C15 pt 2 Flashcards
neoplasia of stomach and intestines
> does behaviour depends on where tumours are found?
o Behaviour of similar tumours is the same regardless of where they arise (anatomical modifiers like ‘gastric’ or ‘colonic’ are only used to describe the tumour and have no prognostic significance)
neoplasia of stomach and intestines
- are they common sites for neoplasia
- malignancy, in general?
- what is a particularly malignant type in all species?
- Both are an uncommon site of neoplasia but still regularly seen as biopsy submissions
o Most stomach and intestinal tumours are malignant
o Usually carcinomas (but lymphoma is also common)
o Scirrhous adenocarcinomas in all species are highly malignant
Non-neoplastic lumps and bumps of the stomach and intestines
- prominent structure in young animals, inflamed intestines
Peyer’s patches very prominent in young animals and inflamed intestines
Non-neoplastic lumps and bumps
> Adenomatous hyperplasia/papillary adenoma/polyps of the intestine / stomach
- what are these
- usually hyperplastic except for what kind?
- common where in dogs?
- cause in small ruminants?
- cat signalment? signs and Tx?
o Projections of surface epithelium anywhere in the GI tract
o Usually hyperplastic except rectal polyps in dogs (look for invasion)
o Most common in the distal rectum of middle aged dogs (rectal papillary adenoma),
usually single, excision is curative, can prolapse
o Can form in lambs and goats with chronic coccidiosis
o Also reported in middle-aged male Asian cat breeds (Siamese, etc), usually present
with vomiting/hematemesis, excision is curative
the most common GI neoplasm in domestic animals
- Lymphoma
Lymphoma, GI
- how common
- types / distribution
- spread?
- looks like what?
- Lymphoma: the most common GI neoplasm in domestic animals
o Can be primary or part of multicentric lymphoma, segmental or diffuse
o Usually only spreads from gut to lymph nodes and/or liver (portal tracts)
o Can be hard to distinguish from inflammatory bowel disease
GI Lymphoma
Dogs - location, signs, cell type
mostly SI, vague clinical signs, usually T cell
GI Lymphoma
Cats - subtypes
> what are they
> cell type
> clinical course
> age group
> notes
Small cell villus:
- T cell
- long clinical course
- old cats
- Patchy (unlike IBD), microscopic infiltrates in other organs but no associated clinical signs
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Large cell lymphoblastic:
- B cell
- rapid clinical course
- old cats
- Palpable masses, similar appearance to canine GI lymphoma
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Large granular cell:
- T cell or NK cells
- rapid clinical course
- old cats
- Distinctive large red cytoplasmic granules, disseminate and may perforate intestine
GI lymphoma in horses
- common?
- cell type?
- looks like?
o Common in horses, usually T
cells and small intestine, can clinically resemble inflammatory bowel disease
GI lymphoma in ruminants
- part of what disease
- type common in cattle, connected to what other condition?
o In cattle and sheep, usually part of adult multicentric disease
o Abomasal common in cattle,
may be part of enzootic bovine leukosis
GI adenocarcinoma
- gastric vs intestinal occurence in dogs vs cats
- where in other species?
- endoscope limitations
- early spread how?
- carcinomatosis if?
- what is most common appearance? looks like what?
in dogs, gastric > intestinal,
in cats intestinal > gastric
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o Mostly small intestinal in other species
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o Endoscopic biopsies cannot show deeper invasion (full thickness best)
o Early spread via lymphatics and veins, carcinomatosis if penetrates serosa
o Scirrhous, mucus-producing carcinomas are most common but can be hard to
tell from mesenchymal tumours (use PAS to see mucus)
GI adenocarcinoma in dogs
- location?
- appearance?
- metastasis?
- carcinomatosis problems?
o Gastric most common in dogs but intestinal also happens
o Firm, grey-white, transmural, may be annular and cause stenosis
o May be ulcerated, some may not be (just thickened and cause loss of rugae)
o Aggressively infiltrative, usually metastasize to lung, liver, spleen by diagnosis
o Carcinomatosis may block lymphatics and cause ascites
GI adenocarcinoma in cats
- location?
- less common than what other cancer?
o Intestinal carcinoma less common than lymphoma in
cats but still more common than in dogs
Adenocarcinoma in sheep
- age?
- metastasis?
relatively common in sheep >5 years old, often
incidental finding at slaughter (metastases rare)
GI adenocarcinoma in horses and cattle
- how common?
- association in cattle?
