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Small Animal (Poppy) > Hepatic Disease > Flashcards

Hepatic Disease Flashcards

1
Q

What is the precursor to bilirubin?

A

Haemoglobin
(Haemoglobin > heme > biliverdin > bilirubin)

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2
Q

Where does haemoglobin metabolism occur?

A

Liver

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3
Q

Where does conjugated bilirubin go?

A

Enters biliary tree then GI tract at duodenal papilla

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4
Q

What do colonic bacteria deconjugate bilirubin into? (Give faeces and urine their colour)

A

Urobilin (wee-bilin)
Stercobilin (poo-bilin)

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5
Q

Is excess haemoglobin/heme a pre-hepatic, hepatic or post-hepatic problem?

A

Pre-hepatic

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6
Q

Pre-hepatic differentials for bilirubin excess (3)

A

Haemolytic anaemia (many causes, most important are primary immune mediated diseases and secondary immune mediated disease e.g. neoplasia)
Internal haemorrhage
Severe myolysis (myoglobin)

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7
Q

Two hepatic causes of increased bilirubin

A

Hepatic disease
Proximal biliary disease (cholangitis/cholangiohepatitis)

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8
Q

Degenerative hepatic diseases (3)

A

Amyloidosis
Lipidosis (cats)
Cirrhosis

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9
Q

Cholangitis

A

Inflammation of the intrahepatic biliary ducts

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10
Q

Cholangiohepatitis

A

When cholangitis leads to secondary inflammation of the surrounding hepatic parenchyma

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11
Q

What occurs in all post-hepatic causes of bilirubin excess?

A

Extrahepatic bile duct obstruction (EHBDO)

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12
Q

Intraluminal differentials for EHBDO (5)

A

Cholelithiasis (stones)
Gall bladder mucocele (Border Terrier)
Inspissated (thickened) bile
Gall bladder polyps
Cysts (cats)

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13
Q

Mural differentials for EHBDO

A

Inflammation (cholangitis/cholecystitis/choledochitis)
Neoplasia

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14
Q

Extramural differentials for EHBDO

A

Pancreatic disease (pancreatitis/neoplasia of pancreas head)
Duodenal disease (infectious/inflammatory/neoplastic)
Porta hepatitis stricture (local inflammation/infectious/neoplasm)

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15
Q

Should there be bile acids in the peripheral circulation?

A

No, never

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16
Q

Tests for pre-hepatic causes of jaundice

A

Haematology (look for anaemia)
Blood smear (spherocytes/autoagglutination)
Gross serum colour (red)
Infectious disease screening
History (toxins?)
Imaging (neoplasia)

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17
Q

What can cause elevations in AST other than liver damage?

A

Muscle damage (concurrent CK elevation)
(Restraining animal for venepuncture?)

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18
Q

Which are the important biochemistry measures for liver function?

A

ALT
ALP

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19
Q

How do urea values reflect hepatic dysfunction?

A

Low
(Urea is the end product of protein metabolism and ammonia production, however can drop for a number of reasons e.g. anorexia)

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20
Q

How do ammonia values reflect hepatic dysfunction?

A

High
(Labile so need point of care testing)

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21
Q

What clinical sign is caused by elevated ammonia?

A

Hepatic encephalopathy (neurological signs)

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22
Q

How does albumin reflect hepatic dysfunction?

A

Low
(Produced by liver, <15g/L there will be failure of endothelial glycocalyx and therefore oedema/ascites)

23
Q

What is a bile acid stim test used to assess?

A

Liver function
Biliary flow

Excellent test of liver function/biliary tract disease but poor at differentiating between hepatic and post hepatic jaundice

24
Q

How is a bile acid stim test done?

A

Take a sample for baseline bile acids, feed patient and take another sample

25
Q

Use of ultrasound when diagnosing hepatic dysfunction

A

Cannot make a diagnosis but it may indicate a problem

26
Q

Main risk of liver biopsy when testing for hepatic dysfunction and how to manage it

A

Risk of bleeding (the liver produces clotting factors so risk increased as patients with liver disease likely to have a coagulopathy)

Test clotting time and give fresh frozen plasma transfusion before the biopsy if there is a prolonged clotting time

27
Q

What is the cholestatic marker in biochemistry?

