C14 pt 2

Question 1

Malignant oral tumours
- common or rare in LA? aggressive?

Answer 1

Malignant oral tumours are rare in large animals and usually not very aggressive when they do occur

Question 2

Clinical signs of oral tumours

Answer 2

• Clinical signs of oral tumours are similar regardless of tumour type
  o Ptyalism, pain, halitosis, dysphagia, anorexia, loose teeth, bleeding, etc

Question 3

Malignant oral tumours
- speed of progression, prognosis

Answer 3

• Malignant tumours progress rapidly with a poor prognosis unless resected early

Question 4

oral Mast cell tumours
- are they worse if affecting mucosa or dermal

Answer 4

• Mast cell tumours affecting mucosa are more malignant than dermal ones

Question 5

oral Melanoma
- how common in dogs?
- how commmon in other species
- what have most done by Dx
- how aggressive
- pigmentation?
- progression?

Answer 5

o Most common oral tumour in dogs (40 % of oral tumours), rare in other species
o Malignant and highly aggressive, most have metastasized by diagnosis
o Variable pigmentation, many at least partly amelanotic
o Necrosis, ulceration, rapid growth, bone invasion

Question 6

oral melanoma in dogs
- what % metastasize
- prognosis
- how to Dx
- breed disposition, age

Answer 6

o 70% metastasize to regional lymph nodes, often also metastasize to lung
o Median survival WITH TREATMENT 3 months (NOT LIKE CUTANEOUS)
o Often need immunohistochemistry to diagnose
o Small, dark coloured breeds predisposed, usually elderly (11-12 years)

Question 7

• Squamous cell carcinoma (SCC)
• most common oral tumour in what species
• 2nd most common in what species?
• resembles what
• metastatic?
• prognosis?
• appearance

Answer 7

o Most common oral tumour in cats
o 2nd in dogs, especially tonsils (increased metastatic risk)
o Resembles gingivitis in early stage but usually advanced by presentation
o Locally invasive, metastasis possible but uncommon
o Poor prognosis due to invasiveness, especially with large masses
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Irregular, nodular, red-grey, friable, often ulcerated and bleed easily

Question 8

oral Fibrosarcoma
- how common in cats? dogs?
- dog signalment
- histo, growth
- recurrence
- metastatic?
- appearance

Answer 8

o Second most common oral tumour in cats (much less common than SCC)
o Third most common in dogs, 15-25 % of oral tumours
o More common in younger dogs, larger breeds predisposed
o Bland histology but aggressive growth, invasion (“hi-lo”)
o Commonly recur following removal
o 20-35 % metastasize to lymph nodes, 10-20% in lung at diagnosis
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Fleshy grey mass, fixed to underlying bone, may ulcerate

Question 9

dental tumors
- common?
- malignant?
- removal?

Answer 9

• Most dental tumours are rare, all are non-malignant
  o Tend to destroy teeth and bone and can be difficult to remove

Question 10

Fibromatous epulis of periodontal ligament origin
- dogs or cats?
- signalment
- what is epulis?
- appearance
- attachment
- prognosis

Answer 10

Fibromatous epulis of periodontal ligament origin: dogs > cats, brachycephalics
o Epulis: generic term for tumour-like masses on the gingiva
o Gross appearance identical to gingival hyperplasia
o Firm, grey-pink, project from between or near teeth, lobulated surface
o Attached to the periosteum, may physically displace teeth but no invasion
o Good prognosis with removal, so distinction from hyperplasia not relevant

Question 11

esophageal diverticula
- etiology
- true vs pseudo

Answer 11

Diverticula: usually acquired, incidental or can impact with feed and rupture
o True diverticulum: all layers of wall involved
o Pseudodiverticulum: mucosa evaginates through defect in muscle layer

Question 12

Vitamin A deficiency and anorexia (lack of abrasion) can lead to what in esophagus?

