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IP 11 Equine Medicine > exam 3 - the stomach > Flashcards

exam 3 - the stomach Flashcards

1
Q

what is the basic structure and function of the equine stomach?

A

single chambered, compound stomach with 2 types of tissues lining it

fxn as a reservoir - relatively small compared to the rest of the GIT

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2
Q

what 2 types of tissue line the equine stomach?

what is the demarcation btwn them?

A

squamous epithelial tissue and glandular epithelial lining

margo plicatus btwn the 2 regions

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3
Q

what types of digestion occur in the stomach?

A

mechanical and enzymatic digestion

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4
Q

t/f

HCl is produced intermittently in the equine stomach, during feeding times

A

false

HCl is produced constantly

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5
Q

what important functions does HCl have in the stomach?

A
  • disinfection

- microbial digestion

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6
Q

what is the function of Ghrelin?

and Leptin?

A

opposing action

Ghrelin: stimulates eating in the brain
Leptin: suppresses appetite

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7
Q

t/f

there is a pH gradient/stratification w/in the equine stomach

A

true

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8
Q

what is the relative pH of the top versus the bottom of the stomach?

A 
top = less acidic [squamous epithelial lining]
bottom  = more acidic
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9
Q

where is HCl secreted from?

by what mechanism of action?

A

sec from parietal cells

via proton pump action

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10
Q

what is the proton pump that secretes HCl stimulated by?

A
  • histamine
  • gastrin
  • acetylcholine
  • prostaglandins
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11
Q

what effect does gastrin have on histamine?

what causes elevation of gastrin?

A

gastrin stimulates histamine release

gastrin is elevated by cortisol

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12
Q

what is the main inhibitor of HCl prduction?

A

somatostatin

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13
Q

what is EGUS?

what % of adult horses are affected?

A

equine gastric ulcer syndrome

common: 60-90% of adult horses

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14
Q

what populations of horses have a higher predisposition of EGUS?

A
  • race and show training horses
  • common in hospitalized horses
  • common in horses affected with colic
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15
Q

t/f

EGUS is a common primary cause of colic

A

false

umcommon primary cause of colic

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16
Q

what are common consequences of colic?

A

being held NPO
stress
drugs

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17
Q

what are 3 types of EGUS?

A
  • 1* squamous ulceration [MC]
  • 1* glandular ‘ulceration’ [2nd MC]
  • 2* squamous ulceration
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18
Q

what causes 1* squamous ulceration?

A
  • excessive exposure to HCl corrodes the lining => bile acids may play a facilitatory role
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19
Q

what causes 1* glandular ulceration?

A

breakdown of bicarbonate-rich mucus layer

may be a role of bacT also

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20
Q

what causes 2* squamous ulceration?

A

pyloric outflow obstruction => excessive exposure to HCl

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21
Q

what is ESGD?

EGGD?

A

equine squamous gastric dz

equine glandular gastric dz

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22
Q

t/f

horses often have both ESGD and EGGD as a part of EGUS

A

false

most horses have 1 or the other - NOT both

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23
Q

what are the mechanisms that lead to squamous epithelial injury?

A

minimally protected

HCl exposure from the fundus

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24
Q

what risk factors contribute to the development of squamous epithelial injury?

A
  • VFAs produced in the stomach of horses assoc with inc ulcer severity
  • pepsin maybe
  • bile salts maybe
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25
Q

what effects might bile have on the squamous cell epithelium?

A
  • detergent action can ‘enable’ H+ to gain access to intercellular squamous epithelial cellular attachments
  • bile may enter stomach during fasting => enterogastric reflux
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26
Q

what are the components of the glandular epithelial protection apparatus?

A
  • bicarbonate rich layer of mucus
  • growth factors [epidermal growth factor]
  • epithelial restitution [stimulated replication]
  • blood flow (NO)
  • PGe2
  • peristalsis
  • saliva production [buffer to acids]
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27
Q

what is the pH in the bicarbonate rich layer of mucus near the glandular epithelium?

A

7

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28
Q

risk factors for EGUS?

A 
low forage ration
intense/inc exercise
high concentration ration
regular / prolonged transport
intermittent fasting [being fed BID]
mgmt / housing change
water deprivaiton
weaning
protracted stable accommodation
stress
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29
Q

approximately what % of horses at pasture have EGUS?

why?

A

11%

b/c continuous flow of saliva -> bicarbonate -> growth factors

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30
Q

what effects does stabiling a horse have on chances for developing EGUS?

A

INCREASED chances of EGUS

d/t stress and acid mobility [altered eating habits]

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31
Q

what effect does NPO for 24 hours have on horse GIT?

A

gastric pH drops to less than 2

squamous ulceration occurs w/in 96 hours

32
Q

BID feeding gives horse ___% chance of developing EGUS

TID feeding gives a horse ___%

A

BID = 75%

TID = 58%

33
Q

unavailability of water inc chances of EGUS by ___ times

A

3

34
Q

why do rations with low roughage content contribute to EGUS?

A
  • VFAs play a role [high NSC (non structural carbohydrate) rations]
  • low dietary fiber [cellulose]
35
Q

what effect does high intensity exercise have on EGUS?

A
  • dec pH to less than 4
  • inc intra abdominal pressure
  • pushes acidic fluid onto squamous epithelium
36
Q

t/f

NSAIDs are commonly linked to EGUS

A

false

ulcers NOT commonly linked to routine NSAID asministration

37
Q

t/f

uremia d/t kidney dz can inc risk of developing EGUS

A

true

38
Q

c/s of EGUS?

A
  • may be sub clin and NO signs
  • behavioral signs
  • poor performance
  • wt loss
  • poor haircoat
  • bruxism [grinding teeth]
39
Q

what behavioral changes may occur with EGUS?

