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what is an important clinical question
whether the horse has an acute liver injury with the potential for recover
or chronic liver disease that has acutely decompensated
what are liver function tests
direct bilirubin, bile acids, blood ammonia, Pt/PTT
When do liver function tests become abnormal
when 70-80% of the hepatic function has been lost
what two types of injury do liver specific enzymes help to characterize
hepatocellular vs biliary
does the magnitude of liver specific enzyme elevation correlate with hepatic function?
no they detect injury but do not assess function, and they should not be interpreted in isolation
what are unique findings of horses with severe liver disease
-increased hematocrit
-serum iron concentration
-transferrin saturation that persists despite rehydration
special consideration for anorexic of fasted horses
fasting induced hyperbilirubenaemia and mild icterus is common
fasting for 2-3 days can also increase serum bile concentrations
special considerations for racehorses
increased GGT activity has been associated with poor performance and maladaptation to training
with GGT lowering during periods of rest
special considerations for foals
GGT is present only in low concentrations in equine oclostrum
therefore increased GGT activity reflects endogenous productions rather than from colostrum
serum ALP is increased bc of growth for first year of life
serum bile acid concentrations are higher than adults for first 6 months
what are the three liver specific enzymes tested in horses
GGT
GLDH
SDH
what are the liver specific hepatocellular enzymes
GLDH and SDH
ALT
How do GLDH and SDH differ
SDH has a shorter half life making it useful for monitoring progress or resolution. common in US
GLDH more common in NZ
what enzyme assess biliary disease
GGT
what are the non liver specific enzymes
ALP and AST
what can affect AST
hepatocellular, muscle or erythrocyte
what affects ALP
liver, bone, corticosteroid
what is the most common metabolic cause of liver failure in horses
hepatic lipidosis and hyperlipemia
when does hepatic lipidosis occur
when a negative energy balance activate hormone sensitive lipase in adipose tissue, resulting in excessive mobilization of NEFAs. the liver becomes overwhelmed by the influx of fat, leading to triglyceride accumulation within hepatocytes and increased circulating triglyceride concentration
what animals are at risk of hepatic lipidosis and hyerpliparmia
Shetland and welsh mountain ponies, mini horses, donkeys, obese animals, horses with EMS or PPID, pregnant or lactating mares, horses experiencing stress
when can hyperlipemia occur as a primary disease
in ponies and donkeys
why is hyperlipemia not a primary disease in horses
usually secondary to an underlying disorder causing negative energy balance
what are the clinical signs of hyperlipemia, and hepatic lipidosis
-progress rapidly from anorexia, lethargy, weakness → ataxia, head pressing, recumbency, seizures, and death
-ventral edema, icterus, and reduced gastrointestinal motility may also be present
-without treatment death often occurs within 6-10 days of onset
how do you diagnose hyperlipemia and hepatic lipidosis
hypertriglyceridaemia (>5mm/L)accompanied by compatible clinical signs is diagnostic
gross lipemia of centrifuged plasma provides a useful stall side clue
liver enzyme activités (GGT, GLDH, SDH) are variably increased
what does lipemia describe
the appearance of serum
will all horses with hypertriglyceridaemia have hyperlipemia
no
but all horses that have hyperlipemia will have severe hypertriglyceridaemia
Treatment of hyperlipaemia and hepatic lipidosis
is challenging and often requires referral for hospitalisation for intensive nutritional support, including enteral or parenteral nutrition and insulin therapy.
careful monitoring of blood glucose is essential to avoid hypoglycemia
identifying the underlying and correcting the identifying cause of the negative energy balance
prognosis of hyperlipaemia and hepatic lipidosis
poor
reported mortality of 57-85%
animals with serum triglyceride concentrations <5mmol/L have substantially greater prognosis
what can be added to treatment for a PPID associated hyperlipemia
pergolide in addition to supportive care
prevention of hyperlipemia
identify at risk animals and manage obesity
recognize and manage endocrine disease
avoid prolonged negative energy balance
monitor serum triglyceride concentrations
a mini horse develops hyperlipemia following several days of anorexia. the primary goal of treatment is to:
increase endogenous insulin secretion to suppress hormone sensitive lipase
how does liver disease often present
subtle, non specific signs such as weightloss, mild colic, icterus, and occasional fever
clinical examination and clinicopathological testing help identify hepatic involvement
what body systems can present with the trait of colic, pyrexia, and icterus
hepatic system (most likely)
GI (severe enteritis or colitis)
respiratory system (pleuritis or pleuropneumonia)
haemopoietic system (IMHA) but colic not typical
what is the most common clinically significant biliary disease in horses
cholangiohepatitis caused by ascending bacterial infection from the duodenum
what does cholangiohepatitis predispose to and why
calcium bilirubinate cholelithiasis
bacterial infection causes bilirubin deconjugation
calcium bilirubinate crystals form
biliary sludge develops
choleliths form around a glycoprotein matrix
clinical signs of cholangiohepatitis
fever, icterus, recurrent (often mild colic), and weightloss
diagnosis of cholangiohepatitis
marked increases in GGT and ALP
conjugated biliruben of >25% of total bilirubin supports biliary obstruction
ultrasound of sludge, dilated bile ducts or choleliths
liver biopsy and culture provide definitive diagnosis
treatment of cholangiohepatitis
prolonged antimicrobial therapy ideally guided by culture
ursodiol may improve bile flow and reduced inflammation
continue treatment until GGT and ALP remain normal for 2-4 weeks
surgery is reserved for complete biliary obstruction or selected cases with accessible choleliths
prognosis of cholangiohepatitis
good if there is clinical improvement within 7-10 days and minimal hepatic fibrosis
and that it has successfully been distinguished from cholelithiasis as these carry a much more guarded prognosis
what is chronic active hepatitis
a progressive peri portal inflammatory liver disease of uncertain cause
clinical signs of chronic active hepatitis
often subtle and intermittent, and may include fever
moist exfoliative dermatitis of the coronary bands can occur and may reflect immune mediated vasculitis or photosensitization
hepatic encephalopathy can develop
clinicopathological findings of chronic active hepatitis
cholestatic liver disease,
evidence of inflammation (leukocytosis left shift and monocytosis)
liver biopsy is essential for diagnosis and prognosis
histopathology of chronic active hepatitis
peri portal fibrosis with neutrophilic or lymphocytic inflammation
concurrent cholangiohepatitis is common and may be either a cause or consequence of the disease
treatment of chronic active hepatitis
corticosteroids (effective but 50% relapse)
antibiotics if concurrent cholangiohepatitis is present
colchicine and zinc if progressive fibrosis is identified
ursodiol for cholestasis
what is equine hepacivirus
a close relative to human hepatitis C, is a recognized cause of acute and chronic hepatitis in horses
what is the expected histopathology of equine hepacivirus
fibrosis, lymphocytic inflammation, hepatocellular necrosis, and ductular reaction
what is the treatment and prognosis of equine hepacivirus
no treatment shown to consistently eliminate infection
guarded prognosis
what are the most common primary hepatic tumors
cholangiocarcinoma
hepatoblastoma
the liver is a frequent site of metastasis for what cancers
lymphoma
SCC
melanoma
what is unique of ascites in relation to the liver in horses
it is uncommon in equine liver failure
its presence should raise suspicion for neoplasia or concurrent peritonitis
is hemorrhage a risk of liver biopsy?
there is no significant association between abnormal coagulation tests and post biopsy complications
what kind of bacteria are equine hepatobiliary infections caused by
enteric gram negative and anaerobic bacteria