EQUINE | CPD Article
Clinical Pathology Basics for Equine
Practitioners - Liver Disease
Dr Rick Last – BVSc; M.Med.Vet (Pathology)
Consulting Specialist Veterinary Pathologist
Introduction
Clinical signs of liver disease in equines are often
vague and non-specific, although there are some
clinical symptoms which are highly suggestive of a
primary hepatopathy, and these include hepatomegaly
/ microhepatica, icterus, ascites and hepatic
encephalopathy. The more common non-specific
clinical signs include depression, weight loss, anorexia,
abdominal pain, polyuria/polydipsia (PU/PD). These
non-specific signs are also frequently observed with
many other diseases.
In the early stages of liver disease, sub-clinical
presentation with non-specific signs is common,
while specific hepatic symptoms are rarely observed.
Therefore, serum biochemical profiling of hepatic
function is extremely useful in identifying the presence
or absence of liver disease and whether any hepatic
dysfunction is acute or chronic. These biochemical
changes may result from either primary liver disease or
are secondary to other primary non-hepatic diseases.
However, when these biochemical tests are interpreted
in conjunction with clinical signs and other laboratory
analyses, they allow for recognition of pattern changes,
from which a number of diagnostic, prognostic and
treatment decisions can be made.
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The diagnosis of liver disease is based on abnormalities
in serum enzymes that are partly or exclusively
associated with hepatocytes and/or epithelial cells
lining the biliary tree as well as some analytes that assess
liver functionality and other more general indicators of
inflammation.
Hepatic enzymes are divided into two categories
• Hepatocellular leakage enzymes (cytoplasmic,
mitochondrial).
• Induced enzymes.
Hepatocellular leakage enzymes are soluble enzymes
that occur normally in the cytoplasm (aspartate
aminotransferase AST; alanine aminotransferase
ALT, sorbitol dehydrogenase SDH) or mitochondria
(glutamate dehydrogenase GLDH and aspartate
aminotransferase AST) of hepatocytes. They are
released with hepatocellular membrane damage with
sublethal injury or hepatocellular necrosis. The serum
activity of these enzymes depends on the number of
hepatocytes injured, the severity of the injury and the
half-life of the enzyme involved.
Induced hepatic enzymes (alkaline phosphatase ALP;
γ-glutamyl transferase GGT) are typically membrane-
bound and not released into the serum with increased
membrane permeability. Increased serum enzymatic
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