropylation pathways → metabolism of various endogenous /xenobiotic compounds, generation of endogenous sulfur compounds, and production of molecules important in cell signaling and gene transcription □ Transsulfuration pathways is glutathione (important endogenous antioxidant system of the liver)

278
Q

Does SAMe prohibit steroid induced hepatic vaculoar change?

A

· Ameliorate oxidative stress induced by corticosteroid administration (dogs), BUT does not prohibit corticosteroid-induced hepatic vacuolar change (Center et al., 2005)

279
Q

Which cells in the liver are responsible for hepatic fibrogenesis?

A

Hepatic stellate cells (Ito cells, lipocytes, perisinusoidal cells)

280
Q

What is the most common antifibrotic?

A

Colchicine = Plant alkaloid
· Inhibit fibrosis by binding selectively/reversibly to microtubules, inhibiting their polymerization and thus collagen secretion
Does not decreased fibrosis

281
Q

Name several other antifibrotics.

A

· Interferon-γ, milk thistle, penicillamine, prednisone, ursodeoxycholic acid, and zinc
§ Not evaluated in dogs and cats with fibrosis but many used for other liver dz (coincidental benefit)

282
Q

Which vitamin K dependent coagulation factors are made by the liver?

A

factors II, VII, IX, and X
§ From lack of dietary vitamin K uptake, poor vitamin K absorption by cholestatsis, altered bacterial flora associated with abx use, hepatic dysfunction–associated impairment of the vitamin K epoxide cycle
□ Identified and monitored with prothrombin time (PT) or proteins induced by vitamin K absence or antagonism (PIVKA)

283
Q

What is the preferred treatment for ascites associated with hepatic disease?

A

Spironolactone (aldosterone receptor antagonist)

284
Q

Where is inherited copper storage diseases copper accumulation located?

A

Centrolobularly

285
Q

Where is secondary copper loading of liver cells during cholestasis?

A

Copper mainly periportal parenchyma

286
Q

Where is copper absorbed?

A

40-60% from small intestine

287
Q

What transport is responsible for hepatocellular uptake of copper?

A

Copper transporter (CTR1)

288
Q

Once copper is within liver cells what happens?

A

· In liver cells copper is immediately bound to transport proteins: COX17, ATOX1, CCS → deliver copper to their target destination in cell
o Targets: Superoxide dismutase, mitochondrial enzymes

289
Q

How is copper excreted from liver cells?

A

· Golgi apparatus the ATPases ATP7A (Menkes disease protein) and ATP7B (Wilson’s disease protein) are responsible for preparation of copper excretion
o Excretion into bloodstream copper bound to ceruloplasmin
o Also if excessive copper excretion within bile via interactions with copper metabolism murr1 domain-containing protein 1 (COMMD1)

290
Q

What is copper bound to in the blood?

A

Ceruloplasmin

291
Q

What is copper stored with?

A

Metallothionein

292
Q

Name 5 breeds that have inherited copper associated chronic hepatitis.

A
  1. Bedlington terriers
  2. WHWT
  3. Skye terriers
  4. Dobermans
  5. Dalmatian
  6. Labs
293
Q

What is responsible for copper associated chronic hepatitis in Bedlington terriers?

A

Deletion of exon 2 in COMMD1 gene (previously MURR1) → accumulation of copper in hepatocytes = chronic hepatitis

294
Q

How much copper is present in breeds that have primary copper storage diseases compared to normal dogs?

A

Primary copper storage disease = 600 to > 2000ppm (vary)

Normal dog = 200-500 ppm/ dry weight (littler variation btwn breeds)

295
Q

Which breed has hemolysis associated with hepatic copper release into blood been described?

A

Bedlington Terrier

296
Q

What is the age of dogs with primary copper storage disease?

A

Accumulate copper at 5-6 months and appear normal for years

297
Q

What is the first and most consistent lab abnormality in Bedlington terriers with inherited copper toxicosis?

A

ALT elevation

298
Q

What is characteristic on histology for primary copper storage diseases?

A

Magnitude and localization of copper within zone 3 in the liver lobule
As copper accumulates in hepatocytes: Hepatocellular inflammation within copper-laden macrophages and chronic hepatitis

299
Q

What are the 2 methods of copper assessment in liver samples?

