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Equine > AOR disease (SA) > Flashcards

AOR disease (SA) Flashcards

1
Q

two common complications to see alongside GDV

A

splenic torsion
ventricular tachycardia (give lidocaine)

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2
Q

causes of septic peritonitis

A

GI perforation
Bactaeremia
UTI and urinary ascension
Penetrating injuries

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3
Q

causes of aseptic peritonitis

A

Inflammatory abdominal disease
gi perforation

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4
Q

Signs of a septic peritonitis on fluid tap

A

Glucose lower than blood
Lactate higher than blood

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5
Q

how to tell if fluid is haemoabdomen

A

PCV
PCV same as blood = acute
PCV higher than blood = semi-acute

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6
Q

3 causes of ahemoabdomen and how to manage

A

Neoplastic bleed: Measure lactate and BP to asses perfusion
Trauma: Often RTA. IVFT, whole blood, tranexamic acid
Coagulopathy: FFP

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7
Q

Signs of uroabdomen on tap

A

High creatinine (double that of blood), urea and potassium

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8
Q

Complication of uroandomen

A

K reabsorbed = hyperkalameia = Brady dysrhythymia

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9
Q

Tx of uroabdomen

A

Catheterise and surgical repair
Give bicarb and Hartmanns to move K into cells

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10
Q

Ascites: Transudate (PP)
Cytology
Cause
Dx

A

Low protein, low TNCC
Due yo hypoalbuminae
From liver disease, PLE, PLN
Dx: Biochem

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11
Q

Ascites: Modified transudate
Cytology
Cause
Dx

A

High protein, moderate TNCC, yellow and turbid
Due to increased hydrostatic pressure => causes a protein leak
CV disease (right sided failure), thrombosis, neoplasia, chronic liver disease causing portal hypertension
Dx: Imagine

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12
Q

Ascites: Septic exudate
Cytology
Cause
Dx

A

Aka pyothorax
High TNCC, high protein, turbid
Penetrating wound, surgical complication, ruptured infected lesion
Dx: Abdomincenteis and cytology

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13
Q

Ascites: Non-septic exudate
Cytology
Cause
Dx

A

High TNCC, high protein, opaque
Neoplasia, FIP, uroabdomen
Dx: abdomincentiwis and cytology

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14
Q

What are the other effusions

A

Chyle and blood

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15
Q

Pathogens of FIP

A

Viraemia => infects moncytes/macropahges => react with endothelial cells => breakdown of junctions => fluid leak => effusions

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16
Q

Signs of FIP

A

80% have an effusion
- abdominal = most common, approximately 80%,
- also thoracic and occasionally cardiac

Non-specific clinical signs are common: lethargy, anorexia and weight loss, fever (non-responsive to treatment), +/- jaundice, +/- lymphadenomegaly

17
Q

What hernia can testosterone lead to

A

Perineal

18
Q

breed and tx for anal furunculosis

A

GSD
Atopica (cyclosporin)
Or preds and hypoallergenic diet

19
Q

anal ademona vs adenocarcinoma

A

AC:
- Adhere to deeper tissue
- Rapidly growing
- Don’t respond to castration to remove testosterone and need radical surgery

20
Q

What do anal sac adenocarcinomas look like and lead to

A

Older females. Small, discrete nodules. aggressive.
Secretes PTH like substance => hypercalcameia and PUPD

21
Q

Tx for colitis

A

`metronidazole and high fibre feed

22
Q

Tx for feline magacolon

A

Laxitives (lactulose), enema, high fibre
may need subtotal colectomy, high risk of infection so give metrinidazole and no enema

23
Q

what probe to use most

A

periodontal
only use explorer when needed as scratches surface

24
Q

gingivitis v peridontitis

A

Gingivitis = inflammation limited to gingiva (gum)
Periodontitis = inflammation of gingiva and additional periodontal tissues (PDL, alveolar bone, cementum)

25
Q

gingivitis grades

A

0-3
2 = bleeds when probed
3 = spontaneous blled

26
Q

how to assess periodontitis

A

assess attachment loss
- periodontal pocket (mm)
- gingival recession (mm)
- furcation involvement (F0-3)
- mobility ( (m0-3)

27
Q

how to tell if discolouration is a dead tooth

A

if bruising colour remains and doesn’t fade
needs removing

radiographs show wide pulp cavity

28
Q

what is caries

A

acidogenic bacteria erodes cementum

29
Q

how does periodontal disease develop

A

combo of gingivitis and periodontitis

gingivitis => gram positives build up => gram negative anaerobes take over => bacteria secrete plaque biofilm => mineralises to calculus => inflammation and recession
reversible if plaque removed

periodontitis = irreversible sequelae
damage => pocketing => gingival recession

30
Q

use of luxator and elevator

A

luxator = sharp = cut fibre
elevator = fatigue fibres
both used to breakdown fibres and expand alveolus

31
Q

what is mucueole

A

build up of saliva in salivary of submandibular gland

32
Q

purpose of scaling polishing flushing

A

Scale: debulking of calculus
Polishing: removal of plaque biofilm (but not much else…)
Flushing: removal of paste and calculus material w/ chlorhexidine

33
Q

when do permanent teeth erupt

A

3-6m

Equine (11 decks)

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