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Year 4 > SA Liver > Flashcards

SA Liver Flashcards

1
Q

When may ammonia be raised?

A

Liver failure

Congenital and acquired portosystemic shunts

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2
Q

How may urine be affected by liver disease?

A

Isosthenuria or inappropriately low USG
Bilirubinuria
Ammonium biurate crystals or uroliths

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3
Q

When investigating liver function, what can we test?

A

Hepatocellular injury
Cholestasis
Hepatocellular function
Hepatic portal circulation

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4
Q

Where are enzymes mostly found?

A

Inside cells (no function in blood)

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5
Q

How are proteases stored?

A

As inactive zymogens

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6
Q

Give 5 changes that indicate reduced hepatocellular function

A

Decreased uptake and excretion of bilirubin and bile acids
Decreased conversion of ammonia to urea
Decreased synthesis of metabolites
Decreased synthesis of coagulation proteins
Decreased immunologic function

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7
Q

Which enzymes are produced by pancreatic acinar cells?

What else do they produce?

A

Proteases (trypsin, chymotrypsin, elastase)
Lipases
Amylase

Also bicarbonate

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8
Q

Give some other functions of pancreatic enzymes

A

Proteases aid B12 absorption
Aid zinc absorption
Antibacterial activity
Intestinal mucosal modulation

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9
Q

What tests can we carry out to test exocrine pancreatic function?

A 
Enzyme assays for amylase and lipase (poor specificity)
DGGR lipase (more specific)
'Specific' canine pancreatic lipase (cPL) (more specific and sensitive than lipase and amylase) (Test available at external labs or in-house SNAP tests)
TLI (trypsin-like immunoreactivity) (not as sensitive as cPL)
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10
Q

What is the function of amylase?

Why may it be increased?

A

Catalyses hydrolysis of complex starches

Can increase due to decreased GFR

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11
Q

What is the function of lipase?

Why may it be increased?

A 
Catalyses hydrolysis of triglycerides 
Can increase (mildly) due to decreased GFR
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12
Q

When testing DGGR lipase, what are the cut-off values for diagnosis of pancreatitis?

A

> 34 U/L in cats

>216 U/L in dogs

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13
Q

After finding an elevation in lipase, what tests would you carry out to confirm a diagnosis of pancreatitis?

A

PLI (specific pancreatic lipase)
Imaging (ultrasound)
Biopsy
Fluid analysis

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14
Q

When would you test for TLI (trypsin-like immunoreactivity)?

A

In animals with clinical signs of maldigestion/malabsorption
High sensitivity/specificity for exocrine pancreatic insufficiency
Less useful for pancreatitis

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15
Q

What does a TLI test detect?

A

Trypsin, trypsinogen, and trypsin bound to protease inhibitors (most TLI in blood is trypsinogen, do not want free trypsin in the blood)

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16
Q

What value of cPL (specific canine pancreatic lipase) indicates pancreatitis?

A

> 400ug/L

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17
Q

Which cells are present in the pancreas?

A 
PP cells (produce pancreatic polypeptides)
B cells (produce insulin)
Delta cells (produce somatostatin)
Alpha cells (produce glucagon)
Acinar cells (produce digestive enzymes)
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18
Q

What can we test to investigate liver function?

A

Hepatocellular injury (damage to hepatocytes -> leakage of enzymes)
Cholestasis (reduced/blocked bile excretion -> release of enzymes induced by retained bile)
Hepatocellular function (decreased production/catabolism of substances)
Hepatic portal circulation (decreased extraction of substances absorbed from the GI)

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19
Q

In which case may increased AST be artefactual?

A

Leakage from RBCs

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20
Q

Which are the liver ‘leakage’ enzymes?

A

ALT (largely liver-specific but also muscle. SA)
AST and LDH (both liver and muscle)
SDH and GLDH (liver specific in all species. Used in LA)

ALP and GGT are indicative of liver damage in horses and ruminants

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21
Q

What is cholestasis?

A

Decreased bile flow and excretion

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22
Q

What are the 3 kinds of cholestasis?

A

Intrahepatic (due to hepatocellular swelling)
Extrahepatic (due to bile duct obstruction)
Functional (nothing mechanically abnormal)

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23
Q

What can you use as markers for cholestasis?

A

Bilirubin
Bile acids (more sensitive)
Cholesterol
ALP and GGT (cholestatic enzymes; GGT is more specific)

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24
Q

What are the 2 major isoforms of ALP?

A

Liver-ALP (L-ALP)

Bone-ALP (B-ALP)

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25
Q

C-ALP is induced by what?

In which species?

