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3. Sys Path > C15 pt 2 > Flashcards

C15 pt 2 Flashcards

1
Q

neoplasia of stomach and intestines
> does behaviour depends on where tumours are found?

A

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)

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2
Q

neoplasia of stomach and intestines
- are they common sites for neoplasia
- malignancy, in general?
- what is a particularly malignant type in all species?

A
  • 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
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3
Q

Non-neoplastic lumps and bumps of the stomach and intestines
- prominent structure in young animals, inflamed intestines

A

Peyer’s patches very prominent in young animals and inflamed intestines

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4
Q

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?

A

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

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5
Q

the most common GI neoplasm in domestic animals

A
  • Lymphoma
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6
Q

Lymphoma, GI
- how common
- types / distribution
- spread?
- looks like what?

A
  • 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
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7
Q

GI Lymphoma
Dogs - location, signs, cell type

A

mostly SI, vague clinical signs, usually T cell

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8
Q

GI Lymphoma
Cats - subtypes
> what are they
> cell type
> clinical course
> age group
> notes

A

Small cell villus:
- T cell
- long clinical course
- old cats
- Patchy (unlike IBD), microscopic infiltrates in other organs but no associated clinical signs

<><><><>

Large cell lymphoblastic:
- B cell
- rapid clinical course
- old cats
- Palpable masses, similar appearance to canine GI lymphoma

<><><><>

Large granular cell:
- T cell or NK cells
- rapid clinical course
- old cats
- Distinctive large red cytoplasmic granules, disseminate and may perforate intestine

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9
Q

GI lymphoma in horses
- common?
- cell type?
- looks like?

A

o Common in horses, usually T
cells and small intestine, can clinically resemble inflammatory bowel disease

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10
Q

GI lymphoma in ruminants
- part of what disease
- type common in cattle, connected to what other condition?

A

o In cattle and sheep, usually part of adult multicentric disease
o Abomasal common in cattle,
may be part of enzootic bovine leukosis

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11
Q

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?

A

in dogs, gastric > intestinal,
in cats intestinal > gastric
<><><><>
o Mostly small intestinal in other species
<><><><>
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)

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12
Q

GI adenocarcinoma in dogs
- location?
- appearance?
- metastasis?
- carcinomatosis problems?

A

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

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13
Q

GI adenocarcinoma in cats
- location?
- less common than what other cancer?

A

o Intestinal carcinoma less common than lymphoma in
cats but still more common than in dogs

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14
Q

Adenocarcinoma in sheep
- age?
- metastasis?

A

relatively common in sheep >5 years old, often
incidental finding at slaughter (metastases rare)

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15
Q

GI adenocarcinoma in horses and cattle
- how common?
- association in cattle?

A

Rare in horses (lymphoma more common) and cattle (bracken fern association)

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16
Q

Gastric squamous cell carcinoma
- how common in horses? anatomic location
- signalment? signs?
- appearance
- possible outcomes?
- metastasis?

A

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)

17
Q

Intestinal stromal tumours
- most common in what animal
- also found in what other species?
- comparison to Leiomyoma/leiomyosarcoma and historical difficulty with this?
- prognosis?

A

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

18
Q

why do intestines autolyse quickly? consequence for samples?

A

Full of bacteria (mostly anaerobes, but diverse)
o Biopsies must be handled with care and fixed quickly

19
Q

why is it hard to interpret histology samples of intestines?

A

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

20
Q

Intestines: Response to injury (SI)
- epithelial damage response
> minutes
> hours-days
> days
> how do deeper ulcers heal? How soon does new mucosa form?

A
  • 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
21
Q

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?

A
  • 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)
22
Q

villous atrophy
- is it common
- causes what?
- types, depending on what?
> what causes each? recovery?

A
  • Villus atrophy: common, causes malabsorption and protein loss
    o 3 types depending on how crypts are doing
    <><><><>
    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
    <><><><>
    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
    <><><><>
    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
23
Q

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?