A

ALP

28
Q

When biochemistry shows elevated liver values how can you differentiate hepatic causes from post hepatic causes of jaundice?

A

Post-hepatic: liver function retained so liver function markers are normal (urea, albumin and clotting times)

29
Q

Test used in dogs/cats for pancreatitis (as a post-hepatic cause of jaundice)

A

cPLI/fPLI (canine/feline Pancreatic Lipase Immunoreactivity)

30
Q

Liver blood supply

A

Double blood supply:
~30% hepatic artery
~70% hepatic portal vein

31
Q

How are infectious/toxic substances drained from the GI tract to the liver?

A

Hepatic portal vein

32
Q

Functions of the liver

A

Digestion/metabolism/storage of nutrients (triglycerides, protein, glycogen, cholesterol, vitamins and minerals)
Waste management (NH3, bilirubin)
Protein metabolism (albumin synthesis)
Production and activation of clot factors
Drug metabolism
Immunoregulation (Kupffer cells)

33
Q

What percentage of liver function must be lost before there are clinical signs of chronic liver failure?

A

70%

34
Q

In acute liver disease are clinical signs seen before there is 70% loss of functional liver mass and why?

A

Yes, because there is last time for adaptation by surviving hepatocytes

35
Q

Which direction does blood flow in?

A

From portal triad to central vein (zone 1 to 3)

36
Q

Where is bile made and which direction does it flow in?

A

Made in zone 3 cells
Flows towards bile duct (opposite direction to blood flow)

37
Q

Disease in which zone causes jaundice earliest?

A

Zone 3

38
Q

Non-specific clinical signs in liver disease

A

Depression/lethargy
Anorexia
Weight loss
Vomiting/diarrhoea
PUPD

39
Q

Clinical signs suggestive of liver disease (although can occur with other disease)

A

Jaundice
Hepatic encephalopathy
Ascites
Drug intolerance
Coagulopathy

40
Q

Why do GI signs occur with liver disease?

A

Portal hypertension leads to vascular stasis and venous congestion which has an adverse effect on the GI tract
(Also increased risk of GI ulceration)

41
Q

Mechanism of ascites in liver disease (two causes)

A

Portal hypertension
Hypoalbuminaemia

42
Q

What presents in the following way:
Waxing and waning
Non-localising on neurological exam
Hyperactive and/or depressed
Circling/pacing
Central blindness
Salivation
Seizures/coma

A

Hepatic encephalopathy

43
Q

Enzymatic markers of hepatocellular injuries (3)

A

ALT/alanine aminotransferase
AST/aspartate aminotransferase
GLDH/glutamate dehydrogenase

44
Q

Where is the liver enzyme (AST) also found and how do you differentiate liver damage as the source?

A

Muscle
In muscle inflammation CK is also present in biochemistry. In liver disease ALT will be elevated

45
Q

In which species is a small increase in levels of ALT always significant

A

Cats (low reference range due to short half life in circulation)

46
Q

Enzymatic markers of cholestasis

A

ALP/alkaline phosphatase
GGT/gamma glutamyl transferase

47
Q

Difference in ALP half life between dogs and cats

A

Long in dogs (66 hours), short in cats (6 hours)

48
Q

Causes of ALP increase

A

Cholestasis
Iatrogenic (corticosteroids and anti-convulsants in dogs)
Secondary ‘reactive hepatopathies’ (hyperthyroidism and DM in cats, bone lesions and young animals as it is a bone isoenzyme of ALP)

49
Q

After hepatic insult, does ALP or ALT rise more slowly?

A

ALP (must be synthesised before release)

50
Q

Which enzyme will rise alongside ALP in cholestasis but will not increase with bone lesions?

A

GGT

51
Q

Causes of increased bile acids (3)

A

Hepatic dysfunction
Cholestasis
Portosystemic shunt

52
Q

What level of bilirubinuria is abnormal in dogs and cats?

A

Any level is abnormal in cat
++ in dog

53
Q

Is USG increased or decreased in liver disease?

A

Decreased

Small Animal (Poppy) (20 decks)

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