A

Corticosteroids

Dogs

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26
Q

Where is haem broken down to bilirubin?

A

Macrophages

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27
Q

What is bilirubin conjugated with in the liver?

A

Glucoronic acid

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28
Q

What are the 3 types of hyperbilirubinaemia?

A

Pre-hepatic: secondary to haemolysis of RBCs
Hepatic: due to decreased bilirubin uptake, conjugation, and excretion. Often due to concurrent hepatocyte dysfunction and intra-hepatic cholestasis
Post-hepatic: Secondary to obstruction of extra-hepatic bile duct

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29
Q

Does conjugated or unconjugated bilirubin predominate with pre-hepatic bilirubinaemia?

A

Unconjugated at first, then an increasing proprotion of conjugated as time passes
Also, some degree of cholestasis

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30
Q

Does conjugated or unconjugated bilirubin predominate with post-hepatic bilirubinaemia?

A

Conjugated

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31
Q

Why may jaundice persist long after liver function has returned to normal?

A

Due to delta-bilirubin, bound to albumin

Will be no bilirubinuria

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32
Q

Give some functions of the liver

A

Removal of bacteria
Produces clotting factors
Storage of glycogen, iron, copper and vitamins
Detoxification of body wastes, drugs, and xenobiotics
Synthesis of cholesterol and bile acids
Synthesis of plasma proteins
Breakdown of RBCs
Carbohydrate, lipid and amino acid metabolism

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33
Q

What produces bile acids?

A

Hepatocytes

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34
Q

Describe the route of bile acids

A

Produced by hepatocytes
Released into biliary system then intestine
Over 90% are reabsorbed from the ileum, enter portal vein, return to liver, recirculated
Small amount lost in faeces; replaced by liver

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35
Q

Why may bile acids be increased?

A

Reduced uptake/excretion by hepatocytes (reduced hepatocyte mass/function)
Disruption of enterohepatic circulation (portosystemic shunts, cholestasis)

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36
Q

Which value for bile acid concentration indicates increased production and hepatobiliary pathology?

A

Values >25-30 mmol/L

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37
Q

How can you test for post-prandial SBA?

A 
(Post-prandial serum bile acids)
Take resting sample
Fatty meal
Post-prandial sample 2 hours after feeding
If >25-30 mmol/L -> abnormal
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38
Q

What is meant by a ‘reactive hepatopathy’?

A

Many extrahepatic diseases cause elevation in liver enzymes

eg hypoxia, GI and pancreatic disease, sepsis

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39
Q

What haematology may we see in liver disease?

A

Often unremarkable but we may see:
Acanthocytes
Microcytosis
Ovalocytes (cats with hepatic lipidosis)

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40
Q

What are the 3 cholestatic markers?

A

Bilirubin, GGT, ALP

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41
Q

What must you always do before taking a liver biopsy?

A

Check clotting profile

Liver makes clotting factors-impaired liver function may result in reduced clotting factors

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42
Q

Where does the liver get its blood supply?

A 
Hepatic portal vein (70-80%)
Hepatic artery (20-30%)
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43
Q

What are the 3 major types of icterus

A

Pre-hepatic (haemolysis)
Hepatic (hepatocyte dysfunction, intrahepatic cholestasis)
Post-hepatic (extra-hepatic cholestasis)

44
Q

Give some clinical signs of metabolic dysfunction

A

Non-specific signs (loss of condition, weight loss)
Hypoglycaemia (can cause seizures/collapse)
Hypoalbuminaemia (only in chronic disease; can contribute to ascites)

45
Q

What do copper-coloured irises indicate in cats?

A

Portosystemic shunt

46
Q

Give some circulatory disturbances caused by liver disease

A

Ascites
PUPD
Portosystemic shunts

47
Q

How do hepatic encephalopathies occur?

A

Liver is unable to turn NH3 into urea (decreased functional liver mass and/or portosystemic shunt)
Increased blood NH3 (plus other toxins)
Leads to altered CNS function

48
Q

Give some CNS signs seen with hepatic encephalopathies

A

Anorexia, vomiting and diarrhoea, PUPD

Dullness, aggression, staggering, blindness, head-pressing, seizures

49
Q

When are hepatic encephalopathies worse?

A

After a high protein meal
GI bleed
Dehydration, acid-base imbalance

50
Q

Why is bleeding seen with liver disease?

A

Defective production and storage of clotting factors
Vitamin K malabsorption
Portal hypertension -> GI bleeding

51
Q

Give some clinical signs of a portosystemic shunt

A 
Ascites
Stunted growth (if young)
Vomiting and diarrhoea
PUPD
Non-specific signs (anorexia, weight loss, weakness, poor coat and skin condition)
52
Q

How can we classify hepatopathies?

