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Liver and Biliary Disease Liver and Biliary Disease

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Liver and Biliary Disease - PPT Presentation

Rob Grogan rjg17icacuk Year 4 BSc Anaesthesia amp Crit Care Disclaimer amp sponsor MedED does not represent the ICSM Faculty or Student Union This lecture series has been designed and produced by students We have made every effort to ensure that the information contained is ID: 933384

hepatitis liver jaundice acute liver hepatitis acute jaundice cirrhosis viral chronic pain bilirubin hep cancer disease bile biliary infection

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Slide1

Liver and Biliary Disease

Rob Grogan rjg17@ic.ac.uk Year 4 BSc Anaesthesia & Crit Care

Slide2

Disclaimer & sponsor “

MedED does not represent the ICSM Faculty or Student Union. This lecture series has been designed and produced by students. We have made every effort to ensure that the information contained is accurate and in line with Learning Objectives featured on SOFIA, however, this guide should not be used to replace formal ICSM teaching and educational materials.”

Slide3

Conditions

Definition, aetiology, epidemiology, symptoms, signs, investigations

+ Management, complications and prognosis

Gallstones

(Biliary colic, cholecystitis, acute cholangitis)

Alcoholic hepatitis

NASH

Viral hepatitis (see infections 2)

Autoimmune hepatitis

Cirrhosis

Liver failure

Neoplasms (HCC, cholangiocarcinoma and pancreatic cancer)

PSC/PBS

Liver cysts/abscess (see slides)

Wilson’s disease (see slides)

Haemochromatosis (see slides)

Slide4

Learning everything for all conditions

Differentiate conditions based on presentation + common managements

Slide5

SBA 1

A 39 year old female attends her GP for a routine check-up. She is obese and has type II diabetes, and been taking metformin and simvastatin for around 2 years. She complains of mild fatigue but has otherwise been well. She says she drinks around 8 units of alcohol per week. On examination there are no signs of chronic liver disease.

Investigations

Albumin 38 g/L (35-51)

ALT 178 IU/L (<40)

AST 154 U/L (<40)

ALP 57 U/L (35-51)

GGT 19 U/L (11-42)

Bilirubin 12

umol

/L (<17)

What is the most likely diagnosis?

Drug-induced hepatitis

Non-alcoholic steatohepatitis

Alcoholic hepatitis

Viral hepatitis

Cirrhosis

Slide6

SBA 2

A 21 year old male student in London was well until 4 days ago when he developed diarrhoea, vomiting and RUQ pain. Yesterday morning, his flatmates noticed that his eyes had turned yellow. He has not lost any weight in the past few months and his stools are brown. LFTs revealed high transaminases, and a viral screen was ordered.

Viral screen

Anti-

HepA

IgM/IgG Negative

Hep C Virus RNA Undetectable

HBsAg (

HepB

surface antigen) Positive

Anti-

HBcAg

IgM Positive

Anti-

HBcAg

IgG Negative

Anti-HBsAg IgG Negative

Given the diagnosis, what is the most likely

prognosis for this patient?

Full recovery

Carrier status

Chronic hepatitis

Cirrhosis

Hepatocellular carcinoma

Slide7

SBA 3

A 59 year old man with a history of long-standing alcoholism and previous episodes of hepatic encephalopathy presents to ED with altered mental status, fever and worsening abdominal distension and tenderness. An ascitic tap shows neutrophil concentration of 345 cells/mm3

Given the most likely diagnosis, how would you manage this patient?

