Hepatobiliary Disease

Dr Rajveer Thethi FY1 Gastroenterology

Aims and Objectives

Liver anatomy Jaundice Gallstones Cirrhosis and liver failure Other liver pathologies

Not to be bored to death... A lot of content just understand the principles

THE LIVER
1 2

3 7 8 6

4 5

9 11 10

Liver Function
Protein synthesis
Clotting factors Albumin

Metabolism
Absorption from GIT Bile production Maintains blood glucose

Immune function Excretion

LFTs
AST & ALT hepatocellular damage ALP & GGT bile duct damage & cholestasis
N.B. ALP also raised in bone placenta related pathology

Albumin and clotting factors

Loss of liver synthetic function (long and short term respectively)

Jaundice
= raised serum bilirubin
(>30 for it to be visible)

Pre-hepatic Intra-hepatic Post-hepatic

Bilirubin cycle

Learning points
Unconjugated HBr- conjugation failure Conjugated HBr excretion failure (DubinJohnson)or post hepatic obstruction Urinary urobilinogen normal finding
Lack of implies bilirubin not getting into bowel or reduced absorption in Terminal ileum and will get pale stools (no stercobilinogen)

Pre-hepatic jaundice
Ask for split bilirubin conjugated and unconjugated Unconjugated hyperbilirubinaemia Other LFTs normal Increased production
haemolysis Br production exceeds conjugation capacity Excess Br refluxes into blood

Reduced conjucation
Drugs e.g. Abx Gilberts syndrome

40yo woman has a hernia operation. D1 post op pt frankly jaundiced all bloods NAD except raised Bili Examination just jaundice Pt says Doc this has happened before, whats going on?

Case

Gilberts syndrome
Reduced expression of UGT 1A1 (enzyme that conjugates bilirubin in liver) Enough action normally However, in stress reduced expression of UGT Stress Fasting, illness, sepsis
(raised unconjugated fraction only)

Anything to worry about?

Intrahepatic jaundice
Almost always conjugated HBr (even with 10% liver function)
Only unconj if severe hepatocyte loss Stools still dark but has DARK urine (from conjugated bili) and jaundiced

Br will be released with hepatocyte necrosis

AST and ALT raised

Causes of intra-hepatic jaundice

Anything that can damage the liver Acute liver failure (e.g. Paracetamol OD) Decompensated cirrhosis Infectious (Hep A - E) Metabolic (NAFLD and ALD) Autoimmune hepatitis Biliary (PSC & PBC) Drugs (esp abx)

Post hepatic jaundice

Normally surgical Conjugated Br No bile in bowel no urobilinogen therefore no stercobilinogen (pale stool) HBr (conjugated) therefore can filter in kidney dark urine ALP and Bili high Br toxic to hepatocytes collateral damage so
Mildly raised ALT and AST

1ST line US look for cause and dilated CBD and IHD

Causes of post-hepatic Jaundice

Intra-luminal gallstones, biliary sludge Intra-mural PSC, CholangioCa, Stricture Extra-mural - CaHoP, lymphadenopathy, Ampullary malignancy, SMA aneurysm

Gallstones

Cholecystolithiasis gall stones in the gallbladder may be asymptomatic or symptomatic (biliary colic)

Biliary colic
Intermittent RUQ pain Can cause nausea and vomiting Related to fatty meals Normal vital signs clinically well Diagnosis - Ultrasound Can have acalculus biliary colic biliary sludge Symptomatic Management n,v &pain No peritonitis US may be normal gb with gs or shrunken gb from repeating isults

Acute cholecystitis inflammation of the gall bladder

Acute Cholecystitis
Can cause mildly deranged LFTs More continuous RUQ pain and clinically UNWELL
(vitals, WCC, SIRS, CRP)

May cause systemic symptoms and fevers Murphys sign +ve, R shoulder tip pain Can be acalculus cholecystitis Need ABx Will need elective cholecystectomy within 6 weeks now evidence for quicker op

Ultrasound

Choledocholithiasis gallstone in the CBD

Choledocholithiasis
Gallstone/s in CHD or CBD About 15% of people with gallstones will develop stones in the common bile duct Can occur even if gall bladder removed stones in biliary tree Intense RUQ/LUQ/epigastic pain Systemic features Jaundice Ultrasound then may require MRCP