Rare in horses (lymphoma more common) and cattle (bracken fern association)
Gastric squamous cell carcinoma
- how common in horses? anatomic location
- signalment? signs?
- appearance
- possible outcomes?
- metastasis?
o Most common stomach tumour of horses, arises from pars esophagea
o Middle aged to old, unexplained anorexia, weight loss, sometimes rapid emaciation
o Cauliflower-like mass, often ulcerative, necrosis, hemorrhage
o May obstruct the oesophagus and can induce desmoplasia (scarring)
o Usually advanced by diagnosis, may have
carcinomatosis (can resemble mesothelioma) and distant metastases (liver, lungs, etc)
Intestinal stromal tumours
- most common in what animal
- also found in what other species?
- comparison to Leiomyoma/leiomyosarcoma and historical difficulty with this?
- prognosis?
Intestinal stromal tumours: most common in dogs, also occur in horses
o Older animals, often incidental, leiomyoma > GIST > leiomyosarcoma
o Leiomyoma/leiomyosarcoma: smooth muscle origin
o Gastrointestinal stromal tumour (GIST): interstitial cells of Cajal (pacemaker
cells of gut)
o Historically under-diagnosed because resembles leiomyosarcoma
o Hard to tell prognosis, can metastasize to lymph nodes, liver, mesentery
why do intestines autolyse quickly? consequence for samples?
Full of bacteria (mostly anaerobes, but diverse)
o Biopsies must be handled with care and fixed quickly
why is it hard to interpret histology samples of intestines?
o Not many established criteria for grading lesions and lots of normal variation
o Orientation is very important
o Endoscopic biopsies can target a lesion, but have limitations (small, partial thickness)
o Full thickness preferred, the more and bigger, the better
Intestines: Response to injury (SI)
- epithelial damage response
> minutes
> hours-days
> days
> how do deeper ulcers heal? How soon does new mucosa form?
- Minutes: adjacent enterocytes flatten and migrate to cover defect
- Hours-days: crypts proliferate
- Days: regenerated cells mature (final stage)
- Deeper ulcers heal by granulation, new mucosa forms in weeks- months
SI villus:crypt ratio
- changes with what?
- normal adult? neonate healing speed?
- what do we see if increased cell loss?
- what do we see if fasting?
- Crypt:villus ratio changes depending on status of gut
- Normal adult ~3:1 (villus = 3 crypt lengths)
> Neonates less proliferative ability – heal slower - Increase cell loss (ex. parasites) = crypts > villi
- Fasting: mature cells lost more slowly= villus > crypts (reversible)
villous atrophy
- is it common
- causes what?
- types, depending on what?
> what causes each? recovery?
- Villus atrophy: common, causes malabsorption and protein loss
o 3 types depending on how crypts are doing
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1. Crypts are fine, too much epithelial loss
o Viruses, coccidia, bacteria and their toxins, ischemia
o Will recover completely if survive effects of malabsorption
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2. Crypts are hypertrophic and there is epithelial loss
o Crypt hypertrophy comes first (not as a response to villus atrophy)
o Immature enterocytes are leaving the crypts too early and are lost faster
o Chronic, persistent problem (parasites, Johne’s, inflammatory bowel disease) o Usually lots of inflammation, resolves if cause is removed
o Crypts may elongate so much that total mucosa thickness is not changed
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3. Crypts are damaged: caused by anything that damages proliferating cells or affects mitosis
o ‘Radiomimetic injury’ (often affects other proliferating cells too)
o Ionizing radiation, parvovirus, BVD, antimitotic toxins, sometimes ischemia
o Crypt lesions are visible before villus lesions
> Existing enterocytes lost at normal rate, but can’t be replaced
Crypts are damaged: caused by anything that damages proliferating cells or affects mitosis
> how can we tell if this villous atrophy is viral or due to ischemia?
> clinical signs?
> sequelae?
> what happens to surviving crypts?
- Severe malabsorption, fluid loss, hemorrhage
- May lead to ulceration
- Prone to pathogen invasion
- Surviving crypts become hyperplastic within days (healing delayed if no survivors)
- Can stricture if circumferential
Intestines: Response to injury (LI)
- differences from SI?
- Similar to SI but no villi
- Proliferative compartment prone to damage by similar causes but less severe
o Ex. Coronaviruses, coccidia
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Minutes: flattening and migration
Damaged areas may have fewer goblet cells
Protein-energy malnutrition
- cause?
- increased susceptibility to what?
- differentiate what primary issues?
