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Chronic GI Disease Flashcards

1
Q

Obj: Given a patient w/ chronic GI signs:

  • Differentiate between primary and secondary GI disease
  • Formulate an empirical treatment plan based on localization of clinical signs, most likely responses, and possible treatment side-effects
A
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2
Q

Obj: For diet trials: describe how different diet types work and identify specific examples in each category

A
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3
Q

Obj: Differentiate how microbiota-targeted therapies work and describe evidence for/against use

A
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4
Q

Obj: For dogs and Cats w/ Idiopathic IBD:

  • Formulate a medication plan based on available clinical and laboratory results
  • Discuss prognosis, including negative prognostic indicators w/ owners
A
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5
Q

Obj: For infectious diseases:

  • List major routes of transmission, tissues affected, SI or LI clinical signs
  • Based on a case scenario, prioritize differentials based on the above and unique systemic or laboratory findings and choose the best diagnostic test
  • For a specific patient, decide whether treatment is needed and formulate a treatment plan
A
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6
Q

What is a ‘Chronic Enteropathy’?

A
  • GI signs ≥ 3-4 weeks duration
    • Non-GI disease has been excluded
  • Includes:
    • GI neoplasia
    • GI infectious disease
    • Idiopathic inflammatory disease
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7
Q

What is the diagnostic approach to chronic GI disease?

A
  • Rule-out systemic disease
    • Baseline blood work
    • Urinalysis
    • Baseline Cortisol (dogs)
    • T4 (cats)
    • specPL (Pancreatic lipase; select cases)
    • Bile acids (select cases)
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8
Q

Obj: For Feline CE:

  • Contrast common imaging and laboratory findings vs dogs
  • Adjust diagnostic and treatment plans based on unique feline physiology, most common differentials, and nutrient deficiencies
A
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9
Q

What are the common enteropathogens? (Viruses, protozoa, bacteria, fungi, parasites, and misc)

A
  • Viruses:
    • Parvovirus
    • Coronavirus
    • Rotavirus
  • Protozoa
    • Giardia
    • Tritrichomonas
    • Cryptosporidium
  • Bacteria
    • Clostridium
    • Campylobacter
    • Salmonella
    • E.coli
  • Fungi
    • Histoplasma
  • Parasites
    • Hookworms
    • Roundworms
    • Stomach worms
    • Whipworms
    • Heterobilharzia
  • Misc:
    • Neorickettsia
    • Prototheca
    • Pythium
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10
Q

What is Helicobacter spp?

A
  • Etiologic agent:
    • Gram negative
    • microaerophilic
    • spiral bacteria
  • Normal Flora in:
    • 70-100% of healthy dogs
    • 40-100% of healthy cats
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11
Q

What are the clinical signs of a Helicobacter infection?

A
  • Most asymptomatic
  • +/- Chronic vomiting
  • No relation to GI ulceration
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12
Q

How is a Helicobacter spp. Infection diagnosed?

A
  • Histopathology
    • Spiral bacteria in association w/ gastric mucosa
  • Squash prep cytology
  • PCR
  • Rapid urease test
    • does have false positives (other urease producing bacteria - E. coli, Proteus)
  • Response to treatment
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13
Q

What is the treatment for Helicobacter spp infections?

A
  • Combination therapy for 3 wks
    • Amoxicillin + azithromycin/clarithromycin + bismuth subsalicylate +/- omeprazole
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14
Q

What is Heterobilharzia?

A
  • Etiology: Trematode parasite (Heterobilharzia americanum)
  • Geographic risk: US Gulf Coast
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15
Q

How is Heterobilharzia americanum transmitted?

A
  1. Cercaria form of organism penetrates dog skin (snail intermediate host)
  2. Organism migration to liver
  3. Eggs laid in mesenteric venules
  4. Migration of organisms through GI wall
  5. Severe granulomatous inflammation
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16
Q

What are the clinical signs of Heterobilharzia?

A
  • LI or SI diarrhea
  • Vomiting
  • Weight loss
  • +/- liver failure, renal failure
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17
Q

How is Heterobilharzia diagnosed?

