Liver diseases

Indika Bandara Gawarammana

Clinical assessment of liver disease

History Physical examination Investigations

Presentation
With obvious signs of liver disease

With abnormal biochemistry

Important factors in the history

Risk factors for Hep A and C ( drug , blood,tatooing) Alcohol history Drug history Family history

Physical examination
Spider naevi Palmar erythema Clubbing Dupuytrens contracture Leuconychia Jaundice Ascites and oedema Hepatic encephalopathy Hepato- splenomegaly Caput Medusae Abdominal masses

Non hepatic disease

Right heart failure and constrictive pericarditis Non alcoholic fatty liver disease

Investigations
Non specific Assesses liver function To detect structural abnormalities To determine the underlying cause

Blood
AP ( liver, Bone, placenta and intestines) and GT are markers of cholestasis In liver disease AP increase with gamma GT Produced locally by the liver in infiltrative diseases(elevates early in metastases and abscess)

 AP and GT elevates disproportionately to AST/ALT in extrahepatic and intrahepatic cholestasis In liver necrosis:

Transaminases
>1000iu/L seen in viral and drug hepatitis and occasionally with cholangitis AST elevates disproportionately with alcohol, not >1000

Abnormal liver function tests

Most chronic LD are identified because of an incidental abnormal LFT Physical examination is normal

Threshold for investigating LFT abnormalities

Abnormal LFT in acute hospital setting is common Causes are multifactorial: including intrahepatic cholestasis from sepsis, hepatic congestion from heart failure and drugs LFT also change secondary to hyper/hypo thyroidism and active RA

In an asymptomatic, non jaundiced patients with abnormal LFT it is worth initially:

Exclude alcohol and stop alcohol Stop drugs started within the last 3 months Exclude drug toxicity from herbal medicine Repeat LFT in 3 weeks If LFT remain abnormal even after 3 weeks, do an appropriate liver disease screen and an USS

Assess the following:

Pattern: hepatocellular or cholestatic Magnitude of elevation Duration of abnormality Associated symptoms Clinical evidence of cirrhosis

Clinical clues:
Alcohol abuse Incresed BMI, lipid Type 2 Diabetes IV drugs, blood
New drugs, herbs F/H of CLD Other autoimmune diseases Recent travel Diarrhoea

ALD NAFLD
Hep B,C Drug induced Haemochromatosis Wilsons PBC,autoimmune hepatitis Hep A,E PSC

Raised transaminases
AST less specific ALT near normal in ALD AST:ALT >2 in ALD

Degree of elevation
Minor < 100 Chronic hep B,C Haemochromatosis Fatty liver
Above Alcoholic hepatitis NAFLD,Autoimmune hepatitis, Wilsons Drug, acute viral hep, Acute autoimmune hep Ischaemic liver

Moderate 100-300

Major >1000

Chronic liver disease screen

Hepatitis C antibody,RNA Hep B Santigen Transferrin saturation >55%, HFE genotype Chronic Hep C Chronic HepB Haemochromatosis

AMA
Anti Sm muscle ab,ANA Immunoglobulin: IgG IgM IgA Low caeruloplasmin level

PBC
Autoimmune hepatitis Autoimmune hepatitis PBC ALD Wilsons disease

Cholestasis: elevated ALP

ALP is produced by bone,intestine and placenta

Associated symptoms
Pain: biliary obstruction Itching in the absence of jaundice suggests intrahepatic disease: PBC, PSC In elderly, biliary obstruction can present with confusion and elevated ALP

Degree of elevation
Very high ( >1000-2000) in the absence of jaundice : hepatic infiltration

Other investigations
All must have USS to exclude obstruction and metastasis Image the biliary tree even if the bile ducts are not dilated when there is cholangitis or pain to exclude CBD stones If uss is normal exclude PBC with AMA Biopsy if ALP more than twice and AMA negative ERCP to exclude PSC as biopsy maybe normal

raised ALP

USS

normal ducts

abnormal

no pain

pain present

stones

metastasis

AMA positive PBC

AMA negative Biopsy

image for CBD stones

ERCP if biopsy is neg to exclude PSC

Gamma glutamyl transferase

Main use is to differentiate liver ALP from bone Elevated in chronic LD and in simple steatosis Not diagnostic of alcohol Isolated GGT elevation with normal PT and Alb: leave alone

Real LFT
Albumin: indicator of CLD PT both chronic and acute LD PT over 20 poor prognosis

Investigation of jaundice
history and ex urine bile blood biochemistry unconjugated others normal conjugated abnormal biochemistry

bld film, retic coombs

hepatitis serology

positive

negative

positive

negative

haemolysis work up

viral hepatitis

ultra sound

biliary obs

no biliary obs

ERCP

iron amd copper

? liver biopsy