GI Pathology Flashcards
plica
folds of the gut wall that include both mucosa + submucosa
villi
fingerlike projections of the gut wall that include mucosa only
- many enterocytes per villi
microvilli
fingerlike projections on the apical surface of each enterocyte –> brush border
function of plica, villi, and microvilli
increase surface area
crypts
intestinal glands; invaginations between each villi
- crypts should be 1/4 the height of a villi
differences in large intestine vs small intestine
large intestine - NO villi/microvilli
functions of the intestines
- absorption of nutrients
- excretion of waste
main GI disease processes
- inflammation
- degeneration
- growth disorders
- developmental disorders
timeline of inflammation
acute, chronic, chronic active
acute inflammation
fibrin, neutrophils, hyperemia, congestion
chronic inflammation
fibrosis, macrophages, giant cells, plasma cells, lymphocytes
chronic active inflammation
combination of acute and chronic features
what is fibrin
acute phase protein that leaks from vessels during inflammation
what is fibrosis
collagen scar tissue; takes weeks to form
what is intussuception
type of degenerative/necrotic disease process
telescoping of proximal intestine into distal intestine
intussuceptum
the (proximal) part of intestine that goes into the intussuscepiens
intussuceptiens
the (distal) part of intestine that receives the intussuceptum
what is fibrinous colitis
type of degenerative/necrotic disease process
common in horses
often caused by C. diff infection
formation of a fibrin pseudomembrane on the mucosal surface of the colon
main consequences of diarrhea
- acid/base imbalance
- electrolyte depletion
- dehydration
normal absorption/secretion in the small intestine
absorption: occurs in cells at the top of the villi
secretion: occurs in cells at the base of the villi/crypts
net ABSORPTION
mechanisms of diarrhea
- secretory
- malabsorptive
- effusive
- osmotic
secretory diarrhea
absorption: normal
secretion: increased
net SECRETION
causes of secretory diarrhea
bacterial endotoxins (cholera, E. coli) on surface of enterocytes
- causes cAMP stimulated Cl- secretion into lumen –> draws water into lumen
disease: colibacillosis
malabsorptive diarrhea
absorption: decreased
secretion: normal
net SECRETION
causes of malabsorptive diarrhea
villus atrophy
causes morphologic damage –> reduced crypt:villi ratio
effusive diarrhea
absorption: normal
secretion: increased
net FIBRINOUS SECRETION
causes of effusive diarrhea
anything that damages endothelium of vessels
osmotic diarrhea
retention of water in the gut lumen
causes of osmotic diarrhea
magnesium sulfate
starch - can’t get broken down
high grain diet in ruminants
salts pull water into the lumen
what is large intestine diarrhea
reduction in the ability of the colon to absorb solute and fluid presented by proximal bowel (osmotic)
what are the mechanisms of large intestine diarrhea
same as small intestine:
1. secretory
2. malabsorptive
3. effusive
4. osmotic
partial obstruction
allows the passage of gas, fluid, or diarrhea
complete obstruction
does not allow the passage of gas or fluids; causes severe distention
strangulated obstruction
compromised blood supply + lumen obstruction
non-strangulated obstruction
lumen obstruction only - no compromised blood supply
mechanical obstruction
obstruction from within the lumen
functional obstruction
diffuse dysfunction of the intestine causing it to not be able to move contents forward
proximal obstruction
stomach or small intestine
more common in small animals
distal obstruction
ascending/descending colon
more common in large animals
simple obstructions in small animals
foreign bodies
simple obstructions in large animals
food/sand impactions
strangulated obstructions in small animals
GDV
strangulated obstructions in large animals
strangulated lipomas, epiploic foramen entrapment, large colon volvulus
non-strangulated infarctions
obstruction of blood supply without luminal obstruction
SA: thromboembolic events
LA: parasitic migrations (strongyles) causing cranial mesenteric arteritis
mechanism of obstruction –> necrosis
intestinal obstruction –> distention –> decreased perfusion to mucosa/serosa/muscularis
causes of distention
gas: aerophagia & bacterial overgrowth –> increased production
fluid: normal secretions, decreased absorption ability
is the small or large intestine more sensitive to pressure necrosis
small intestine b/c it has villi –> takes longer to regenerate
what layer of the intestinal wall is most sensitive to pressure necrosis
seromuscular layer
prone to neutrophilic infiltrate and mesothelial cell loss
hemorrhagic strangulating obstructions
veins: compressed
arteries: not compressed
arteries continue pumping blood in –> compressed veins prevent blood from leaving
causes congestion & ischemia
examples of hemorrhagic strangulating obstructions
intussusceptions
partially strangulated hernias
ischemic strangulating obstructions
veins: compressed
arteries: compressed
complete lack of blood supply causes rapid degeneration of mucosa
examples of ischemic strangulating obstructions
large colon volvulus
what part of the intestinal wall is most prone to ischemic injury
villi
already hypoxic under normal conditions due to exchange of arteries and veins as they travel up villi
has a high energy requirement to power Na/K ATPases
mechanism of ischemic injury in villi
hypoxia –> loss of oxidative phosphorylation –> failure of ATPases –> anaerobic glycolysis –> cell dies and detaches from basement membrane
what can be used as an indicator of tissue perfusion
lactate (produced by anaerobic glycolysis)
serum lactate in SA
compare serum and fluid lactate in LA
gruenhagen’s space
space that forms as epithelium begins to pull away from basement membrane
cells eventually slough off and can break all the way down to crypts
ischemia
oxygen deprived cell death
ischemia-reperfusion injury
local and systemic inflammatory response that occurs once blood flow is restored following an ischemic event
causes toxins that built up to be released all at once
what toxin is generated during ischemia
superoxide
superoxide
reactive metabolite that is generated during ischemia
targets cell membranes –> activates arachidonic acid pathway –> produces pro-inflammatory cytokines
effect of NSAIDs on arachidonic acid pathway
blocks COX pathways
decreases PGE nad TXE production
effect of corticosteroids on arachidonic acid pathway
blocks phospholipase A2
decreases all cytokine production
epithelial restitution
the reformation of the mucosal barrier:
- tight junctions
- apical membrane
- mucous layer
when does epithelial restitution occur
immediately after acute injury (18-24 hrs)
is epithelial restitution faster in the small intestine or colon
colon (no villi)
steps of epithelial restitution
- crypt cells proliferate and replace lost cells
- villi contract to decrease surface area that needs to be restored
- epithelial cells migrate to seal the basement membrane
- tight junctions and intracellular spaces close
what is the number 1 prognostic indicator that a colicking horse needs to go to surgery
persistent pain after time/meds
colic qualifications for surgical repair
usually small intestine or strangulated lesions
1. persistent pain
2. enteroliths
3. strangulated lesions
4. exploratory laparotomy
non surgical colics
usually large intestine or non-strangulated lesions
medical management - fluids, electrolytes