A
  • Chemistry panel
    • Hypercalcemia
    • Hypoalbuminemia +/- hyperglobulinemia
    • Elevated liver enzymes
    • Azotemia
  • Cytology or histopathology from liver
  • Intestinal biopsies
  • Fecal sedimentation or PCR
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18
Q

What is the treatment for Heterobilharzia?

A
  • Praziquantel
  • Fenbendazole
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19
Q

What is the prognosis of Heterobilharzia?

A
  • Acute: Good
  • Chronic: Guarded-poor
  • Chronic Carriers possible
  • Hypercalcemia, acute azotemia do NOT affect prognosis
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20
Q

What is Giardia?

A
  • Etiologic Agents: Giardia duodenalis (Binucleated flagellate)
  • Pathogenesis:
    • 2 forms: trophozoite and cyst
      • Trophozoite lives in Small intestine
    • Fecal oral transmission
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21
Q

What is the common signalment of animals w/ Giardia?

A
  • Young (<1-2 years)
  • Immunocompromised
  • Steroids (recrudescence)
  • Group-housed animals
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22
Q

What are the clinical signs of Giardia?

A
  • Small intestinal diarrhea (acute or chronic)
  • Cats may have mucoid diarrhea
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23
Q

How is Giardia diagnosed?

A
  • ZnSO4 centrifugation-flotation
    • Intermittent shedding
    • 95% sensitivity w/ 3 repeated tests
  • Immunoassays (fecal antigen)
    • SNAP point-of-care: good sensitivity (90%) and specificity (99%)
  • Direct IFA (fecal cysts)
    • High discordance between antigen and cyst-based tests
    • false negatives common
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24
Q

What is the treatment/prevention for Giardia?

A
  • Treatment: Fenbendazole 50 mg/kg q24h for 5 days
  • Prevention:
    • Treat all group-housed animals
    • Clean/disinfect environment
    • Bathe at beginning/end of treatment
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25
Q

How is Histoplasmosis transmitted?

A
  • Inhalation or ingestion
  • Intracellular yeast replication
    • results in Granulomatous inflammation
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26
Q

What are the clinical signs of Histoplasmosis?

A
  • GI histoplasmosis more common in dogs
    • SI or LI diarrhea
  • Protein-losing enteropathy - Panhypoproteinemia, effusion, edema
  • Weight loss
  • Concurrent respiratory disease, ocular disease, cytopenia, fever
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27
Q

How is Histoplasmosis diagnosed?

A
  • Urine histoplasma antigen
  • Cytology/Histopathology
    • Rectal scrape
    • Intra-abdominal LN, liver, spleen
    • GI endoscopy
    • If systemic: Bone marrow aspirate, lung aspirate, skin lesion impression cytology, aqueocentesis
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28
Q

What is the treatment for Histoplasmosis?

A
  • Itraconazole 10 mg/kg q24h for at least 6 months
  • Fluconazole 5 mg/kg q12h for at least 6 months
    • treatment of choice w/ ocular or CNS involvement
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29
Q

What is the prognosis for Histoplasmosis?

A

Guarded to poor for severe GI involvement

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30
Q

What is Pythium insidiosum? hosts? location?

A
  • Aquatic oomycete organism
  • Causes GI infiltration and pyogranulomatous inflammation
  • Located in the Gulf States
  • Come from warm, swamp water or fields post-flooding
  • Large breed, male dogs, less than 3yo most commonly affected
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31
Q

What are the clinical signs of a Pythium insidiosum infection?

A
  • Mass lesions resulting in partial or complete GI obstruction
    • transmural pyloric-duodenal thickening
  • Small intestinal diarrhea
  • Weight loss
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32
Q

How is a Pythium insidiosum infection diagnosed?

A
  • Baseline bloodwork
    • CBC: Eosinophilia
    • Chemistry: Panhypoproteinemia, hypercalcemia
  • Histopathology:
    • Granulomatous inflammation with special stains to identify organism
      • branching, non-septate or poorly septate hyphae
  • Serum ELISA or PCR
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33
Q

What is the treatment for a Pythium insidiosum infection?

A
  • Combination of:
    • surgical excision
    • +herbicide (mefenoxam)
    • +antifungals (itraconazole, terbinafine)
    • +/- Vaccination
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34
Q

what is the prognosis for a Pythium insidiosum infection?

A
  • Poor to grave
  • Poorly responsive to therapy
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35
Q

What is Prototheca?