A
  • abnormal / dec appetite **
  • slow eating **
  • girthing pain or stretching
  • abnormal attitude / personality
  • uncharacteristic protracted recumbency
40
Q

dx of EGUS based on:

A

Hx
c/s
gastric endoscopy
trial Tx and response

41
Q

complications commonly assoc w EGUS?

A 
aspiration pneumonia
reflux esophagitis
peritonitis
blood loss
hypoproteinemia
cholangiohepatitis 
gastrorrhexis
42
Q

when does EGUS and reflux esophagitis occur?

2* to what?
c/s?
prognosis?

A
  • 2* to gastric outflow obstruction: severe acid reflux erosive ulceration
  • c/s: dysphagia, ptyalism, wt loss, inappetence, lethargy
  • more severe ulceration at gastric aspect
  • unfavorable prognosis
  • indicator of severe dz
43
Q

what abnormalities may be seen on blood work for EGUS?

A

presence of inflammation

44
Q

t/f

a fecal occult blood test is helpful in Dx of EGUS?

A

false

is unhelpful

45
Q

what is the typical protocol for gastro-esophageal endoscopy?

A
  • NPO at least 15 hours
  • restraint - twitch, stocks, experienced assistants, tranquilization
  • pass line NG tube
  • gastruc infufflation and deflation
46
Q

EGUS Tx and Px?

A

risk reduction and pharmaceuticals

47
Q

prognosis of EGUS?

A
  • squamous ulceration tends to heal better than glandular ulcers
  • extensive squamous ulcers heal better than deeper focal ulcers
48
Q

what is essential to follow up of EGUS treatment?

A

ENDOSCOPY

49
Q

how to reduce risks of EGUS?

A
  • mirrors in stables and during transport - horse feels less lonely - dec stress
  • provide plenty of water - promotes salivary flow
  • use haying nets to promote smaller feedings and foraging behavior
  • dec risk factors for stereotypical behavior
  • alfalfa for forage
  • offer small forage feeding 30 mins prior to exercise
50
Q

why is alfalfa a good feed for an EGUS animal?

A

has high Ca - neutralizing effect on gastric acid

51
Q

what is the drug of choice for EGUS?

Tx dose? Px dose?

A

Omeprazole

gastro gard to Tx: 4 mg/kg PO SID
ulcer gard to Px: 1 mg/kg PO SID

4 wk duration

52
Q

what is mechanism of omeprazole?

A

must be absorbed into circulation from duodenum / SI - circulates back and works systemically on gastric mucosa

53
Q

what is the mechanism of action of Ranitidine for Tx of EGUS?

A

histamine inhibitor

54
Q

how does sucralfate work?

A

promotes PGe2 production

most helpful in glaudular ulcers

55
Q

t/f

antacids are effective Tx for EGUS

A

false

right idea but you would need very large amounts to be effective

56
Q

how commonly is Sx a Tx option for EGUS?

A

rarely

57
Q

what role do oils have in Tx of EGUS?

A

corn oil or rapeseed oil

promote PGe2 prod
help gastric glanduular dz

58
Q

EGGD is easier or more difficult to resolve than ESGD?

why?

A

more difficult

b/c does not respond as well to fast and simple Tx with omeprazole

needs longer term Tx

59
Q

how common is gastric neoplasia in horses?

A

RARE

60
Q

what types of neoplasia occur in equine stomach?

A

gastric squamous cell carcinoma
lymphosarcoma
leiomyoma

61
Q

common presentation for gastric squamous cell carcinoma?

A
  • old horse
  • wretched halitosis
  • weight loss and inappetance d/t pain upon eating
  • colic: post prandial
  • episodes of choke
62
Q

dx of gastric squamous cell carcinoma?

A

enodscopy
u/s of cavities
analysis of peritoneal fluid

63
Q

what is behavior typical of gastric squamous cell carcinoma?

A
  • may only involve the stomach
  • may spread to involve abdominal vescera and ascites
  • may spread to invade chest
64
Q

why might a horse with gastric squamous cell carcinoma experience inc respiratory rate and effort?

A

if tumor has metastasized to the chest

puts pressure on diaphragm

65
Q

what causes a 1* gastric distension disorder to occur?

A

ingestion of fermentable food => food impaction [simple grain ingestion]

66
Q

what causes a 2* gastric distension disorder to occur?

A

small intestinal obstruction

67
Q

what might cause a gastric / pyloric outflow obstruction?

A

ulceration

neoplasia

68
Q

what is a phytobezoar?

clinical significance?

A

hair ball

horses will eat whole persimmons and get a large mass of “persimmon-bezoar” in their stomach

69
Q

in the event of a gastric distension disorder, what MUST be done?

if this is not done, the patient will die.

A

STOMACH TUBE

necessary to relieve fluid accumulation

70
Q

what occurs if a horse consumes too many persimmons?

A

foreign body mass in stomach
outflow obstruction and colic
spontaneous reflux common

consider location and time of year for Dx / case presentation

71
Q

dx persimmon problem?

A

geographic location and season first

endoscopy
exploratory coeliotomy

72
Q

tx for persimmon-boezer?

A

Sx

anecdotal - coca cola - questionable

73
Q

t/f

gastric impaction may be primary OR 2* d/t hepatic dz

A

true

74
Q

what is gastric impaction?

A
  • outflow obstruction

- risk of rupture

75
Q

predisposing factors to gastric impaction?

A

dental
gastritis
ulceration

76
Q

dx of gastric impaction?

A

difficulty passing NG tube

x ray evidence

77
Q

what is gastrorrhexis?

caused by?

A

gastric rupture

may be spontaneous or idiopathic
2* to weakness in wall or to distension

potentially but invariably fatal

IP 11 Equine Medicine (10 decks)

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