osce stuff Flashcards
How would you define jaundice?
Jaundice is the yellowish discolouration of the skin, sclera and mucous membranes due to hyperbilirubinaemia
How is bilirubin produced?
Bilirubin is the end product of haem metabolism
80% of bilirubin is produced from the breakdown from haemobglobin in RBCs and 20% from the breakdown of haem in myoglobin and cytochromes.
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.
How would you investigate patients with jaundice?
FBC, LFTs, hepatoglobulins, reticulocytes, coom’s test, clotting profile, autoimmune screen, viral screen. Urine test. Further: USS abdo, CT abdo, ERCP, MRCP, liver biopsy
What is Gilbert’s syndrome?
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 is Dubin-Johnson syndrome?
Autosomal recessive defect in molecular transporters responsible for excreting conjugated bilirubin out of hepatic cells. → ↑levels of conjugated bilirubin and pigmentation of the liver
Cirrhosis is what?
It’s a consequence of chronic liver disease. Characterised by a replacement of normal liver tissue by fibrous scar tissue and regenerative nodules, which leads to a loss of liver function.
Complications of liver cirrhosis?
Ascites Spontaneous bacterial peritonitis Coagulopathy Portal HTN Hepatic encephalopathy Hepatorenal syndrome HCC
What can precipitate hepatic encephalopathy?
Infection Drugs: diuretics and sedatives Upper GI bleed Abdo paracentesis Surgery
Signs of decompensated liver failure:
encephalopathy Asterixis Jaundice Ascites Hepatic fetor Constructional apraxia
Causes of ascites:
Transudative: chronic liver disease, nephrotic syndrome, CCF, hypoalbuminaemia, myxoedema, meig’s
Exudative: malignancy, pancreatitis, TB, Budd-Chiari, portal vein thrombosis.
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.
Alpha-1-antitrypsin deficiency is what?
Defective production of alpha-1-antitrypsin, which is a protease inhibitor. There are several forms and degrees of deficiency. Deficiency results in cirrhosis, increased risk of HCC, emphysema. Tx by liver and lung transplantation.
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 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.
