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GI2 > Smallies 5 - Liver > Flashcards

Smallies 5 - Liver Flashcards

1
Q

Briefly discuss the structure of the classical liver lobule

A

Hepatocytes are organized in radial cords forming a six-sided polyhedral prism with portal triads at each of the corners and a single central vein

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2
Q

What is defined as the functional unit of the liver?

A

Hepatic acinus

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3
Q

What is the significance of zones 1,2&3?

A

Blood flows from portal triad to central vein (zone 1 to zone 3)
Bile is made by zone 3 cells and flows in the opposite direction to blood
Hypoxic damage primarily affects zone 3
Metabolic & toxic damage primarily affects zone 1

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4
Q

What are the liver’s coping strategies in the face of disease?

A

Massive structural and functional reserve
- Clinical signs not seen until >70% of functional liver mass lost  liver failure
- Signs seen earlier in acute disease because less time for adaptation by surviving hepatocytes
Significant capacity to regenerate – up to a point

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5
Q

What are the functions of the liver?

A

•Crucial role in many metabolic processes
•Digestion/metabolism/storage of nutrients including
o Fat/triglycerides – liver is really important in fat digestion
o Protein
o Carbohydrate/glyocgen
o Cholesterol
o Vitamins and minerals
•Waste management e.g. NH3, bilirubin etc
•Immunoregulation especially Kupfer cells, IgA
•Protein metabolism including albumin synthesis
•Production and activation of coagulation factors and blood proteins
•Drug metabolism/detoxification – consideration when giving drugs to animals with liver disease

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6
Q

What is more common in dogs - primary or secondary liver disease?

A

Secondary liver disease

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7
Q

Why do we need to identify if liver disease is primary or secondary?

A

To help with investigations of the underlying cause and for deciding treatment plans

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8
Q

List common causes of secondary hepatopathies?

A

•GI disease
•Pancreatitis – especially in cats
•Endocrine disease
o Hyperadrenocorticism (very rare in cats)
o Diabetes mellitus
o Hypothyroidism (dogs)/hyperthyroidism (cats)
•Right-sided congestive heart failure
•Hypoxia e.g. secondary to shock, anaemia – anything that causes hypoxia will have a detrimental effect on the liver (all of the metabolic processes in the liver are very energy/oxygen dependent)
•Toxaemia
•Sepsis/bacteraemia
•Drug induced e.g steroids, phenobarbitone

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9
Q

What is the focus of treatment for secondary liver disease?

A

• If liver disease is secondary, we need to consider underlying causes of the secondary hepatopathy and tackle those. Secondary disease should resolve with management of the underlying disease

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10
Q

What are clinical signs of early primary liver disease?

A

o Minimal/not evident
o Subtle and non-specific
o Waxing and waning e.g. huge overlap with primary GI disease/IBD
o We may not see much until >70% loss of liver function

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11
Q

List non-specific signs of liver disease

A 
Depression/lethargy
Anorexia
Weight loss
Vomiting/diarrhoea
PU/PD
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12
Q

List clinical signs that are suggestive of liver disease

A 
Jaundice
Hepatic encephalopathy
Ascites
Drug intolerance
Coagulopathy
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13
Q

How can portal hypertension lead to vomiting and diarrhoea?

A

Leads to vascular stasis and venous congestion –> adverse effect on GI tract
Increases the risk of GI ulceration

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14
Q

What are the mechanisms of ascites?

A

o Portal hypertension – increased portal flow and increased resistance to flow e.g. cirrhotic liver (Fluid will be a modified transudate)
o Hypoalbuminaemia - has to be significantly low e.g. < approximately 15g/l (Fluid will be pure transudate – rarer as the liver can often just make enough protein)
o Dogs with ascites and mild hypoalbuminaemia: the low albumin alone will not be the cause of the ascites

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15
Q

What are neurological signs of hepatic encephalopathy?

A

o Waxing and waning, non-localising on neuro exam
o May be associated with feeding – may be comatosed after a meal (some owners don’t recognise this in puppies because they think this is normal, so a cPSS may not be diagnosed quickly)
o Hyperactive and/or depressed/dull/clumsy
o Circling, pacing, central blindness, salivation (especially cats)
o Seizures –> coma

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16
Q

What normally happens to ammonia and other encephalopathic toxins originating from the GIT?