A

Unicellular, achlorophyllous organism related to green algae

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36
Q

What is the pathogenesis of Prototheca?

A
  • pyogranulomatous inflammation and ulceration
  • Dissemination to:
    • eyes
    • CNS
    • skin
    • lymph nodes
37
Q

What are the clinical signs of a Prototheca infection

A
  • Enterocolitis - hemorrhagic, LI diarrhea
  • Ocular - Chorioretinitis, uveitis
38
Q

How is prototheca diagnosed?

A
  • Cytology or histopathology
  • Sabouraud culture
39
Q

What is the treatment for Prototheca?

A
  • no effective treatment
  • Anti-fungals?
    • Amphotericin - treatment of choice in humans
    • Itraconazole or fluconazole
40
Q

What is the prognosis of prototheca?

A
  • Poor to grave
  • almost 100% fatal
41
Q

What is the pathogenesis of inflammatory enteropathies?

A
  • Multifactorial
  • Abnormal GI immune response
    • immune system dysregulation
    • increased inflammatory mediators
    • loss of GI mucosal tolerance
    • genetics
  • Immune system interaction with:
    • dietary antigens
    • GI bacterial microbiota
  • GI mucosal barrier disruption
42
Q

How are Inflammatory Enteropathies diagnosed?

A
  • Rule-out non-intestinal disease
    • CBC and Chem often normal in uncomplicated cases. May see:
      • Mild, non-regenerative anemia (of chronic disease)
      • Hypoalbuminemia and electrolyte abnormalities with PLE
      • Hypokalemia w/ inappetence or severe vomiting/diarrhea
  • Rule-out infectious disease:
    • Fecal float + deworming (fenbendazole)
      • others on a per-patient basis
  • Abdominal imaging
  • GI function testing
  • GI biopsies
    • Gold standard
    • Evaluates primary vs secondary causes
  • Treatment trials
43
Q

FYI

What are some breed-specific inflammatory enteropathies?

A
  • German shepherd IgA deficiency
  • Irish Setter Gluten Sensitivity
    • (Wheat, barely, rye)
  • Shar-pai Congenital Cobalamin Deficiency + Idiopathic IBD
  • Basenji Immunoproliferative Disease, increased serum IgA
44
Q

How is treatment response categorized for Inflammatory enteropathies?

A
  • Food-responsive
  • Nutrient-responsive
  • Microbiome-targeted therapies
  • Steroid/immunosuppression responsive
45
Q

What food treatments are used for inflammatory enteropathies? (Broad categories)

A
  • Highly digestible
  • Novel protein/limited ingredient
  • Hydrolyzed
  • Elemental
46
Q

What is the theory behind Highly digestible diets for treatment of inflammatory enteropathies?

A
  • Diets are low-fat and contain easily digestible carbohydrate sources, so less antigen is present to GI lymphoid cells
47
Q

Do Highly digestible diets work for treatment of inflammatory enteropathies?

A
  • Palatable
  • unable to induce long-term remission in dogs with FRE (Food Responsive enteropathies)
    • may have good short-term response
48
Q

What is the theory behind Novel protein/limited ingredient diets for treatment of inflammatory enteropathies?

A
  • Presentation of antigens to GI lymphoid cells that are not “primed for reaction”
49
Q

Do Novel protein/limited ingredient diets work for treatment of inflammatory enteropathies?

A
  • Palatable
  • Equal response in dogs with true “novel” diet and hydrolyzed diet
  • May be challenging to find a novel diet
    • OTC diets are not limited
    • Consider homemade limited ingredient diet for short-term trial
  • Some protein sources are higher in fat (especially canned)
  • Examples: Duck/pea, venison/potatoes, Salmon, rabbit, kangaroo
    • novel proteins vary w/ geographic location
    • Fish is NOT a novel protein for cats
50
Q

What is the theory behind Hydrolyzed Diets as treatment for inflammatory enteropathies?

A
  • Avoids GI hypersensitivity response by including protein/carbohydrate components that are broken down into particles that are too small to cause a reaction
51
Q

Do Hydrolyzed diets work as treatment for inflammatory enteropathies?

