Liver Disease Lab Dx Flashcards

1
Q

What 3 substances can be used to evaluate the liver?

A
  • Enzymes
  • Metabolites
  • Function tests
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2
Q

Give 4 enzymes which indicate hepatocellular damage. Why are they seen in association with hepatocellular damage?

A
  • ALT
  • AST
  • SDH
  • GLDH
    > leak directly from cells when hypoxia/oxidants/mitochondrial toxins -> ATP depletion -> membrane “blebbing” and production of blebosomes or necrosis of the cell
    > levels increase rapidly with cell damage as substances already produced and contained in cells
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3
Q

Which is the most common enzyme looked at in cats and dogs? When will levels rise/fall? Is it liver specific?

A

ALT - also found in muscle but only at v. low levels

  • ^ within 12hours injury
  • peak 1-2d
  • falls over 2-3w
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4
Q

Is the same most common enzyme analysed in large and small animals?

A

No - ALT activity in large animals is very low

  • Use SDH or GLDH
  • GLDH = liver specific but rarely available to look at in smallies
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5
Q

Which hepatocellular enzyme is found in high levels but is not liver specific? Where else is it found?

A

AST - also derived from muscle and RBCs in fairly high concentration (~= ALT)

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6
Q

Which enzyme is muscle specific? When will levels rise/fall?

A
CK (more rapid changes)
- ^ within 1-2hrs 
- Peak 6-12hrs
- Decrease over 24-48hrs 
> If persistently high indicates ongoing damage
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7
Q

Give 2 enzymes that indicate cholestasis. Where are they derived from?

A
  • ALP
  • GGT
    > derived from bile duct epithelium (amongst oher places)
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8
Q

Define cholestasis

A

Obstruction of bile flow with regurgitation of biliary substances into he blood

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9
Q

Where else is ALP found and hwo may this influence results?

A

> Bone - will be higher in young growing animals

> Steroid induced isoform in DOGS only (due to stress or dugs)

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10
Q

In which species is any increase in ALP particularly significan?

A

Cats (no steroid induced isoform, short half life)

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11
Q

What is the most common cause of ALP in cats?

A

Hyperthyroidism

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12
Q

When would “induction” related increases be seen vs “leakage”?

A

Induction eg. after steroid injection = 1 week later

Leakage = instantaneously

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13
Q

Which enzyme is a more sensitice indicator of cholestasis in large animals?

A

GGT (ALP has a v. large range)

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14
Q

Where is GGT found other than bile duct epithelium?

A
  • Colostrum -> ^ in nursing animals

- renal tubular cells -> urine if tubular damage present

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15
Q

How can differences in ALT and ALP be remembered?

A
  • alT = trauma [not related to liver FUNCTION]

- alp = production [induction]

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16
Q

Give 7 measures of hepatic FUNCTION

A
  • bilirubin
  • albumin
  • urea
  • glucose
  • cholesterol
  • ammonia
17
Q

What is the average lifespan of a red blood cell?

A

120d

18
Q

Outline the pathway of RBC breakdown

A
  • RBC breakdown
  • Hbg -> bilirubin (not water soluable
  • Albumin bound unconjugated bilirubin transported in blood -> liver, dissociates
  • Hepatocytes uptake and conjugate -> bile -> gut
  • Converted to urobiligen and stercobiligen for excretion
19
Q

How does dogs metabolism of bilirubin differ to other species?

A

Capable of excreting small amouns of unconjugated bilirubin directly from he kidneys

20
Q

Why is serum/plasma yellow?

A

Bilirubin”

21
Q

In which species does bilirubin increase dramatically with fasting?

A

Horses (fasting >24 huors)

22
Q

What effect on bilirubin levels would ^ haemolysis have a) initially? b) longterm?

A

a) ^ UNconjugated bilirubin

b) ^ conjugated aswell (due to rate limiting step being excretion -> bile)

23
Q

What is the rate limiting step of bilirubin metabolism?

A

excretion -> bile

24
Q

In which species is low level bilirubinuria found normally?

A

Dogs (canine renal tubular epithelium can conjugate bilirubin)

25
Q

In which species is bilirubinaemia always significant?

A

Cats (may be seen before ^ levels deeced in the blood)

26
Q

What are he 2 products of protein metabolism?

A

Ammonia and Urea (ammonia derived from gut, travels -> liver via poral circulation and converted to urea)

27
Q

Which system does v/^ urea in the blood/urine(?) indicate a problem in? What else may be seen with liver disease?

A

v = liver
^ = kidney
- ammonium biurate crystals in urine due to high ammonia levels

28
Q

Are glucose levels often affected by hepatic disease?

A
  • Not sensitive - decreases only with end stage liver disease
  • hypoglyceamia caused by neoplasia and bacterial sepsis
  • hyperglycaemia caused by stress and diabetes mellitits
29
Q

Is cholesterol a useful biomarker of liver function?

A

NO! Can be
- increased (cholestasis and v excretion)
- decreased (v synthesis)
- the same if both parts diseased!
> ^ with endocrine disorders (DM, Cushings)
> varies inversely with T4 (^hypothyroidism, v hyperthyroidism)

30
Q

WHy are bile acids recycled in enterohepatic recirculation?

A

High energy for production

31
Q

How is bile acid concentration used to monitor hepatic function in different species?

A
  • measure fasted
  • measure post-prandial
    > tests hepatic uptake
  • horses: measure single sample as no gall bladder
  • not often used in ruminants (range too wide)
32
Q

What 2 major pathologic processes does ^ [BA] indicate?

A
  1. v clearance from portal blood, v functional mass [ie. not being reuptaken by hepatocytes] or PSS
  2. v BA excretion via bile ( Obstructive cholestasis)
33
Q

Which parameter can be measured to evaluate hepatic function but rarely is?

A

Ammonium (NH4+) concentration [indications similar to bile acids]
- test not feasible as stability poor

34
Q

Are liver enzymes and function tests sufficient to determine the undelying cause of liver lesion?

A

No - FNA or biopsy required

35
Q

Look at lecture for other lab findings to take into account

A