A

They are normally detoxified in the liver

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17
Q

Why might liver detoxification fail?

A

o Congenital portosystemic shunts (cPSS) - Toxins bypass the processing plant of the liver
o Fulminant acute liver disease - Detoxification processes in the liver are compromised and overwhelmed
o Acquired portosystemic shunts - Chronic fibrotic/cirrhotic liver disease shuts down normal HPV supply

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18
Q

How might the drug Cimetidine influence metabolism of other drugs?

A

Cimetidine binds cytochrome P450 which decreases oxidative metabolism of other drugs by the liver leading to increased plasma levels (E.g. propranolol, metronidazole, phenobarbitone)

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19
Q

How might the drug Phenobarbitone influence metabolism of other drugs?

A

Phenobarbitone can enhance the metabolism of some drugs i.e. decreased effect (E.g. corticosteroids, metronidazole)

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20
Q

Which drugs are directly hepatotoxic?

A

Potentiated sulphonamides
Azathioprine
Take care with paracetamol and diazepam in cats

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21
Q

If you see jaundice what is the first thing you need to establish?

A

Immediately try to work out if it is pre, hepatic or post

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22
Q

What are possible causes of pre-hepatic jaundice?

A

Due to haemolytic anaemia (always associated with significant anaemia)
Bilirubin production exceeds liver’s capacity to excrete it

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23
Q

What are possible causes of hepatic jaundice?

A

Decreased uptake, conjugation and excretion of bilirubin

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24
Q

What are causes of post-hepatic jaundice?

A

Obstruction of the biliary tree or common bile duct e.g. pancreatitis, cholelith, duodenal mass etc
Prevention of excretion via faeces

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25
Q

In which species may you see cutaneous signs associated with liver disease?

A

Horses
Cattle
Sheep
Dogs - rare

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26
Q

How can liver disease lead to photosensitisation?

A

o Compromised liver function results in phylloerythrin production (a photodynamic metabolite of chlorophyll) which enters the skin
o Phylloerythrin in the skin reacts with UV light releasing energy -> inflammation and skin damage

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27
Q

What is the pathophysiology of hepatocutaneous syndrome?

A

Similar to Zn deficiency on histopathology

Malnutrition of the skin due to abnormally low circulating amino acids

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28
Q

What will a dog with hepatocutaneous syndrome?

A

Usually dogs present due to skin disease rather than liver disease
o Erythema, crusting and hyperkeratosis
o Affects footpads (painful), nose, periorbital, perianal and genital regions
o Sometimes noticed on pressure points – often worse at these points
o Often associated with secondary infection
Presents as a really difficult pyoderma case that doesn’t completely respond to antibiotics

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29
Q

What are the liver findings with a case of hepatocutaneous syndrome?

A

Characteristic ‘swiss cheese liver’ on ultrasound - distinctive appearance
Biopsy of liver will show macronodular cirrhosis

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30
Q

What is the standard diagnostic path in the investigation of liver disease?

A

Blood tests/clinical pathology
o Measurement of liver enzymes expresses liver enzyme activity
Diagnostic imaging e.g. radiography or ultrasound
Biopsy

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31
Q

What do we have as markers of hepatobiliary disease?

A

Enzyme activities

Serial evaluation of liver enzymes to look at trends often give the best method of assessment

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32
Q

What are the downsides of using enzyme activities as markers of hepatobiliary disease?

A

They are not specific for primary liver disease
The magnitude of elevation may reflect degree of damage but is not prognostic due to regenerative capacity of the liver
In end stage disease, liver enzymes may be within the reference range due to the decreased liver mass leading to a decreased number of cellular enzymes available

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33
Q

What are markers of hepatocellular injury on biochemistry

A

ALT
AST
GLDH

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34
Q

What are markers of cholestasis on biochemistry?

A

ALP

GGT

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35
Q

What are specific markers of liver function?