A
  1. Quantitative: Spectrophotometric method

2. Semiquantitative: Histochemical stains - Rubeanic acid and rhodanine, detects when > 400 mcg/g DW

300
Q

What is the underlying pathophysiology of copper accumulation in Bedlington terriers?

A

§ Inherited autosomal-recessive defect of MURR1 gene → COMMD1
§ Hepatic damage parallels ↑ hepatic copper concentrations from ¯ copper excretion into bile in COMMD1-deficient liver cells
§ Accumulated copper = dense granules in lysosomes within CENTROLOBULAR region

301
Q

What are the 3 clinical stages that are described in Bedlington terriers with copper storage disease?

A

□ 1. Hepatic Copper: 400 to 1500 ppm DW; within centrolobular hepatocytes (zone 3) – clinically silent, only on liver bx (liver structure normal but copper in granules)
□ 2. Hepatic Copper: 1500 to 2000 ppm DW; copper within midzonal and periportal hepatocytes (zones 2 and 1), inflammation in bx, mixed cells in centrolobular region (necrotic hepatocytes, lymphocytes, plasma cells, neutrophils, and copper-laden macrophages)
□ 3. Hepatic Copper: Exceeds 2000 ppm DW = CLINICAL; bx = hepatic and cirrhosis; Cholestasis/bile duct proliferation occur along with fibrosis possibly dt compression exerted on bile ducts in a distorted fibrotic liver and cytokine-induced proliferation of bile ducts

302
Q

What happens with heterozygous carriers in copper hepatopathy in Bedlington terriers?

A

§ Heterozygous carrier dogs →↑ hepatic copper concentrations (out of RR) until 6-9 months before concentrations fall back to normal
□ THUS liver bx in dogs < 1 yr do NOT differentiate carrier dog from affected dogs

303
Q

In which sex of dobermans is copper storage disease more common?

A

Females, young (1-3 yrs) ↑ ALT, centrolobular copper, subclinical hepatitis ® Copper increased before development of hepatitis (Mandigers et al., 2004)
□ Liver dz by 4-7 yrs = Chronic hepatitis and cirrhosis

304
Q

In which sex of labs is copper storage disease more common?

A

§ Females more affected; 7 yrs (2-10 yrs)

Copper in centrolobular region = Primary copper accumulation

305
Q

What are the 3 main chelators used to treat copper storage disease?

A
  1. Penicillamine
  2. Trientine
  3. Zinc
    Need lifelong therapy
306
Q

What is penicillamine used to treat, how does it work, and which breeds has it been used in?

A

§ Chelates metals → Copper
§ Mobilization of copper from tissues and promotes copper excretion in urine
§ ↑ Synthesis of metallothionein (a copper-binding protein)
§ Antiinflammatory, immunosuppressive, and antifibrotic effects
Used in Bedlington terriers, Dobermans, and Labs in studies

307
Q

Which chelator may be superior copper chelator and thus better for acute hemolytic crisis?

A

Trientine (increased urinary excretion of copper and may help to decrease intestinal absoprtion of copper)

308
Q

What is the MOA of zinc as a chelator?

A

Oral zinc to decreased copper absorption from diet
Induced production of metallothionein in intestinal mucosal cells
□ Metallothionein binds copper from diet → prevents uptake of copper into circulation

309
Q

What is imperative to monitor when a patient is on zinc for chelation?

A

§ Plasma zinc (dogs): 90-120 mcg/dl
□ Need > 200 mcg/dl required to suppressed copper uptake
□ >1000 mcg/dl hemolysis may occur
□ NEED to monitor zinc monthly for several months to check concentration in therapeutic range

1 study: Minimum of 3 months of zinc needed BEFORE copper uptake from intestines blocked

310
Q

Name several foods that are high in copper.

A

Foods high in copper: eggs, liver, shellfish, organ meats, beans, mushrooms, chocolate, nuts, and cereals

311
Q

How are bile acids made?

A

· Primary bile acids synthesized from cholesterol (liver) → chenodeoxycholic acid and cholic acid
· Conjugated in liver by glycine or taurine

312
Q

What is the MAJOR circulating bile acid in dogs and cats?

