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Y4 SA - Clinical pathology > Tests for hepatic and pancreatic function and integrity 1 + 2 > Flashcards

Tests for hepatic and pancreatic function and integrity 1 + 2 Flashcards

1
Q

Name 4 factors that can be tested to assess liver function/integrity

A
  • Hepatocellular injury
  • Cholestasis
  • Hepatocellular function
  • Hepatic portal circulation
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2
Q

What is hepatocellular injury?

A

Damage to hepatocytes leading to leakage of enzymes

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3
Q

How can cholestasis be used to assess liver function?

A

Reduced/blocked bile excretion
Release of enzymes induced by retained bile

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4
Q

How can hepatocellular function be used to assess liver function?

A

Decreased production or catabolism of substances

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5
Q

How can hepatic portal circulation be used to assess liver function?

A

Decreased extraction of substances absorbed from the GI

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6
Q

How are liver enzymes assessed?

A
  • Very difficult to measure in amount directly, so expressed as activity rather than concentration
  • Different localisation within the cell
  • Not usually present in blood
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7
Q

What are liver ‘leakage’ enzymes?

A

Found in the blood when the cells are damaged

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8
Q

Name and describe the liver enzymes

A
  • ALT: largely liver specific, but also from muscles. SA only.
  • AST: liver and muscle so not liver specific
  • LDH: liver and muscle so not liver specific
  • SDH: liver specific in all species. unstable
  • GLDH: liver specific in all species
  • ALP and GGT: indicative of liver damage in horses and ruminants
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9
Q

What is the significance of increased liver ‘leakage’ enzymes?

A
  • Indicative of hepatocellular damage
  • Magnitude of increase correlates with degree of hepatocellular damage but NOT with reversibility of injury, prognosis or hepatic function
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10
Q

Myocyte damage can lead to a mild increase in which liver enzymes?

A

AST, LDH +/- ALT

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11
Q

How can myocyte damage be differentiated from liver damage?

A

Check creatine kinase when liver enzymes are increased

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12
Q

Other than liver and muscles damage, why else might liver enzymes be increased?

A

Artefact (haemolysis) can increase AST and LDH

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13
Q

How can you differentiate an artefact from liver damage?

A

Check serum/plasma quality

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14
Q

Give two examples of when the increase in liver enzymes doesn’t correlate with the reversibility of injury, prognosis or hepatic function

A
  • Chronic hepatopathies
  • When there is a reduction of the overall hepatocellular mass (cirrhosis, PSS)
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15
Q

Describe the half life of liver enzymes in small animal species

A

Short half-life: days in dogs, hours in cats, thus even small increases may be significant in cats

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16
Q

Name the 2 cholestatic enzymes

A

ALP
GGT

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17
Q

Which liver enzyme has a good sensitivity for canine liver-disease, poor sensitivity for feline liver-disease?

A

ALP

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18
Q

List the components of bile

A

Bilirubin
Bile acids
Cholesterol

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19
Q

Describe the isoenzymes and isoforms of ALP

A

Two isoenzymes (intestinal and non-tissue specific)
Several isoforms (produced from post-translational modification of isoenyzmes)

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20
Q

Describe the major measurable isoforms of ALP

A

Liver-ALP (L-ALP) and bone-ALP (B-ALP)
B-ALP causes usually only mild increases
- Negative prognostic marker in osteosarcoma
- Partially responsible for the increased ALP in cats with hyperthyroidism

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21
Q

Describe C-ALP

A

Unique to dogs and is induced by corticosteroids (endogenous or exogenous).
Product of the I-ALP gene, but produced in hepatocytes

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22
Q

Describe I-ALP

A

Intestinal-ALP (I-ALP) produced by intestinal ALP gene
- Short half-life (minutes) and lost in GI tract
- Not generally detected in plasma

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23
Q

Name the three types of hyperbilirubinaemia

A

Prehepatic
Hepatic
Post-hepatic

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24
Q

Describe the cause of prehepatic hyperbilirubinaemia

A

Secondary to haemolysis
Check for anaemia!

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25
Q

Describe the causes of hepatic hyperbilirubinaemia

A

Can be due to decreased bilirubin uptake, conjugation, and excretion (so hepatocyte dysfunction and intrahepatic cholestasis)
- Viral hepatitis
- Drugs
- Cirrhosis
- Tumours

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26
Q

Describe the cause of post-hepatic hyperbilirubinaemia

A

Secondary to obstruction of the extrahepatic bile duct.
- Gallstones
- Cancer of the bile duct

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27
Q

How is post-hepatic hyperbilirubinaemia diagnosed?

