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Equine Med & Surgery > GI diseases > Flashcards

GI diseases Flashcards

1
Q

Infectious causes of acute diarrhea in adult horses

A
  • Salmonella (S. typhimurium, others)
  • Neorickettia risticii
  • Clostridium difficile
  • Clostridium perfringens
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2
Q

Toxic causes of acute diarrhea in adult horses

A
  • NSAID overdose (right dorsal or generalized colitis)
  • Cantharadin (blister beetle) toxicity
  • arsenic
  • antibiotic associated
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3
Q

Misc. causes of acute diarrhea in adult horses

A
  • grain overload
  • sand enteropathy
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4
Q

What factors determine infection risk with Salmonella?

A
  1. organism virulence
  2. if horse has any risk factors
    • antibiotic administration
    • immunocompromised
    • underlying GI disease (colic)
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5
Q

Pathogenesis/dissemination of salmonella infection

A

invades epithelial cells, causes massive inflammation in lamina propria, often found in mesenteric LN & liver, may cause septicemia (particularly foals)

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6
Q

What organism causes Potomac Horse Fever?

A

Neorickettsia risticii

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7
Q

What cytotoxins are involved in the pathogenesis of clostridiosis?

A

Cytotoxin A, Cytotoxin B

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8
Q

How does the life cycle for Neorickettsia risticii and infection of horses work?

A
  • infects trematodes
  • aquatic snails, and aquatic insects are intermediate hosts for infected trematode larvae
  • horses ingests aquatic insects affected with trematode metacercaria
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9
Q

What cells does Neorickettsia risticii infect?

A

macrohages, monoctyes

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10
Q

What is the primary cause of clostridiosis in adult horses?

A

Clostridium difficile

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11
Q

What factor predisposes horses to development of clostridiosis?

A

antibiotic treatment

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12
Q

What is the pathogenesis of clostridiosis?

A

severe epithelial damage -> hemorrhagic colitis

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13
Q

What would be contraindicated in a cantharidin toxicity case?

A

mineral oil-will INCREASE absorption

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14
Q

What are some specific ways mucosal injury occurs when talking about specific causes of acute diarrhea in adult horses?

A
  • Damage to enterocytes by microbial or chemical toxins (clostridia, cantharidin, arsenic, lactic acid from fermented carbohyrates)
  • cell death of enterocytes (Salmonella)
  • NSAIDs damage mucosa by inhibition of homeostatic prostaglandins
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15
Q

Hypersecretion is what type of fluid loss?

A

isotonic

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16
Q

Consequences of high volume fluid loss include:

A
  • dehydration
  • electrolyte & acid/base imbalances
  • hypoproteinemia
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17
Q

Laboratory findings associated with acute diarrhea

A
  • mature neutropenia & leukopenia (early) or neutrophilia with leukocytosis (late)
    • usually left shift
  • thrombocytopenia
  • hyperfibrinogenemia
  • hypoproteinemia
  • hypoglycemia
  • hyponatremia
  • hypokalemia
  • hypocalcemia
  • metabolic acidosis (if poor perfusion or bicarb loss)
  • azotemia
  • high anion gap/lactic acidosis
  • elevated liver function tests
  • relative polycythemia
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18
Q

Diagnosis for Salmonella

A
  • fecal culture-at least five samples
  • +/- fecal PCR
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19
Q

Diagnosis of Potomac Horse Fever

A
  • buffy coat PCR
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20
Q

Diagnosis of Clostridiosis

A
  • C. difficile*
  • fecal cytotoxin immunoassay best
  • C. perfringens*
  • culture & PCR for toxins
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21
Q

Diagnosis of cantharadin toxicity

A
  • ID blister beetles in the hay
  • catharidin assay-urine best/preferred, especially if alive; can do feces or GI contents
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22
Q

Situations where colloids are beneficial

A
  • vascular leak syndrome
  • tissue edema
  • poor cardiac output/perfusion
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23
Q

Appropriate fluid therapy if dehyration is mild (<5%)

A
  • oral fluids with salt supplementation
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24
Q

Appropriate fluid therapy if dehydration is moderate (6-8%)

A
  • oral fluids with salt supplementation
    • might need to administer by NG as well
    • stimulation of thirst with salt paste
  • IV administration may or may not be needed; may consider colloids
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25
Q

Appropriate fluid therapy if dehydration >8% or horse is hypotensive

A
  • IV fluids necessary
    • isotonic crystalloid bolus then constant infusion
    • hypertonic saline mayb e useful to restore circulating volume and increase BP
    • colloids
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26
Q

What are anti-inflammatory/analgesic considerations with acute diarrhea situations?