Reassure and discharge

IM chlordiazepoxide and IV rifaximin

Large volume paracentesis

IV Cefotaxime and oral lactulose

IV vancomycin and IV albumin

Slide8

Jaundice

Increased bilirubin concentration in the blood

Liver

Unconjugated bilirubin

– albumin

Unconjugated bilirubin

Conjugated bilirubin

UDPGT

uridine-

diphosphoglucuronic

glucuronosyltransferase

Conjugated bilirubin in bile

Biliary system

Duodenum

Haeme

Unconjugated bilirubin

and iron

Spleen

Urobilinogen

Stercobilinogen

Slide9

Jaundice

Pre-hepatic

Haemolysis/Gilbert’s

Hepatocellular

Hepatitis

Cirrhosis

Liver mass

Haemochromatosis

Post-hepatic

Gallstone

Pancreatic cancer/(bile duct cancer)

PSC/PBS

Drugs

Bilirubin

(unconjugated)

(mainly conjugated)

(conjugated)

Slide10

Jaundice

Pre-hepatic

Haemolysis/Gilbert’s

Dark urine

(

conj

bilirubin)

Dark urine

(

conj

bilirubin)

+

pale stools

(lack of stercobilin)

+

pruritus

(bile salts)

Post-hepatic

Gallstone

Pancreatic cancer/(bile duct cancer)

PSC/PBS

Drugs

Normal urine

Hepatocellular

Hepatitis

Cirrhosis

Liver mass

Haemochromatosis

Slide11

Jaundice- raised bilirubin

Pre-hepatic

Haemolysis/Gilbert’s

Hepatocellular

Hepatitis

Cirrhosis

Liver mass

Haemochromatosis

Raised bilirubin only

Raised ALP/GGT

Hepatocyte damage

Bile duct damage

Raised AST/ALT

Post-hepatic

Gallstone

Pancreatic cancer/(bile duct cancer)

PSC/PBS

Drugs

Slide12

Hepatitis

Alcoholic

NASH

Viruses

Autoimmune

Inflammation of the liver

Causes?

Drugs

RUQ pain, jaundice, hepatomegaly, joint pain, nausea, fatigue, dark urine

Acute or chronic (<6 months)

Raised AST and ALT

Acute hepatitis

C

hronic hepatitis

Cirrhosis

Recovery

Liver failure

Slide13

Alcoholic liver disease

Steatosis (fatty)

Alcoholic Hepatiti

s

(inflammation)

Completely reversible

Reversible

, especially if mild Irreversible

After few days of heavy drinking

No symptoms

After

long term alcohol use

, rarely after

binge

Nausea, anorexia, weight loss, hepatomegaly

Severe:

fever, jaundice, tachycardia, tender hepatomegaly, bruising, encephalopathy, ascites

Cirrhosis

Come to later

Damage mediated by consumption of NAD+ which promotes fatty infiltration

inflammation

Slide14

Alcoholic hepatitis

InvestigationsFBC: macrocytic anaemia

LFTs: AST/ALT ratio >2,

↑bilirubin, -/↑ALP,

↑GGT

, ↓ albumin

Clotting:

↑ prothrombin time sensitive marker of significant liver damage

Imaging: hepatic USS

Liver biopsy (diagnostic, rarely needed) and histology: ballooning,

Mallory bodies indicates hepatitis

Management

Alcohol abstinence

+ withdrawal management (diazepam)

Nutrition (enteral preferred, calories

and vitamins)

Weight loss/stop smoking

Steroids in severe alcoholic hepatitis

Alcohol then to

ast

Slide15

Non-alcoholic fatty liver disease (NAFLD)

Steatosis (fatty)

Steatohepatitis

(NASH)

(inflammation)

Fatty liver in those who do not consume alcohol in amounts generally considered harmful to the liver

RFs:

Obesity

(truncal),

insulin resistance/diabetes

,

hyperlipidaemia

, hypertension, metabolic syndrome, short bowel syndrome, TPN.

Signs of insulin resistance (polyuria, polydipsia, acanthosis nigricans)

Ix

LFTs: AST:ALT elevated <1, GGT/ALP may also be elevated. Check glucose

Mx

Diet and exercise; controlling RFs (e.g., statins for

hypercholesterolaemia

, good blood sugar control for diabetics with metformin/thiazolidinediones)

Cirrhosis

Completely reversible

Reversible

, especially if mild Irreversible

Slide16

SBA 1

A 39 year old female attends her GP for a routine check-up. She is obese and has type II diabetes, and been taking metformin and simvastatin for around 2 years. She complains of mild fatigue but has otherwise been well. She says she drinks around

8 units of alcohol per week. On examination there are no signs of chronic liver disease.

