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SMALL ANIMAL > 9.5.4: Acute hepatobiliary disease > Flashcards

9.5.4: Acute hepatobiliary disease Flashcards

1
Q

Diseases in which zone produce jaudice earliest?

A

Zone 1
Due to local cholestasis

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2
Q

Metabolic and toxic damage primarily affects which zone?

A

1

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3
Q

Hypoxic damage primarily affects which zone?

A

3

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4
Q

Non-specific signs of liver disease

A
  • Depression/lethargy
  • Anorexia
  • Weight loss
  • Vomiting/diarrhoea
  • PUPD
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5
Q

-
More specific signs of liver disease

A
  • Jaundice
  • Hepatic encephalopathy
  • Ascites
  • Drug intolerance
  • Coagulopathy
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6
Q

Describe how liver disease can cause GI signs

A
  • These signs probably reflect the metabolic derangements in the liver
  • Sometimes due to portal hypertension
  • Portal hypertension -> leads to vascular stasis and venous congestion (not well tolerated by GIT)
  • Portal hypertension increases the risk of GI ulceration
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7
Q

Describe how liver disease leads to PUPD

A

Various reasons suggested:
* Decreased urea production -> decreased medullary solute gradient -> impaired renal concentrating mechanism -> dilute urine and compensatory
* Psychogenic component -> linked to hepatic encephalopathy
* Reduced hormone metabolism e.g. cortisol

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8
Q

Describe how liver disease leads to ascites

A
  • Portal hypertension -> increased portal flow -> increased resistance to flow e.g. in cirrhotic liver
  • Hypoalbuminaemia - albumin has to be significantly low to cause ascites
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9
Q

How low does albumin have to be to cause ascites?

A

Serum albumin <15g/l

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10
Q

Where can we localise the cause of jaundice to?

A
  • Prehepatic: bilirubin production exceeds the liver’s capacity to excrete it
  • Hepatic: decreased uptake, conjugation and excretion of bilirubin
  • Post-hepatic : obstruction of the biliary tree/prevention of excretion via faeces
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11
Q

Describe how liver disease causes neurological signs (hepatic encephalopathy)

A
  • Ammonia and other encephalopathic toxins originate in the GIT
  • Normally, they are detoxified in the liver
  • In abnormal situations, detoxification fails e.g. toxins bypass liver or the liver is overwhelmed
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12
Q

How does hepatic encephalopathy develop in congenital portosystemic shunts (cPSS)?

A

Toxins bypass the processing plant of the liver

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13
Q

How does hepatic encephalopathy develop in fulminant acute liver disease?

A

Detoxification processes in the liver are compromised and overwhelmed

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14
Q

How does hepatic encephalopathy develop in acquired portosystemic shunts?

A
  • Chronic fibrotic/cirrhotic liver disease leads to multiple tortuous anastomotic vessels opening up, diverting blood from the hepatic portal vein to bypass the liver
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15
Q

Why is PCV helpful in localising the cause of jaundice?

A
  • If jaundice is pre-hepatic, this means bilirubin is overwhelming the liver
  • Bilirubin is formed from breakdown of RBCs e.g. haemolytic anaemia
  • If PCV is normal, we can rule out pre-hepatic causes of jaundice
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16
Q

Which is more common in dogs: primary or secondary liver disease?

A

Secondary liver disease

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17
Q

What are some differentials/possible causes of secondary hepatopathies?
(i.e. what would damage the liver?)

A
  • GI disease
  • Pancreatitis
  • Endocrine disease: HAC, DM, HypoT4 (dogs), HyperT4 (cats)
  • Right-sided congestive heart failure
  • Hypoxia e.g. secondary to shock, trauma, anaemia
  • Toxaemia
  • Sepsis/bacteraemia
  • Drug-induced e.g. corticosteroids, phenobarbitone
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18
Q

True/false: if you suspect secondary liver disease, a good first step is to biopsy the liver.

A

False
* Biopsy is very invasive and if disease is secondary, it is not necessary and will not help get us to a diagnosis.
* Biopsy may show changes in the liver, but if we treat the primary cause/underlying disease, the secondary liver disease should resolve

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19
Q

True/false: liver enzymes are highly sensitive and specific marker of primary liver disease.

A

False
Liver enzymes are sensitive markers of hepatic injury, but they are not specific for primary liver disease.

20
Q

True/false: the magnitude of the elevation of liver enzymes may reflect the degree of damage to the liver.

A

True
For example, a large elevation in liver enzymes may correlate with marked damage. However, this is not prognostic, due to the regenerative capacity of the liver.

