T2 Exam Flashcards
Corneal Ulcer Classification
Superficial/uncomplicated
Complicated
- Non-healing >7days
- Penetrating
- Perforating
Corneal ulcer diagnosis
History, CS, ocular exam, positive fluorescein stain
How to treat a superficial, small, non-complicated ulcer sustained <2days ago?
- ABs e.g. chloramphenicol, tricin
- Systemic analgesia e.g. phenylbutazone
- Atropine (once off)
revisit in 2-3days
Corneal ulceration surgical options?
- debridement of melting and stromal abscesses
- Grafting
- Temporary tarsorrhaphies
- Enucleation
Steps when presented with a pruritic horse. (6)
- Skin scraping (superficial & deep)
- ectoparasites
Positive: treat
Negative: ascaricidal trial - Fungal culture
- detrmatophyte
Positive: treat
Negative: rule out - Bacterial infection
- cytology of papule fluid
- AB trial - Consider allergies
- insect bite trial - Adverse food reactions (food allergy)
- elimination diet - Atopic dermatitis
- serological/intradermal allergy testing
- response to therapy
Drugs for pain relief in a colic case
xylazine: 0.4-0.6mg/kg IV
(double dose for IM)
Flunixin 1.1mg/kg
- Only if we have a diagnosis otherwise masks pain so can’t cage prognosis
Fluid Therapy Calculation
Deficit= %dehydration x BW
Maintenance= 60ml/kg/day (adult)
= 100ml/kg/day (foal)
Ongoing losses= estimated NG reflux, Diarrhea frequency x volume
First half within first 3-6hrs (~5-10l/hr)
second half within 24hrs (1-2l/hr)
How much fluid would a 500kg horse require if its 10% dehydrated with high volume diarrhoea (1L every 2hrs) in the first 24hrs?
Deficit
= 0.1 x 500
= 50L
maintenance
= 0.06x500
= 30L
Deficit
= 1 x 12
= 12L
total = 92L
What are the radiographic signs of physeal dysplasia? (7)
- Physeal widening
- Irregular physis outline
- Sclerosis
- Bone lipping
- Asymmetry of metaphysis
- Wedging of epiphysis
- Asymmetry of cortical bone
At what age must you correct angular limb deformities of the Fetlock and Carpus/Tarsus?
Fetlock = 30-60days (closes ~90days)
Carpus/Tarsus = 6weeks-4m (closes around 6m)
Pyrrolizidine Alkaloid Toxicosis pathogenesis.
PAs alkylate nucleic acids and protein prevents cell division and protein synthesis results in formation of MEGALOCYTES. Fibrous tissue replaces parenchyma when megalocytes die = liver fibrosis CHRONIC NODULAR LIVER HYPOPLASIA
PA toxicosis Histopathological findings (3)
megalocytosis, bridging portal fibrosis and biliary hyperplasia.
Common plants containing PAs
- Paterson’s curse (Echium plantagineum)
- Rattlepod (Crotalaria crispata)
- Ragwort (Senecio spp) - not in AU
CS of hepatobiliary disease (6 common/6 uncommon)
Common = Icterus, weightloss, depression/lethargy, anorexia, colic, fever.
Less common = photosensitization, diarrhea, ventral oedema, ascites, encephalopathy, bleeding diathesis.
Liver enzymes for hepatocellular injury
AST, SDH, GLDH