A
  • Equal response in dogs with true ‘novel’ diet and hydrolyzed diet
  • Many are lower in fate and more digestible compared to novel protein diets
  • may be less palatable
  • Components may need to be smaller (3-5kDa)
    • most available diets (10kDa)
  • availability of ‘multifunction’ diets
52
Q

What is the theory behind Elemental diets as treatment for inflammatory enteropathies?

A
  • Contains only individual amino acids, glucose polymers, avoiding hypersensitivity response
  • low fat
53
Q

Do Elemental diets work as treatment for inflammatory enteropathies?

A
  • Humans: induction of remission in Crohn’s disease in 6-8wks
    • ability to transition to highly digestible diet long-term
    • no difference in remission rates compared to steroids
  • Human elemental diets CANNOT be used in cats
    • Arginine, Taurine, Carnitine, and other AA too low
54
Q

What recommendations need to be followed to allow for the best possible response to diet trials for inflammatory enteropathies?

A
  • No other protein/carbohydrate sources
    • No oral treats, flavored supplements, toothpaste, preventatives
      • Dry kibble or baked canned food (special diet) can be used for treats
    • Flea/heartworm prevention can be administered at the beginning, then transitioned to topical if patient responds to food trial
  • Consider e-tube for ‘picky’ patients
55
Q

What is the expected response to food trials for treatment for inflammatory enteropathies?

A
  • 6 weeks for remission
    • improvement in 2 wks
  • Dogs 60-90% response rate
    • response more likely in:
      • younger dogs w/ LI or mixed bowel diarrhea
      • dogs with vomiting alone
      • Patients w/ lower disease severity scores
      • Patients with normal albumin
    • Only 5% response in cases w/ only SI diarrhea
  • Cats: response more likely in:
    • <5yrs old
    • Patients w/ concurrent dermatologic signs
    • 30% Food responsive overall
      • >50% w/ only LI disease
56
Q

When should food trials be considered as failed treatment for inflammatory enteropathies?

A
  • If following fail:
    • 2 novel protein diets
      • hydrolyzed
    • +/- homemade diet
57
Q

What are the microbiome-targeted therapies for treatment of inflammatory enteropathies?

A
  • Fiber
    • second preferred treatment option
  • Probiotics
    • Continuous therapy likely needed
    • More likely to be an ancillary therapy
  • Fecal microbiota transplantation
    • limited evidence
    • more likely to be an ancillary therapy
  • Antibiotics
    • Antibiotic-responsive diarrhea (ARD) or chonic diarrhea responding to antibiotic therapy, was historically considerd a response categorey
    • Due to negative side effects, long-term treatment is no longer recommended
58
Q

What is the pathogenesis of ARD?

A
  • Increased total number GI bacteria
  • Bacterial dysbiosis
  • GI mucosal barrier defects
  • Contact with pathogenic bacteria
59
Q

What are the cons of an antibiotic trial for inflammatory enteropathies?

A
  • No controlled studies evaluation dogs with chronic enteropathies and treatment with metronidazole
  • Microbiome changes persist in healthy dogs for >1-2 months with metronidazole and tylosin, respectively
  • Worse fecal score in healthy dogs given tylosin or metronidazole
  • Microbiome alterations are NOT corrected with antibiotics and clinical signs return in many dogs after discontinuation
60
Q

What is Idiopathic Inflammatory bowel Disease (IBD)?

A
  • GI signs ≥3-4 wks + exclusion of other causes + lac of response to diet/antibiotics + response to immunomodulation
  • Interplay of Dietary antigens + Enteric bacteria + Mucosal immune response
61
Q

What type of inflammation are found in GI biopsies of IBD animals?

A
  • Lymphoplasmacytic
  • Eosinophilic
  • Granulomatous
  • Neutrophilic
62
Q

What are the alternative diagnoses (other than IBD) for cats with lymphoplasmacytic GI inflammation?

A
  • 50:50 IBD: Small cell lymphoma
  • PCR for antigen receptor rearrangements (PARR) may be needed to completely distinguish these etiologies in addition to histopathology
63
Q

When GI biopsy reveals Eosinophilic Inflammation what other diseases have to be ruled-out before calling it IBD?

