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ACVIM Generals Revision MS > Hepatic Disease > Flashcards

Hepatic Disease Flashcards

1
Q

Which type of PSS is more commonly seen in cats?

A

EHPSS

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2
Q

Why does clinical icterus take 2 weeks to resolve?

A

It binds irreversibly to albumin and can be deposited in tissues

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3
Q

At what level of bilirubin does clinical jaundice become noticeable?

A

>50umol/L

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4
Q

How might protein content of ascitic fluid due to portal hypertension help in refining differential diagnoses?

A

Typical anything gpost-sinosoidal (e.g. hepatic/post-hepatic) has a higher protein content (>25g/dL).

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5
Q

Accumulation of which amino acid is implicated in ammonia’s effect on neuronal cells?

A

Glutamine (as NH3 can be combined with glutamate) GLutamin acts as an osmotic agent.

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6
Q

ALT half life

  • Dog
  • Cat
A

48-60h in the dog
6h in the cat

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7
Q

ALP half life

  • Dog
  • Cat
A
  • 70h
  • 6 hours
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8
Q

How is ALP bonded to the cell membrane?

A

Via glucose phosphatidyllinositol bonds - these can be degraded in there presence of bile acids.

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9
Q

Other than the liver, what alternative sources for ALP are there?

A

Intestine, renal cortex, placenta, liver, bone

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10
Q

AST half life and alternative sources

A

22h dog, 6 minutes cat
Red blood cells and muscle.

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11
Q

What does it mean if ALP is increased by GGT is not in a cat?

A

This can be indicative of hepatic lipidosis.

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12
Q

Why is GGT more useful than some other liver enzymes in cats?

A

It has a longer half life than ALP

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13
Q

What part of the liver do GLDH and LDH give information about?

A

Both are indicative of hepatocellular injury

GLDH is more specific to the liver and LDH is less so.

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14
Q

Which liver enzymes should be interpreted alongside CK?

A

Mostly AST but also ALT as this is found in muscle to some degree too.

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15
Q

What is the normal function of CK?

A

It releases ADP from phosphocreatine, creating ATP.

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16
Q

At what degree of elevation might CK elevation make you suspicious for muscle disease?

A

>5x elevations repeatedly.

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17
Q

What can happen to ALP concentrations with improvement of chronic hepatitis and why?

A

It can increase due to induction from the regenerative response.

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18
Q

How much functional hepatic loss must there be, generally, before significant hypoalbuminaemia may develop?

A

70%

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19
Q

Which globulins are produced in the liver?

A

Alpha and beta. Gamma are produced by B and plasma cells.

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20
Q

Which of the following is most correct about the sensitivity and specificitty of serum bile acids for the diagnosis of PSS?

a) neither is improved by addition of the fasting sample
b) the post-prandial sample improves sensitivity
c) the post-prandial improves specificity

A

c)

Although both sensitivity and specificity is improved.

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21
Q

Ammonia is more [sensitive than it is specific/specific than it is sensitive] for PSS

A

Ammonia is more sensitive than specific.

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22
Q

Which coagulation factors are NOT produced by the liver?

A

vWB, VIII

23
Q

What % activity of protein C is likely a result of PSS?

A

<70%

24
Q

What are the reasons which PU/PD may develop in a patient with hepatic disease?

A
  1. Loss of medullary hypertonicity from reduced medullary urea concentration
  2. Impaired hormone metabolism (lack of cortisol breakdown)
  3. Psychogenic (HE)
  4. Fanconi-like disease if copper accumulation is impaired
25
Q

The spleen should normally be —echoic to the liver?

A

Hyper

26
Q

What is the sensitivity of abdominal ultrasound for MAPSS?

A

67%

27
Q

How much discrepency is there between tract liver biopsy findings and wedge biopsy histopathology?

A

Approximately 50-60% depending on what you are looking for. Try-cut is probably best when there is a neoplastic cause.

28
Q

Which hepatoprotectant has specific veterinary evidence behind its use?

A

Silmaryn - used IV to treat amanita phalloides toxicity.

29
Q

Which anti-oxidant is SAMe a precursor of?

A

Glutathione

30
Q

What are the four different types infectious/inflammatory cholangitis?

A

Neutrophilic
Lymphocytic
Destructive
Chronic (associated with fluke)

31
Q

Which CAV subtype can give rise to hepatitis?

