prehepatic hepatocellular cholestatic

Jaundice (and viral hepatitis) Flashcards by Ailsa Bell

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

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types of jaundice?

prehepatic
hepatocellular
cholestatic

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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

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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

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hepatocellular causes of jaundice?

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

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

Hep A

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does Hep A cause chronic liver disease?

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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

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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

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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)

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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

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

hepatocellular jaundice

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

cholestatic jaundice
(itch due to bile salts not bili)

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

cholestatic jaundice (obstructive if bilirubin rises)

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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

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

kids

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Hep C acute Sx? prognosis?

usually Asx

* 80 percent become chronic

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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

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which viral Heps have a vaccine?

Hep A

* Hep B

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

• Hepatitis B

acute or decompensated

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how is Hep B transmitted?

hematogenously (IVDU, needlestick, tattoos, blood transfusions, piercings)
sexually
vertically

risk of chronicity in Hep B?

less than four percent

higher if acquired perinatally or in early childhood

Tx Hep B?

oral antiviral therapy (suppressing viral replication)

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

Hx: IVDU - which viral hep is common?

Hep C

also Hep B

natural history of Hep B infection from childhood?

* 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

diagnostic test for Hep A?

IgM

diagnostic test for Hep B?

HBs Ag (surface antigen)

diagnostic test for Hep C?

Ab (screening) | PCR (confirmation)

diagnostic test for Hep E?

IgM

Ix: monitoring investigations in chronic viral hep?

* LFTs, coag, AFP * liver US * fibroscan (transient elastography)

Ix acute hep?

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)

Ix: ? | • HBs Ag +ve

incubating Hep B | infective if also HBe Ag +ve

``` Ix: ? • HBs Ag +ve • HBc IgM • HBc IgG • HBe Ag • ↑↑↑ LFTs ```

acute hep B infection

Ix: ? • HBs Ag • HBc IgG • ↑ LFTs

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

Ix: ? • HBs Ab • HBc IgG

recovered from hep B | no surface antigen, only Ab

Ix: ? | • HBs Ab

vaccinated against hep B

Tx viral hep?

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

which viral heps can Become Chronic?

* 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

if hep B/C cirrhosis - screening?

HCC: • 6 monthly US and AFP varices: • 3 yearly OGD

complications of acute viral hep?

* ALF * GN (hep B) * 20 percent of pregnant ladies die in hep E

danger of Hep E?

pregnancy (20 percent die)

prognosis chronic Hep C?

* 20 percent will have cirrhosis in 20 years | * 2 percent HCC

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

hep C

how is Hep C transmitted?

* blood mostly | * rarely, sex/vertical

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?

hep E

how is Hep E transmitted?

* 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)

when might Hep E become chronic?

* organ transplant recipients * haematological malignancy requiring chemotherapy * HIV

ΔΔ cholestatic causes of jaundice?

• 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)

ΔΔ jaundice in pregnancy?

* gallstones * PET * /HELLP * obstetric cholestasis

Ix jaundice?

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)

Tx obstructive jaundice? | complications?

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

difference between cholestatic and obstructive jaundice?

* 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