Jaundice Flashcards
Important Hx points in Precenting complaint
How did you discover the change in colour? Was it you or someone else?
Could you tell me when and how it started?
ONSET AND DURATION
Has it been intermittent or constant? Has it been getting worse? Fevers Pains Pruritus Bruising
Any other symptoms?
Any recent illnesses?
Any previous episodes of jaundice?
Family members or contacts with similar symptoms?
Acute onset jaundice (days) DDx
Gallstones
Acute hepatitis
Acute Budd-Chiari
Haemolysis
Subacute onset of jaundice (weeks-months) DDx
Pancreatic / hepatobiliary malignancy
Intrahepatic cholestasis
Right sided heart failure
Recurrent episodes of jaudice DDx
Gallstones
Disorder of bile transport (Gilbert’s)
features if gallstones/biliary causes
Abdominal pain (RUQ) Pale stools Itching Change in bowel habit: diarrhoea Dark urine
Features of liver causes
Abdominal swelling
Ankle swelling
Bleeding/ bruising
Features of autoimmune causes
Joint pains
Rashes
Hepatitis B and C risk factors
IVDU Blood transfusions Tattoos Piercings Needlestick injuries if healthcare professional
SIGNPOST Sexual history: Number of sexual partners New sexual partners: do you have a regular sexual partner? What type of contraception do you use?
Hepatitis A risk factors
Recent travel
Shellfish eating
COntact with affected individuals
Red flags
No abdo pain
Weight loss
PMHx
Previous jaundice Previous surgery Autoimmune conditions (PBC, AIH) UC/ or IBD for(PSC) Haemolytic anaemia
drugs
Haemolysis • Antimalarials (eg dapsone) Hepatitis • Paracetamol overdose • Isoniazid, rifampicin, pyrazinamide • Monoamine oxidase inhibitors • Sodium valproate • Halothane • Statins
Cholestasis • Flucloxacillin (may be weeks after •Fusidic acid, co-amoxiclav, nitrofurantoin • Steroids (anabolic; the Pill) • Sulfonylureas • Prochlorperazine
• Chlorpromazine
What are the causes of BUDD-CHIARI?
Hypercoagulabloe states: pregnancy, contraceptive pill, PRV, essential thrombocythaemia, antiphospholipid syndrome, Protein C, S or antithrombin III deficiency
HCC
Hepatic infections such as hydatid disease
Renal and adrenal tumours
Congenital venous webs
What is BUDD-CHiari>
Characterised by thrombosis of the hepatic veins, resulting in: abdo pain, ascites, hepatomegaly
Jaundice usually absent
No cutaneus features of liver disease as the onset of liver failure is rapid
Liver is smoothly enlarged and tender
When can liver be palpable without being enlarged?
Emphysema – overinflated lungs#
Reidel’s lobe
R-sided pleural effusion
What are the causes of hepatomegaly?
Cirrhosis – look for signs of chronic liver disease/
Carcinoma – usually secondary tumours
cCF – liver is firm, smooth, may be pulsatile if tricuspid regurg
Infections – HAV, HBV, HCV, EBV, leptospirosis, pyogenic
Metabolic cuases: haemochromatosis, Wilson’s
PBC
Lymphoproliferative disorders
Sarcoidosis, amyloidosis
Budd-Chiari syndrome
What is Hep C?
It is an RNA virus. Main routes of transmission: through needles in IVDU, blood transfusions, blood products. Sexual transmission is low. Complicaitons: liver cirrhosis, HCC. Tx: interferon-alpha and ribavarin.
What is Hep B>
It is a DNA virus
Transmitted perenterally or by sexual contact. Complications include liver cirrhosis and HCC. Tx with interferon-alpha is successful in about 40% of cases. SEs include flu-like sx, depression, fatigue, haematological abnormalities. Other drugs: lamivudine, adefovir, entecavir.
What is AIH?
More common in females. Associated with autoimmune conditions such as type 1 diabetes, thyroiditis, RA, scleroderma, IBD.
Presents with fatigue, RUQ pain, arthralgia, abnormal LFTs
Tx with immunosuppressive drugs (steroids, azathioprine)
80% are associated with HLA B8/DRw£, ANA, anti-smooth muscle antibodies and polyclonal hypergammaglobulinaemia.
WHat is Gilbert’s syndorme?
Autosomal dominant condition resulting in reduced levels of the enzyme glucuronyltransferase. This results in reduced conjugation of bilirubin.→ lvls of unconjugated bilirubin ↑. Precipitated by stress, fasting, infection. Condition is benign and asymptomatic, no treatment necessary
What causes jaundice?
The causes can be classified as Pre-hepatic , hepatic and post-hepatic causes.
Prehepatic: when bilirubin production is increased through exercise, haemoglobin breakdown (haemolysis) or myoglobin breakdown (rhabdomyolisis). Haemolysis can be intrinsic where the RBC is defective or extrinsic, where RBC is normal.
Hepatic: bilirubin increases in any process in which cell necrosis reduces liver’s ability to metabolize and excrete bilirubin such as:
Acute hepatitis and liver cirrhosis of any cause, enzymopathies such as Gilbert’s syndrome and Crigler-Najjar syndrome.
Posthepatic: when there is an obstruction of biliary drainage system causing their reflux to blood. Within the liver: PBC, PSC, drugs. Extrahepatically: gallstones, pancreatic Ca, parasites.