A

NSAID

  • could impede mucosal repair and potentially nephrotoxic
  • use at lowest dose possible if used

Lidocaine

  • very good analgesic (inhibits afferent neurons, sympatholytic), anti-inflammatory, promotes mucosal healing
  • but must be given by CRI and monitored closely
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27
Q

What are some compounds that are sometimes given to aid mucosal healing?

A
  • bismuth subsalicylate
  • psyllium
  • misopostol
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28
Q

Describe nutritional support for acute diarrhea cases in adult horses

A
  • need to eat SOMETHING
  • good quality grass hay/grass-best
  • pelleted diet-reduces mechanical load on colon & readily digestible(should be high in roughage & low in soluble CHO)
  • avoid grains-fermented to lactate
  • enteral nutrition should be avoided
  • parenteral nutrition is cost effective in severely hypermetabolic patients or neonates
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29
Q

When are absorbant powders indicated?

A

Cantharadin toxicity, clostridiosis(reduce absorption of endotoxins); only given to horses with intestinal motility

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30
Q

Metronidazole may be indicated for __________

A

clostridiosis

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31
Q

What is one undesirable side effect of metronidazole in some horses?

A

horses may stop eating

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32
Q

What antibiotic is recommended for Neorickettsia risticii?

A

Oxytetracycline IV preferred

can give Doxycycline PO

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33
Q

Possible antibiotics indicated for salmonellosis

A
  • Chloramphenicol
  • Enrofloxacin
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34
Q

What are some possible causes of chronic diarrhea?

A
  • #1-parasites (particularly cyathostomes)-cause large intestinal inflammation & PLE
  • inappropriate diet
  • sand accumulation in ventral colon & cecum
  • chronic salmonellosis
  • right dorsal ulcerative colitis
  • neoplasia-colon
  • chronic peritonitis
  • chronic liver or heart disease
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35
Q

Diagnostic plan for chronic diarrhea

A
  • fecal exam for parasites
  • evaluate for sand
  • salmonella culture/PCR
  • peritoneal fluid analysis for peritonitis or neoplasia
  • rectal biopsy for IBD or neoplasia
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36
Q

Drug of choic for deworming cyathostomes

A

moxidectin

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37
Q

What is a good treatment approach for sand?

A

psyllium powder

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38
Q

What types of diets are appropriate choices for chronic diarrhea treatment?

A
  • all hay
  • complete pelleted feed
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39
Q

What are risk factors for NSAID toxicity?

A
  • dehydration
  • reduced blood flow to colon
  • underlying disease
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40
Q

What is a classic finding associated with RDUC?

A

hypoproteinemia/hypoalbuminemia-d/t PLE

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41
Q

Differentials for intermittent colic with or without weight loss

A
  • obstructive disease of GI tract
  • gastric ulcers
  • IBD
  • neoplasia
  • sand enteropathy
  • parasites (cyathostomiasis)
  • peritonitis
  • dental disease
  • EIA
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42
Q

What are the two cornerstones for treatment of RDUC?

A
  1. diet modification
    * low fiber roughage: pelleted; avoid hay, avoid grain, avoid grass
  2. misoprostol to promote mucosal healing
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43
Q

What is the role of corn oil in RDUC treatment?

A

provides calories and possibly promotes healing by promoting prostaglandin production

44
Q

What are the two forms of equine gastric ulcer disease?

A
  1. squamous disease (EGUS)
  2. glandular disease

*can coexist

45
Q

Perforating ulcers are most common in what age horses?

A

weanlings (4-6 months of age)

46
Q

What are the normal protective factors to acid injury of stomach?

A
  • saliva
  • roughage mat
  • mucus, epithelial integrity-PGs
  • gastric emptying
47
Q

Risk factors for squamous disease

A
  • occupation/training (race & show horses)
  • intermittent feeding, anorexia, withholding food
  • stress (environment, hauling, stall confinement)
48
Q

Risk factors for glandular disease

A
  • Illness
    • ICU foals
    • post-op colics
  • gastric outflow obstruction
  • NSAID toxicity
  • maybe Helicobacter infection
49
Q

What is a classic sign of gastric pain?

A

pain associated with eating-may be reluctant to eat

50
Q

What type of ulcers seem to be more painful?

A

glandular

51
Q

What type of hay is the best as a buffer?

A

alfalfa

52
Q

What is the H2 antagonist of choice in horses?

A

ranitidine

53
Q

What is the most specific therapy to reduce acid production?

A

proton pump blocker-omeprazole(Gastroguard)

54
Q

Sucralfate is most effective for ulcers in what part of the stomach?