A

bilirubin
bile acids
ammonia

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36
Q

What are non-specific markers of liver function?

A 
albumin
urea
glucose
cholesterol
coagulation factors
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37
Q

Which species are changes in GLDH important in?

A

Horses

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38
Q

Why are ALT, AST and GLDH markers of hepatocellular injury?

A

Cell necrosis or changes in membrane permeability cause enzyme leakage

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39
Q

With end stage liver disease what do the levels of ALT look like?

A

Levels can be normal or only a small increase

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40
Q

With liver regeneration what happens to ALT levels?

A

Increased

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41
Q

What are important species differences we should consider when interpreting ALT?

A

Cats: small increases are always significant because of a low reference range and a short t ½ in circulation
Horses: limited use

42
Q

Which is more liver specific and why - ALT or AST?

A

ALT is more specific - there are small amounts in red cells, heart and skeletal muscle but these do not cause a significant increase in clinical disease
AST is also found in muscle (skeletal and cardiac)

43
Q

What other biochemistry reading can we use to work out if changes in AST are more likely to be related to liver pathology than muscle pathology?

A

CK
Muscle inflammation causes increased AST with no increase in ALT, but CK may also be elevated in muscle inflammation
Increased AST with normal CK, is more likely to be liver disease

44
Q

What are two cholestatic enzymes that can be measured on biochemistry?

A

ALP

GGT

45
Q

Where are ALP and GGT found?

A

Found on bile canalicular membrane

46
Q

What leads to an increase in cholestatic enzymes?

A

Impaired bile flow leads to increased synthesis and release of enzymes

47
Q

Why is there a time lag between impaired bile flow and an increase in ALP/GGT?

A

The enzymes need to be made before they are released into the blood stream

48
Q

Which is the last enzymes to be normalised after acute liver insult?

A

ALP

49
Q

What are important species differences we should consider when interpreting ALP?

A

Long t ½ in dogs (66 hrs) vs. 6 hours in cats
Dogs ALP increase is more marked and prolonged vs. cats
In cats, small increases are always significant due to short half life
T 1/2 in horses and LA unclear

50
Q

What else (non-hepatic) can cause an increase in ALP?

A

Drug induction in dogs e.g. corticosteroids
Secondary reactive hepatopathies e.g. hyperthyroidism
Bone lesions/young animals (bone isoenzyme of ALP)

51
Q

Why is GGT more specific than ALP as a marker of cholestasis?

A

No increase with bone lesions
Located lower down biliary tree, further from the liver - less affected by primary hepatocellular damage so is more likely to increase with biliary disease rather than liver disease

52
Q

What are important species differences we should consider when interpreting GGT?

A

Cats: more sensitive but less specific indicator of cholestasis than ALP. “Picks up” more cases (few false negatives) but gives more false positives
Most horses with significant liver disease have increased GGT. A marked increase in GGT gives a poor prognosis

53
Q

What are measurable markers of protein metabolism?

A

Plasma proteins
Urea
Clotting factors
Ammonia

54
Q

Where are plasma proteins synthesised?

A

Albumin and all the globulins except gamma globulins are synthesised exclusively in the liver

55
Q

When is hypoalbuminaemia related to hepatic disease?

A

Hypoalbuminaemia due to reduced hepatic function is only seen when the liver loses more than 70% of its function

56
Q

Which hepatic diseases is low urea most commonly seen with?

A

cPSS

End stage liver disease

57
Q

Why is urea a marker of protein metabolism?

A

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

58
Q

Why does urea have a low sensitivity and specificity in regards to being a marker of protein metabolism?

A

Influenced by many extrahepatic variables e.g. hydration status, recent meal (increases after high protein meal), GI bleeding

59
Q

Which clotting factors does the liver make?

A

All clotting factors except FVIII and vWF

60
Q

Which clotting factors are activated in the liver?

A

The liver is the site of activation of vitamin-K dependent clotting factors (II, VII, IX, X, protein C)

61
Q

What does decreased production of clotting factors in chronic end-stage liver disease lead to?

A

Prolonged clotting times (APTT and OSPT (PT))
Risk of spontaneous bleeding
Complications in liver biopsy

62
Q

Is ammonia a good marker of liver function?