Answer 12

hyperkeratosis

Question 13

bloat line in esophagus is a sign of:

Answer 13

increased abdominal pressure
‘Red = head’

Question 14

esophageal ulceration _____ with viral diseases

Answer 14

common

Question 15

Liquefactive necrosis due to ____; coagulative necrosis due to ____

Answer 15

alkalis
acids

Question 16

Reflux esophagitis
- what is it?
- species?
- sequelae
- predisposing condition

Answer 16

Reflux esophagitis: loss of sphincter integrity, mostly non-ruminants
o Squamous epithelium is not acid-resistant
o Chronic acid exposure leads to columnar and/or mucous
metaplasia (like stomach)
o Hiatal hernia can predispose (usually intussusception of
stomach into esophagus or esophagus into itself)

Question 17

Esophagus: Obstruction
- intrinsic vs extrinsic
- what is ‘choke’
- locations
- 2 populations?
- sequelae

Answer 17

• Intrinsic (within lumen) or extrinsic (space-occupying)
• Choke: feed impaction, areas of narrowing or change in direction predisposed
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  1. Over the pharynx
  2. Thoracic inlet
  3. Heart base
  4. Diaphragm
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  Oral to obstruction: dilation
  o May be food-filled, ulcerated
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  Can cause pressure necrosis
  o May lead to perforation or diverticula
  o If impaction is removed, can lead to scarring and stricture

Question 18

Esophagus: Obstruction
- result of perforation

Answer 18

• If esophagus perforates, severe cellulitis results
  o Can track along fascia into the pleural space

Question 19

Esophagus: Obstruction
- Extrinsic usually due to what in carnivores?

Answer 19

Extrinsic usually due to vascular ring anomalies in carnivores
o Persistent right aortic arch

Question 20

Megaesophagus
- cause
- result

Answer 20

• Due to muscular dysfunction, leads to food impaction and regurgitation

Question 21

Congenital idiopathic megaesophagus
- what species?
- progression over time?
- vs adult onset?

Answer 21

o In dogs, can improve with age
o Also seen in cats, foals, calves (acquired more common)

• Adult-onset idiopathic megaesophagus can also occur in dogs
• Possible sequelae?

Question 22

Ruminant forestomachs
- after death, how fast does epithelium slough
- if remains attached, suspect what?

Answer 22

• Epithelium sloughs within hours of death
  o If it remains attached, there may be adhesions (rumenitis) – suspect acidosis

Question 23

rumen contents PM
- appearance for vagus indigestion
- toxins?
- pH after death?

Answer 23

• Always examine rumen contents – hydration, froth, odour (ammonia, acidosis), pH
  o Contents are abundant and watery in vagus indigestion
  o Look for toxic plant material in suspected toxicity
  o pH can increase after death (interpret with caution, normal 5.5-7.5 depending on diet)

Question 24

Rumen papilla development is dependent on what?
- and how?

Answer 24

• Rumen papilla development is dependent on diet
  o High concentrates: blunted, hyperkeratotic, clumped papillae
  o High forages: longer papillae

Question 25

foreign bodies in ruminants
- what species?
- what are common in young animals, with what diet? consequences?

Answer 25

Foreign bodies very common in cows, rare in other ruminants
o Important if cause toxicity (ex. lead) or traumatic reticuloperitonitis
o Trichobezoars common in young animals, especially on low fibre diets, usually incidental

Question 26

Rumenitis: Carbohydrate overload
- species?
- tolerance?
- animals commonly affected?
- acute death due to what?
- lesions and consequences?
- PM clues?

Answer 26

• Primarily a disease of cattle, possible but rare in small ruminants
  o In all ruminants, tolerance of high CHO levels is possible if introduction is gradual
  o Especially common in feedlot cattle due to introduction to high CHO diet
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• Acute deaths are usually due to lactic acidosis rather than rumenitis
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• In survivors, lesions act as a portal for pathogen entry
  o Can also develop laminitis, encephalopathy
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• Gross lesions are nonspecific – history is key!
  o Low postmortem rumen pH is confirmatory but high
  does not rule it out (recall: pH can rise after death)

Question 27

Rumenitis: Carbohydrate overload
- pH & motility relationship
- pathogenesis

Answer 27

pH 7.5:
- Increased VFAs
- Decreasing pH
- Altered flora

pH 5:
- Gram –ves die
- Streptococci increase
- Lactic acid produced

pH 4.5:
- Streptococci die
- Lactobacillus spp increase

pH 4:
- fatal

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as pH decreases:
- Decreasing motility
- Increasing osmotic pressure
- Fluid drawn from blood to lumen - dehydration

Question 28

Rumenitis: Carbohydrate overload
- PM Dx?
- what happens as acidic rumen contents move into intestines?
- what is needed for recovery?