Cholestatic jaudice biliary stasis and hyperbilirubinaemia

Ascending Cholangitis and biliary sepsis

Ascending Cholangitis
Charcots triad RUQ pain, jaundice & fever (rigors)
(Reynolds pentad)= Charcots triad + haemodynamic compromise and altered mental status

Can be life threatening medical emergency May be due to malignancy in HoP/CBD or stricture formation USS dilated CBD (<6mm) and IHD dilation Needs Abx (C&M), fluids, paracetamol MRCP Gold standard Rx ERCP Needs cholecystectomy later LFTs High ALP, GGT, Bili, WCC, CRP

MRCP

ERCP

Courvoisier's law
Courvoisier's law states that, in the presence of jaundice, an enlarged gallbladder is unlikely to be due to gallstones; rather carcinoma of the pancreas or the lower biliary tree is more likely.

Cirrhosis
A pathological term NOT A DIAGNOSIS Architectural disruption Fibrosis with fibrous bands (cause PHT) Regenerative nodules (HCC risk) Chronic damage
Inflammation (not acute damage)

Causes of Cirrhosis
Anything that can CHRONICALLY damage the liver Metabolic (NAFLD, ALD or other) Autoimmune hepatitis Hepatitis B&C Biliary (PSC & PBC) Drugs (esp abx)

Cirrhosis
Compensated First Decompensated Later

Portal Hypertension

Hepatic Failure

Features of chronic liver disease

Portal Hypertension
Ascites
Peritoneal Tap to Dx Paracentesis to drain Spironolactone Diuretic Intollerant Diruetic Resistant Risk of Spontaneous Bacterial Peritonitis (SBP) Portal Vein Thrombosis Hepato-renal syndrome

Oesophageal Varices
Described as columns on endoscopy Managed with betablockers Monitoring using regular OGD Banding / sclerotherapy Different grades Common cause of upper GI bleeds

Causes of Ascites
NOT ALWAYS LIVER Can split into:
Transudates
Hydrostatic pressure
Cardiac Failure Hepatic Failure

Hypoalbuminamia

Exudates
Malignancy (e.g. Ovarian Ca) Inflammatory (infective)

Iatrogenic causes

Compensated cirrhosis
Liver can still meet functional demands No features of failure Can have signs of portal hypertension and be completely stable Normally a stimulus for decompensation to start
e.g. Bleed, alcohol, infection, OD

Decompensated Hepatic Failure

3 CARDINAL FEAUTRES OF DECOMPENSATION ENCEPTHALOPATHY COAGULUPATHY HYPOGLYCAEMIA

and
Worsening Jaundice Worsening ascites Infection (inc SBP) Hypoalbuminaemia

Coagulopathy of liver disease

Impairment of synthetic function
Cannot make clotting factors

Low platelets
Large spleen + portal hypertension

Toxin impairs Platelet function Reduced bile flow

Reduced fat soluble vitamin absorption Reduced Vit D hence reduced clotting factors Which ones?

Hepatitis
Inflammation of the liver not necessarily infective Raised LFTs Very high AST and ALT High Br Viral serology essential Autoantibodies for autoimmune hepatitis Plasma paracetamol

Hepatitis viruses
A&E
Acute only Faeco-oral tansmission

C
Chronic only
Blood transfusions (iatrogenic) Sexual contact IVDU

B
Acute or chronic Acute blood/sex Chronic perinatally
High risk chronicity Low risk acute illness

D
Acute and chronic Only in the presence of HepB

http://epi.publichealth.nc.gov/cd/lhds/manuals/hepb/docs/hbv_serology.pdf

PSC & PBC

Primary Sclerosing cholangitis
Strong link with IBD (UC) Inflammation & strictures Intra & extra hepatic Male more common Intrahepatic only Autoimmune AMA+ve Granuloma formation Women 9:1

Primary Bilairy Cirrhosis

Both lead to cirrhosis and increase risk of HCC

Metabolic diseases
Wilsons Disease
Copper accumulation ATP27B mutation Cannot excrete from hepatocytes

Alpha-1- antitrypsin deficiency Inactivates neutrophil enzyme Absence of lung enzymes too Emphysema Mortality normally from lung not from liver

 Haemochromatosis
Mutation in HFE gene Excessive iron absorption NOT Lack of excretion
we simply cant

Slate grey / tanned complexion

Thanks for listening.... Any questions?

r.thethi@doctors.org.uk