A

tri-hydroxy bile acid taurocholate

313
Q

What loosely correlates with degree of toxicity of bile acids?

A

hydrophobicity (conjugation/hydroxylation decreased toxicity)

314
Q

How does UCDA affect circulating bile acid pool?

A

PROTECTIVE: Replacing more hydrophobic hepatotoxic bile acids (chenodeoxycholate) from circulating bile acid pool
NOT a huge deal in dogs/cats since major circulating bile acid is nontoxic

315
Q

How does UCDA result in potent choleresis?

A

§ Induction of choleresis stimulated by biliary excretion of bile acids other toxic endogenous metabolites that are retained (copper, leukotrienes, bilirubin, and cholesterol)
§ 2 Mechanisms:
1. ↑ Plasma membrane expressed of membrane transporter necessary to generate bile flow
□ Mobilizing intracellular stores of transporters → activation of signal transduction molecules (protein kinase C)
2. Cholehepatic shunting
□ Unconguated UDCA secreted in bile, becomes protonated, leading to generation of bicarbonate ion
□ Protonated UDCA passively absorbed by biliary epithelial cells → net secretion of 1 bicarbonate ion (osmotic draw for biliary water secretion)

316
Q

How does UCDA result in prevent apoptosis?

A

§ Mechanism = Stabilizing mitochondrial function
□ If cell gets “death signal” (Fas, TNF = death receptor) or intracellular stress (Bcl-2 family, Bax, Bid translocate to cytosol to mitochondria)
® Proteins integrate into mitochondrial membranes = disrupt membrane permeability → release of apoptogenic factors = Cell death
□ UDCA: ¯ cellular expression of Bax and preventing Bax translocation to the mitochondria
· Directly interact with mitochondrial membrane to inhibit Bax-mediated membrane changes
· ↑ mitochondrial glutathione levels: stabilizing mitochondrial membrane transporters or by increasing the activity of methionine adenosyltransferase
· ↑ S-adenosylmethionine: metabolized by transsulfuration to glutathione
· Glutathione = major antioxidant in the liver, esp important free-radical scavenger in the mitochondria
· Stimulation of cellular survival signaling

317
Q

How is Ursodeoxycholic acid absorbed?

A

o Oral administration of UCDA: 30-60% absorbed by SI (80%) and colon (20%)
§ Enhanced absorption if given with a meal
§ High hepatic first pass metabolism (70%)
§ Once in hepatocytes → conjugated to taurine or glycine → enterohepatic circulation
§ Bioavilability UCDA may ¯ with advanced cholestasis (¯ hepatic extraction, ↑ renal elimination)
§ UDCA metabolized to lithocholate (colon), eliminated in feces

318
Q

How does UDCA afect total serum bile acids in healthy animals?

A

May ↑ preprandial and postprandial total serum bile acids in healthy animals, BUT not above RR

319
Q

What is known about UDCA therapeutic benefit in dogs and cats?

A

UNKNOWN!

320
Q

If liver injury occurs randomly when a medication is given, it is known as….

A

Idiosyncratic hepatotoxin

321
Q

Name 4 mechanisms that can occur with drug associated liver disease.

A
  1. Cytopathic change on hepatocytes (lysis, necrosis)
  2. Induction of cholestasis and metabolic dysfunction
  3. Induction of immune system activity against hepatocytes
  4. Production of proinflammatory response to liver
322
Q

What is a poor prognostic indicator in humans with drug assoicated liver disease?

A

Progressive elevation in bilirubin

323
Q

What is the pathophysiology of feline hepatic lipidosis?

A

Excessive accumulation of lipids in hepatocytes
• Catabolic state = enhances mobilization of peripheral fat stores to the liver and impaired dissemination of lipid from hepatocytes - Not completely understood

324
Q

What is classic signalment for feline hepatic lipidosis?

A

Overweight cat with period of recent anorexia - Middle aged to older cats

325
Q

What are the 2 main goals of diagnosis in feline hepatic lipidosis?

A

to identify lipidosis in the liver and rule in/out an underlying disease process

326
Q

Which liver enzyme is NOT normally elevated in feline hepatic lipidosis?