- Protein-energy malnutrition: insufficient feed or nutrient intake
o Increases susceptibility to infections
o Can be due to GI disease or systemic illness (cachexia – mechanisms poorly understood)
o Must differentiate starvation, cachexia, and primary GI issues
Lesions of starvation:
liver atrophy and serous atrophy of epicardial fat
Malassimilation
- due to problems in what phases of digestion?
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- what are the phases of digestion
- what nutrients they uptake
- possible causes?
- species
o Problems in any of the 3 phases of digestion
1) luminal (breakdown),
2) epithelial (absorption), and
3) delivery (uptake into blood or lymph)
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LUMINAL:
- Fats, proteins, polysaccharides
- Possible causes: Exocrine pancreatic insufficiency (either due to juvenile atrophy or acquired atrophy/fibrosis in chronic pancreatitis)
- mostly dogs
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EPITHELIAL:
- Fats, proteins, polysaccharides
- Possible causes: Villus atrophy, Short bowel syndrome (removal of >75-85% of small intestine)
- any species
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DELIVERY:
- fats
- Possible cause: lymphangiectasia
- dogs
- Consequences of fat malassimilation
o Diarrhea
o Steatorrhea (fat in feces) in monogastrics (especially dogs)
o Fat-soluble vitamin deficiency
Altered protein metabolism
- cause of what in livestock?
- causes? how common?
o Important cause of lost productivity in livestock
o Reduced intake (anorexia): important in chronic GI disease but nonspecific
o Malabsorption: uncommon because widespread villus atrophy required
o Loss: important in many GI diseases, mostly due to plasma protein loss
o 3 categories of GI protein loss
- ulceration
- abnormal permeability
- lymphatic disruption
does location of protein loss matter?
- what if lost in stomach or SI?
- what if lost in colon?
Stomach and SI
* Digested
* Absorbed as ammonia from colon
* Liver converts ammonia to urea (can see elevated urea in GI disease)
Colon
* No digestion possible
GI protein loss
- When plasma protein is lost into gut, is loss selective?
- signs are due to what protein loss, mostly?
*When plasma protein is lost into gut, loss is nonselective
o Clinical signs mostly due to albumin loss
Protein-losing enteropathy (PLE): 3 phases of disease
- clinical signs vary with what?
o 1) Protein loss without compensatory production (decreased albumin)
o 2) Compensatory production equivalent to losses (normal albumin)
o 3) Losses exceed production (decreased albumin)
o Clinical signs vary depending on rate and severity of loss and adaptation
signs of protein losing enteropathy?
top Ddx?
- Protein intake not enough to replace losses = catabolic state (muscle and bone loss, fat OK)
+/- diarrhea
+/- edema
+/- hydrothorax
+/- ascites
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Top differential: glomerular disease
Diarrhea
- what is it? can cause what problems?
- SI vs LI diarrhea definition
- what animal has no SI diarrhea and why?
- Diarrhea: excess water in feces (usually due to excess fluid loss)
o Can cause electrolyte disturbances, acid-base imbalance, dehydration
<><><> - Most fluid secreted by SI normally resorbed there as well
- Colon handles the rest, but has a limit
- If limit exceeded = SI diarrhea
- If abnormal handling of normal fluid = LI diarrhea
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horse has no SI diarrhea
> Massive colon in adults
SI diarrhea characteristics
- 3 overlapping categories
> causes
> examples
- Small intestine diarrhea: generally infrequent and large volumes
o 3 overlapping categories
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SECRETORY: - Imbalance of secretion > absorption
eg. Bacterial enterotoxins block Na/Cl absorption and increase Cl secretion -> water follows
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MALABSORPTIVE: - Villus atrophy of any cause
> Osmotic retention – unabsorbed nutrients/electrolytes pull fluid into lumen
eg. Viral, bacterial, etc… Magnesium sulfate laxatives
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EFFUSIVE: - Increased permeability allows solutes and fluids back into lumen from mucosa after absorption
eg. Portal hypertension, right sided heart failure, hypoalbuminemia, inflammation
Large intestine diarrhea
- possible with what alterations in absorption?
- character?
- types, examples?
- Large intestine diarrhea: possible with small reductions in absorption
o Frequent, small volumes, +/- blood and mucus
o Secretory: ex. laxatives, steatorrhea cause increased water secretion
o Osmotic overload: too much fermentable substrate (CHO) from SI (malabsorption
more common than excess intake) -> increased short chain fatty acids -> overload buffering capacity -> pH decreases -> flora altered, produces lactic acid -> draws water into lumen
o Bacterial enterotoxins not as important as in SI diarrhea
