vet clinics liver Flashcards

1
Q

name the blood markers for Hepatocellular Injury and their half life

what is their specificity and sensibility like?

A

GLDH: 12-24h

SDH <12h

AST 7 days

all very sensitive

highest specificity: SDH BUT very unstable in samples!!

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2
Q

markers of Biliary Injury/Cholestasis, their half life and their sensitivity/specificity

A

GGT: 3d

sens ++++, spec: +++

AP: 3d

sens: +++/ spef: +

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3
Q

GGT in training horses

A

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

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4
Q

bile acids and colic

A

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.

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5
Q

when do liver function tests become abnormal?

A

only after 70% or more of hepatic function is lost.

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6
Q

bile acids are a good predictor of liver disease?

A

Bile acid concentrations above 20 μmol/L are a good predictor of liver failure

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7
Q

What is a mild increase in bile acids and what mght this indicate?

A

Milder increases (up to 20 μmol/L) may occur in a few horses without hepatic disease that are anorexic for 2 or more days

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8
Q

Can bile acid concentrations predict outcome of liver disease?

A

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._

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9
Q

Albumin concentration in liver failure

A

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.

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10
Q

Why is Vit K important?

A

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

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11
Q

are liver biopsies safe in chronic hepatic failure?

A

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

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12
Q

lactic dehydrogenase is present in

A

in almost all living cells

very unspecific

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13
Q

Cause of theiler’s disease? consequences?

A

suspected to be parvovirus

occurring several weeks after administration of a biological substance of equine origin

fulminant hepatic necrosis, often fatal

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14
Q

For both equine pegiviruses, it was recently demonstrated that they are

A

not hepatotropic and not associated with hepatitis, but instead cause persistent infection of bone marrow

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15
Q

prevalence of EqPV H

A

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

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16
Q

EqPV-H:

experimental infection of horses

A

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!!!)

17
Q

Can EqPV H be transmitted from horses to donkeys?

A

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

18
Q

Liver biopsies as prognostic indicator for liver disease

A

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

19
Q

Best prognostic indicator for liver disease outcome?

A

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.

20
Q

what happens with increased serum iron levels ?

A

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

21
Q

how to treat iron intoxication

is liver damage reversible?

A

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
22
Q

Stability of SDH in blood samples

A

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.

23
Q

amyloidosis definition

A

extracellular deposition of protein fibrils resistant to proteolysis

24
Q

What is AL amyloidosis?

A

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
25
Q

What is AA amyloidosis?

A

derived from the circulating acute phase reactant serum amyloid A (SAA) by proteolytic cleavage

associated with

nasal amyloidosis

splenic amyloidosis

hepatic am

26
Q

treatment and outcome of hepatic amyloidosis

A

1 case report

treatment with dexamethasone

dead after 7 months

hepatic rupture??

27
Q

Does a positive PCR eqPV H mean active infection?

Is there a risk factor?

A

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)

28
Q

causes of hepatitis in horses

A

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)

29
Q

Nonprimate hepacivirus

A
  • 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.
30
Q

Theiler disease–associated virus

A

not clinically relevant

31
Q

pegivirus in horses

A

not clinically relevant

32
Q

how long does it take for theiler’s to occur?

A

90% of cases occurring 40–70 days after the antiserum inoculation

also kann ÜBER 2 MONATE NACHHER sein

90% mortality