A

glandular

55
Q

What is a specific therapy you could try in refractory cases of ulcers?

A

oral doxycycline-use as anti-inflammatory

56
Q

Causes of primary impaction (choke)

A
  • poor quality feed
  • poor mastication
  • dehydration/lack of saliva
  • greedy eaters
57
Q

Causes of secondary impaction/obstruction (choke)

A
  • corn cob, apple, other FB
  • stricture (congenital or acquired)
  • diverticulum
  • neoplasia
  • abscess or granuloma
  • inclusion cysts
  • vascular ring anomaly
  • motility dysfunction-megaesophagus
58
Q

Prepharyngeal dysphagia is called _______

A

“quidding”

59
Q

Clincal signs associated with choke

A
  • anxiety
  • hypersalivation
  • nasal discharge including feed material, saliva, water
  • cough
  • gag, extend neck when eating
  • mass/swelling in cervical region
  • dehydration
60
Q

What could cause a functional obstruction leading to choke?

A

esophagitis

61
Q

Treatment plan for choke

A
  • Clear obstruction:
    • lavage under heavy sedation (detomidine)-single NG tube; keep head lower than thoracic inlet
    • lavage under general anesthesia-double NG tube
    • sugery may be necessary to remove FB, masses, etc.
  • hydrate
62
Q

Fluid of choice when dealing with choke

A

0.9% saline with bicarbonate added as needed

63
Q

What effect does detomidine have on esophageal motility?

A
  • decreases waveform duration
  • increases transit time
64
Q

Dietary management of horse after choke

A

Remember esophageal motility will be reduced for a few days post-obstruction

  • pelleted diet slurry-may need to feed permanently if choke was secondary (e.g. stricture, mass)
    • 2-3% BW per day divided into six feeedings
    • corn oil supplemenation
  • avoid hay, grass until function is normal; reintroduce slowly when appropriate
  • salt supplementation if salivary loss continues
65
Q

Complications of choke

A
  • aspiration pneumonia-can be severe if bacterial infection occurs
  • rupture-proably fatal
66
Q

Follow-up protocol for choke

A
  • re-scope after relieving obstruction-look for mucosal injury or underlying disease/causes
  • if ulcerated:
    • NSAIDs??-prevent stricture
    • sucralfate
  • re-scope 14-30 days if injury to mucosa is seen
67
Q

Etiology of proximal enteritis

A

none definitively known:

possibly C. difficile, other bacteria, mycotoxins suggeted

68
Q

Pathophysiology of proximal enteritis

A
  • mucosal barrier damage
  • hypersecretion (due to inflammation)
  • functional ileus of proximal GI tract–>gastric fluid accumulation
69
Q

Distinguish between proximal enteritis and small intestinal obstruction

A
  • Fever with proximal enteritis; not with SIO
  • loops on rectal palpation are non-turgid with PE but turgid with SIO
  • Peritoneal fluid of SIO (if strangulating) has high WBC/RBC; PE does not
  • animals with PE will respond to gastric decompression while animals with SIO remain painful after gastric decompression
  • gastric fluid with PE-fetid, orange-red, large volume (>10L); SIO-green-yellow fluid (bile)
  • ultrasound: PE-thicker wall and smaller diameter than SIO, some motility. SIO: diameter 6-10 cm, wall
  • PE-GGT, Tbili, ALP, AST usually elevated; not with SIO
70
Q

Therapeutic principles for PE

A
  • analgesia
    • usually flunixin meglumine (low dose) & lidocaine CRI; butrophanol also option
  • gastric decompression
  • fluids-hydration/electrolyte balance
  • sepsis/endotoxemia
  • prokinetics
71
Q

Differential diagnosis for proximal enteritis

A
  • peritonitis
  • small intestinal obstruction
  • gastric outflow obstruction
  • salmonellosis
72
Q

Antibiotics given in the case of proximal enteritis? rationale?

A
  • Metronidazole is given sometimes since Clostridiosis is potential etiology
  • give broad spectrum antibiotics if neutrophil count is very low (b/c increased risk of infections)
73
Q

Why is it useless to give omeprazole when horse is still refluxing?

A

it needs to be absorbed in SI to have effects; omeprazole is drug of choice once motility has returned

74
Q

What are some prokinetics that may be tried to return motility and combat functional ileus?

