C15 Gastrointestinal Pathology II Flashcards

1
Q

Stomach/abomasum
If empty, normal pH:
- carnivores
- herbivores

A
  • Carnivores <3
  • Herbivore <3.5-4.0
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2
Q

what type of epithelium is prone to acid damage?

A

Stratified squamous epithelium

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3
Q

Stomach: Response to injury
- superficial damage repair?
- how?

A
  • Superficial damage is rapidly repaired by epithelial migration
    <><><><>
  • Fibrin, sloughed cells, mucus Cover defects and protect from acid, allow healing
  • Flattened epithelium = ‘stretched’ to cover defects
  • Progenitor cells in isthmus proliferate later
  • Increased blood flow
    > Dilutes and removes excess acid absorbed by damaged areas
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4
Q

Stomach: Response to injury
> Mucous metaplasia/hyperplasia
- associated with?
- how can achlorhydria arise?
- common causes
- seen near what?

A

Mucous metaplasia/hyperplasia: associated with chronic inflammation
o Parietal cells are replaced with goblet cells, can lead to achlorhydria
o Many possible causes, but nematodes (Ostertagia spp.) most common
o Also seen near healing ulcers

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5
Q

Stomach: Response to injury
> Achlorhydria
- what is it
- how bad can it get and why thats a problem
- main issue?
- additional issues? signs?

A

Achlorhydria: insufficient acid production
o If severe, gastric pH can approach neutral (allows microbial growth)
o Main problem is inappetence, NOT impaired digestion
o Protein lost through mucosa -> loss of efficiency +/- weight loss
o Can also predispose to invasion of pathogens (bacteria, fungi)

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6
Q

Stomach: Dilation and displacement in the horse
- causes
- types
- survivors may get what?
- sequelae?

A
  • Usually due to ileus or grass sickness (secondary dilation)
  • Primary dilation due to excess carbohydrates, water, or lush pasture forage
    o Survivors may develop laminitis
  • Either may lead to rupture (idiopathic rupture also possible)
    o Fairly common cause of colic
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7
Q

stomach rupture in horse
- where? how can we tell vs perforation?
- how can we tell not post mortem lesion
- bloat line?
- cause of death?
<><><><>
- causes of perforations? occurence?

A
  • Usually greater curvature
  • Tear longer on serosa than mucosa
  • Surrounding hemorrhage = not postmortem
  • May have a bloat line
  • Cause of death?
    o Shock
    o Peritonitis
    <><><><>
    Perforations less common
    o Ulcers
    o Parasites
    o Neoplasia
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8
Q

Gastric dilation and volvulus in dogs
- signalment
- associated with?
- rotates how?

A
  • Gastric dilation and volvulus: common in deep chested breeds, rare in cats o Usually associated with eating +/- aerophagia
    o Predisposing factors poorly understood
    <><><>
    Gradual dilation, if unresolved….
    …rotates clockwise from transverse to longitudinal orientation
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9
Q

Gastric dilation and volvulus
- simple dilation vs volvulus > where are esophagus and spleen?
- splenic infarct risk?

A

o In simple dilation, esophagus is patent and spleen stays on the left
o Recurrent dilation predisposes to splenic infarcts
o In volvulus, the spleen ends up on the right with venous infarction +/- rupture

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10
Q

Complete occlusion of esophagus
- causes what effect on stomach?
- how do we get to hemoabdomen, and death?
- what animals?

A

Complete occlusion of esophagus -> venous infarction of stomach due to obstruction
> Stomach becomes red-black, bloody contents, can rupture
> Can cause blood vessel avulsion and hemoabdomen
> Venous obstruction and pressure from distended stomach decrease venous return
> Circulatory shock, respiratory distress from pressure on diaphragm
> Death if not treated quickly!
<><><><>
dogs?
Adult sows fed infrequently

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11
Q

Abomasal displacement and volvulus
- signalment
- timing?
concurrent conditions

A

Abomasal displacement and volvulus: common in intensively managed dairy cows
o Most common around parturition, atony likely involved
o Often concurrent metritis, ketosis, hypocalcemia +/- retained placenta

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12
Q

LDA
- common? hard to treat?
- possible complications of surgery?
- PM > watch out for what?

