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Year 3 - Met3a > Jaundice > Flashcards

Jaundice Flashcards

1
Q

Define jaundice

A
  • yellowing of the skin, sclera and mucosa from an increase in plasma bilirubin
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2
Q

At what level of plasma bilirubin does jaundice become visible

A

visible at > 60umol/L

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3
Q

Describe how bilirubin is broken down

A
  • bilirubin is conjugated with glucuronic acid by hepatocytes making it water soluble
  • conjugated bilirubin is secreted into bile and passes into gut
  • some is taken up by the liver again (enterohepatic circulation) and the rest is converted to urobilinogen by gut bacteria
  • Urobilinogen is then either reabsorbed and excreted by the kidneys or converted into stercobilin which colours the faeces brown
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4
Q

What are the two cases of jaundice

A
  • Unconjugated hyperbilirubinaemia - water insoluble so does not enter urine
  • Conjugated hyperbilirubinaemia - water soluble so enters the urine and makes the urine dark, less conjugated bilirubin enters the gut (due to cholestasis) and the faeces become pale
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5
Q

Describe the pathophysiology of pre hepatic jaundice

A
  • excess red blood cell breakdown overwhelms the livers ability to conjugate bilirubin this leads to unconjugated hyperbilirubinaemia
  • this is not water soluble so cannot be excreted into the urine
  • intestinal bacteria convert some of the extra bilirubin into urobilinogen which is reabsorbed and is excreted by the kidney therefore urinary urobilinogen is increased
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6
Q

Name the pre-hepatic cause of jaundice

A 
Congenital RBC issues 
Cell shape 
- sickle cell disease 
- hereditary spherocytosis 
- hereditary elliptocytosis 
Enzyme 
- GP6D deficiency 
- pyruvate kinase deficiency 
Haemoglobin 
- thalassaemia

Autoimmune haemolytic anaemia

Drugs

  • penicillin
  • sulphasalazine
  • antimalarials

Infections
- malaria

Mechanical

  • metallic valve prostheses
  • DIC

transfusion reaction s

paroxysmal nocturnal haemoglobinuria

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7
Q

describe the pathophysiology of hepatocellular causes of bilirubin

A
  • disorders of uptake, conjugation or secretion of bilirubin leading to mixed conjugated and unconjugated hyperbilirubinaemia
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8
Q

name the conjugated causes of hepatocellular jaundice

A
  • cirrhosis
  • malignancy - primary or metastases
  • viral hepatitis
  • Drugs
  • Enzymes
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9
Q

Name the drugs that can cause hepatitis

A
  • isoniazid
  • rifampicin
  • atenolol
  • enalapril
  • verapamil
  • nifedipine
  • amiodarone
  • ketoconazole
  • cytotoxic
  • halothane
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10
Q

What drugs cause cholestasis

A
  • ciclosporin
  • azathioprine
  • chlorpromazine
  • cimetidine
  • erythromycin
  • nitro
  • ibuprofen
  • hypoglycaemics
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11
Q

What is Dubin-Johnson syndrome

A
  • Autosomal recessive (cMOAT gene) with excretion of conjugated bilirubin – leads to pigmented liver
  • Increase in conjugated bilirubin with no other enzyme changes
  • High coproporphyrin
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12
Q

What is Rotor syndrome

A
  • Similar to DJS
  • Liver not pigmented
  • Normal coproporphyrin
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13
Q

Name the unconjugated causes of hepatocellular jaundice

A
  • Gilbert’s syndrome

- Crigler-Najjar syndrome

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14
Q

What is Gilbert’s syndrome

A
  • Congenital hypo-activity of conjugation enzyme UGT-1; benign and common (5%)
  • Normal LFTs except mildly elevated bilirubin, especially in times of physiological stress/illness
  • Normal life expectancy; benign condition
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15
Q

What is Crigler-Najjar syndrome

A
  • autosomal recessive (type I) or dominant (type II)
  • congenial absence in type 1 or decrease of glucoronyl transferase in type 2
  • leads to severe unconjugated hyperbilirubinaemia
  • normal liver histology
  • treatment is liver transplant; only type II survive to adulthood
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16
Q

Describe the pathophysiology of post hepatic jaundice

A
  • obstruction of biliary drainage - this leads to conjugated hyperbilirubinaemia
17
Q