Answer 28

• Rumen epithelium may be hard to peel off, but histology is more reliable
• As liquid, acidotic rumen contents move into the intestines, it causes diarrhea
• Recovery requires normal flora to be re-established

Question 29

Rumenitis: Sequelae
> Fusobacterium necrophorum
- where found normally?
- issues with rumenitis?
- what does it cause?
- appearance of lesions?

Answer 29

o Normal part of rumen flora, invades damages epithelium (especially ventral sac)
o Causes necrosis and sloughing of papillae (ulcers)
o Healing by contraction and epithelial migration (papillae may not regrow)
o Can seed to liver via portal vein and form abscesses
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- Stellate scars of old ulcers
- liver abscess

Question 30

Rumenitis: Sequelae
> Mycotic invasion
- severity?
- when to consider?
- progression?
- appearance?

Answer 30

o More severe than Fusobacterium spp., often fatal
o If inflammation extends to serosa, consider fungal infection
o Produce submucosal venous thrombi and infarction, can also seed to liver
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- Circular, transmural red-black lesions with pale centre
- Often serosal fibrin (peritonitis)

Question 31

Bloat
- most common form?
> cause?
- effect?
- pathogenesis
- PM evidence? timing?
- progression

Answer 31

• Acute/primary bloat: most common form
  o High concentrate or legume diets
  o Decreased saliva production (low forage diet)
  o Microbiota disruptions
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  Normally little foam is produced and it is unstable (breaks apart)
  In bloat, foamy contents can’t be eructated May disappear if PM delayed 10-12 hours
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• Cardiorespiratory collapse due to increased abdominal pressure
• Found dead in sawhorse stance, congested head and neck
• Bloat line in esophagus

Question 32

Chronic/secondary bloat
- cause?
- common signalment?

Answer 32

Chronic/secondary bloat: free gas retention due to defect in eructation
o Esophageal obstruction, vagus indigestion, etc (rule out postmortem bloat)
o Often has periods of acute exacerbation
o Bucket-fed calves with ruminal drinking – milk ferments in rumen, produces gas (also
causes lesions of acidosis)

Question 33

Traumatic reticuloperitonitis
- cause
- progression
- late stages
- PM, what may be gone?
- can lead to…

Answer 33

• Perforation of the reticulum by a long, thin, sharp foreign body
• Followed by acute local peritonitis, potentially fibrinopurulent pericarditis if it penetrates the diaphragm and pericardium
  (Sudden death if heart or large vessels involved)
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• Later stages: adhesions, often can find a tract with suppurative material
• Foreign body may be absent by the time of diagnosis
• Can lead to vagal indigestion
  o Not fully understood, believed to be functional or structural problem with
  forestomach outflow
  o May not be associated with lesions of the vagus nerve itself

Question 34

Ruminant forestomachs: Neoplasia
- common?
- possible sequelae

Answer 34

• Rare, can interfere with eructation and cause bloat

Question 35

Ruminant forestomachs: Neoplasia
> papillomas
- agent
- sometimes affects what else
- severity
- progression

Answer 35

Papillomas: bovine papillomavirus-4
o Sometimes also affects esophagus
o Usually mild in healthy animals, masses are mostly small
o Regress in ~12 months due to cell-mediated immunity
o Can progress to SCC in immunosuppressed animals or bracken fern exposure

Question 36

Ruminant forestomachs: Neoplasia
> Fibropapillomas
- agent
- anatomic location
- SCC association

Answer 36

Fibropapillomas: bovine papillomavirus-2
o Esophagus, esophageal groove and rumen in cattle
o Not associated with squamous cell carcinoma

Question 37

• Lymphoma can affect the _____ in cows

Answer 37

forestomachs