21
Q

Which liver enzymes are markers of hepatocellular injury?

A
  • ALT
  • AST
  • GLDH

These are released from hepatocytes following damage, when cell necrosis/changes in membrane permeability cause the enzymes to leak out.

22
Q

Which liver enzymes are markers of cholestasis?

A
  • ALP
  • GGT
23
Q

What are some relatively non-specific markers of liver function?

A
  • Albumin
  • Urea
  • Glucose
  • Cholesterol
  • Coagulation factors
24
Q

What are some specific markers of liver function?

A
  • Bilirubin
  • Bile acids
  • Ammonia
25
Q

What levels of ALT might you expect in end-stage liver disease?

A

In end stage liver disease, ALT may be normal or only slightly increased.

26
Q

Liver regeneration might cause levels of which enzyme to be high?

A

ALT

27
Q

True/false: AST is a highly specific liver enzyme.

A

False
AST is found in the liver, but also in skeletal and cardiac muscle.
It is found in the mitochondria, so more damage (compared to ALT) might be required before AST leaks out of cells.

28
Q

If you see elevations in AST with no change to ALT, what might this be suggestive of? There might also be elevations in CK with these cases.

A

Muscle inflammation (skeletal and cardiac muscle contain AST)

29
Q

Which enzymes are consider markers of cholestasis and why is this?

A

Enzymes = ALP and GGT
* These enzymes are found on the bile canalicular membrane and normally secreted in small amounts into bile
* Impaired bile flow leads to increased synthesis and release of these enzymes

30
Q

Which liver enzyme is usually the last to normalise after acute hepatic insult?

A

ALP

31
Q

True/false: ALP is liver specific.

A

False
ALP may increase with acute hepatic insult, but also with:
* drug administration in dogs (e.g. corticosteroids, anticonvulsants)
* secondary reactive hepatopathies (e.g. hyperT4)
* bone lesions
* in young animals.

32
Q

What are the species differences to be aware of when assessing ALP?

A
  • ALP has a long T1/2 in dogs (66hrs) but short in cats (6hrs)
  • Therefore in dogs, increases of ALP are more marked and prolonged than in cats
  • In cats, small increases in ALP are always significant
33
Q

When does GGT increase?

A
  • GGT increases in cholestasis, in parallel with ALP
34
Q

What percentage of hepatic function must be lost to generate hypoalbuminaemia?

A

Liver must lose more than 70% of function to cause hypoalbuminaemia.
i.e. there must be very bad liver disease/damage for this to be the cause of low albumin!

35
Q

How do urea levels relate to hepatic function?

A

Low urea indicates decreased ability to synthesise urea from ammonia in the hepatic urea cycle.

36
Q

True/false: urea levels are specific for hepatic disease.

A

False
Urea levels are poorly sensitive and specific for hepatic disease because they are influenced by many extrahepatic variables, e.g.:
* hydration status
* recent meal
* GI bleeding

37
Q

Which liver conditions is low urea most commonly seen with?

A
  • Congenital portosystemic shunts
  • End-stage liver disease
38
Q

The liver makes all clotting factors except…

A

Factor VIII and vWF

39
Q

Which anti-clotting factors and fibrinolytic proteins are made by the liver?

A

All of them

40
Q

Where it the site of activation for Vitamin K-dependent clotting factors?

A

The liver

41
Q

Decreased production of clotting factors (e.g. in end-stage liver disease) leads to:

A
  • Prolonged clotting times (APTT and PT)
  • Risk of spotaneous bleeding
  • Risk of complications in liver biopsy
42
Q

When might we see increased bile acids?

A
  • Hepatic dysfunction
  • Cholestasis
  • PSS
43
Q

True/false: if we have a jaundiced patient, a bile acid stim test could be undertaken to provide more info.

A

False
No point doing a bile acids stim test in this patient.

44
Q

Describe how to undertake a bile acid stim test, and what the normal and abnormal findings might be

A
  • Take blood sample, feed patient, take 2nd blood sample 2 hrs later
  • Normal = bile acids have returned to normal levels by 2hrs after feeding
  • Abnormal = bile acids remain elevated 2hrs after feeding
45
Q

How can bilirubin act as a marker of liver function and what are the limitations of this?

A
  • Bilirubin is produced from the breakdown of heme-containing compounds (hence marker of liver function)
  • However we have to rule out pre- and post-hepatic jaundice
46
Q

How does bilirubin relate to jaundice?

A

Jaundice is caused by the retention of bilirubin in soft tissues

SMALL ANIMAL (90 decks)

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