Jaundice (and viral hepatitis) Flashcards
what causes high bilirubin levels?
- bilirubin from breakdown of haem in rbcs
- unconjugated bilirubin is lipid soluble
- easily enters blood
- conjugated with glucuronic acid in hepatocytes
- water-soluble, allowing excretion in bile
- ↑rbc destruction / ↓conjugation
- = ↑unconjugated bilirubin
- hepatocellular damage / biliary tract damage
- ↑conjugated bilirubin
types of jaundice?
- prehepatic
- hepatocellular
- cholestatic
prehepatic causes?
HAEMOLYSIS: (hereditary:)
• spherocytosis
• enzyme deficiencies (G6PD deficiency, pyruvate kinase deficiency)
• abnormal Hb (sickle cell anaemia, thalassaemia)
(acquired:)
• AI (SLE, RA, scleroderma)
• lymphoproliferative (usually non-Hodgkin’s lymphoma or CLL)
• transfusion reactions (ABO incompatibility)
• drugs
• infection (CMV, EBV, toxoplasmosis, and leishmaniasis)
• microangiopathic haemolytic anaemias: (DIC, TTP, HUS, PET)
• GILBERT’S syndrome
Hx: pt complains of jaundice precipitated by dehydration, fasting, menstrual periods, or stress, such as an intercurrent illness or vigorous exercise? Episodes resolve spontaneously.
Ix:
• unconjugated hyperbilirubinaemia
• but LFTs otherwise normal
Diagnosis?
Gilbert’s disease
hepatocellular causes of jaundice?
- viral (Hep A-E, HIV, parasites)
- toxins: alcohol, drugs
- HCC, liver mets
- AI Hep
- Wilson’s (genetic)
commonest cause of acute viral hepatitis, particularly common among children and young adults?
Hep A
does Hep A cause chronic liver disease?
no
Hx: 20 yr old patient develops jaundice over a few weeks, fever, malaise, has recently been to Bangladesh, and eaten some dodgy shellfish?
- Hep A
* 70-80 percent of newly infected patients aged >14 years develop jaundice
how does Hep A spread?
- primarily by faecal-oral contact
- may occur in areas of poor hygiene
- water-and food-borne epidemics occur
- eating contaminated raw shellfish is sometimes the cause
Hx: patient presents jaundiced, but with no changes to colour of urine or stool?
- prehepatic
- ↑ unconjugated bilirubin
- ↑ urobilinogen (product of conjugated bilirubin in GI tract, gives urine yellow colour)
- brown faeces (colour given by conversion of bilirubin to stercobilinogen in GI tract)
Hx: patient presents jaundiced, with normal colour stools but dark urine?
- hepatocellular jaundice
- some conjugated bilirubin is being produced still (hence normal faeces)
- but ↑ unconjugated levels being excreted leads to dark urine
Ix findings:
• ↑ conjugated and ↑ unconjugated bilirubin
• urine: some urobilinogen, conjugated bili
hepatocellular jaundice
Hx: patient jaundiced, with pale poo and dark urine, and itch?
cholestatic jaundice (itch due to bile salts not bili)
Ix show:
• LFTs (↑ conjugated bili)
• urine (↓ urobilinogen, ↑ conjugated)
cholestatic jaundice (obstructive if bilirubin rises)
Hx: patient presents with fever, malaise, anorexia, N and arthralgia, followed by jaundice, pale poo and dark pee, and itch.
Ex: RUQ pain, hepato +/- splenomegaly, lymphadenopathy.
What is it? Prognosis?
• ACUTE hepatitis
- Hep A (most likely)
- Hep B (more arthralgia and urticaria)
- Hep E
usually self-resolves in 2-6 weeks
in Hep B, are kids or adults more likely to be chronically infected?
kids
Hep C acute Sx? prognosis?
- usually Asx
* 80 percent become chronic
ΔΔ acute hepatitis?
- viral: Hep A-E, CMV, EBV, HSV, yellow fever
- bacterial: leptospira, brucella, coxiella, mycobacteria
- NASH
- alcoholic hep
- AI hep
- drugs: rifampicin, isoniazid, NSAIDs
- ischaemic hep
- Wilson’s
which viral Heps have a vaccine?
- Hep A
* Hep B
Hx: (40 percent) patient develops jaundice, V, fatigue, and abdominal pain, with a history of IVDU and unprotected sex?
• Hepatitis B
acute or decompensated