Jaundice (and viral hepatitis) Flashcards

1
Q

what causes high bilirubin levels?

A
  • 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
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2
Q

types of jaundice?

A
  • prehepatic
  • hepatocellular
  • cholestatic
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3
Q

prehepatic causes?

A

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

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4
Q

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?

A

Gilbert’s disease

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5
Q

hepatocellular causes of jaundice?

A
  • viral (Hep A-E, HIV, parasites)
  • toxins: alcohol, drugs
  • HCC, liver mets
  • AI Hep
  • Wilson’s (genetic)
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6
Q

commonest cause of acute viral hepatitis, particularly common among children and young adults?

A

Hep A

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7
Q

does Hep A cause chronic liver disease?

A

no

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8
Q

Hx: 20 yr old patient develops jaundice over a few weeks, fever, malaise, has recently been to Bangladesh, and eaten some dodgy shellfish?

A
  • Hep A

* 70-80 percent of newly infected patients aged >14 years develop jaundice

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9
Q

how does Hep A spread?

A
  • 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
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10
Q

Hx: patient presents jaundiced, but with no changes to colour of urine or stool?

A
  • 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)
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11
Q

Hx: patient presents jaundiced, with normal colour stools but dark urine?

A
  • hepatocellular jaundice
  • some conjugated bilirubin is being produced still (hence normal faeces)
  • but ↑ unconjugated levels being excreted leads to dark urine
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12
Q

Ix findings:
• ↑ conjugated and ↑ unconjugated bilirubin
• urine: some urobilinogen, conjugated bili

A

hepatocellular jaundice

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13
Q

Hx: patient jaundiced, with pale poo and dark urine, and itch?

A
cholestatic jaundice
(itch due to bile salts not bili)
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14
Q

Ix show:
• LFTs (↑ conjugated bili)
• urine (↓ urobilinogen, ↑ conjugated)

A

cholestatic jaundice (obstructive if bilirubin rises)

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15
Q

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?

A

• ACUTE hepatitis

  • Hep A (most likely)
  • Hep B (more arthralgia and urticaria)
  • Hep E

usually self-resolves in 2-6 weeks

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16
Q

in Hep B, are kids or adults more likely to be chronically infected?

A

kids

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17
Q

Hep C acute Sx? prognosis?

A
  • usually Asx

* 80 percent become chronic

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18
Q

ΔΔ acute hepatitis?

A
  • 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
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19
Q

which viral Heps have a vaccine?

A
  • Hep A

* Hep B

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20
Q

Hx: (40 percent) patient develops jaundice, V, fatigue, and abdominal pain, with a history of IVDU and unprotected sex?

A

• Hepatitis B

acute or decompensated

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21
Q

how is Hep B transmitted?

A
  • hematogenously (IVDU, needlestick, tattoos, blood transfusions, piercings)
  • sexually
  • vertically
22
Q

risk of chronicity in Hep B?

A

less than four percent

higher if acquired perinatally or in early childhood

23
Q

Tx Hep B?

A
  • oral antiviral therapy (suppressing viral replication)

* undetectable HBV DNA in approximately 95% of patients who are treated

24
Q

Hx: IVDU - which viral hep is common?

A

Hep C

also Hep B

25
Q

natural history of Hep B infection from childhood?

A
  • Asx throughout childhood with normal LFTs and +ve eAg, +ve Hep B DNA
  • then in the 20s the immune system tries to clear infection causing acute hep (↑↑↑ALT) and drop in hep B DNA
  • eAg becomes eAb
  • become inactive carriers
  • can reactivate later
26
Q

diagnostic test for Hep A?

A

IgM

27
Q

diagnostic test for Hep B?

A

HBs Ag (surface antigen)

28
Q

diagnostic test for Hep C?

A

Ab (screening)

PCR (confirmation)

29
Q

diagnostic test for Hep E?

A

IgM

30
Q

Ix: monitoring investigations in chronic viral hep?

A
  • LFTs, coag, AFP
  • liver US
  • fibroscan (transient elastography)
31
Q

Ix acute hep?

A

BEDSIDE:
• urine (toxin screen)
• DHx

BLOODS:
• paracetamol level
• serology
- hep A (IgM)
- hep B (HbsAg)
- hep C (Ab, PCR)
- hep D (if hep B +ve)
- hep E (IgM)
- EBV (IgM)
- CMV (IgM)
- auto-Ab (AI)
- ferritin (haemachromatosis)
- ceruloplasmin (Wilson's)
• LFTs
• coag (PT, INR)
• albumin

IMAGING:
• US
• MRCP (obstructive)
• CT (CA, etc)

32
Q

Ix: ?

