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Clinical pathology > Investigation of liver and pancreatic disease > Flashcards

Investigation of liver and pancreatic disease Flashcards

1
Q

Liver function

A
  • Glycogen storage and synthesis
  • Synthesis and catabolism of clotting factors, amino acids and urea
  • Lipoprotein and cholesterol synthesis; fatty acid metabolism; bile acid synthesis
  • bile acid and bilirubin excretion; Drug detoxification and excretion; Steroid hormone inactivation and excretion
  • Iron storage, B12 storage and metabolism
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2
Q

Signs of liver disease

A
  • Neonatal jaundice: Yellowing of sclera and skin
  • Jaundice
  • Finger clubbing: alterations to vascular network = lack of nutrients/oxygen to the nail bed
  • Spider naevi: liver metabolises oestrogen, damage = excess so affects capillaries = vasodilation
  • Gynaecomastia: binding proteins affected, increased oestrogen and therefore breast tissue caused
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3
Q

Routine liver function tests

A
  • Alkaline phosphate
  • alanine aminotransferase (ALT)
  • AST
  • biliruibin
  • gamma glutamyl transferase (GGT)
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4
Q

Hepatocyte damage test

A
  • ALT + AST
  • Enzymes found in the cell only released by cellular damage
  • ALT is more specific for liver than AST as AST also found in muscle and RBCs
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5
Q

Tumour markers:

A

alpha fetoprotein for primary hepatocellular carcinoma

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6
Q

When is ALT commonly raised

A
  • Epstein-Barr virus
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7
Q

Biliary tract damage

A
  • increased conjugated bilirubin in blood and liver

- Increased synthesis of enzymes ALP and yGT

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8
Q

Alkaline phosphate (ALP)

A
  • Elevated due to increased production by cells lining the bile canaliculi and overflow into blood
  • Due to: cholestasis, cirrhosis, tumours, lesions
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9
Q

Gamma glutamyltransferase (yGT)

A
  • Can support a liver source of raised ALP; elevated due to structural damage
  • Can be induced by alcohol, diabetes, obesity, pancreatic or kidney damage
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10
Q

Biochemical markers of fibrosis

A

ELF score: predicting the likelihood of fibrosis without imaging or invasive tests

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11
Q

Bilirubin

A

Measured as:

  • Total
  • Unconjugated: pre-hepatic and hepatic
  • Conjugated: post-hepatic (obstructive) and hepatic
  • Jaundice at serum bilirubin >40-50umol/L
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12
Q

How is bilirubin metabolised

A
  • Bilirubin is insoluble in water and has to go around body in blood plasma
  • Taken up in the liver and conjugated by UDP GT - makes it more soluble
  • Excreted in the bile and is used in fat digestion/absorption
  • Colon conjugated bilirubin is acted on by bacteria to make stercobilinogen = brown colour - excreted in faeces
  • Some bilirubin absorbed and excreted in urine as urobilinogen which makes urine darker
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13
Q

Hyperbilirubinemia

A
  • Characterised by jaundice

- Can have pre-hepatic, post-hepatic or hepatic causes

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14
Q

Pre-hepatic aetiology of Hyperbilirubinemia

A
  • Haemolysis e.g. rhesus incompatibility

- Ineffective erythropoiesis (breakdown of BRC) e.g. spherocytosis (sphere shaped RBC not biconcave)

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15
Q

Post-hepatic aetiology of Hyperbilirubinemia

A
  • obstructive causes

- Gallstones, bliary stricture, cancer e.g. cholangiocarcinoma, head of pancreas, cholangitis

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16
Q

Hepatic aetiology of Hyperbilirubinemia

A

Unconjugated:
- decrease in activity of UDP GT
- Gilbert’s syndrome – benign inherited disorder of bilirubin conjugation
Conjugated:
- inherited disorders of excretion e.g. Dubin-Johnson
- reduced ability to excrete the bilirubin out of the liver via the bile ducts
- Check urea levels

17
Q

Urea levels and hyperbilirubinemia

A
  • If exit of conjugates bilirubin is blocked, it will be reabsorbed and thereby increase reabsorption in urine
  • There would be dark urine because of the urobilinogen, but pale stools because of the lack of stercobilinogen.
18
Q

Inborn Errors of Bilirubin Metabolism

A
  • Decreased activity of UDP GT: Gilbert’s, Crigler-Najjar syndromes
  • Reduced ability to excrete bilirubin glucuronide: Dubin-Johnson, ROTOR syndroes
19
Q

Blood tests with jaundice

A
  • AST/ ALT elevated and normal ALP: approx. 90% have hepatitis
  • AST or ALT normal and elevated ALP: approx. 90% have obstructive jaundice
20
Q

Urine tests

A
  • Prehepatic: unconjugated bilirubin – no urinary bilirubin
  • Hepatic - variable depending on degree of obstruction
  • Post-hepatic: obstruction – dark urine (& pale stools)
21
Q

How Useful are routine LFTs

A
  • Only 3-4% of subjects with abnormal LFTs have liver disease - can be due to many other reasons
22
Q

When to measure LFTs

A
  • Signs - Pain, itchy, jaundice, TATT, bruising
  • Lifestyle - Alcohol, obesity, diabetes, recent travel, drug use
  • Disease present – hepatitis, haemochromatosis, liver cancer, drugs
  • Severity – chronic hepatitis vs acute onset
23
Q

Acute pancreatitis definition

A
  • pancreas becomes inflamed (swollen) over a short period of time
24
Q

Acute pancreatitis symptoms

A
  • Severe epigastric pain

- sudden onset, radiating to the back

25
Q

Acute pancreatitis diagnosis

A

raised serum amylase or lipase, imaging, clinical history

26
Q

Acute pancreatitis potential biochemical features

A
  • Uraemia
  • Hypalbuminaemia
  • Hypocalcaemia
  • Hyperglycaemia
  • Metabolic acidosis
  • Abnormal LFTs
27
Q

Chronic pancreatitis definition

A
  • Inflammation of the pancreas with progressive loss of both islet cells and acinar tissue
28
Q

Chronic pancreatitis presentation

A
  • Abdominal pain, Malabsorption, Impaired glucose tolerance, Alcohol often important factor
  • Malabsorption often presenting feature - think of weight loss, malaise, fatty/foul stools, vitamin deficiencies
29
Q

Chronic pancreatitis diagnosis

A
  • Imaging
  • Pancreatic Function test for investigating insufficiency; Direct or Indirect
  • Vitamin D, calcium, FBC, LFTs, glucose, lipids
30
Q

Direct (invasive) pancreatic function test

A
  • Gold standard tests
  • Intubation to collect aspirates in the duodenum
  • Secretin, CCK, Lundh Tests: stimulate pancreatic production and measure duodenal fluid for bicarbonate
31
Q

Indirect (non-invasive) pancreatic function tests

A
  • Pancreatic enzyme analysis in stools (Elastase)
  • Trypsinogen (IRT) measured in blood
  • Pancreolauryl & NBT-PABA tests – labelled compound given as a meal and enzyme activity is measured.

Clinical pathology (69 decks)

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