Name the causes of post hepatic jaundice

A
  • Hillary tree obstruction
  • primary biliary cirrhosis (ANA and anti-microbial Abs)
  • primary sclerosis cholangitis (ANCA, anti-smooth muscle Abs, 80% have UC, association with cholangiocarcinoma)
  • Drugs
18
Q

what can cause biliary tree obstruction

A
  • common bile duct gallstones
  • compression of the bile duct e.g. pancreatitis, pancreatic cancer, lymph nodes, biliary atresia
  • cholangiocarcinoma
  • post-operative stricture
  • choledochal cyst
  • Caroli’s disease
  • Mirizzi’s syndrome
19
Q

What is Caroli’s syndrome

A

multiple segmental cystic or saccular dilatations of intrahepatic bile ducts with congenital hepatic fibrosis; may present in 20yo with portal HTN ± recurrent cholangitis/cholelithiasis

20
Q

What is Mirizzi’s syndrome

A

common bile duct compression by a gallstone impacted in the cystic duct, often associated with cholangitis

21
Q

What are the drugs that can cause obstruction of biliary drainage

A
  • flucloxacillin
  • fusidic acid
  • Co-amoxiclav
  • nitrofurantoin
  • steroids
  • sulfonylureas
  • prochlorperazine
  • chlorpromazine
22
Q

What are the causes of jaundice in a previously stable patient with cirrhosis

A
  • Sepsis (UTI, pneumonia, peritonitis)
  • malignancy (hepatocellular carcinoma)
  • alcohol
  • Drugs
  • GI bleeding
23
Q

What should you ask in a history of a patient that is jaundice

A
  • blood transfusions
  • IV drug use
  • body piercing
  • tattoos
  • sexual activity
  • travel
  • jaundiced contacts
  • family history
  • alcohol use
  • ALL medications - old drug charts, GP records
24
Q

What should happen in an examination of a jaundice patient

A
  • signs of chronic liver disease
  • hepatic encephalopathy
  • lymphadenopathy
  • hepatomegaly
  • splenomegaly
  • ascites
  • palpable gallbladder - if seen with painless jaundice the cause is not gallstones - more likely pancreatic or gallbladder cancer as stones lead to fibrotic unexpandable gallbladder
  • pale stools and dark stools - cholestatic jaundice
25
Q

What should you check the urine for in jaundice patients

A
  • Prehepatic causes (unconjugated): absent bilirubin

- obstructive causes (conjugated): absent urobilinogen

26
Q

What should be in the haematology in a jaundice patient

A
  • FBC
  • Clotting film
  • Reticulocyte count
  • Coombs’ test
  • Haptoglobins for haemolysis
  • Malaria parasites (e.g. if unconjugated hyperbilirubinaemia/fever)
  • Paul Bunnell (suspected EBV)
27
Q

what should you check in chemistry in a jaundice patient

A
  • U&Es
  • LFT
  • total protein
  • serum albumin
  • paracetamol level
28
Q

What microbiology should be tested in a jaundice patient

A
  • blood and other cultures

- hepatitis serology

29
Q

What imaging should be used in a jaundice patient

A
  • Ultrasound – Are bile ducts dilated? Are there gallstones, metastases, or a pancreatic mass?
  • ERCP – If bile ducts are dilated and LFTs not improving
  • MRCP or EUS – if US shows gallstones but no definite common bile duct stones
  • Liver biopsy – If bile ducts are normal
  • CT/MRI abdo – if abdominal malignancy is suspected
30
Q

What causes unconjugated hyperbilirubinemia

A
  • water insoluble so does not enter the urine
  • Gilbert’s syndrome – mutation of UGT-1
  • Crigler Najjar syndrome – split into type 1 (autosomal recessive) and type 2(autosomal dominant), only type 2 survive till adulthood -leads to congenial absence in type 1 or deficiency in type 2 of glucornyl transferase – treatment is liver transplant
  • Overproduction – haemolysis, ineffective erythropoiesis
  • Impaired hepatic uptake – drugs, ischaemic hepatitis
  • Impaired conjugation – Gilberts and Crigler Najjar
  • Physiological neonatal jaundice
31
Q

What causes conjugated hyperbilirubinaemia

A
  • water soluble so enters the urine and makes the urine dark
  • Hepatocellular dysfunction – hepatocyte damage, virus hepatitis, autoimmune hepatitis, alpha 1-antirypsin deficiency, Wilsons disease, Dubin Johnson and Rotor syndrome, haemochromatosis
  • Impaired hepatic excretion – BC, PSC, drugs, common bile duct obstruction, Mirrizi syndrome

Year 3 - Met3a (43 decks)

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