A
  • Often cholestatic enzymes (ALP and GGT) much higher than leakage enzymes (ALT and AST)
  • Serum cholesterol often high
  • Ultrasound very helpful
28
Q

Describe measuring bilirubin levels

A

Total and conjugated can be measured directly

29
Q

Conjugated bilirubin is also called ..?

A

Direct bilirubin

30
Q

Unconjugated bilirubin is also called …?

A

Indirect bilirubin

31
Q

Determination of relative amounts of conjugated and unconjugated bile is not very useful to classify … ?

A

Hyperbilirubinaemia

32
Q

Determination of relative amounts of conjugated and unconjugated bile is not very useful to classify hyperbilirubinaemia except in?

A

Horses
fasting hyperbilirubinaemia is mostly due to unconjugated bilirubin

33
Q

What are the clinical signs of hyperbilirubinaemia?

A
  • Jaundice persists long after liver function has returned to normal due to delta-bilirubin, bound to albumin
  • If jaundice is due to delta-bilirubin, there will be no bilirubinuria
34
Q

List the functions of the liver (8)

A
  • Detoxification of body wastes and drugs
  • Synthesis of cholesterol and bile acids
  • Synthesis of plasma proteins
  • Breakdown of RBCs
  • Carbohydrate, lipid and amino acids metabolism
  • Removal of bacteria
  • Production of clotting factors
  • Storage of glycogen, iron, copper and vitamins
35
Q

List the factors that can be used to test hepatocellular function

A
  • Decreased uptake and excretion of bilirubin and bile acids increased (unconjugated) bilirubin and bile acids
  • Decreased conversion of ammonia to urea: increased ammonia, decreased urea
  • Decreased synthesis of metabolites, decreased albumin, cholesterol, coagulation factors and inhibitors, glucose
  • Decreased synthesis of coagulation proteins decreased fibrinogen, increased PT, PTT
  • Decreased immunologic function decreased clearance of toxins and antigens -> systemic stimulation -> increased immunoglobulins
36
Q

What are the consequences of altered hepatic blood flow?

A
  1. Decreased uptake and excretion of bile acids
  2. Decreased conversion of ammonia to urea
  3. Decreased immunologic function
37
Q

Describe ammonia metabolism in the body

A
  • Produced in the GIT by protein digestion or bacteria metabolism
  • Enters the liver via portal vein
  • Uptake by hepatocytes to synthesise urea, amino acids, proteins
  • Urea diffuses to sinusoidal blood or bile canaliculi and is excreted through kidneys or intestine, respectively
38
Q

When are the levels of ammonia significant?

A

When raised - hepatic encephalopathy?

39
Q

When are the levels of ammonia raised?

A

Congenital and acquired portosystemic shunts
Liver failure

40
Q

Describe bile acid metabolism in the body

A
  • Bile salts are produced by hepatocytes
  • Released into biliary system and then intestine: allow fat absorption and digestion
  • More than 90% of BAs then reabsorbed from the ileum, enter portal vein, return to liver, re-circulate
  • Small amounts lost in faeces; replaced by liver
41
Q

List the causes of increased bile acids

A
  • Reduced uptake/excretion by hepatocytes due to: reduced hepatocellular mass or impaired hepatocyte function
  • Disruption of enterohepatic circulation due to: portosystemic shunts or cholestasis/bile obstruction
42
Q

If bilirubin levels are already increased why do you not need to measure bile acid levels?

A

Bile acid test if more sensitive than bilirubin

43
Q

Describe how you would interpret fasting serum bile acid results

A
  • Values > 25-30 mmol/L are abnormal and indicate hepatobiliary pathology: many underlying causes possible and cannot differentiate between cholestasis and liver failure
  • Values < 25-30 mmol/L: cannot completely exclude portosystemic shunt, perform a bile acid stimulation test (BAST) if still suspecting hepatic pathology
44
Q

What is a post prandial serum bile acid test?

A
  • BA stimulation test/dynamic BA
  • Take resting sample
  • Fatty meal
  • Post-prandial sample 2 hours after feeding
45
Q

List some extrahepatic diseases that can cause an elevation in liver enzymes

A
  • Hypoxia
  • GI and pancreatic disease
  • Endocrine diseases (fat or glycogen accumulation)
  • Sepsis (can also cause functional cholestasis)
46
Q

What are reactive hepatopathies?