A
  • Rule out other hyper-eosinophilic disorders:
    • Dietary sensitivity
    • parasites
    • hyper-eosinophilic syndrome
64
Q

What animals more commonly have Eosinophilic IBD

A
  • Young animals
  • Boxers, German Shepherd, Dobermans
65
Q

What other GI conditions are frequently associated with Eosinophilic IBD?

A
  • GI erosions
  • GI ulcerations
66
Q

What Is Eosinophilic Sclerosing Fibroplasia? Etiologies?

A
  • Affects felines
  • Inflammatory enteropathy resulting in GI mass-like lesions, which histopathologically consist of eosinophilic inflammation and collagen
  • Etiology: Unknown, suspect Immune-mediated
67
Q

What sites are more often affected by Eosinophilic sclerosing fibroplasia

A
  • Pylorus
  • ileocaecocolic junctions
68
Q

What exam findings are common with Eosinophilic sclerosing fibroplasia?

A
  • Many 85% have a palpable abdominal mass
  • Complete loss of GI wall layering on ultrasound
  • enlarged intra-abdominal lymph nodes common
  • Cytology can be concerning for neoplasia, making hitopathology extremely important
69
Q

What is the treatment for Eosinophilic Sclerosing Fibroplasia

A
  • Surgery (if possible)
  • immunosuppression (steroids)
70
Q

What is the prognosis for Eosinophilic Sclerosing Fibroplasia

A
  • Guarded
  • If full resection is possible - cats often do well
    • predilection sites make complete resection difficult
    • many cats present in advanced stages
71
Q

What are the rule outs for GI Granulomatous Inflammation?

A
  • Fungal
  • Feline Infectious peritonitis
  • Granulomatous colitis
72
Q

What are the primary medications used for Immunosuppression in IBD?

A
  • Prednisone - dogs
    • 2 mg/kg q24h max of 40-50 mg dose
  • Prednisolone - cats
    • 2 mg/kg q 24h
  • Budesonide
    • 0.3mg/m2 q24h - dogs
    • 0.5-0.75 mg q24h - cats
73
Q

What are secondary options for immunosuppression?

A
  • Dogs
    • Cyclosporine 5 mg/kg q12h
    • Chlorambucil 2-4 mg/m2 q24h
    • Mycophenolate 10 mg/kg q12h
  • Cats:
    • # 2 - Chlorambucil 15-20 mg/m2 q14days
    • # 3 - Cyclosporine 5 mg/kg q12h
74
Q

What supportive medications can be used in conjunction with immunosuppressants for IBD?

A
  • Cobalamin if deficient
  • Anti-nausea/anti-emetic medications
    • Maropitant
    • Ondansetron
    • Metaclopramide
  • Appetite stimulants
    • Mirtazapine
    • Capromorelin
    • Cyproheptadine
  • Mucosal protection
    • acid suppression
      • famotidine
      • Omeprazole / Esomeprazole
    • Gastroprotectants
      • sucralfate
      • Barium
      • Misoprostol
  • Promotility drugs
    • Metaclopramide
    • Cisapride
    • Erythromycin
75
Q

How is Cobalamin used for IBD?

A
  • if cobalamin deficient
  • Weekly SQ dose for 6 wks then monthly - OR daily dosing
  • Cats are more likely - can develop within 1 month
76
Q

Why are cats with IBD more likely to develop Cobalamin deficiency?

A
  • Shorter serum half-life in cats with chronic GI disease
    • vs 5-7 days in healthy cats
77
Q

What Anti-nausea/antiemetic medications are used as ancillary treatment For IBD? How do they work?

A
  • Maropitant - Centrally-acting [Neurokinin 1 (NK1)]’ Chemoreceptor trigger zone (CRTZ)
    • Better anti-emetic than anti-nausea
    • Does not increase appetite in cats
  • Ondansetron - Centrally and peripherally acting [Serotonin (5HT3) receptors in the GI tract, & CRTZ]
    • Better anti-nausea than anti-emetic
    • Poor oral bioavailability
  • Metoclopramides: Centrally and peripherally acting [5HT3 and dopamine (D2) receptors in GI tract, & CRTZ)
    • weak anti-emetic, especially in cats
    • more commonly used for prokinetic properties
78
Q

What Appetite stimulants are used as ancillary treatment For IBD? How do they work?

