69. Jaundice Flashcards

1
Q

24 year old man with jaundice, fever, very raised ALT, raised bilirubin, mildly raised ALP

a) Describe the liver problem
b) Qs to ask
c) Tests to perform

A

a) Hepatitis
b) Travel history, occupational history, sexual history, IVDU, etc.

c) - Clotting test (for acute liver failure eg fulminant hepatitis, paracetamol overdose)
- Antibody test:
1. Look for core antibody for infection and surface antigen - IgM for acute; IgG for chronic
2. Look for surface ANTIBODY for immunity
(note: you cannot have surface antibody and surface antigen at the same time)
- Non-invasive liver screen (USS; as opposed to an invasive liver screen - biopsy)

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2
Q

Acute liver failure.

a) Define
b) Classification
c) Causes
d) Presentation
e) Social Hx - Qs to ask
f) Non-invasive liver screen + other tests to do
g) Score for mortality in cirrhosis

A

a) Acute encephalopathy, coagulopathy and jaundice without previous cirrhosis
b) < 7 days: hyperacute, 7-14: acute
c) Paracetamol OD, alcohol, viral hepatitis (ABCDE, CMV, EBV), NASH, autoimmune, ischaemic hepatitis
d) Jaundice, abdominal pain, bruising/bleeding, confusion, drowsiness, slurred speech (DDx - stroke), hepatomegaly, ascites
e) Alcohol, IVDU, foreign travel, tattoos, sexual activity

f) NILS: FBC, clotting, LFTs, HepBsAG, Anti-HCV, EBV/CMV serology, caeruloplasmin (Wilson), transferrin (Haemochromatosis), antibodies (AMA, ASMA, ANA - PBC, PSC, etc.), alpha-1-antitrypsin
- Other: UEs, CRP, amylase, Ca2+, glucose, paracetamol levels

g) Child Pugh score

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3
Q

Management of acute liver failure

a)

A
A-E
Stop hepatotoxic drugs
prophylactic abx
IV fluids
Monitor glucose/ PT
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4
Q

Decompensated chronic liver failure.

a) 4 key features
b) Causes (acute +….?)
c) Management

A

a) Cirrhosis: variceal bleeding, encephalopathy, coagulopathy, hypoalbuminaemia (ascites)
b) Wilson’s, haemochromatosis

c) - Pabrinex, chlordiazepoxide reducing regime
- SBP (>250 white cells/mm3): abdo pain in presence of ascites (+ sepsis signs) - IV ABx
- GI bleeding management + prophlaxis (propranolol, TIPS)
- Manage any AKI

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5
Q

Pre-hepatic jaundice.

a) Pathophysiology
b) Presentation
c) LFTs
d) Differentials

A

a) Increased haemolysis:
- Often causes ANAEMIA + JAUNDICE

b) - Anaemia signs and symptoms (pale and yellow)
?splenomegaly (from increased haemolysis)

c) - UNCONJUGATED hyperbilirubinaemia
- Normal LFTs
- Anaemia !

d) - Gilbert’s syndrome
- Sickle cell crises/ thalassaemia
- Sepsis
- Transfusion reactions: ABO/Rhesus incompatibility
- Haemolytic drug reaction

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6
Q

Hepatic jaundice.

a) Pathophysiology
b) Presentation
c) LFTs
d) Differentials

A

a) Hepatocellular dysfunction

b) - ?dark urine, pale stools (may be normal)
- ?RUQ pain
- ?hepatomegaly

c) - Conjugated/unconjugated hyperbilirubinaemia
- AST/ALT raised > GGT/Alk Phos

d) - Hepatitis: infective, alcoholic, drug-induced, autoimmune,
- Dysfunction: cirrhosis, ALD, CLD
- Malignancy: HCC, liver mets

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7
Q

Post-hepatic jaundice.

