marked steatosis (fatty liver disease, pootly controlled diabetes)

hepatic venous outflow limitation - congestive cardiac failure and bud chiari syndrome

liver infiltration - lymphoma, glycogen storage diseases (Eg gaucher's disease), amyloid

• palp spleen = consider cirrhosis, haematological malignancy, amyloid or unusual infections

inc production of unconjugated bilirubin from excessive destruction of RBC in haemolysis exceeds ability of liver to conjugate so unconjugated accumulates in blood so none found in urine.

however there is an inc in the amount of urobilinogen produced in gut so more resorbed and overflows into systemic circulation where it is excreted by kidney

in presence of hepatocellular damage - liver unable to conjugate bilirubin efficiently and less excreted into canaliculi

thus both unconjugated and conjugated accumulate in the blood

Obstruction of intrahepatic or extrahepatic bile ducts prevents excretion of conjugated bilirubin

conjugated bilirubin builds up in blood and is excreted in urine = dark brown

HAEMOLYSIS eg spherocytosis or incompatible blood transfusion

hepatitis: viral (A, B, C, E), Leptospirosis, glandular fever (infectious mononucleosis)

liver poison - paracetamol od, chlorinated hydrocarbons eg carbon tetrachloride, chloroform and halothane, phosphorus

liver tumours =, most of parenchyma replaced by deposits

2) pathology in wall

congenital atresia of CBD
traumatic stricture
1o or 2o sclerosing colangitis
tumour of bile duct (cholangiocarcinoma)

3) external compression

pancreatitis
tumour of head of pancreas
tumour of ampulla of vater
hilar lymphadenopathy

LEMONY YELLOW TINGE SUGGESTS HAEMOLYTIC JAUNDICE

DEEP JAUNDICE SUGGESTS HEPATIC OR POSTHEPATIC TYPES

urinary urobilinogen may be raised as unable to re-excrete the urobilinogen reabsorbed from bowel

haptoglobin level (low in haemolysis), reticulocyte count, coombs test, split bilirubin (conjug/unconjug)

liver synthetic function (hepatocellular dysfunction) - prothrombin time, albumin

ALP, GGT, US of bile ducts, MRCP, PTC, ERCP, CT for pancreatic lesion

intrahepatic mass - cross sectional imaging, such as US and CT, w/ needle biopsy

treat with metronidazoleor US guided percutaneous drainage if not responding

hepatocellular failure - impaired protein synthesis: prolonged prothrombin time and low albumin

gynaecomastia, testicular atrophy, amenorrhoea, spider naevi, finger clubbing, palmar erythema

idiopathic hepatic venous thrombosis in young adults of both sexes - this is a manifestation of a prothrombotic tendency, which may be hereditary or acquired due to myeloproliferative disease, other systemic conditions or drugs

result of portal congestion and hypertrophy of splenic subtance itself

often assoc w/ haematological changes of hypersplenism: leucopenia and thrombocytopaenia

anaemia accompanying splenomegaly can be accounted for by GI bleeding and is not necessarily a result of splenic enlargement

serum albumin synthesis (via liver) is reduced = lower serum osmotic pressure

splanchnic vasodilation = blood pools = systemic hypotension = renal hypoperfusion = trigger RAAS = retain water and Na

inferior vena cavagram - can demonstrate hepatic venous occlusion

treat uncomplicated portal htn involves treatment of the underlying condition eg abstinence of etoh, treat underlying viral infection, metabolic condition or autoimmune liver disease

if large oesophageal varices are visible on endoscopy, prophylaxis with medication or band ligation of varices is performed, since first episode of variceal haemorrhage is associated with a 15-20% mortality

encephalopathy may be precipitated by absorbing meal of blood within intestine

prophylaxis against haemorrhage varices- beta blocker = reduce splanchnic blood flow and lower portal venous pressure

endoscopic band ligation in larger varices

prone to bleeding from gastric erosions and commonly affected by peptic ulceration

airway protection, emergency resuscitation, stabilise prior to endoscopy

prevent aspiration - pts with liver disease have impaired consciousness = risk of aspirate

reduce intrarenal blood flow - inc glomerular afferent arteriolar tone

fibroalmellar carcinoma, uncommon variant of hepatoma affecting young adults and children

systemic blood spread (from lung, breast, testis, melanoma, etc)

direct spread (from gallbladder, stomach and hepatic flexure of colon)

in absence of cirrhosis = massive liver swelling, weight loss, ascites possibly

in presence of advanced disease - rapid deterioration, decompensation with encephalopathy ascites and impaired synthetic function

serum alpha fetoprotein raised but not sens or spec for carcinoma, rises in other diseases

cross sectional imaging US and contrast enhanced CT or MR confirm tumour presence

selective hepatic angiography distinguish generative nodules from small HCCs or reveal multifocal

in absence of cirrhosis, 1o hepatocellular carcinoma confined to one lobe treat by hemi-hepatectomy

in presence of cirrhosis, removing liver substance may precipitate hepatic decompensation and death = do radiofrequency ablation or transarterial chemoembolisation (TACE) - further lesions are likely to develop - only alternative is liver transplant

present with jaundice and may complicate primary sclerosing cholangitis

resection of these tumours not appropriate in disseminated malignancy

but maybe when deposits can be surg excised leaving adequate residual liver