A

GGT!

327
Q

In which spp does bilirubinuria proceed hyperbilirubinemia?

A

Cats!

328
Q

What is the correlation btwn degree of elevation in ammonia and CS of hepatic encephalopathy?

A

POOR correlation!

329
Q

In order to diagnose feline hepatic lipidosis on FNA of liver what needs to be present?

A

cytosolic vacuolization of at least 50% of cells

330
Q

What is the mainstay of treatment for feline heaptic lipidosis?

A

nutritional support to reverse catabolic state - Need high quality protein

331
Q

What two amino acids would need to be supplemented it not giving a feline diet to a hepatic lipidosis cat?

A

Taurine and arginine

332
Q

What is a potential complication with chronic Vitamin K administration?

A

Oxidation injury to organs and RBCs

333
Q

What two amino acids are thought to be low in feline hepatic lipidosis?

A

L-carnitine and Taurine

334
Q

What should be given to prevent Heinz body anemia in cats with hepatic lipidosis?

A

SAMe = Essential for hepatocellular production of glutathione

335
Q

What is the most common electrolyte abnormality in feline hepatic lipidosis?

A

Hypokalemia

336
Q

What are 3 electrolyte abnormalities that can occur with refeeding syndrome?

A

Hypokalemia, Hypomagnesium, hypophosphatemia

337
Q

What are the 4 classifications of feline inflammatory liver disease.

A
  1. Neutrophilic cholangitis (acute and chronic forms)
  2. Lymphocytic cholangitis
  3. Cholangitis associated with liver flukes
  4. Lymphocytic portal hepatitis
338
Q

Based on WSAVA what term should be used in cats instead of cholagniohepatitis?

A

Cholangitis - IN cats the primary inflammatory changes are centered or surrounding the bile ducts
Unlike in dogs where cholangiohepatitis with hepatic inflammation is the most common inflammatory liver disease

339
Q

What is the most common feline biliary tract disease?

A

Neutrophilic cholagnitis (when acute mainly neutrophils but mixed inflammatory cells once chronic) - thought to be related to ascending biliary tract infection from GIT

340
Q

What is the most common bacteria associated with acute neutrophilic cholangitis in cats?

A

E. coli

Others: Enterococcus, Bacteroides, Clostridia, Staphylococcus and alpha-hemolytic Streptocooccus

341
Q

What two other diseases have been noted in cats with acute neutrophilic colangitis?

A

Pancreatitis (50%)and IBD (83%)

342
Q

What is the most common signalment for neutrophilic cholangitis in cats?

A

Young to middle age male cats (3-5 yrs)

343
Q

What is the most common CS in cats with cholangitis?

A

Vomiting

344
Q

What is the treatment of choice for feline neutrophilic cholangitis?

A

Antibiotic against G- enteric aerobes with good hepatic and biliary penetration § Cephalasporins, amoxicillin or amoxicillin-clavulanic acid
At least 4 weeks (duration is not known)

345
Q

What cells are present in chronic neutrophilic cholangitis in cats?

A

Mild to marked infiltration of portal areas by lymphocytes, plasma cells and neutrophils

346
Q

What is the treatment of choice for feline chronic neutrophilic cholganitis?

A

Unknown since the etiology is unknown - Try course of antibiotics then consider steroids

347
Q

Which breed of cat is over-represented for lymphocytic cholangitis?

A

Persians

348
Q

What is lymphocytic cholangitis in cats?

A

Moderate to marked infiltrates of small lymphocytes – predominantly restricted to portal areas – often associated with variable portal fibrosis and biliary proliferation

349
Q

In which feline hepatic disease is acites a prominent feature?

A

Lymphocytic cholangitis

350
Q

Which feline disease is similar to human chronic primary biliary cirrhosis?

A

Lymphocytic cholangitis

351
Q

What is the liver fluke that results in chronic cholangitis in cats?

A

Trematode - Platynosomum spp (2 intermediate hosts - snail/slug and lizard/gecko/toad
Diagnosis: Operculated fluke eggs on fecal or in bile
Tx: Praziquantel

352
Q

What are common findings in cats with lymphocytic cholangitis?

