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Yr 3 Oxford Clinical Cases > Jaundice > Flashcards

Jaundice Flashcards

1
Q

What are the three steps of bilirubin metabolism?

A

Production of unconjugated bilirubin

Conjugation of bilirubin

Excretion of bilirubin

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2
Q

How does unconjungated bilirubin travel to the liver?

A

Bound to albumin

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3
Q

Where are blood cells normally broken down?

A

In the spleen by splenic macrophages

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4
Q

What is bilirubin conjugated with in the liver?

A

Glucuronic acid

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5
Q

What is conjugated bilirubin converted to within the intestines and what happens to these products?

A

Urobilinogen and stercobilinogen

Some of the urobilinogen is reabsorbed by the intestines and excreted by the kidneys

Stercobilinogen gets converted to stercobilin, which gives faeces its brown colour

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6
Q

What are the three main types of jaundice?

A

Pre-hepatic = excessproduction of bilirubin

Hepatic= pathology in hepatocytes or bile cannaliculi in liver

Post-hepatic (obstructive)= blockage of bile ducts outside of liver

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7
Q

What characteristic clinical features are associated with obstructive jaundice?

A

Dark urine

Pale stools

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8
Q

What are the two causes of cholestatic jaundice?

A

Obstruction (gallstones)

Paralysis (ileus) of common bile duct = drug induced

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9
Q

What are the two mechanisms of unconjugated hyperbilirubinaemia?

A

Increased production of bilirubin (increased haemolysis) Decreased capacity to conjugate bilirubin (hepatic pathology)

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10
Q

Why might patients who are undergoing intravascular haemolysis have dark urine?

A

Free haemoglobin from the haemolysis is degraded into haemosiderin, which is water soluble and very dark

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11
Q

List some congenital causes of intravascular haemolysis.

A
  • G6PD deficiency
  • Pyruvate kinase deficiency
  • Sickle cell disease
  • Thalassemia
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12
Q

List some acquired causes of intravascular haemolysis.

A
  • Artificial heart valves
  • Blood group mismatch
  • DIC
  • Malaria
  • Medications
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13
Q

What might be seen on the blood film of a patient undergoing intravascular haemolysis?

A

Schistocytes

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14
Q

Which clinical sign is likely to be seen in patients undergoing extravascular haemolysis?

A

Splenomegaly

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15
Q

List a congenital and acquired cause of extravascular haemolysis.

A

Congenital – hereditary spherocytosis

Acquired – autoimmune haemolytic anaemia

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16
Q

State 2 mechanisms leading to a decreased conjugation of bilirubin

A
  • Reduced unconjugated bilirubin getting into hepatocytes (redcued hepatocyte uptake)
  • Decreased conjugation of bilirubin (enzymatic defects)
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17
Q

What can cause reduced uptake of bilirubin by the liver?

A

TIPS (transjugular intrahepatic portosystemic shunt)

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18
Q

Name two congenital enzymatic problems that lead to unconjugated hyperbilirubinaemia.

A

Gilbert’s syndrome

Crigler-Najjar syndrome

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19
Q

Name a congenital cause of obstructive jaundice.

A

Dubin-Johnson syndrome

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20
Q

Using the surgical sieve, list causes of obstructive jaundice.

A
  • Infection – hepatitis, ascending cholangitis, liver abscess
  • Neoplasia – HCC, cholangiocarcinoma, pancreatic cancer
  • Vascular – Budd-Chiari syndrome
  • Inflammation/Autoimmune – PBC, PSC, autoimmune hepatitis, pancreatitis
  • Trauma – gallstones, strictures (post ERCP)
  • Endocrine – intrahepatic cholestasis of pregnancy
  • Degenerative
  • Metabolic – haemochromatosis, Wilson’s disease
  • Drugs – alcohol, paracetamol, sodium valproate, co-amoxiclav, nitrofurantoin
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21
Q

List some key features of the history of presenting complaint that you should ask a patient with jaundice.

A
  • Acute or chronic
  • RUQ pain, nausea and vomiting – suggests hepatitis of any cause
  • Fever and diarrhoea – suggest infection (viral hepatitis)
  • Steatorrhoea, dark urine, pruritus – suggests obstructive
  • Weight loss, fever, night sweats – systemic features of malignancy (hepatitis, cholgeocarcinoma, pancreatic)
  • Bronzed skin and signs of diabetes mellitus – haemochromatosis
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22
Q

List three diseases, exclusive to pregnancy, that can cause jaundice.