A
  • lidocaine CRI
  • Metaclopramide-CRI best to avoid neurologic side effects, mania
  • Erythromycin
  • Bethanechol used to be used
75
Q

How to institute feed/water back to horses recoving from proximal enteritis

A
  • NPO while refluxing >2-4L q4 hr
  • can give small amounts of water when no significant amount of reflux for 24 hours
  • water tolerated–>graze every few hours for 24 hours
  • grazing tolerated–>small amounts of hay/complete pelleted feeds, slowly increasing over 2-3 days
  • parenteral nutriaion is an opeion if NPO >72 hours
76
Q

Complications that can arise from proximal enteritis

A
  • laminitis
  • ulcers
  • peritonitis
  • adhesions
  • renal failure
  • DIC
  • liver fibrosis
77
Q

Etiology of proliferative enteropathy?

A

Lawsonia intracellularis

78
Q

Transmission of proliferative enteropathy

A

fecal-oral from horse to horse

79
Q

Lay term for proliferative enteropathy

A

“hose pipe gut”

80
Q

Pathophysiology of proliferative enteropathy

A

infection of GI epithelial crypt cells–>epithelial proliferation in small intestine–>secretion, malabsorption, PLE

81
Q

What age horses are affected by proliferative enteropathy

A

1-7 months old

82
Q

Clinical signs associated with proliferative enteropathy

A
  • rapid weight loss
  • diarrhea, often + melena
  • peripheral edema
  • mild to severe colic
  • lethargy
  • anorexia
83
Q

Lab findings associated with proliferative enteropathy

A
  • panhypoproteinemia
  • leukocytosis
  • anemia of chronic inflammation/blood loss(non-regenerative)
  • maybe electrolyte and acid base imbalances, depending on diarrhea
84
Q

Antemortem test of choice for proliferative enteropathy

A

serology

85
Q

Why is fecal PCR for L. intracellularis not very sensitive?

A

animals are not frequently shedding

86
Q

Ultrasonographic findings assoc. with proliferative enteropathy

A
  • thickened small intestine
  • limited motility
87
Q

Treatment options for proliferative enteropathy

A
  • erythromycin, may be combined with rifampin
  • azithromycin
  • oxytetracycline or doxycycline
  • chloramphenicol if erythromycin fails
  • colloids (plasma or hetastarch)
  • fluid support if needed
88
Q

Causes of IBD

A
  • an inappropriate immune response to a pathogen or antigen
  • appropriate immune response to a persistent pathogen or antigen
89
Q

How does the segment affected by IBD impact clinical signs seen?

A

Small intestine–> malabsorption syndrome

Large intestine –> diarrhea

Protein-losing enteropathy regardless of segment

90
Q

What is a differential for IBD?

A

alimentary lymphosarcoma

91
Q

What is the most common form of IBD?

A

lymphocytic/plasmacytic

92
Q

Classifications of IBD

A

Eosinophilic

Granulomatous

Lymphocytic/plasmacytic

93
Q

Pitting edema under the chin is often seen with what disease?

A

IBD

94
Q

Lab findings associated with IBD

A
  • anemia of chronic inflammation
  • hypoalbuminemia, hypoglobulinemia
  • possible leukocytosis
    • eosinophilia-rarely, but lucky if found
    • lymphocytosis-rarely
95
Q

Weight loss is NOT common with what form of IBD?

A

eosisinophilic colitis

96
Q

Dermatitis may be an associated finding with what form(s) of IBD

A
  • granulomatous enteritis
  • multisystemic eosinophilic epitheliotropic disease
97
Q

What type of IBD is most likely to have diarrhea as a clinical sign?

A

MEED

98
Q

Which form of IBD is most likely to produce colic?

A

eosionophilic colitis

99
Q

Chronic weight loss in an adult horse should prompt what diagnostic test?

A

coggins

100
Q

How does peritoneal fluid analysis help determine peritonitis vs. neoplasia?

A
  • neoplasia: glucose and pH similar to that of plasma
  • peritonitis: glucose and pH lower than plasma
101
Q

What immunosuppressive treatments can be given in the case of IBD?

A
  • Dexamethasone IV or IM since oral abs. poor
  • Prednisolone PO
102
Q

Causes of peritonitis

A
  • intestinal rupture
  • internal abscess (usu. mesenteric LN or liver)
    • gram negative enteric bacteria, Actinobacillus equuli mixed with Streptococcus zoopidemicus or equi, R. equi in foals)
  • primary infection
  • cholangiohepatitis & bile duct rupture
103
Q

Peritoneal fluid findings with peritonitis

A

High WBC, protein, fibrin present

104
Q

What antibiotics are often first choice in the treatment of peritonitis?

A

aminoglycoside/penicillin combination

105
Q

What antibiotic would be indicated with peritonitis due to suspected peforation?

A

metronidazole

106
Q

When might a rectal biopsy be helful in making a diagnosis?

A

MEED or granulomatous enteritis

Equine Med & Surgery (11 decks)

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