A
  • Mirtazapine - Centrally and peripherally acting (5HT3 antagonist; CRTZ)
    • transdermal and oral forms increase food intake
    • low dose (1.875 mg PO q24h) in cats
  • Capromorelin - Central (ghrelin) agonist
    • Increased insulin like growth factor, food intake, weight gain
    • Side-effect: Diarrhea
  • Cyproheptadine - Centrally and peripherally acting [Histamine (H1) receptors]
    • relatively poor stimulant
    • Side-effect: sedation
    • can NOT be combined with mirtazapine
79
Q

What Mucosal protectants are used as ancillary treatment for IBD? How do they work?

A
  • Acid suppression:
    • Famotidine - H2 blocker
    • Omeprazole - Proton pump inhibitor
  • Gastroprotectants:
    • Sucralfate - coating agent, stimulates prostaglandin secretion
    • Barium - coating agent, stimulates prostaglandin protection
      • Can be given as enema w/ lower GI bleed
      • caution in vomiting/regurgitating patients
    • Misoprostol: PGE1 analog
      • NSAID-induced ulceration or gastroprotection with NSAID overdose
80
Q

When would Acid suppression or Gastroprotectants be used for ancillary IBD treatment

A
  • Acid Suppression:
    • Overt GI ulceration
    • “At-risk” patients:
      • GI neoplasia w/ hyperacidity
      • ulcerogenic drugs + other “high risk” disease
        • intervertebral disk disease, intrahepatic portosystemic shuts, portal hypertension
    • Short-term for Esophagitis
  • Gastroprotectants:
    • Overt GI bleeding/ulceration
81
Q

What Promotility drugs are used as ancillary treatment For IBD? How do they work?

A
  • Metoclopramide - act on pylorus and SI
  • Cisapride - act on LES (cats), pylorus, SI, colon
  • Erythromycin - motilin agonist - acts on LES (cats), pylorus, colon (dogs)
82
Q

What parameters should be used to monitor patients with inflammatory enteropathies?

A
  • Body Weight
  • BCS
  • MCS
  • Fecal scores: subjective measure of fecal water content
  • Disease Severity Scores
    • Additive assessment of disease severity based on a combination of clinical signs and lab findings
      • higher cumulative score = more severe disease
    • Canine IBD activity Index
    • Canine Chronic enteropathy activity index
    • Feline Chronic enteropathy activity index
  • Lab work abnormalities
83
Q

What is the prognosis for inflammatory enteropathies for dogs?

A
  • For Idiopathic IBD:
    • 70-80% response w/ immunosuppression
      • only 30% complete remission
    • 25% euthanasia rate for uncontrollable disease
    • Dogs responding to diet trials do better
      • failure to adhere to diet trial is associated w/ relapse
84
Q

What are the negative prognostic indicators in dogs for Inflammatory Enteropathies?

A
  • Hypocobalaminemia
  • Hypoalbuminemia (<2 g/dL)
  • Effusion or edema
  • Severe duodenal mucosal lesions on histopathology
  • Crypt abscesses on histopathology
  • Chronic enteropathy activity index score > 12
  • Abdominal US changes suggestive of lymphoma
    • GI thickening + loss of wall layering + hyperechoic mucosa + enlargement mesenteric lymph nodes
  • Higher fecal S100A12 (calprotectin)
  • Decreased Serum Vit D (259Oh)D)
85
Q

What is the prognosis for cats with Inflammatory enteropathies?

A
  • Few prognostic studies on idiopathic IBD
    • Variable response rates: 50- >90% w/ steroids
    • MST >2yrs
86
Q

What is the etiology of Bilious vomiting syndrome?

A
  • Unknown - possibly:
    • motility disorder w/ duodenogastric reflux of bile
    • Association with hyperacidity
87
Q

What are the clinical signs of Bilious vomiting syndrome?

A
  • Vomiting in the morning or after long periods of fasting
  • Vomit contains bile-stained fluid
  • Otherwise healthy
88
Q

How is Bilious vomiting syndrome diagnosed?

A
  • Diagnosis of exclusion and response to treatment
89
Q

What is the treatment for Bilious vomiting syndrome?

A
  • Late night meal, snacks during the day
  • smaller, lower fat meals
  • Promotility medications
  • Omeprazole

Medicine II (46 decks)

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