A

Acute fatty liver of pregnancy

Intrahepatic cholestasis of pregnancy

HELLP syndrome (haemolysis, elevated liver enzymes, low platelets)

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23
Q

Why is it important to check for signs of diabetes mellitus?

A

Haemochromatosis can lead to diabetes mellitus

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24
Q

List some key features of the past medical history and explain why they might be significant.

A
  • Gallstones - obstructive jaundice
  • Liver disease
  • Haemophilia – may have received contaminated blood products
  • Recent blood transfusion or surgery – possible transfusion reaction
  • Ulcerative colitis - PSC association
  • Diabetes mellitus - haemochromatosis association
  • Emphysema - a1- antitrypsin deficiency
  • Psychosis – may result from Wilson’s disease
25
Q

List some drugs that increase the risk of jaundice by the following mechanisms: Intravascular haemolysis Autoimmune, extrvascular haemolysis Hepatitis Cholestasis

A
  • Intravascular haemolysis: Sulphonamides, aspirin in G6PD patients
  • Autoimmune, extravascular haemolysis: Methyldopa
  • Hepatitis: Paracetamol overdose, sodium valproate
  • Cholestasis: Co-amoxiclav, nitrofurantoin
26
Q

List some significant diseases causing jaundice which might be obtained whilst taking the family history

A
  • Gilbert’s
  • Haemochromatosis
  • Wilson’s Disease
  • SCD
  • Thalassaemia
  • Hereditary spherocytosis
  • G6PD
27
Q

List some features of the social history that would be significant in a patient with jaundice.

A
  • Alcohol abuse
  • IV drug use
  • Tattoos
  • Unprotected sex with multiple partners
  • Recent foreign travel (malaria, Hep A+ E East Asia)
28
Q

List some features that you might see on inspection of a patient with jaundice.

A
  • Signs of dehydration
  • Fever
  • Conjuctival icterus
  • Cachexia
  • Scratch marks
  • Needle tracks
  • Signs of chronic liver disease (spider naevi, palmar erythema, clubbing, bruising and gynaecomastia)
  • Bronzed tan (haemochromatosis)
  • Kayser-Fleischer rings (Wilsons)
29
Q

List some features you might feel on palpation of someone with Jaundice

A
  • Organomegaly- splenomegaly (extravascular haemolysis), epigastric mass (pancreatic/hepatic malignancy), hepatomegaly (hepatitis)
  • RUQ tenderness- Biliary disease, hepatitis
  • Ascites- chronic liver disease
  • Lymphadenopathy- malignancy
30
Q

Which causes of jaundice are supported by RUQ tenderness?

A
  • Hepatitis
  • Gallbladder disease – cholecystitis, ascending cholangitis
31
Q

List some blood tests that may be useful in a patient with jaundice.

A
  • FBC and reticulocyte count
  • Serum bilirubin levels
  • Liver enzymes (AST, ALT, ALP, GGT)
  • Serum amylase or lipase
32
Q

State which liver disease is likely if:

Elevation of AST > ALT

Elevation of ALT > AST

Elevation of ALP + GGT

Isolated elevation of GGT

A
  • Elevation of AST > ALT Alcoholic liver disease
  • Elevation of ALT > AST Viral hepatitis
  • Elevation of ALP + GGT Biliary pathology
  • Isolated elevation of GGT Recent alcohol consumption (note isolated ALP elevation= increased bone turnover)
33
Q

What does the finding of bilirubin in the urine indicate?

A

Post-hepatic obstruction

34
Q

Which test must be performed in young women presenting with jaundice? List some causes of jaundice in these people

A

Pregnancy test – there are some causes of jaundice that are exclusive to pregnant women

  • pre-eclampsia HELLP syndrome
  • Intra-hepatic cholestasis of pregnancy
  • Acute fatty liver of pregnancy
35
Q

List the components of the haemolysis screen.

A
  • Haptoglobins – these bind to free Hb and, hence, will be low in haemolytic states
  • Lactate dehydrogenase (LDH) – released by red cells when they lyse
  • Direct Antiglobulin test (Coombs test) – tests for autoantibodies against red cells (AIHA)
  • Blood film – look for schistocytes, sickle cells, spherocytes, malaria
36
Q

Which diseases are tested for in viral serology?

