vet clinics liver Flashcards
name the blood markers for Hepatocellular Injury and their half life
what is their specificity and sensibility like?
GLDH: 12-24h
SDH <12h
AST 7 days
all very sensitive
highest specificity: SDH BUT very unstable in samples!!
markers of Biliary Injury/Cholestasis, their half life and their sensitivity/specificity
GGT: 3d
sens ++++, spec: +++
AP: 3d
sens: +++/ spef: +
GGT in training horses
small number of racehorses may have moderate increases in GGT (50–140 IU/L)
GGT activity is correlated to cumulative training load and racing frequency and considered a maladaptation to training
bile acids and colic
Bile acid concentrations can be increased in some horses with intestinal disorders, such as
colic, enteritis, and equine dysautonomia.
Moderate to markedly increased bile acid concentrations in horses with colic are associated with a guarded prognosis.
when do liver function tests become abnormal?
only after 70% or more of hepatic function is lost.
bile acids are a good predictor of liver disease?
Bile acid concentrations above 20 μmol/L are a good predictor of liver failure
What is a mild increase in bile acids and what mght this indicate?
Milder increases (up to 20 μmol/L) may occur in a few horses without hepatic disease that are anorexic for 2 or more days
Can bile acid concentrations predict outcome of liver disease?
yes, in chronic liver disease: persistently increased bile acid concentrations greater than 20 μmol/L have a guarded to poor prognosis.
Bile acid concentrations s_hould not be used as a predictor of prognosis in horses with acute liver disease._
Albumin concentration in liver failure
Albumin concentrations rarely are low in horses with
acute (6%) or
chronic (18%) liver failure,
and hypoalbuminemia is neither a sensitive nor specific test for liver failure in the horse.
Why is Vit K important?
vitamin K (bile avids needed for absorption)
aids in synthesis of activated coagulation factors II, VII, IX, and X, along with the inhibitors proteins C and S
are liver biopsies safe in chronic hepatic failure?
Clotting times often are increased in horses with liver failure due to insufficient hepatic synthesis of clotting factors II, V, VII, IX, X, XI, and XII.
Regardless, clinical bleeding is uncommon and liver biopsies can be performed safely in most cases
lactic dehydrogenase is present in
in almost all living cells
very unspecific
Cause of theiler’s disease? consequences?
suspected to be parvovirus
occurring several weeks after administration of a biological substance of equine origin
fulminant hepatic necrosis, often fatal
For both equine pegiviruses, it was recently demonstrated that they are
not hepatotropic and not associated with hepatitis, but instead cause persistent infection of bone marrow
prevalence of EqPV H
clinically healthy horse populations in the USA, China, Germany, and Austria have demonstrated
DNA prevalence between 7.1% and 17%
and seroprevalence between 15% and 34.7%
higher in farms with reported theiler’s disease
EqPV-H:
experimental infection of horses
resulted in subclinical hepatitis, demonstrated by increased liver enzymes, without clinical signs in most cases
onset of hepatitis: 5-8 weeks after infection
viral DNA remained detectable in different organs for at least 15 weeks after infection
(in natural cases up to 20 months!!!)
Can EqPV H be transmitted from horses to donkeys?
Unlike EqHV – for which detection of antibodies and nucleic acid in samples from donkeys confirmed cross-species transmission [46] – there is currently no evidence of EqPV-H transmission to other species of equines
Liver biopsies as prognostic indicator for liver disease
Durham:
Histo Grading system: 0-14
scores 2 - 6: 12 times less likely to survive to 6 months than horses with biopsy scores of 0
scores 7 - 14: 46 times less likely to survive
Best prognostic indicator for liver disease outcome?
Based on the available evidence,
histological evaluation of hepatic biopsies provides better prognostic information than does the results of blood tests.
Of the routinely performed blood tests, SBA concentration provides the best prognostic information.
what happens with increased serum iron levels ?
The majority of iron in mammals (approximately 80%) is
- bound to heme in erythrocytes, and the
- remaining variable portion mainly to transferrin in blood or
- ferritin or haemosiderin intracellularly (Kohgo et al. 2008).
if transferrin in plasma is saturated -> liver tends to take up unbound iron more than erythrocytes-> hepatic accumulation = haemosiderinosis
how to treat iron intoxication
is liver damage reversible?
2 case reports with poneys
- phlebotomy (8% of blood volume)
- deferoxamine:
- inhibits cell iron uptake by binding to intraand extra-cellular unbound iron which is then excreted in bile or urine
- reduction of hepatic stellate cell activation and fibrogenesis
- attenuation of lipid peroxidation
- damage reversible if acute hepatopathy, not with chronic
Stability of SDH in blood samples
stable in heparinized plasma stored under all temperature conditions for 4 h
at 4 ◦C for 24 h,
but changes in enzyme activity may only be considered clinically relevant if they exceed 25% of previously measured activity.
amyloidosis definition
extracellular deposition of protein fibrils resistant to proteolysis
What is AL amyloidosis?
protein deposition derived from the N-terminal region of monoclonal immunoglobulin light chains
associated with
- localised accumulations within the upper respiratory tract and combined nasal and conjunctival infiltration
- as well as systemic accumulation with the development of visceral masses
- associated with multiple myeloma (Kim et al. 2005), and finally in the cutaneous form,
- associated with histiolymphocytic lymphoma
What is AA amyloidosis?
derived from the circulating acute phase reactant serum amyloid A (SAA) by proteolytic cleavage
associated with
nasal amyloidosis
splenic amyloidosis
hepatic am
treatment and outcome of hepatic amyloidosis
1 case report
treatment with dexamethasone
dead after 7 months
hepatic rupture??
Does a positive PCR eqPV H mean active infection?
Is there a risk factor?
Apparently yes, but
EqPV-H antibodies and DNA are frequently detected in Austrian horses, without associated hepatitis in horses with active infection.
The risk of active EqPV-H infection increases with increasing age. (16- to 31-year-old horses)
causes of hepatitis in horses
Toxic: eg, pyrrolizidine alkaloids, Panicum grasses, aflatoxins
Metabolic: hepatic lipidosis
Bacterial: ascending cholangiohepatitis, Tyzzer disease in foals (Clostridium piliforme)
Idiopathic: Chronic active hepatitis, (Theiler disease)
Neoplastic: lymphoma, hepatocellular carcinoma
Viral: nonprimate hepacivirus (NPHV), equine parvovirus-hepatitis (EqPV-H)
Nonprimate hepacivirus
- Virus prevalence: 2% to 7% (based on serum PCR). Seroprevalence: w40%.
- Transmission: iatrogenic through biologic products, vertical, otherwise unknown.
- Disease association in experimental models: subclinical hepatitis with mild elevations in liver enzymes.
- Disease association in clinical cases: 1 report of suspected NPHV–associated hepatitis.
- Clinical implications: likely a relevant cause of mild liver disease. Capacity to cause clinical hepatitis, liver failure, or chronic diseases, such as cirrhosis, chronic active hepatitis, and neoplasia, is unknown.
Theiler disease–associated virus
not clinically relevant
pegivirus in horses
not clinically relevant
how long does it take for theiler’s to occur?
90% of cases occurring 40–70 days after the antiserum inoculation
also kann ÜBER 2 MONATE NACHHER sein
90% mortality