a) Pathophysiology
b) Presentation
c) LFTs
d) Differentials

A

a) Cholestasis - obstruction of the common bile duct

b) - Dark urine, pale stools
- Pruritis
- ?RUQ pain

c) - CONJUGATED hyperbilirubinaemia
- GGT/Alk Phos raised >ALT/AST

d) Gallstones (choleithiasis), acalculous cholecystitis, cholangitis (and biliary sepsis), pancreatic cancer, cholangiocarcinoma, biliary stricture, PSC/PBC

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8
Q

Courvoisier’s law.

a) Law
b) Why this happens?
c) Exceptions

A

a) The presence of a palpable non-tender gallbladder in a jaundiced patient is more likely to be due to malignancy than gallstones
b) Gallstones are a chronic inflammatory diseases, causing gallbladder fibrosis, meaning it is unable to distend (so won’t be palpable)

c) Double gallstones:
- One blocking the common bile duct (responsible for jaundice)
- One at the cystic duct (causing a palpable non-tender gallbladder)

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9
Q

Jaundice: history.

a) Onset
b) Associated symptoms to ask about
c) PMHx
d) FHx
e) DHx
f) SHx

A

a) - Sudden (and painful) - more likely gallstones
- Gradual (and painless, or vague abdominal discomfort, weight loss/anorexia) - more likely malignancy

b) - PAIN (especially RUQ/other abdominal)
- Obstructive: dark urine, pale faeces
- Systemic: fever, nausea, vomiting (?hepatitis), weight loss/ anorexia (?malignancy), pruritis
- Anaemia symptoms: pale, SOB, dizziness/LOC, fatigue
- Current pregnancy (?obstetric cholestasis)

c) - Gallstones
- IBD (can cause PSC)
- Surgery
- Malignancy
- Haematological disease

d) - Sickle cell, thalassaemia, etc.
- Hereditary jaundice (eg. Gilbert’s)

e) - Recent antibiotics (eg. erythromycin)
- Known hepatotoxics/ enzyme inducers
- Allergies

f) - Foreign travel (?hepatitis)
- Alcohol
- Smoking (?malignancy)
- IVDU
- Sexual history

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10
Q

Jaundice: examination.

a) Best way of examining
b) Chronic jaundice causes what appearance?
c) Inspection
d) Palpation

A

a) - Natural light
- Best seen in sclera, frenulum of tongue and abdomen

b) Greenish-yellow (biliverdin)

c) - Signs of chronic liver disease: clubbing, asterixis, palmar erythema (thenar and hypothenar eminences), spider naevi (chest), gynaecomastia, ascites, peripheral oedema
- Signs of malignancy: cachexia

d) - Tenderness
- Murphy’s sign (cholecystitis)
- Organomegaly: gallbladder (?malignancy), liver (tender = ?hepatitis), spleen (?haemolysis), pancreatic tumour
- Lymphadenopathy - ?malignancy

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11
Q

Jaundice and LFTs.

a) Mixed hyperbilirubinaemia, AST raise > ALT, GGT high, normal Alk Phos, macrocytosis
b) Mixed hyperbilirubinaemia, ALT raise > ALT, GGT and Alk Phos mildly raised, tender hepatomegaly
c) Unconjugated hyperbilirubinaemia, other LFTs normal, intermittent jaundice with intercurrent illness

A

a) Alcoholic liver disease
b) Acute hepatitis
c) Gilbert’s syndrome

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12
Q

Investigating jaundice.

a) Bedside
b) Bloods
c) Imaging
d) Special tests

A

a) - Urine dip
- Pregnancy test

b) - LFTs (C+UC bilirubin, liver enzymes, PT, albumin)
- FBC, haematinics, CRP, U+Es
- ?septic screen
- ?Hepatitis serology
- ?Antibodies (eg. ANA, AMA, ANCA) - PSC, PBC, etc.

c) - Abdominal USS (good at detecting gallstones, fluid, masses)
- MRCP (if high suspicion of gallstones not detected on USS)
- CT TAP - if malignancy suspected

d) - ERCP - diagnosis and intervention for gallstones
- Liver biopsy
- Ascitic tap (if present)