• HBs Ag +ve

A

incubating Hep B

infective if also HBe Ag +ve

33
Q
Ix: ?
• HBs Ag +ve
• HBc IgM
• HBc IgG
• HBe Ag
• ↑↑↑ LFTs
A

acute hep B infection

34
Q

Ix: ?
• HBs Ag
• HBc IgG
• ↑ LFTs

A

chronic hep B infection
(if infective, HBe Ag)
(if acute insult, HBc IgM)

35
Q

Ix: ?
• HBs Ab
• HBc IgG

A

recovered from hep B

no surface antigen, only Ab

36
Q

Ix: ?

• HBs Ab

A

vaccinated against hep B

37
Q

Tx viral hep?

A

conservative
• notify Public Health England
• screen and vaccinate contacts if hep A/B

medical
• IVT/supportive Tx
• antivirals if hep B (lowers complications), C (curative)

long-term
• avoid alcohol, IVDU, unprotected sex
• monitoring for cirrhosis, HCC

38
Q

which viral heps can Become Chronic?

A
  • A? no
  • B? yes, but <4 percent
  • C? yes, > 70 percent
  • D? (doesn’t count)
  • E? not really (only if immunocompromised)

so mostly C, and some B

39
Q

if hep B/C cirrhosis - screening?

A

HCC:
• 6 monthly US and AFP

varices:
• 3 yearly OGD

40
Q

complications of acute viral hep?

A
  • ALF
  • GN (hep B)
  • 20 percent of pregnant ladies die in hep E
41
Q

danger of Hep E?

A

pregnancy (20 percent die)

42
Q

prognosis chronic Hep C?

A
  • 20 percent will have cirrhosis in 20 years

* 2 percent HCC

43
Q

Hx: (in 20-30 percent) patient develops jaundice, anorexia, malaise, N, with history of IVDU, multiple tattoos + body piercings?

A

hep C

44
Q

how is Hep C transmitted?

A
  • blood mostly

* rarely, sex/vertical

45
Q

Hx: patient presents with jaundice, malaise, N, having drank dodgy water in developing country (type 1/2), or eaten dodgy pork in a developed country (type 3/4)?

Ex: ranging from neurological syndromes, renal injury, pancreatitis, and haematological disorders?

A

hep E

46
Q

how is Hep E transmitted?

A
  • water-borne and linked to faecal contamination of the water supply (hep E 1/2, developing countries)
  • in developed countries, transmitted zoonotically from animal reservoirs like PORK (type 3/4)
47
Q

when might Hep E become chronic?

A
  • organ transplant recipients
  • haematological malignancy requiring chemotherapy
  • HIV
48
Q

ΔΔ cholestatic causes of jaundice?

A

• benign biliary obstruction:

  • choledocholithiasis
  • postoperative stricture
  • biliary duct injury
  • ascending cholangitis
  • PSC
  • IgG4 cholangiopathy

• malignant biliary obstruction

  • CA head of the pancreas
  • cholangiocarcinoma
  • mets
  • lymphoma

• intrahepatic causes:

  • PBC, PSC
  • drugs
  • (most causes hepatocellular jaundice can damage intrahepatic ducts, like alcohol and viruses)
49
Q

ΔΔ jaundice in pregnancy?

A
  • gallstones
  • PET
  • /HELLP
  • obstetric cholestasis
50
Q

Ix jaundice?

A

BEDSIDE:
• urine (toxin screen)
• DHx
• +/- ascitic tap

BLOODS:
• paracetamol level
• serology
- hep A (IgM)
- hep B (HbsAg)
- hep C (Ab, PCR)
- hep D (if hep B +ve)
- hep E (IgM)
- EBV (IgM)
- CMV (IgM)
- auto-Ab (AI)
- ferritin (haemachromatosis)
- ceruloplasmin (Wilson's)
• LFTs
• coag (PT, INR)
• albumin

IMAGING:
• US
• MRCP (obstructive)
• CT (CA, etc)

51
Q

Tx obstructive jaundice?

complications?

A
  • IV fluids
  • vit K
  • Abx (cholangitis prevention)
  • ERCP
  • impaired Vit K absorption in GI tract (raised INR)
  • hepatorenal syndrome
  • cholangitis
52
Q

difference between cholestatic and obstructive jaundice?

A
  • cholestatic is like when it all just halts (drugs can cause it and shit, like co-amox)
  • obstructive is when there is an actual blockage (pancreatic Ca, etc) you’d expect bilirubin to rise in this case