A
  • Hepatitis A, B and C
  • EBV and CMV
  • HIV
37
Q

Which antibodies should be tested for in an autoimmune screen of a jaundice patient?

A
  • Anti-smooth muscle antibodies (ASMA) – type 1 autoimmune hepatitis
  • Anti-mitochondrial antibodies (AMA) – primary biliary cirrhosis
  • Anti-nuclear antibodies (ANA)
38
Q

Which test results would be consistent with:

  1. Haemochromatosis
  2. Alpha-1 anti-trypsin deficiency
  3. Wilson’s disease
A
  • Haemochromatosis: High ferritin High transferrin saturation
  • Alpha-1 anti-trypsin deficiency: Low alpha-1 anti-trypsin
  • Wilson’s disease: High serum copper, Low caeruloplasmin
39
Q

What is the earliest maker of compromised liver function?

A

Prolonged clotting times

40
Q

Why is PTT a better indicator of liver dysfunction than albumin?

A
  • Elevated PTT is one of the earliest signs of liver dysfunction whereas alumin takes 20days to fall
  • Low Albumin could be caused by decreased sythesis (hepatic dysfunction) or increased excretion (Nephrotic syndrome)
41
Q

What are the four possible outcomes for patients with acute viral hepatitis B?

A
  1. Full clinical recovery (virus is rarely completely cleared)
  2. Carrier status
  3. Chronic hepatitis B (some will end up developing cirrhosis and HCC)
  4. Fulminant hepatitis (rare but 80% mortality)
42
Q

Describe the inheritence of Gillbert’s syndrome

A

Autosomal Recessive

43
Q

Describe the typical presentation of a patient with obstructive jaundice.

A
  • Jaundice
  • RUQ pain
  • Steatorrhoea + dark urine
  • Nausea
  • Raised ALP + GGT
44
Q

Which investigation can be performed to visualise gallstones?

A

Biliary ultrasound => MRCP if inconclusive

45
Q

Which intervention can be performed to remove gallstones from the CBD and drain pus?

A

ERCP

46
Q

Describe the presentation of acute cholecystitis.

A
  • Constant
  • unresolving fever (> 6 hrs)
  • Tender abdomen
  • Positive Murphy’s sign
  • Nausea and (maybe) vomiting
47
Q

Outline the management of acute cholecystitis.

A
  • Antibiotics + analgesia
  • NBM
  • IV fluids
  • Cholecystectomy
48
Q

What is Charcot’s triad?

A

Sign of Ascending Cholagitis which is a surgical emergency:

  • RUQ pain
  • Jaundice
  • Fever with rigors
49
Q

Outline the management of ascending cholangitis.

A

EMERGENCY

  • Blood cultures
  • Careful monitoring
  • Broad-spectrum antibiotics
  • ERCP if necessary – to drain pus from the CBD
50
Q

What is Primary Biliary Cirrhosis (PBC)?

A

Autoimmune disorder characterised by T-cell mediated destruction of the biliary ducts

51
Q

Explain why a patient with PBC might have a higher brusing tendency?

A
  • Reduced bile outflow
  • Vitamin K is a fat soluble enzyme which binds to bile miscelles in the intestines during absorption
  • Vitamin K essential for production of clotting factors.
52
Q

Which liver enzymes will be deranged in PBC?

A

High ALP + GGT because these are stored within the epithelial cells of the biliary tree. Since these cells are being destroyed, these enzymes will be released

53
Q

Which autoantibody is the hallmark of PBC?

A

Anti-mitochondrial antibodies (AMA)

54
Q

Outline the management of PBC.

A
  • Confirm diagnosis – MRCP and biopsy
  • Immunosuppression- corticosteroids, methotrexate, ciclosporin
  • Bile salt replacement- urodeoxycholic acid
  • Fat-soluble vitamin supplementation
  • Pruritus management – with cholestyramine
  • Liver transplantation
55
Q

What is Primary Sclerosing Cholangitis (PSC)?

A

Autoimmune disorder that lead to T-cell mediated destruction of biliary epithelial cells, leading to multifocal scarring of biliary ducts

56
Q

Which disease is PSC strongly associated with?

A

Ulcerative colitis

57
Q

Which antibody is often elevated in PSC patients?

A

pANCA

58
Q

What Autoimmune screening test is performed for patients with suspected haemolytic anaemia

A

DAT or Coombe’s test

Yr 3 Oxford Clinical Cases (28 decks)

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