A
  • 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
24
Q

Intestines: Response to injury (LI)
- differences from SI?

A
  • Similar to SI but no villi
  • Proliferative compartment prone to damage by similar causes but less severe
    o Ex. Coronaviruses, coccidia
    <><><><>
    Minutes: flattening and migration
    Damaged areas may have fewer goblet cells
25
Q

Protein-energy malnutrition
- cause?
- increased susceptibility to what?
- differentiate what primary issues?

A
  • 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
26
Q

Lesions of starvation:

A

liver atrophy and serous atrophy of epicardial fat

27
Q

Malassimilation
- due to problems in what phases of digestion?
<><><><>
- what are the phases of digestion
- what nutrients they uptake
- possible causes?
- species

A

o Problems in any of the 3 phases of digestion
1) luminal (breakdown),
2) epithelial (absorption), and
3) delivery (uptake into blood or lymph)
<><><><>
LUMINAL:
- Fats, proteins, polysaccharides
- Possible causes: Exocrine pancreatic insufficiency (either due to juvenile atrophy or acquired atrophy/fibrosis in chronic pancreatitis)
- mostly dogs
<><><><>
EPITHELIAL:
- Fats, proteins, polysaccharides
- Possible causes: Villus atrophy, Short bowel syndrome (removal of >75-85% of small intestine)
- any species
<><><><>
DELIVERY:
- fats
- Possible cause: lymphangiectasia
- dogs

28
Q
  • Consequences of fat malassimilation
A

o Diarrhea
o Steatorrhea (fat in feces) in monogastrics (especially dogs)
o Fat-soluble vitamin deficiency

29
Q

Altered protein metabolism
- cause of what in livestock?
- causes? how common?

A

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

30
Q

o 3 categories of GI protein loss

A
  • ulceration
  • abnormal permeability
  • lymphatic disruption
31
Q

does location of protein loss matter?
- what if lost in stomach or SI?
- what if lost in colon?

A

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

32
Q

GI protein loss
- When plasma protein is lost into gut, is loss selective?
- signs are due to what protein loss, mostly?

A

*When plasma protein is lost into gut, loss is nonselective
o Clinical signs mostly due to albumin loss

33
Q

Protein-losing enteropathy (PLE): 3 phases of disease
- clinical signs vary with what?

A

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

34
Q

signs of protein losing enteropathy?
top Ddx?

A
  • Protein intake not enough to replace losses = catabolic state (muscle and bone loss, fat OK)
    +/- diarrhea
    +/- edema
    +/- hydrothorax
    +/- ascites
    <><><><>
    Top differential: glomerular disease
35
Q

Diarrhea
- what is it? can cause what problems?
- SI vs LI diarrhea definition
- what animal has no SI diarrhea and why?

A
  • 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
    <><><>
    horse has no SI diarrhea
    > Massive colon in adults
36
Q

SI diarrhea characteristics
- 3 overlapping categories
> causes
> examples

A
  • Small intestine diarrhea: generally infrequent and large volumes
    o 3 overlapping categories
    <><><><>
    SECRETORY:
  • Imbalance of secretion > absorption
    eg. Bacterial enterotoxins block Na/Cl absorption and increase Cl secretion -> water follows
    <><>
    MALABSORPTIVE:
  • Villus atrophy of any cause
    > Osmotic retention – unabsorbed nutrients/electrolytes pull fluid into lumen
    eg. Viral, bacterial, etc… Magnesium sulfate laxatives
    <><>
    EFFUSIVE:
  • Increased permeability allows solutes and fluids back into lumen from mucosa after absorption
    eg. Portal hypertension, right sided heart failure, hypoalbuminemia, inflammation
37
Q

Large intestine diarrhea
- possible with what alterations in absorption?
- character?
- types, examples?

A
  • 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

3. Sys Path (28 decks)

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