A

Jaundice, ascites and hypergammaglobulinemia (almost all cases)

353
Q

What is the major difference with lymphocytic portal hepatitis in cats?

A

As opposed to cats with cholangitis there is no inflammation that is centered at bile ducts

354
Q

What is the common signalment for lymphocytic portal hepatitis in cats?

A

Older, > 10 yrs

355
Q

What is the underlying etiology of feline lymphocytic portal hepatitis?

A

• Etiology not known – suspect immune mediated disease or non-specific ‘reactive’ change possibly reflecting extrahepatic disease processes

356
Q

Discuss the anatomy of a portosystemic shunt.

A

• Ductus venosus (Carries blood oxygenated placenta blood to fetal systemic circulation bypassing hepatic circulation) normally closes in 10 days of birth = abnormal patency leads to congenital shunts

357
Q

What breed is the most common to have PSS?

A

Yorkies (59X more likely than mixed breed and 36X more likley than all breeds)

358
Q

Which cat breed is likely to have PSS?

A

Himalayan cats

359
Q

Which dog breed is known to have familial PSS that have been reduced with breeding?

A

Irish Wolfhound

360
Q

What can occur if you breed a dogs with congenital port vein hypoplasia (hepatic microvascular dysplasia)?

A

Offspring can have PSS = Suggestive that diseases may be related

361
Q

What type of PSS is found in large breed dogs?

A

Intrahepatic PSS

362
Q

What type of PSS is found in cats and small breed dogs?

A

Extrahepatic PSS

363
Q

What should a cat with copper colored iris make you think of?

A

PSS!! Esp if hypersalivation

364
Q

Which amino acid deficiency is thought to precipitate hepatic encephalopathy?

A

Arginine deficiency in cats

365
Q

What can be found on CBC, Chemistry, urinalysis of animals with PSS?

A

CBC: Microcytosis, leukocytosis, anemia
Chemistry: Low BUN, cholesterol. Protein. Albumin, glucose with increased ALT and ALP (bone)
UA: Low USG and ammonium biurate crystals

366
Q

What is the expected result of serum ile acids in PSS?

A

Normally VERY high > 100umol/L, some as low as 25umol/L

367
Q

What percentage of dogs can have postpranial bile acids that are less than fasting and why?

A

About 20%, related to interdigestive contraction of GB or prolonged gastric empyting or intestinal transit times

368
Q

What percentage of dogs with PSS can have normal ammonia levels?

A

About 21% of dogs with PSS will have normal ammonia levels, esp if after fasting or medical management

369
Q

Why is holding of an ammonia sample so important?

A

RBCs have 2-3X ammonia as what is in plasma, therefore if prolonged time, hemolysis plasma not separated = Increased ammonia readings

370
Q

What was developed to provide a more accurate diagnosis of liver dysfunction?

A

Ammonia tolerance test

371
Q

If a small liver, large kidneys, uroliths, and reduced portal vein to aorta ratio is noted, what should you be suspicous of?

A

PSS

372
Q

What is the benefit of percutanous splenic scintigraphy?

A

About 90% of the dose of technetium 99m (99mTc) can be used compared to rectal

373
Q

What is another imgaing modality that requires celiotomy?

A

Intraoperative mesenteric portography

374
Q

How can Protein C levels help with portal vein hypoplasia vs PSS?

A

Protein C >70% in dogs with portal vein hypoplasia

Protein C< 70% in dogs with PSS

375
Q

What percentage dogs can do well with medical management only with PSS?

A

About 1/3, many living as long as 7 yrs

Over 50% were euthanized within 10 months for progressive neurologic signs

376
Q

What are 2 factors that have been assoicated with better response to medical management in PSS?

A

Older animal

High BUN

377
Q

Which dogs with PSS have the best prognosis with surgery?

A
  1. Extrahepatic shunts
  2. Undergo complete shunt closure
  3. Urinary tract signs with no HE
378
Q

What percetnage of animals with PSS cannot tolerate complete closure of their shunt and why?

A

About 30-60%, related to increased in portal pressures

379
Q

Which surgery for PSS Is associated with high complications?

A

Complete or partial occlusion, compared to gradual occlusion
periopertive death 14-22%
Seizures 7-11%
Recurrence of CS 40%

380
Q

How does an meroid constrictor work for PSS?

