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Hepatobiliary disease - Coggle Diagram
Hepatobiliary disease
Clinical findings
Chronic liver signs
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Photosensitive dermatitis
-Non-pigmented areas only
-Due to phyloerrythrin – should be degraded by liver
CBC & biochem
Increased bilirubin
o Indicates liver function
o Also increase with blood cell destruction & decreased excretion
o Can increase with anorexia
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Hepatic encephalopathy
• Increased ammonia
• Cytotoxic oedema, impaired cerebral function
• Can lead to vasogenic oedema
Early signs: yawning, aimless wandering, mild ataxia, decreased awareness
Later signs: head pressing, aggression, recumbency **may just progress straight to this
=poor px
Tx
o Sedation
o Reduce absorption of protein: mineral oil, lactulose
o correct hypoglycaemia
Diagnostic investigation
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Serum bile acids
• Don’t measure pre & post prandial, its secreted continuously as don’t have gall bladder
• Used to assess liver function
• Bad if high
US
• May not see any changes
• Echogenicity – is liver more hyperechoic
• Evidence of masses
• Usually do from right side
Liver biopsy
• Can do blind or US guided
• Block skin & muscle
• Take multiple samples
• Don’t need to assess clotting ability before taking
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Diseases
Pyrrolizidine alkaloid toxicity
• Most common cause of chronic liver
• Plant Paterson’s curse
• Unpalatable so wont eat unless deprived or pasture covered
• Toxic dose 200mg/kg – also cumulative
• Don’t see signs until 4 weeks – months after ingestion
• Inhibit liver cell synthesis – so swell and form megalocytes > progress to fibrosis
• Classic histo presentation: biliary hyperplasia
Bacterial cholangiohepatitis
• Dx – histo, culture & sensitivity
• Actinobacillus, E. coli
• Tx – long term AB’s
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Theiler's disease
• Acute hepatitis
• Caused by biological products
• Common in USA
• Signs – anorexia, icterus, bleeding etc
• Rapid progression to failure