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Equine Medicine > Diseases of the Esophagus & Stomach > Flashcards

Diseases of the Esophagus & Stomach Flashcards

1
Q

What is the equine esophagus like?

A
  • not covered by serosa
  • left side of the neck, not typically palpable
  • 2/3 skeletal muscle, 1/3 smooth muscle
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2
Q

What are the 3 most common situations which horses develop esophageal obstruction (choke)?

A
  1. ravenous eaters (grain, hay, beet pulp, carrots)
  2. geriatric and young horses where dental pain is more common = decreased chewing
  3. sedated or exhausted
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3
Q

What should be asked before treating esophageal obstruction (choke)?

A
  • cause of the obstruction - normal feed given to horse, pellets vs grain vs apples/carrots
  • prior history, other times this happened
  • how often/long this has been happening
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4
Q

In what 3 situations is choke harder to treat?

A
  1. pieces of food (apples, carrots) > accumulated grain
  2. repeated obstructions resulting in repeated damage and stricture
  3. long duration leading to dehydration and aspiration
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5
Q

What are the most common clinical signs associated with choke?

A
  • anxiety
  • extended neck
  • gagging, retching
  • coughing, ptyalism, dysphagia
  • (palpable) distended esophagus
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6
Q

How is choke most commonly diagnosed?

A
  • clinical signs
  • NG tube
  • endoscopy in esophagus to observe lesions and trachea to evaluate for aspiration
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7
Q

What are the 3 steps to treating choke?

A
  1. remove all feed and water from stall
  2. make the patient comfortable and left the esophagus relax with alpha-agonists, like Acepromazine, Xylazine, and Detomidine (low head carriage = avoids aspiration)
  3. pass tube up to obstruction and gently lavage while tracking water intake and outflow
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8
Q

Other than alpha-agonists, what medications are used during NG tube placement for choke?

A
  • oxytocin
  • lidocaine
  • buscopan
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9
Q

What after care is required after treating choke?

A
  • restrict food for 48 hr and progressively re-feed with soft mashes
  • endoscopy to observe possible damage in esophagus and trachea
  • NSAIDs
  • antibacterials
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10
Q

What are 6 complications associated with choke?

A
  1. ulceration
  2. aspiration pneumonia
  3. metabolic alkalosis
  4. stricture due to circumferential ulcer
  5. perforation
  6. stomach rupture
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11
Q

What is avoided when treating choke? Specific treatments?

A
  • leave food or water in stall
  • push aggressively
  • flush without lowered head
  • forget followups and risks
  • refeed too soon (within 48 hr)

butorphanol (suppressed cough) and mineral oil (aspiration causes irreversible respiratory lesions)

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12
Q

What has increased the prevalence of equine gastric ulcer syndrome?

A
  • intense exercise in sporting horses
  • horses are easily stressed?
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13
Q

What are the 2 regions of the equine stomach? What are they separated by?

A
  1. non-glandular/squamous - pale, white; incoming food, microbial fermentation, saliva buffering acid
  2. glandular - pink; highly acidic, thick mucus layer

margo plicatus - common area for ulcers

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14
Q

What is the main etiology of equine squamous gastric ulcer syndrome? What 3 risk factors are associated?

A

acidic conditions

  1. intense exercise/training
  2. stress - fasting, transport, stabling, work
  3. NSAIDs
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15
Q

What are the 3 main etiologies of equine glandular gastric ulcer syndrome? What are 3 risk factors?

A
  1. acidic conditions
  2. NSAIDs
  3. Helicobacter
  • gender
  • training, exercise
  • no grass turn out, no roughage, unprocessed grain
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16
Q

What is unique about a risk factor in equine glandular gastric ulcer syndrome compared to squamous?

A

time in work does not have as much of an effect in EGGUS compared to ESGUS

17
Q

What are the overall 2 risk factors associated with EGGUS/ESGUS?

A
  1. stress
  2. nutrition
18
Q

What are the most common clinical signs associated with EGUS?

A
  • colic
  • poor appetite, weight loss
  • pain on tightening of girth

signs more commonly seen in foals, horses with ulcers may have no clinical signs

19
Q

What are 2 ways to diagnose EGUS? Two other possible ways?