A

Gradual closes over 2-3 wks from device swelling and local inflammation/tissue reaction
Excellent outcome sin 80-85% of dogs, bit persistent shunting noted in 17-21%

381
Q

What are common complications in cats undergoing sx for PSS?

A

Blindness and seizures

382
Q

What is a potential reason that Yorkies may have persistent elevation in bile acids despite clinical improvement after PSS sx?

A

They may also have congenital portal vein hypoplasia

383
Q

What is the pathogenesis of biliary mucoceles?

A

• Accumulation of mucous component of bile within the GB
○ Initially thought to be due to obstruction of the cystic or CBD (like humans)
○ This theory not supported by histopathology
○ More likely due to an abnormality in the mucous secreting glands of the GB mucosa
UNKNOWN

384
Q

Name 3 diseases that may be predisposing dogs to biliary mucoceles.

A
  1. Chronic pancreatitis
  2. HAC
  3. Liver dz
385
Q

What are the 4 breeds that are over-represented for biliary mucoceles?

A
  1. Shelties (shetland sheepdogs)
  2. Cockers
  3. Dachshunds
  4. Mini Schnauzer
386
Q

What is the diagnostic of choice for biliary mucoceles?

A

AUS = nongravity dependent kiwi, varying degrees of EHBO ○ Prognosis hard to determine (can’t see pressure necrosis of GB wall or cystic duct)

387
Q

What is the treatment of choice for biliary mucoceles?

A

Cholecystectomy (majority are sterile bur still get cultures)

388
Q

What is the perioperative mortality of biliary mucoceles?

A

About 20-25%, no risk factors have been identified

Even biliary tract rupture or bile peritonitis did not affect survival!

389
Q

What is common complication of biliary mucoceles?

A

Pancreatitis (pre-op and post op)

390
Q

What does E-tube stand for?

A

Esophagostomy tube

391
Q

Where should you measure for an E-tube?

A

Btwn ribs 7-8

392
Q

Name 2 techniques for placing E tubes.

A
  1. Eld Device (used to place gastrostomy tubes)

2. Curved forceps technique

393
Q

What is Type I canine parvovirus (CPV-1)?

A

Isolated from healthy dogs and considered to be nonpathogenic except in neonates

394
Q

What is Type 2 canine parvovirus (CPV-2)?

A

Severe enteritis

395
Q

What cells does CPV-2 infect?

A

Rapidly dividing cells
Intestinal - Hemorrhagic diarrhea
Lympoid system - Leukopenia
Bone Marrow

396
Q

What can occur in neonates with CPV-2?

A

It can infect the myocytes, resulting myocarditis = Death

397
Q

What is a major risk factor for CPV-2?

A

Non-vaccination

398
Q

What breeds have an increases risk of infection of CPV-2?

A

Rotties
Dobermans
Pitties

399
Q

How is CPV-2 diagnosed?

A

ELISA for parvovirus antigen (fecal material, rectal swab, bx)

400
Q

What can result in a false positive Parvo ELISA?

A

Vaccination with MLV - Weak positive test rresult from 5-15 days

401
Q

If an animal with parvovirus is not hospitalized with is the survival rate?

A

About 50%, if hospitalized 80-90% survival

402
Q

What is known about the used of Nuprogen (granulocyte colony-stimulating factor) for parvovirus?

A

Based on a study, there was no survival advanatage was noted

403
Q

What is oseltamivir and how is it used for CPV-2?

A

Neuraminidase inhibitor that inhibits viral replication in specific cells (Tamiflu) - thought to help in parvovirus

404
Q

What is the classic signalment for constipation and megacolon?

A

Middle aged (6 yrs), male cats (70% males), DSH (46%)

405
Q

Which breed of cat has increased constipation and megacolon?

A

Siamese (12%)

406
Q

What is the mechanism of cisapride for colonic prokinetic?

A

Enhances colonic propulsive motility trhough activation of colonic smooth m. (5-hydroxytryptamine)

407
Q

What is considered to be abnormal for gastric emptying?