A

Primary (inflammatory or non-inflammatory)

Secondary

53
Q

Give some causes of reactive hepatopathies

A 
IBD
Bacterial infections
Periodontal disease (can cause bacteraemia)
Riskettsial infections
Acute pancreatitis 
Diabetes mellitus
Hyper/hypoadrenocorticism
R-HF
Hyperthyroidism 
Septicaemia
54
Q

Give some bacterial causes of an inflammatory, infectious hepatopathy

A 
Leptospirois
Bacterial cholangiohepatitis (ascending infection from intestines)
55
Q

Give some viral causes of an inflammatory, infectious hepatopathy

A

Infectious canine hepatitis
Canine herpes virus
FIP

56
Q

Give a protozoal cause of an inflammatory, infectious hepatopathy

A

Toxoplasma

57
Q

Give some causes of an inflammatory, non-infectious hepatopathy

A

Toxic hepatic disease
Drug-induced hepatic disease
All forms of chronic hepatitis (canine chronic hepatitis, feline lymphocytic cholangitis)

58
Q

Give some causes of a non-inflammatory hepatopathy

A 
Congenital portosystemic shunt
Juvenile hepatic fibrosis
Feline hepatic lipidosis (rare)
Neoplasia
Telangiectasia (permanent dilation of blood vessels) and peliosis (blood-filled cavities throughout liver) -> fragile liver
Surgical: trauma, liver lobe torsion
Amyloidosis
59
Q

Which enzyme are cats deficient in which makes them more sensitive to certain toxins/drugs?

A

Glucuronyl transferase (results in difficulty conjugating toxins)

60
Q

How does paracetamol toxicity occur in cats?

A

Deficient in glucuronyl transferase therefore deficiency of glucuronidation
Results in methaemoglobinaemia -> haemolytic anaemia, facial oedema, hepatocellular damage (liver failure and icterus)

61
Q

What is the treatment for paracetamol poisoning in cats?

A

N-acetlycysteine
S-adenosyl methionine
Vitamin C
Supportive care: ABs, IV fluids, activated charcoal if recent ingestion

62
Q

Give some differentials for icterus in cats, starting with the most common (*)

A

*Cholangitis complex
*FIP (dry form)
*Lymphoma
*Lipidosis
*Pancreatitis
Cirrhosis
Neoplasia
Toxoplasmosis
Haemolytic anaemia
Toxic hepatopathy
Panleucopenia
Biliary obstruction/ bile duct rupture

63
Q

What will you see first- an increase in serum bilirubin or visible icterus?

A

Increase in serum bilirubin

64
Q

What is microhepatica a sign of?

A

Portosystemic shunt

65
Q

What should you always do before taking a liver biopsy?

A

Coagulation tests/check clotting profile

66
Q

What do liver enzyme tests tell you?

A

If liver is affected by something, NOT if its function is impaired

67
Q

Which liver enzymes can you test?

A

Hepatocellular markers: ALT, AST

Cholestatic markers: ALP, GGT

68
Q

Which liver function tests can you do?

A 
Bile acids (most sensitive)
Serum proteins (esp. albumin)
Glucose, urea, cholesterol (produced in liver)
Bilirubin
Ammonia
69
Q

What do you see first with chronic hepatitis: altered lab results or clinical signs?

A

Altered lab results

70
Q

When might you typically do a portovenogram?

A

Looking for a portosystemic shunt

71
Q

What can you look at on a radiograph to give you an idea of liver size?

A

Position of gastric axis

72
Q

What is the best way to diagnose most liver conditions?

A

Liver biopsy

73
Q

Give some indications for a liver biopsy

A

Persistent increase in liver enzymes
Altered liver size
Monitoring progressive liver disease
To evaluate response to treatment

74
Q

How can you perform a liver biopsy?

A

Percutaneous (blind; US-guided with ‘Tru-cut’)
Laparoscopy
Coeliotomy

75
Q

Give some contraindications for doing a percutaneous liver biopsy

A 
Lack of operator experience
Small liver (unless US-guided)
Focal disease (easy to miss)
Extrahepatic cholestasis
Bleeding disorder
Severe anaemia
76
Q

Which dog breeds are more prone to juvenile hepatic fibrosis?

A

GSD, Rottweiler

77
Q

Describe the pathology of juvenile hepatic fibrosis

A
  • Progressive fibrosis
  • Minimal inflammatory reaction
  • Central vein fibrosis and occlusion most common
78
Q

How do acquired shunts occur?

