Icterus in horses Flashcards Preview

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Flashcards in Icterus in horses Deck (36)
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1
Q

pre-hepatic icterus

A

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

2
Q

haemolysis in horses

A

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

3
Q

hepatic icterus

A

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

4
Q

anorexia + icterus

A

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

5
Q

post-hepatic icterus

A

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

6
Q

common clinical signs of liver dysfunction

A
depression
anorexia
colic
abnormal behaviour
weight loss
icterus
7
Q

less common clinical signs of liver dysfunction

A
photosensitization 
diarrhoea 
bilateral laryngeal paralysis
haemorrhagic diathesis
ascites
dependant oedema
8
Q

colic - suggests which hepatic dysfunction

A

hepatocellular swelling

biliary obstruction

9
Q

weight loss - suggests which hepatic dysfunction

A

Chronic disease
Decreased intake
Metabolic dysfunction

10
Q

hepatic encephalopathy

A

Severe hepatic dysfunction

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

11
Q

hepatic encephalopathy - pathogenesis

A

decr ammonia clearance

amino acid alterations - creates false neurotransmitters

12
Q

photosensitisation

A

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

13
Q

liver specific components of blood test

A

bile acids
SDH
GGT

14
Q

what to look for on a hepatic ultrasound

A

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

15
Q

hepatic biopsy can provide info for ___

A

diagnosis
prognosis
treatment options

16
Q

treatment of HE

A

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

17
Q

dietary modification

A

High carbohydrate, limited protein – protein source rich in BCAA

18
Q

anti-inflammatories

A

NSAIDS - Flunixin meglumine
DMSO
Corticosteroids - dexamethasone, prednisolone

19
Q

pyrrolizide alkaloid toxicity - aetiology

A

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

20
Q

pyrrolizide alkaloid toxicity - pathogenesis

A

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

21
Q

pyrrolizide alkaloid toxicity - clinical signs + diagnosis

A

non-specific clinical signs

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

22
Q

pyrrolizide alkaloid toxicity - treatment + prognosis

A

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

23
Q

theiller’s disease a.k.a

A

serum sickness
acute necrotic hepatitis
serum associated heptitis

24
Q

theiller’s disease

A
unknown cause
widespread hepatic necrosis
small liver at post mortem
no specific treatment
prognosis - poor if severe HE
25
Q

tyzzers disease - cause by which bacteria

A

Clostridium piliformis

26
Q

tyzzers disease - clinical signs

A

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

27
Q

tyzzer’s - diagnosis

A

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

28
Q

tyzzer’s - treatment + prognosis

A

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

29
Q

cholelithiasis - diagnosis

A

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

30
Q

cholelithiasis - treatment + prognosis

A

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

31
Q

hyperlipaemia

A

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

32
Q

hyperlipaemia - clinical signs

A
Lethargy 
Anorexia 
Weakness 
Icterus 
Mild colic, diarrhoea 
Recumbency 
\+/- more severe signs of liver disease
33
Q

hyperlipaemia - diagnosis

A
Breed 
History 
Clinical signs 
Measure Tg in serum - Hyperlipidaemia, Hyperlipaemia 
\+/- liver biopsy
34
Q

hyperlipaemia - treatment

A

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

35
Q

hyperlipaemia - prognosis

A

poor once clinical signs seen

36
Q

hyperlipaemia - prevention

A

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