A

It is an insensitive marker of liver function because massive functional reserve

63
Q

What happens in icterus?

A

It results from retention of bilirubin in soft tissues

64
Q

What are bile acids formed from?

A

Cholesterol

65
Q

How can you use bile acids as an assessment of liver function?

A

Can take fasting and/or post-prandial (2 hrs) bile acids to assess some liver function

66
Q

When might you see increased bile acids?

A

Hepatic dysfunction
Cholestasis (not worthwhie when bilirubin already increased)
PSS

67
Q

What RBC morphology changes might you see with chronic hepatitis and why?

A

Acanthocytes and target cells

Due to alteration in membrane phospholipids

68
Q

What might happen to USG with liver disease and why?

A

Often decreased due to various mechanisms causing PUPD

69
Q

How will you interpret bilirubinuria in a cat compared to a dog?

A

Normal to find some bilirubin in dogs’ urine but can be increased
Always abnormal in cat’s urine – investigate further if you see bilirubin in the urine and slight changes on liver enzymes on blood results, patient probably has liver disease

70
Q

What might you see in a sediment analysis with a patient with liver disease?

A

Ammonium biurate crystals

71
Q

Describe the normal appearance of the liver on lateral radiography?

A

Contained within the costal arch
The caudal border appears angular
Stomach axis is parallel to the ribs

72
Q

What is the normal appearance of the liver on ultrasound?

A

Moderately and uniformly echoic - less echoic than spleen
Coarsely granular parenchyma
Uniform texture

73
Q

Why is biopsy important when working up a liver case?

A

Provides a definitive diagnosis
Gives an indication of prognosis – can assess level of fibrosis/cirrhosis
Enables us to select the most effective treatment

74
Q

What techniques are available for liver biopsy?

A

Ultrasound guided - tru-cut biopsy, but get really small samples and can lacerate structures accidentally e.g. biliary tree
Laparotomy - wedge biopsy
Laparoscopy - cup biopsy forceps or ligating loop techniques

75
Q

What are the advantages and disadvatages of an FNA when working up a liver disease case?

A

Disadvantages:
o Rarely provides a definitive diagnosis in many liver conditions
Advantages:
o Safe and quick procedure
o Useful for diagnosis of lipidosis, lymphoma and amyloidosis

76
Q

Why must cats have protein included in their diet?

A

In cats, hepatic gluconeogenesis relies on protein
o Protein calorie malnutrition occurs if they are fed a low protein diet
Cats rely on dietary taurine and arginine (can’t synthesis these essential amino acids)
o Arginine deficient diet  increased NH3 (i.e. compromises urea cycle)
o Taurine essential for conjugation of bile salts

77
Q

Why are portal hypertension and acquired portosystemic shunts uncommon in cats?

A

Cats rarely progress to severe fibrosis and cirrhosis

78
Q

List non-specific clinical signs of liver disease in cats

A
  • Lethargy
  • Change in appetite - Inappetance? Occasional polyphagia?
  • Weight loss - BCS often reflects duration of disease
  • Vomiting and diarrhoea
  • Polyuria and polydipsia
  • Pyrexia
79
Q

List more specific clinical signs of liver disease in cats

A
  • Jaundice
  • Ascites – inflammatory response to liver disease, different mechanism to dogs
  • Hepatomegaly
80
Q

Define cholangitis

A

Indicates biliary disease that goes on to affect the hepatic parenchyma

81
Q

What is the common signalment of acute neutrophilic (suppurative) cholangitis?

A

Young/middle aged cats

82
Q

What are the clinical signs of acute neutrophilic (suppurative) cholangitis?

A

Usually acute onset so present within a day or two of becoming unwell
Anorexia/food aversion – act keen to eat then walk away (owners perceive this as normal cat behaviour)
Vomiting/nausea
Diarrhoea
Lethargy

83
Q

What are physical exam findings of acute neutrophilic (suppurative) cholangitis?

A

Dehydration – do to it being an acute illness
Pyrexia
Jaundice – not in all cases
Abdominal discomfort

84
Q

What is the cause of acute neutrophilic (suppurative) cholangitis?