A

CAV-1

32
Q

Histologic findings that indicate primary vs. secondary copper accumulation

A

Primary:

  • Centrilobular (near the central vein)
  • Can be found both in damaged and non-damaged areas

Secondary:

  • Periportal (zone 1) accumulation
  • Accumulation only in damaged areas
33
Q

Liver architechtur eand histopathology

A

Lobule consists of:

  1. Portal triads
  2. Liver sinudoids, arranged in sheets around the;
  3. Central vein

The limiting plate is the are surrounding the lobules (I think).

Liver Zones - this is based on the acinum model.

The periportal have the most oxygen rich blood and are also exposed to the most toxic blood. The zone 3 hepatocytes are most at risk of hypoxic injury.

  1. Closest to the portal triad (periportal)
  2. Intermediate
  3. Closest to the central vein (perivenular)
34
Q

How do cats get liver fluke?

A

Eating the paratenic hosts = lizardsm terrestrial snails, isopods.

35
Q

Deficiencies in which amino acids are thought to contribute to hepatic lipidosis in cats?

A

Carinitine and taurine

36
Q

Why does protein deficiency and negative nitrogen balance predispose to feline hepatic lipidosis?

A

It means there is less ability to produce apolipoproteins which allow the liver to export fat via vLDLs

37
Q

What is the main defining histopathologic feature of chronic hepatitis?

A

Fibrosis

38
Q

What is meant by lobar dissecting hepatitis?

A

It is characterised by fibrotic dissection of the lobules, a particularly severe form of chronic hepatitis.

39
Q

What histopathologic feature on a hepatic biopsy should prompt a hunt for infectious aietiologies?

Bonus = the infectious agents that seem more likely in CH

A

Granulomatous or pyogranulomatous inflammation

Better evidence for leptospirosis and leishmania. Viral has no evidence.

40
Q

Which (4) drugs have strongly been associated with chronic hepatitis?

A

Phenobarbital
Primidone
Phenytoin
Lomustine

41
Q

Which breeds have a predilaection to copper associated hepatitis - include known genetic association?

A

Bedlington terrrier (Autosomal recessive deletion at exon 3 of the ATP7B associated protein COMMD1)
Labrador retriever (ATP7B and 7A have been implicated)
Dalmation
Doberman
WHWT

42
Q

What are the main diagnostic criteria for Copper associated hepatitis (histologic)?

A
  1. Centrilobular (zone 3; around the central venin) copper accumulation.
  2. Quantitative copper of >1000ug/g dry weight.
43
Q

What type of immune response is characterised by human immune mediated liver disease?

A

T-cell

44
Q

What is the screening criteria for chronic hepatitis outlined in the 2017 ACVIM consensus statement?

A

Elevated ALT for > 2months with no other cause identified.

45
Q

What portal blood flow changes suggest portal hypertension?

A

Portal blood flow <10m/s

Hepatofugal flow (portal flow from peripheral to central)

46
Q

What is the approximate risk of bleeding following liver biopsy?

A

1.2-3.3%

47
Q

What is the minimum number of liver biopsy specimens according to the ACVIM 2017 consensus?

A

5 biopsies across 2 lobes:

  • 3 for histopath
  • 1 for anarobic and anaerobic culture
  • 1 for copper quantification
48
Q

Minimum number of portal triads required to make an acurate histologic diagnosis in liver speciment

A

12-15

49
Q

How much liver is required for copper quantification by atomic absorption spectroscopy?

A

20-40ug wet weight. This corresponds to:

  • 1 14G TruCut (2cm length)
    1/2 of a 5mm biopsy cup
50
Q

Reccomended monitoring for patients post liver biopsy

A

q2h PCV, vital signs until 6h post-procedure

51
Q

Main things to include in histopathologic evaluation of the liver

Bonus = other useful stains

A
  1. Inflammation: type and extent: H & E stain
  2. Copper accumulation: rhonadine or rubeanic acid
  3. Assessemnt of fibrosis: picrosirius red or masson’s trichrome

Others:
Reticulin = gordon and sweet

Iron = Perles

Lipofuscin = Schmorl’s

PAS = glycogen
Oil Red O = lipid
Halls = Bile
Others for organisms

52
Q

Recc. treatment for copper hepatitis

a) Short term
b) Long term

A

a) Cu restriction and D-penicillamine (may be required for 6-9 months)
b) Cu restriction +/- zinc +/- D-pen

53
Q

Strongest poor prognostic indicators for chronic hepatitis

A

Hyperbilirubinaemia
Increased PT/aPTT
Hypoalbuminaemia
Ascites
Degree of fibrosis on biopsy

ACVIM Generals Revision MS (32 decks)

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