Icterus in horses Flashcards
pre-hepatic icterus
problem with the rbc breakdown-haemoglabin-unconjugated bilirubin part of bile production
haemolysis - incr bilirubin production
primarily unconjugated bilirubin
haemolysis in horses
Neonatal isoerythrolysis - immunocompatibility between foeal + mothers RBCs
Infections eg EIA
Drugs eg penicillin
Toxins eg onion
Autoimmune HA – relatively rare in horses
hepatic icterus
Impaired hepatic uptake or conjugation
Increased unconjugated bilirubin
Common causes in horses : anorexia, acute hepatocellular disease
anorexia + icterus
anorexia is most common cause of icterus in horses
10-15% horses look mildly icteric
may be due to ligandin shortage - protein needed for uptake of unconjugated bilirubin into liver
post-hepatic icterus
Impaired excretion of bilirubin
Cholangitis, cholangiohepatitis etc
Cholestasis if conjugated bilirubin >30% of total bilirubin shunts very uncommon
common clinical signs of liver dysfunction
depression anorexia colic abnormal behaviour weight loss icterus
less common clinical signs of liver dysfunction
photosensitization diarrhoea bilateral laryngeal paralysis haemorrhagic diathesis ascites dependant oedema
colic - suggests which hepatic dysfunction
hepatocellular swelling
biliary obstruction
weight loss - suggests which hepatic dysfunction
Chronic disease
Decreased intake
Metabolic dysfunction
hepatic encephalopathy
Severe hepatic dysfunction
clinical signs of cerebral disease vary - mild depression–head pressing
hepatic encephalopathy - pathogenesis
decr ammonia clearance
amino acid alterations - creates false neurotransmitters
photosensitisation
Phylloerythrin - photodynamic, made by bacteria in gut + excreted by liver
liver dysfunction = more phylloerythrin
UV exposure causes cell membrane damage + necrosis
liver specific components of blood test
bile acids
SDH
GGT
what to look for on a hepatic ultrasound
size
Changes in echogenicity
Dilated bile ducts, choleliths, abscesses, neoplasia
hepatic biopsy can provide info for ___
diagnosis
prognosis
treatment options
treatment of HE
Sedation – care
Mannitol/hypertonic saline: cerebral oedema
Oral lactulose: limit ammonia absorption
Oral BCAA (branched chain amino acids): no evidence that this is beneficial
dietary modification
High carbohydrate, limited protein – protein source rich in BCAA
anti-inflammatories
NSAIDS - Flunixin meglumine
DMSO
Corticosteroids - dexamethasone, prednisolone
pyrrolizide alkaloid toxicity - aetiology
Ingestion of plants containing pyrrolizidine alkaloids - Ragwort
Usually unpalatable
Long term ingestion (cumulative) – 4-12 weeks
pyrrolizide alkaloid toxicity - pathogenesis
Pyrrolizidine alkaloids metabolized by liver to toxic pyrrole derivatives
Pyrroles are antimitotic: cross link DNA + bind to nucleic acid and proteins within hepatocytes
Cells can’t divide - megalocyte production (large RBC) - megalocyte death - fibrosis
pyrrolizide alkaloid toxicity - clinical signs + diagnosis
non-specific clinical signs
diagnosis - History of ingestion, Blood work, Biopsy - megalocytosis
pyrrolizide alkaloid toxicity - treatment + prognosis
no specific treatment
Poor prognosis
Typically death within 10 days of clinical signs of liver failure
Regeneration not possible if fibrosis present + megalocytosis extensive
theiller’s disease a.k.a
serum sickness
acute necrotic hepatitis
serum associated heptitis
theiller’s disease
unknown cause widespread hepatic necrosis small liver at post mortem no specific treatment prognosis - poor if severe HE
tyzzers disease - cause by which bacteria
Clostridium piliformis
tyzzers disease - clinical signs
May be none – found dead
Non-specific
Loss of suckle, depression, recumbency
tyzzer’s - diagnosis
antemortem – difficult
Definitive diagnosis – post mortem identification of organism
Multifocal hepatitis and enteritis
tyzzer’s - treatment + prognosis
treat - antibiotics + supportive, only 1 ever successful case
prognosis - grave
cholelithiasis - diagnosis
Liver enzyme activity: GGT, SDH, AST
Ultrasound: ? Dilated bile ducts, cholelith
Biopsy: histopathology, culture
cholelithiasis - treatment + prognosis
treat - Antimicrobials: long term (weeks – months) Supportive care
prognosis - Depends on fibrosis, number and extent of choleliths, severity of clinical signs
hyperlipaemia
mostly in miniature breeds
incr risk of obese
due to -ve energy balance - disease, stress, pregnancy, lactation
hyperlipaemia - clinical signs
Lethargy Anorexia Weakness Icterus Mild colic, diarrhoea Recumbency \+/- more severe signs of liver disease
hyperlipaemia - diagnosis
Breed History Clinical signs Measure Tg in serum - Hyperlipidaemia, Hyperlipaemia \+/- liver biopsy
hyperlipaemia - treatment
reverse -ve energy balabnce
treat hepatic disease
eliminate stress/treat disease
inhibit further fat mobilization - insulin
incr triglyceride uptake by peripheral tissue - heparin
hyperlipaemia - prognosis
poor once clinical signs seen
hyperlipaemia - prevention
monitor at risk animals
measure Tg level in sick ponies
prevent obesity