A

Normally starts within 15 mins (should have started by 45mins), normally completely empty by 1-2 hrs but at the latest by 4 hours

408
Q

What is the principal behind hydrolyzed diets?

A

Peptides are too small to cross-link IgE on sensitized MC

409
Q

What is the MOA of metoclopramide?

A

Dopaminergic (D2) antagonist

410
Q

How is metoclopramide an antiemetic?

A

Dopaminergic (D2) antagonist = CRTZ

411
Q

What is the MOA of erythromycin?

A

Motilin agonist (cats), 5-HT3 antagonist (dogs) - Stomach and intestines

412
Q

What is the MOA of ranitidine?

A

Acetylcholinesterase inhibitors, M3 muscarinic cholinergic agonist = Stomach, intestine, colon

413
Q

Where does metoclopramide result in prokinetics effects?

A

Stomach - Agonism of serotongeric 5-HT4

414
Q

What are the effects of metoclopramide on the LES?

A

Increases pressure in gastroesophageal sphincter and accelerates gastric emptying

415
Q

Which drug is more potent at increasing gastroesophgeal sphincter tone and promoting gastric emptying?

A

Cisapride

416
Q

Name other reasons for hypergastrinemia.

A
  1. Gastrinoma
  2. Nonfasting sample
  3. Renal Failure
  4. Achlorhydria (primary or secondary omeprazole)
  5. Besenji enteropathy
  6. G- cell hyperplasia
  7. Liver disease
  8. Helicobacter infection
417
Q

Name two breeds that have a Zone 3 hepatopathy: Cyclic increased in LE.

A

Maltese and Bichon frise

418
Q

What is microvascular dysplasia?

A

Permanent aberration of hepatic microcirculation that is clinically characterized by high SBA concentrations

419
Q

What is the current success rate to reduce motioning in dogs with Heicobacter?

A

40-78%

420
Q

What is the current recommendation (new CVT) for tx of Helicobater?

A

Amoxicillin
Clarithromycin
Omeprazole
For 3 weeks

421
Q

What is the current recommendation (new CVT) for tx of Helicobater?

A

Amoxicillin
Clarithromycin
Omeprazole
For 3 weeks

422
Q

What type pf diet is ideal fro gastric emptying?

A

Liquid, low fat and low protein

423
Q

What is the current success rate to reduce motioning in dogs with Helicobacter?

A

40-78%

424
Q

How is B12 absorbed?

A

• CBL homeostasis = Complex, multisteps (within stomach, pancreas, intestines, and liver)
○ CBL is released from food in stomach
○ Bound to nonspecific CBL-binding protein (Haptocorrin) - Salivary and gastric origin
○ Intrinsic factor (IF) - CBL binding protein that promotes CBL absorption in ileum
§ Produced by pancreas (NOT stomach in cats!)
§ Humans = Only gastric production (def from atrophic gastritis
○ High affinity of CBL for haptocorrin in acid pH (binds in stomach)
○ Duodenum: Haptocorrin is degraded by pancreatic proteases → CBL transferred from haptocorrin to IF
§ Facilitated by high affinity of IF for CBL at neutral pH
○ Cobalamin-IF complexes then bind to specific receptors (intrinsic factor cobalamin receptor, aka cubilin) - Located in microvillus pits of apical brush border membrane of ileal enterocytes
○ CBL transcytose to portal bloodstream bound to transcoablamin 2 (TC II) = mediated CBL absorption by target cells
○ Portion of CBL taken up by hepatocytes = Re-excreted rapidly in bile bound to haptocorrin
§ CBL of hepatobiliary origin and dietary derived CBL thought to undergo transfer to IF and receptor mediated absoprtion →ENTEROHEPATIC RECIRCULATION

425
Q

IN cats what is B12 turn over?

A

Rapid, can be depleted in 1-2 months

426
Q

What diseases are thought to increase B12 in cats?

A

High dietary content
Paraenteral supplementation
Cholestatic liver dz

427
Q

What diseases are thought to decrease B12 in cats?

A 
Dietary deficiency
IBD
GI LSA (mutlicentric LSA)
EPI
Pancreatitis
Cholangitis
HyperT4
Intestinal Bacterial Utilization
Receptor Abnormalities

ACVIM Reading List (27 decks)

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