A

Ascending bacterial infection from the gut to the biliary system (via common biliary duct)
- E Coli from small intestine is the most common organism involved
- Mixed infection from other commensals is not unusual
Concurrent disease common e.g. IBD or pancreatitis

85
Q

What is the common signalment of chronic lymphocytic cholangitis?

A

Any cat of any age

Persians predisposed but breed less often seen, also seen in other more common breeds

86
Q

What are clinical signs of chronic lymphocytic cholangitis?

A

Wax and wane
Often bright and alert – won’t be pyrexic or as sick as the acute cholangitis cases
Weight loss
Appetite variable - Intermittent anorexia/lethargy, but appetite can be normal or increased

87
Q

What are physical exam findings of chronic lymphocytic cholangitis?

A

Ascites
Jaundice
Hepatomegaly

88
Q

What is the common signalment of hepatic lipidosis in cats?

A

Increased risk in obese cats but can occur in any shape or size

89
Q

What are clinical signs of hepatic lipidosis in cats?

A 
May be secondary to other illness
Weight loss
Anorexia
Vomiting/nausea/ptyalism
Diarrhoea
Lethargy -> depression/hepatic encephalopathy
90
Q

What are physical exam findings of hepatic lipidosis in cats?

A

Jaundice
Signs of hepatic encephalopathy
Evidence of coagulopathy?

91
Q

What is the cause of hepatic lipidosis in cats?

A

Any cause of sudden loss of appetite e.g. pancreatitis, IBD or cholangitis
Starvation
Excessive peripheral mobilisation of lipid

92
Q

Where are key sites to detect jaundice in cats?

A

Key sites for detecting jaundice in cats include the mucous membranes, sclera of the eye or pinna of the ear - the hard palate can also be a good place to look

93
Q

What level does bilirubinaemia have to be before jaundice is detectable on clinical exam?
And what is normal?

A

Usually >50 umol/l

Reference ranges suggest normal is <10umol/l

94
Q

What are differentials for prehepatic jaundice in cats?

A

Immune mediated: Primary IMHA or Secondary IMHA (FIV/FeLV)

Non-immune mediated: Mycoplasma hemofelis, hypophosphataemia or oxidative damage (HB anaemia, onion toxicity)

95
Q

What are differentials for hepatic jaundice in cats?

A

Inflammatory liver disease e.g. Acute neutrophilic cholangitis or Chronic lymphocytic cholangitis
Hepatic lipidosis (bilirubin can be >200 umol/l)
FIP
Lymphoma
Hepatotoxicity – Paracetamol, carbimazole/methimazole, diazepam
Amyloidosis
Sepsis – jaundice is just another part of the inflammatory response and rapid organ dysfunction
Hepatic jaundice is usually associated with intrahepatic cholestasis rather than reduced liver function

96
Q

What are differentials for post hepatic jaundice in cats?

A

Pancreatitis
Cholecystitis
Cholelithiasis - often associated with neutrophilic cholangitis and an ascending infection
Hepatobiliary mass
Duodenal mass – blocking the entry point of the common biliary duct into the duodenum
Trauma e.g. ruptured biliary tract
Extrahepatic bile duct obstruction

97
Q

What may you see on biochemistry and ultrasound with an extrahepatic bile obstruction?

A

Bilirubin often >250μmol/l

Gall bladder and common bile duct grossly distended

98
Q

List types of ascites in cats

A 
Blood
Urine
Bile
Transudate
Modified transudate
Exudate
99
Q

List differentials for weight loss and polyphagia in cats?

A 
Malabsorption/maldigestion
 o Inflammatory bowel disease, 
 o Exocrine pancreatic insufficiency
 o Intestinal lymphoma
Endocrine disorders 
 o Diabetes mellitus
 o Hyperthyroidism
Neoplasia
Lymphocytic cholangitis
100
Q

What changes are seen on haematology and biochemistry with neutrophilic cholangitis?

A

Haematology - increased neutrophils, left shift, toxic change
Increased ALT, ALP, GGT, bilirubin

GI2 (27 decks)

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