A

Secondary to liver disease (juvenile hepatic fibrosis, cirrhosis)

79
Q

Where do acquired shunts develop?

A

From redundant vessels (between portal vein and caudal vena cava)

80
Q

Which clinical sign is often seen with acquired portosystemic shunts but rarely congenital?

A

Ascites

81
Q

What is the most common canine chronic liver disease?

A

Canine chronic hepatitis

82
Q

Give some types of canine chronic hepatitis

What may they all lead to?

A

-Idiopathic chronic hepatitis
-Lobular dissecting hepatitis
-Drug-induced chronic hepatitis
-Copper-associated hepatitis
May all lead to cirrhosis

83
Q

Which 3 factors may lead to a shorter survival time for canine chronic hepatitis?

A

Hypoalbuminaemia
Severe necrosis and fibrosis in biopsy
Bridging fibrosis

84
Q

What is cirrhosis?

A

Shrunken liver from fibrosis (micro/macro-nodular regeneration)
End-stage of many diseases

85
Q

Which breeds are more affected by hepatic portal hypoplasia?

A

Small terrier breeds

86
Q

What makes up feline cholangitis complex?

A
  • Suppurative cholangitis (neutrophils)
  • Lymphocytic cholangitis (lymphyocytes and plasma cells; indicates immune-mediated)
  • (Sclerosing cholangitis- end stage of others)
  • Can get both in combination with IBD and pancreatitis
87
Q

What does idiopathic hepatic lipidosis lead to?

A

Biliary stasis
Liver failure
Anorexia
Death

88
Q

Give some examples of primary liver tumours

A 
Hepatocellular carcinoma
Hepatoma
Cholangiocarcinoma
Fibroma/sarcoma
Haemangioma/haemangiosaecoma
89
Q

How do you treat hepatic encephalopathy?

A

Low protein diet
Lactulose
ABs (ampicillin or metronidazole)

90
Q

How do you treat chronic active inflammation of the liver?

A

Glucocorticoids

Diet: low copper, high zinc, high protein quality, anti-oxidants. Taurine and L-carnitine for cats

91
Q

Which liver conditions can you treat with glucocorticoids?

A

Chronic active inflammation

Hepatic fibrosis

92
Q

Which dog breeds are affected by copper-associated hepatopathies?

A 
WHWT
Skye and Bedlington terrier
Labrador
Dalmation
Doberman
93
Q

Which agents are ‘de-coppering agents’?

A

Copper chelators: D-penicillamine, Trientine (222-tetramine)

Copper absorption blocker: oral zinc

94
Q

What is UDCA?

A

Ursodeoxycholic acid

Alters bile composition and stimulates bile flow (CI if complete biliary obstruction)

95
Q

What is SAMe?

A

S-Adenosyl methionine

Precursor for GSH production (molecule central to hepatic metabolism and detoxification)

96
Q

How do you treat bacterial cholangiohepatitis?

A

Do culture and sensitivity and give appropriate ABs

97
Q

How do you treat an immune-mediated process in the liver?

A

Prednisolone +/- azathioprine

98
Q

How do you treat liver fibrosis?

A

Prednisolone +/- alter the diet/ give UDCA (modulates immune response)

99
Q

How do you treat copper accumulation?

A

Penicillamine, trientine, zinc

100
Q

Give some complications of liver disease

A

Hepatic encephalopathy and coma
Ascites and oedema
Haemorrhage and anaemia

101
Q

How can we treat ascites and oedema caused by liver disease?

A

Low sodium diet
Diuretics (spironolactone)
Paracentesis (only drain a minimal volume, as can worsen bodywide protein status)

102
Q

Which two liver leakage enzymes indicate hepatocellular damage?

A

ALT (largely liver-specific)

AST (not liver-specific; also to muscle)

103
Q

How would you identify cholestasis on cytology?

A

Presence of dark green-black granular pigment between hepatocytes

104
Q

What in unconjugated bilirubin bound to in the blood?

A

Albumin

105
Q

Which haematology changes might you see with liver disease?

A

Microcytosis (PPS or severe liver insufficiency, likely due to altered iron transport/metabolism)
Ovalocytes/elliptocytes (cats with hepatic lipidosis)
Acanthocytes (spiked cell membrane; lipid disorders, disruption of normal vasculature)

106
Q

What may you see on a urinalysis of a pet with liver disease?

A

Isosthenuria or low SG
Bilirubinuria (>2 in dogs, any in cats)
Ammonium biurate crystals or uroliths (40-70% of patients with PSS)

Year 4 (51 decks)

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