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13
Q

Liver cirrhosis: scoring

a) Non-invasive fibrosis / cirrhosis severity scores
b) Childs-Pugh (3 biochemical, 2 clinical)
c) Paracetamol OD - urgent liver transplant criteria (CHAI)

A

a) NAFLD score (used in NAFLD patients):
- Age, BMI, diabetes, AST, ALT, albumin, platelets

Fib-4 score (used in Hep B/ Hep C)
- Age, AST, ALT, platelets

b) Childs-Pugh (prognosis of patients with cirrhosis):
- Bilirubin level
- Albumin
- INR
- Ascites
- Encephalopathy

c) - Creatinine > 300
- Hepatic encephalopathy grade III or IV
- INR > 6.5
- Acidosis (pH < 7.3)

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14
Q

Abnormal LFTs: history and examination

a) Red flags in HPC
b) PMHx - things to consider
c) Drug history - possible causes of liver injury
d) Family history
e) Social history

A

a) - UGIB: haematemesis, melaena, shock!
- Decompensated LD - jaundice, encephalopathy, ascites, clotting abnormality/ bleeding
- Malignancy - weight loss, anorexia, fatigue, weakness, focal signs (eg. haemoptysis, neurology, bowel habit)

b) - Diabetes, hypertension, obesity (risks for NAFLD)
- Autoimmune disease (eg. IBD, RA)
- Infections - Hep B/C, HIV
- Psych conditions - substance misuse, etc.

c) - Antiepileptics (valproate)
- Oestrogens (COCP, HRT), tamoxifen
- Corticosteroids, anabolic steroids
- Antibiotics (tetracycline, macrolides)
- Cirrhotics (amiodarone, methotrexate)
- Paracetamol overuse

d) - Inherited - haemochromatosis, Wilson’s disease, alpha-1-antitrypsin

e) - Alcohol - overuse (consider alcoholic LD) or normal use (consider NAFLD)
- IVDU
- Social problems

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15
Q

Abnormal LFTs: investigations and management

a) NILS
b) Dominant ALP abnormality - ?
c) Dominant ALT abnormality - ?
d) Dominant bilirubin abnormality - ?
e) Confirming diagnosis of steatosis or cirrhosis
f) Management

A

a) USS liver and blood tests:
- Immunoglobulins
- Hep serology
- Autoimmune screen (Primary biliary cholangitis)
- Raised ferritin and high transferrin saturation
- Low caeruloplasmin
- Low alpha 1 anti-trypsin protein

b) - Raised GGT - ?biliary pathology, ?liver disease
- Normal GGT - ?bone disease, vit D deficiency, normal variant (third trimester pregnancy, growth spurts)

c) - Signs of decompensated LD - ?cirrhosis
- No signs of decompensated LD - ?steatosis

d) - Raised ALT or ALP - consider liver disease
- Normal ALT/ALP, raised CB - consider Gilbert’s
- Normal ALT/ALP, raised UCB or anaemia - consider haemolysis

e) - ELF blood test
- FIbroscan (transient elastography)
- If these suggest cirrhosis, do liver biopsy to assess extent of damage

f) - Weight loss
- Manage risk factors - HTN, diabetes, obesity
- Nutritional management
- Regular bowel opening if encephalopathic (laxatives may be required)
- Diuretics if ascites (spironolactone)
- Monitor renal function
- Pioglitazone useful in biopsy-proven NASH

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16
Q

Stages of fatty liver disease

A
  • Steatosis (alcoholic fatty liver or NAFLD)
  • Steatohepatitis (NASH or alcoholic steatohepatitis) - active inflammation
  • Cirrhosis
  • End stage (decompensated) liver disease
17
Q

Hepatorenal syndrome: pathogenesis

A
  • Portal hypertension*
  • Reduces effective circulating blood volume
  • Leads to activation of RAAS
  • Causes renal artery vasodilatation
  • Leads to reduced renal perfusion and reduced GFR (pre-renal failure)

*Note: generally only occurs in advanced cirrhosis with patients who have portal HTN and ascites. Often leads to hyponatraemia also (fkuid overload and kidneys unable to excrete sodium)