A
  • Left displacement: most common, easily treated
    o Can lead to fistulas if sutures penetrate the mucosa
  • Like all displacements, can reduce during PM positioning!
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13
Q

RDA
- common?
- proportion combined with volvulus?
- metabolic consequence?
- other consequences? sequelae?
- twist orientation?

A

Right displacement (15% of cases):
o Simple right displacement can be complicated by volvulus (20% of cases)
o Duodenal outflow obstructed -> chloride sequestration -> alkalosis
o Can also obstruct blood vessels and damage nerves
<><><><>
- Blood-tinged fluid and gas
- Venous infarction can lead to rupture and peritonitis
- If there is nerve damage, motility cannot be restored: vagal indigestion
<><><><>
Counterclockwise when viewed from right side

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14
Q

Pyloric stenosis
- species?
- congenital vs acquired causes
<><><><>
- what is Chronic hypertrophic pyloric gastropathy
> signalment?
> signs?
- appearance

A
  • Common in dogs, rare in cats and horses
    <><><><>
  • Congenital: poor growth, recurrent vomiting post-weaning
    o May have smooth muscle hypertrophy
    <><><><>
  • Acquired: stricture, foreign bodies, polyps, neoplasia
    o Chronic hypertrophic pyloric gastropathy in dogs
    <><><><>
    Chronic hypertrophic pyloric gastropathy
    o Mucosal and/or muscular hypertrophy
    o Middle aged, small breed dogs, males > females
    o Chronic, intermittent vomiting, weight loss, +/- gastric distention
  • Enlarged mucosal folds obstruct the pylorus
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15
Q

Stomach: Foreign bodies
- can cause

A

*Often incidental and can be virtually anything
* Low roughage Rumen more common
*Can cause vomiting, gastritis, ulcers
* Rare causes of pyloric obstruction and death

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16
Q

Stomach: Impaction - horse, cow, sheep
- cause?
- may cause what? R/O?

A
  • Fibrous feed, poor chewing, low water intake
  • May cause colic, loss of condition, anorexia; rule out dilation
17
Q

Stomach: Impaction - horse, cow, sheep
- primary vs secondary
- sequelae?
- possible breed assoc?

A
  • Primary: low water intake or fibrous feed
  • Secondary: stenosis, vagus indigestion
    <><>
  • Can rupture (especially primary), causing peritonitis
  • Often severe metabolic alkalosis and reduced K+ from inanition
    <><><><>
  • Abomasal dilation and emptying defect in Suffolk and Hampshire breeds
  • Massive abomasal distention, contents are similar to normal rumen content
  • Cause unknown – genetic predisposition to dysautonomia?
18
Q

Gastritis
- Presumptive diagnosis for:

A
  • Presumptive diagnosis for vomiting believed due to gastric irritation
19
Q

Uremic gastritis
- species
- can cause what
- lesions?

A

Uremic gastritis: some dogs, cats, horses with uremia
o Severe congestion and hemorrhage, often causes hematemesis, melena
o Variable lesions, from minimal to gritty, red-black necrosis

20
Q

Mechanical gastritis
- what animals?

A

o Most common in dogs with foreign bodies, cats with hairballs

21
Q

chemical gastritis
- cause in horses?
- cause generally?

A

o Cantharidin toxicity from blister beetles in horses
o Zinc toxicity (causes gastric necrosis)

22
Q

True inflammatory gastritis
- species?
- associated with?

A

o Mostly carnivores, not usually infectious
o Usually associated with systemic inflammation (ex. food allergy)

23
Q

helicobacter as a cause of gastritis in animals
- is it?

