Obstructive jaundice Flashcards

1
Q

What are the borders of Calot’s triangle and what is found within the triangle?

A
  1. Inferior border of the liver
  2. Cystic duct
  3. CBD

Contains cystic artery, Lund’s lymph node (can be enlarged in cholangitis or cholecystitis)

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2
Q

What effect does cholecystokinin have on the gallbladder and sphincter of oddi?

A
  • gallbladder contract
  • sphincter of oddi relaxes
  • therefore bile exits the gallbladder and flows into the duodenum
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3
Q

Explain the metabolism of bilirubin.

A
  • unconjugated bilirubin is formed mainly in the spleen via breakdown of Hb
  • it is insoluble and transported in the plasma bound to albumin
  • taken up by the liver via active transport
  • converted in the hepatocytes into conjugated bilirubin (water soluble)
  • excreted into the bile canaliculi and via main bile ducts into duodenum
  • 10% of the conjugated bilirubin is reduced to urobilinogen and excreted
  • 90% of converted by colonic bacteria into stercobilinogen which is excreted in the faeces
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4
Q

What are the S+S of obstructive jaundice?

A
  • yellowing of the skin (jaundice)
  • pale bulky stools
  • dark urine
  • pruritis
  • abdo distension (acute hepatitis)
  • abdo pain (gallstones)
  • painless palpable gallbladder (carcinoma of the head of pancreas)
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5
Q

What are the different types of jaundice?

A
  1. Pre-hepatic: occurs when he rate of production of bilirubin is sufficiently fast to saturate the uptake-conjugation mechanisms of the liver
  2. Hepatic: caused by some disorder of the hepatocytes at the stages of uptake, conjugation or secretion of bilirubin
  3. Post-hepatic: occurs when there is obstruction to the CBS
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6
Q

What can cause pre-hepatic jaundice?

A
  • Haemolysis
  • Haemolytic anaemias (spherocytosis, pernicious anaemia)
  • Thalassaemia
  • Trauma
  • Gilbert’s syndrome most common inherited cause of unconjugated hyperbilirubinaemia).
  • Crigler-Najjar syndrome (rare autosomal recessive disorder of bilirubin metabolism, caused by deficient diphosphate glycosyltransferase)
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7
Q

What can cause hepatic jaundice?

A
  • Congenital defect of hepatocyte function
  • Hepatocellular injury or infection
  • Viral hepatitis (including type A and type B). Other possible infective causes include leptospirosis, brucellosis, Coxiella burnetii) and glandular fever.
  • Alcoholic hepatitis.
  • Autoimmune hepatitis
  • Drug-induced hepatitis: (paracetamol = most common cause of drug-induced liver disease)
    Hepatotoxic chemicals (phosphorous, carbon tetrachloride and phenol)
  • Decompensated cirrhosis.
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8
Q

What can cause post-hepatic jaundice?

A

Can be intrahepatic (metabolic) or extra hepatic (mechanical)

  1. Intrahepatic:
    - Primary Biliary Cirrhosis (PBC)
    - Primary sclerosing cholangitis
    - Drugs (for example, phenothiazines)
    - Dubin-Johnson syndrome: autosomal recessive disorder characterised by conjugated hyperbilirubinaemia and deposition of pigment in hepatocytes
    - Rotor’s syndrome
  2. Extrahepatic:
    - Bile duct strictures (can be benign or malignant)
    - Common duct stone
    - Cancer of the head of the pancreas
    - Tumour of the ampulla of Vater
    - Pancreatitis
    - Cancer of the gallbladder
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9
Q

What is Courvoisier’s sign and what does it indicate?

A
  • painless jaundice and palpable gallbladder

- indicates malignancy of the pancreas

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10
Q

What blood tests should be carried out to determine the cause of jaundice?

A
  1. Haemolytic causes:
    - increased unconjugated bilirubin
    - normal alkaline phosphatase
    - normal gamma glutamyl transferase
    - normal transaminases
    - normal lactate dehydrogenase
  2. Hepatocellular causes:
    - increased unconjugated bilirubin
    - normal alk phos
    - increased GGT
    - increased transaminases
    - increased LDH
  3. Obstructive causes:
    - normal unconjugated bilirubin
    - much increased all phos
    - much increased GGT
    - normal transaminases
    - normal LDH
  • Reticulocytosis (haemolysis)
  • Raised prothrombin time (parenchymal liver disease or cholestasis)
  • Hepatitis screen (hepatocellular)
  • Serum antibodies (PBC)
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11
Q

What is the role of ERCP in diagnosing and managing obstructive jaundice?

A
  • accurate at diagnosing benign and extra hepatic obstruction and can be combined with procedures to relieve obstruction
  • if bile ducts are dilated and LFTs are not improving then it is an indication of ERCP
  • if the patient has dilated ducts, it is likely to be gallstones, a bile duct stricture, or pancreatic cancer
  • sphincterectomy: used for CBD stone extraction, treatment of ampullae strictures due to tumours or inflammation
  • stent insert (plastic or expanding metal): used for bile duct stones that cannot be removed easily, post-op or benign strictures, malignant strictures, external compression of bile duct
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12
Q

What is the role of surgery in treating obstructive jaundice?

A
  • Surgical resection (Whipple’s pancreaticoduodenectomy): used from selected cases where pancreatic or distal bile duct tumours are benign or malignant
  • Surgical drainage (choledochoduodenostomy or cholecystojejunostomy): very rarely used if other interventions have failed due to very high mobility and mortality
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