A
  1. endoscopy - withhold food for 16 hr and water for 1 hr
  2. therapeutic trial with Omeprazole
  • fecal occult blood
  • sucrose marker
20
Q

Squamous ulcers:

A

pale, white

21
Q

Glandular ulcers:

A

red, pink

22
Q

What are the 2 major ways to treat EGUS?

A
  1. suppression of acid production + protectants
  2. change in management practices
23
Q

What 2 families of drugs are used to suppress gastric acid secretion?

A
  1. PPI - Omeprazole (Gastrogard, Ulcergard) for one month, Esomeprazole, Pantoprazole
  2. H2R antagonists - Cimetidine, Ranitidine, Famotidine
24
Q

What 2 families of drugs are used to protect ulcerated mucosa?

A
  1. protection/repair - Sucralfate, Misoprostol
  2. antacids - Mg(OH)2, Al(OH)3, Lidocaine
25
Q

What drugs are used to stimulate gastric emptying?

A

gastric prokinetics

  • Bethanechol
  • Metoclopramide
  • Erythromycin
  • Cisapride
26
Q

What prophylactic treatment is available to prevent EGUS? What version treats present ulcers?

A

Omeprazole —> OTC Ulcergard

Omeprazole —-> Rx Gastrogard

27
Q

How does the treatment of ESGUS compare to EGGUS?

A

ESGUS - high % heals with Omeprazole SID for 4 weeks and changes in management practices; can add H2 antagonists

EGGUS - low % heals with Omepraxole BID for 6 weeks with Doxycycline, Sucralfate/Pectin-Lecithin, and Misoprostol BID

28
Q

What are 4 ways to prevent ESGUS?

A
  1. management changes - roughage, concentrate, turnout
  2. Omeprazole
  3. Pectin-Lecithin
  4. supplements
29
Q

What are 3 ways to prevent EGGUS?

A
  1. biopsy for gastric hyperplasia
  2. dietary modification - corn oil, Pectin-Lecithin
  3. supplements
30
Q

What causes acute grain overload? What are some clinical signs?

A

accidental ingestion of large amounts of grain (carbs)

  • red-purple mucus membranes (endotoxemia)
  • tachycardia, tachypnea
  • colic, abdominal distension
  • severe lameness caused by laminitis
  • trembling, sweating
  • diarrhea, no intestinal sounds
31
Q

How is acute grain overload diagnosed?

A
  • history, clinical signs
  • polycythemia and neutropenia with left shift and toxic changes
  • gastric reflux
  • tight bands on rectal exam
32
Q

What are the 2 major ways of treating asymptomatic acute grain overload?

A
  1. prevent absorption - lavage stomach, give Epsom salts or activated charcoal if there’s no reflux, mineral oil/biosponge
  2. prevent endotoxemia and sequelae - Flunixin meglumine, diphenhydramine/doxylamine, remove all feed, cryoprophylaxis for laminitis
33
Q

What 8 things are done to treat symptomatic acute grain overload?

A
  1. IV fluid therapy - hypertonic saline then polyionic
  2. IV plasma administration
  3. Flunixin meglumine
  4. Lidocaine - motility, analgesia, neutrophil margination
  5. leave NG tube in place to relieve gas and administer Mg sulfate, charcoal, or warm water (if there’s no reflux)
  6. polymixin to bine endotoxins
  7. pentoxifylline
  8. laminitis prevention with cryotherapy
34
Q

What are primary and secondary causes of gastric dilatation and rupture?

A

PRIMARY - impaction, grain overload, water/air intake

SECONDARY - ileus, obstruction

35
Q

What are the most common clinical signs associated with gastric dilatation? Rupture?

A

acute colic and reflux with hemoconcentration, hypokalemia, and hypochloremia

  • septic shock (pain may suddenly stop)
  • tachypnea, tachycardia
  • sweating
  • muscle fasiculations
36
Q

How is gastric dilation and rupture diagnosed? Treated?

A

NG tube, U/S, abdominocentesis

NG tube, pain medication, euthanasia with rupture

37
Q

Which of the depicted ulcers will take the longest to treat?

A

A —> in the glandular portion of the stomach

38
Q

Which of the following is recommended to treat a horse with a stomach rupture?

a. IV fluid therapy, endotoxemia prevention
b. surgery to repair the tear
c. euthanasia

A

C

Equine Medicine (33 decks)

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