A

o Implicated in human gastritis but more tenuous link in other species
o Most mammals have their own Helicobacter species but most are nonpathogenic
o Exceptions: ferrets and cheetahs
o No evidence these predispose to neoplasia

24
Q

Gastroduodenal ulceration
- pathogenesis (peptic ulcer)

A
  • Peptic ulcer: imbalance between mucosal integrity and effects of gastric acid

o Usually problems with repair rather than acid secretion
o Acid hypersecretion: gastrinoma, histamine release from mast cell tumours
o Impaired protection: NSAIDs (inhibit bicarbonate, alter blood flow)
o Duodenal reflux: bile salts damage cells
o Regardless of cause, breach of mucosa can lead to ulceration
<><>
Ulceration progresses via coagulative necrosis (recall it is acid damage)

25
Q

Duodenal ulcers for where?
- pathogenesis?

A
  • Duodenal ulcers usually form between the pylorus and bile/pancreatic duct
    o Pathogenesis similar to gastric ulcers
26
Q

signs of repairing gastroduodenal ulcer

A
  • Raised edges
  • Granulation tissue bed
27
Q

possible sequelae of gastroduodenal ulcers

A
  • Ulcers that reach the submucosa are at increased risk of hemorrhage
  • ulcers at proximal duodenum / pyloris can lead to stricture
  • If they erode all the way through = perforation
  • In the pylorus or duodenum can cause thrombosis
28
Q

Gastroduodenal ulceration
- Glucocorticoids released during stress can have what impact?
- how does blood from a gastric ulcer look on its way out?

A
  • Glucocorticoids released during stress can cause gastric hemorrhage
    o Ex. surgery, trauma; related to effects of reduced perfusion?
  • Blood from damaged mucosa turns brown-black when exposed to acid
  • If enough digested blood reaches the intestines = melena
29
Q

Gastroduodenal ulceration in dogs
- how common? what location?
- can cause what blood vessel related issue?
- what happens if perforation?

A
  • Uncommon, usually in the pylorus or duodenum and cause thrombosis
  • Perforation releases feed into abdomen, chronic inflammation if blocked by omentum
30
Q

mast cell tumours contribution to peptic ulceration in dogs

A
  • Mast cell tumours can cause peptic ulcers, even if not directly involving stomach!
    o Usually clinically silent
31
Q

Zollinger-Ellison syndrome in dogs
- what is this?
- consequences?

A

Zollinger-Ellison syndrome: ulcers due to gastrin-secreting neoplasm
o Pancreatic neoplasia or gastrinoma
o Metastasis common, often also have reflux esophagitis

32
Q

Gastroduodenal ulceration in cows
- how common? locations
- signalment?
- contributing factors?
- relatively common outcome?

A
  • Common in abomasum, rare in duodenum
    o Veal calves > > > other calves, dairy cows, feedlot cattle
  • Often stress-related and subclinical, tend to present with melena
  • Perforation is a relatively common cause of death in calves
    o Lethal hemorrhage +/- peritonitis
33
Q

Gastroduodenal ulceration in pigs
- location?
- how common?
- clinical signs?
- age?
<><><><>
- pathogenesis for pigs, esp.
- outcome? signs?

A
  • Limited to pars esophagea (squamous), very common and usually subclinical
    o Weaned growers and feeders
  • Sometimes cause runting, anorexia, anemia, and sudden death
    <><><><>
  • Finely ground feed
    > Watery contents that equalize pH instead of partitioning
    > Parakeratosis, fissures, erosion (yellow, thick, irregular, peels easily)
    > Ulceration (deeper bleeding, may stricture if heal via scarring)
    > Fatal hemorrhage (relatively common, look for clots, melena, pallor)
34
Q

Gastroduodenal ulceration in horses
- cause?
- what can it cause?
- most common in what signalment?
- anatomical location
- pathogenesis?
- possible outcomes

A
  • Often incidental but can cause colic in adults and foals
  • Very common in <4 month old foals, performance horses (stress-related?)
  • Often form in squamous epithelium near margo plicatus
  • Similar pathogenesis and progression to pigs
  • Sometimes can perforate or form strictures