C14 pt 2 Flashcards

(37 cards)

1
Q

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

A

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

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2
Q

Clinical signs of oral tumours

A
  • Clinical signs of oral tumours are similar regardless of tumour type
    o Ptyalism, pain, halitosis, dysphagia, anorexia, loose teeth, bleeding, etc
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3
Q

Malignant oral tumours
- speed of progression, prognosis

A
  • Malignant tumours progress rapidly with a poor prognosis unless resected early
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4
Q

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

A
  • Mast cell tumours affecting mucosa are more malignant than dermal ones
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5
Q

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

A

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

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6
Q

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

A

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)

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7
Q
  • Squamous cell carcinoma (SCC)
  • most common oral tumour in what species
  • 2nd most common in what species?
  • resembles what
  • metastatic?
  • prognosis?
  • appearance
A

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
<><><><>
Irregular, nodular, red-grey, friable, often ulcerated and bleed easily

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8
Q

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

A

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
<><><>
Fleshy grey mass, fixed to underlying bone, may ulcerate

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9
Q

dental tumors
- common?
- malignant?
- removal?

A
  • Most dental tumours are rare, all are non-malignant
    o Tend to destroy teeth and bone and can be difficult to remove
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10
Q

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

A

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

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11
Q

esophageal diverticula
- etiology
- true vs pseudo

A

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

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12
Q

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

A

hyperkeratosis

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13
Q

bloat line in esophagus is a sign of:

A

increased abdominal pressure
‘Red = head’

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14
Q

esophageal ulceration _____ with viral diseases

A

common

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15
Q

Liquefactive necrosis due to ____; coagulative necrosis due to ____

A

alkalis
acids

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16
Q

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

A

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)

17
Q

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

A
  • Intrinsic (within lumen) or extrinsic (space-occupying)
  • Choke: feed impaction, areas of narrowing or change in direction predisposed
    <><><><>
    1. Over the pharynx
    2. Thoracic inlet
    3. Heart base
    4. Diaphragm
    <><><><>
    Oral to obstruction: dilation
    o May be food-filled, ulcerated
    <><><><>
    Can cause pressure necrosis
    o May lead to perforation or diverticula
    o If impaction is removed, can lead to scarring and stricture
18
Q

Esophagus: Obstruction
- result of perforation

A
  • If esophagus perforates, severe cellulitis results
    o Can track along fascia into the pleural space
19
Q

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

A

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

20
Q

Megaesophagus
- cause
- result

A
  • Due to muscular dysfunction, leads to food impaction and regurgitation
21
Q

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

A

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?
22
Q

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

A
  • Epithelium sloughs within hours of death
    o If it remains attached, there may be adhesions (rumenitis) – suspect acidosis
23
Q

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

A
  • 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)
24
Q

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

A
  • Rumen papilla development is dependent on diet
    o High concentrates: blunted, hyperkeratotic, clumped papillae
    o High forages: longer papillae
25
foreign bodies in ruminants - what species? - what are common in young animals, with what diet? consequences?
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
26
Rumenitis: Carbohydrate overload - species? - tolerance? - animals commonly affected? - acute death due to what? - lesions and consequences? - PM clues?
* 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 <><><><> * Acute deaths are usually due to lactic acidosis rather than rumenitis <><><><> * In survivors, lesions act as a portal for pathogen entry o Can also develop laminitis, encephalopathy <><><><> * 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)
27
Rumenitis: Carbohydrate overload - pH & motility relationship - pathogenesis
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 <><><><> as pH decreases: - Decreasing motility - Increasing osmotic pressure - Fluid drawn from blood to lumen - dehydration
28
Rumenitis: Carbohydrate overload - PM Dx? - what happens as acidic rumen contents move into intestines? - what is needed for recovery?
* 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
29
Rumenitis: Sequelae > Fusobacterium necrophorum - where found normally? - issues with rumenitis? - what does it cause? - appearance of lesions?
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 <><><><> - Stellate scars of old ulcers - liver abscess
30
Rumenitis: Sequelae > Mycotic invasion - severity? - when to consider? - progression? - appearance?
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 <><><><> - Circular, transmural red-black lesions with pale centre - Often serosal fibrin (peritonitis)
31
Bloat - most common form? > cause? - effect? - pathogenesis - PM evidence? timing? - progression
* Acute/primary bloat: most common form o High concentrate or legume diets o Decreased saliva production (low forage diet) o Microbiota disruptions <><><><> 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 <><><><> - Cardiorespiratory collapse due to increased abdominal pressure - Found dead in sawhorse stance, congested head and neck - Bloat line in esophagus
32
Chronic/secondary bloat - cause? - common signalment?
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)
33
Traumatic reticuloperitonitis - cause - progression - late stages - PM, what may be gone? - can lead to...
* 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) <><><><> * 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
34
Ruminant forestomachs: Neoplasia - common? - possible sequelae
* Rare, can interfere with eructation and cause bloat
35
Ruminant forestomachs: Neoplasia > papillomas - agent - sometimes affects what else - severity - progression
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
36
Ruminant forestomachs: Neoplasia > Fibropapillomas - agent - anatomic location - SCC association
Fibropapillomas: bovine papillomavirus-2 o Esophagus, esophageal groove and rumen in cattle o Not associated with squamous cell carcinoma
37
* Lymphoma can affect the _____ in cows
forestomachs