Icterus in horses

Question 1

pre-hepatic icterus

Answer 1

problem with the rbc breakdown-haemoglabin-unconjugated bilirubin part of bile production
haemolysis - incr bilirubin production
primarily unconjugated bilirubin

Question 2

haemolysis in horses

Answer 2

Neonatal isoerythrolysis - immunocompatibility between foeal + mothers RBCs
Infections eg EIA
Drugs eg penicillin
Toxins eg onion
Autoimmune HA – relatively rare in horses

Question 3

hepatic icterus

Answer 3

Impaired hepatic uptake or conjugation
Increased unconjugated bilirubin
Common causes in horses : anorexia, acute hepatocellular disease

Question 4

anorexia + icterus

Answer 4

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

Question 5

post-hepatic icterus

Answer 5

Impaired excretion of bilirubin
Cholangitis, cholangiohepatitis etc
Cholestasis if conjugated bilirubin >30% of total bilirubin shunts very uncommon

Question 6

common clinical signs of liver dysfunction

Answer 6

depression
anorexia
colic
abnormal behaviour
weight loss
icterus

Question 7

less common clinical signs of liver dysfunction

Answer 7

photosensitization 
diarrhoea 
bilateral laryngeal paralysis
haemorrhagic diathesis
ascites
dependant oedema

Question 8

colic - suggests which hepatic dysfunction

Answer 8

hepatocellular swelling

biliary obstruction

Question 9

weight loss - suggests which hepatic dysfunction

Answer 9

Chronic disease
Decreased intake
Metabolic dysfunction

Question 10

hepatic encephalopathy

Answer 10

Severe hepatic dysfunction

clinical signs of cerebral disease vary - mild depression–head pressing

Question 11

hepatic encephalopathy - pathogenesis

Answer 11

decr ammonia clearance

amino acid alterations - creates false neurotransmitters

Question 12

photosensitisation

Answer 12

Phylloerythrin - photodynamic, made by bacteria in gut + excreted by liver
liver dysfunction = more phylloerythrin
UV exposure causes cell membrane damage + necrosis

Question 13

liver specific components of blood test

Answer 13

bile acids
SDH
GGT

Question 14

what to look for on a hepatic ultrasound

Answer 14

size
Changes in echogenicity
Dilated bile ducts, choleliths, abscesses, neoplasia

Question 15

hepatic biopsy can provide info for ___

Answer 15

diagnosis
prognosis
treatment options

Question 16

treatment of HE

Answer 16

Sedation – care
Mannitol/hypertonic saline: cerebral oedema
Oral lactulose: limit ammonia absorption
Oral BCAA (branched chain amino acids): no evidence that this is beneficial

Question 17

dietary modification

Answer 17

High carbohydrate, limited protein – protein source rich in BCAA

Question 18

anti-inflammatories

Answer 18

NSAIDS - Flunixin meglumine
DMSO
Corticosteroids - dexamethasone, prednisolone

Question 19

pyrrolizide alkaloid toxicity - aetiology

Answer 19

Ingestion of plants containing pyrrolizidine alkaloids - Ragwort
Usually unpalatable
Long term ingestion (cumulative) – 4-12 weeks

Question 20

pyrrolizide alkaloid toxicity - pathogenesis

Answer 20

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

Question 21

pyrrolizide alkaloid toxicity - clinical signs + diagnosis

Answer 21

non-specific clinical signs

diagnosis - History of ingestion, Blood work, Biopsy - megalocytosis

Question 22

pyrrolizide alkaloid toxicity - treatment + prognosis

Answer 22

no specific treatment
Poor prognosis
Typically death within 10 days of clinical signs of liver failure
Regeneration not possible if fibrosis present + megalocytosis extensive

Question 23

theiller’s disease a.k.a

Answer 23

serum sickness
acute necrotic hepatitis
serum associated heptitis

Question 24

theiller’s disease

Answer 24

unknown cause
widespread hepatic necrosis
small liver at post mortem
no specific treatment
prognosis - poor if severe HE

Question 25

tyzzers disease - cause by which bacteria

Answer 25

Clostridium piliformis

Question 26

tyzzers disease - clinical signs

Answer 26

May be none – found dead
Non-specific
Loss of suckle, depression, recumbency

Question 27

tyzzer’s - diagnosis

Answer 27

antemortem – difficult
Definitive diagnosis – post mortem identification of organism
Multifocal hepatitis and enteritis

Question 28

tyzzer’s - treatment + prognosis

Answer 28

treat - antibiotics + supportive, only 1 ever successful case
prognosis - grave

Question 29

cholelithiasis - diagnosis

Answer 29

Liver enzyme activity: GGT, SDH, AST
Ultrasound: ? Dilated bile ducts, cholelith
Biopsy: histopathology, culture

Question 30

cholelithiasis - treatment + prognosis

Answer 30

treat - Antimicrobials: long term (weeks – months) Supportive care
prognosis - Depends on fibrosis, number and extent of choleliths, severity of clinical signs

Question 31

hyperlipaemia

Answer 31

mostly in miniature breeds
incr risk of obese
due to -ve energy balance - disease, stress, pregnancy, lactation

Question 32

hyperlipaemia - clinical signs

Answer 32

Lethargy 
Anorexia 
Weakness 
Icterus 
Mild colic, diarrhoea 
Recumbency 
\+/- more severe signs of liver disease

Question 33

hyperlipaemia - diagnosis

Answer 33

Breed 
History 
Clinical signs 
Measure Tg in serum - Hyperlipidaemia, Hyperlipaemia 
\+/- liver biopsy

Question 34

hyperlipaemia - treatment

Answer 34

reverse -ve energy balabnce
treat hepatic disease
eliminate stress/treat disease
inhibit further fat mobilization - insulin
incr triglyceride uptake by peripheral tissue - heparin

Question 35

hyperlipaemia - prognosis

Answer 35

poor once clinical signs seen

Question 36

hyperlipaemia - prevention

Answer 36

monitor at risk animals
measure Tg level in sick ponies
prevent obesity