A
  • Most reactive hepatopathies have normal (or mildly elevated) bile acids
  • Other markers of liver function will be normal
47
Q

Describe what may be seen on haematology of patients with liver disease

A

Often unremarkable, but we may see:
- Microcytosis (portosystemic shunts or severe liver insufficiency, likely due to altered iron transport or metabolism)
- Ovalocytes (elliptocytes) are frequently seen in cats with hepatic lipidosis
- Acanthocytes: lipid disease, disruption of normal vasculature

48
Q

Describe what may be seen on urinalysis of patients with liver disease

A

Often unremarkable, but we may see:
- Isosthenuria or inappropriately low USG
- Bilirubinuria (more than 2+ in dogs, any in cats)
- Ammonium biurate crystals or uroliths (40-70% of patients with portosystemic shunts)

49
Q

Describe the microscopic anatomy of the pancreas

A

Each pancreatic lobule is composed primarily of acinar cells (that synthesize digestive enzymes) and smaller cells of the branching duct system.
The pancreas also contains islets of Langerhans (1-2% of the glands), that carry out endocrine functions

50
Q

List the functions of the pancreas

A

Alpha cells produce glucagon
Beta cells produce insulin
Delta cells produce somatostatin

51
Q

List the functions of the exocrine pancreas

A
  • Secrete digestive enzymes, zymogens produced by pancreatic acinar cells
  • Enzymes: proteases (trypsin, chymotrypsin, elastase), lipases, amylase
  • Also high concentration of bicarbonate in secretions
  • Aids B12 and zinc absorption
  • Antibacterial activity
  • Intestinal mucosal modulation
52
Q

Specific enzymes assay for … and … are used to identify injury to pancreatic cells

A

Amylase
Lipase

53
Q

Injury to pancreatic cells is most commonly due to?

A

Inflammation (pancreatitis)

54
Q

How is pancreatitis diagnosed?

A
  • Specific enzyme assays
  • Imaging
55
Q

Describe the main features of amylase

A
  • Catalyses hydrolysis of complex starches
  • Short half-life (hours)
  • Salivary and intestinal not found in serum
  • More useful in dogs than other species
  • Can increase due to decreased GFR
56
Q

Describe the main features of lipase

A
  • Catalyses hydrolysis of triglycerides
  • Very short half-life (2 hours)
  • Mostly from pancreas
  • Can increase (mildly) due to decreased GFR
  • Different tests have different positive and negative predictive value
57
Q

Is lipase useful in diagnosing pancreatitis?

A

Elevation in lipase is suggestive but:
- Other causes possible
- Higher the increase higher the likelihood
- Degree of increase doesn’t equal severity of disease

58
Q

How can pancreatitis be diagnosed?

A
  • Clinical signs
  • PLI (specific pancreatic lipase): not to be used on isolation!
  • Imaging (ultrasound), fluid analysis, biopsy
59
Q

Describe the possible haematology changes seen in a patient with pancreatitis

A

Often leucocytosis, neutrophilia and left shift, due to the presence of inflammation

60
Q

Describe the possible biochemistry profile changes seen in a patient with pancreatitis

A
  • Hyperglycaemia due to transient or true diabetes mellitus
  • Hyperlipidaemia due to primary, or secondary to pancreatitis, Cushing’s etc
  • Hypocalcaemia due to saponification of fat, glucagon release -> increased release of calcitonin
61
Q

Name 2 tests used to assess exocrine pancreas function

A

TLI = trypsin-like immunoreactivity
Exocrine pancreatic insufficiency test

62
Q

The TLI (trypsin-like immunoreactivity) test can be used in which spp?

A

Dogs
Cats
Horses
- species specific assays needed

63
Q

Describe the features of the TLI (trypsin-like immunoreactivity) test

A
  • Detects trypsinogen, trypsin, and trypsin bound to protease inhibitors (most TLI in blood is trypsinogen; do not want free trypsin in the blood)
  • Pancreas normally leaks some trypsinogen into blood
  • In animals with clinical signs of maldigestion/malabsorption, (decreased activity) high sensitivity and specificity for exocrine pancreatic insufficiency
  • Less useful for pancreatitis (increased activity)
64
Q

Describe the exocrine pancreatic insufficency test

A

Serum TLI < 2.5 ug/L in dogs (< 5 ug/L equivocal/subclinical)
TLI < 8 mg/L in cats

65
Q

Exocrine pancreatic insufficency can be excluded if?

A

TLI is normal

Y4 SA - Clinical pathology (1 decks)

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