Investigations

Albumin 38 g/L (35-51)

ALT 178 IU/L (<40)

AST 154 U/L (<40)

ALP 57 U/L (35-51)

GGT 19 U/L (11-42)

Bilirubin 12

umol

/L (<17)

What is the most likely diagnosis?

Drug-induced hepatitis

Non-alcoholic steatohepatitis

Alcoholic hepatitis

Viral hepatitis

Cirrhosis

Slide17

Viral hepatitis A and hepatitis E

Hepatitis A&E –

Acute

F

ae

co

-oral spread (sex/contaminated water)

Management –

Supportive. Avoid alcohol/excess paracetamol

Slide18

Viral hepatitis

See infections 2 for Mx

Serology- Hep A Hep E

IgM- Now

IgG- Gone

Slide19

Viral hepatitis B, C and D

Hepatitis B&C – Acute or chronic C

most commonly becomes chronic

B usually stays acute (80-90%)

As can be chronic, risk of cirrhosis/HCC (hep C)

Hep D Coinfection/superinfection of hep B.

Increases risk of liver failure for hep B

Management

Hep B: Acute

 supportive Chronic  antiviral

(e.g., peginterferon-a-2a OR tenofovir)

Hep C: Acute  antiviral Chronic  antiviral

(e.g., sofosbuvir, ledipasvir)

Slide20

Viral hepatitis

Serology- Hep B

Slide21

Serology- Hep B

Anti-HBs antibody from vaccine OR cleared infection

HBeAg

represents degree of replication and thus infectivity, HBV DNA shows viral load

Slide22

Serology- Hep D (firstly, confirm Hep B, then:

Serology- Hep C

HDV IgG

Slide23

SBA 2

A 21 year old male student in London was well until 4 days ago when he developed diarrhoea, vomiting and RUQ pain. Yesterday morning, his flatmates noticed that his eyes had turned yellow. He has not lost any weight in the past few months and his stools are brown. LFTs revealed high transaminases, and a viral screen was ordered.

Viral screen

Anti-

HepA

IgM/IgG Negative

Hep C Virus RNA Undetectable

HBsAg (

HepB

surface antigen) Positive

Anti-

HBcAg

IgM Positive

Anti-

HBcAg

IgG Negative

Anti-HBsAg IgG Negative

Given the diagnosis, what is the most likely

prognosis for this patient?

Full recovery

Carrier status

Chronic hepatitis

Cirrhosis

Hepatocellular carcinoma

Slide24

Viral hepatitis

Key features

Mx

A + E

Acute

F

ae

co

-oral

spread (

oro

-anal sex; dirty water)

E can be chronic in immunocompromised

E can be severe in pregnancy (

 liver failure)

Supportive for A & E

Avoid alcohol

Antiviral (ribavirin) for immunocompromised with hep E

BAcute or chronicMost adults clear it (full recovery); 10% become carriers; 10% get chronic hep BChildren more likely to be carriers/chronicSexually transmitted; IVDU; vertical

Acute:

supportive (most will clear)

Chronic:

Peginterferon-a-2a

C

Acute

or

c

hronic

Most adults develop chronic

hepatits

(80%), only 30% clear it

. Usually asymptomatic infection.

HCCBlood product spread (IVDU/transfusion)Acute: Antivirals (do not wait for natural clearance)Chronic: Antivirals

(see notes for choice)DSuperinfection of B- requires

HbSAg to infect cellsPeginterferon-a AND tenofovir

Slide25

Hepatitis- distinguishing features

Alcoholic

NASH

Viral

Drug

AI

Hx

Long term

alcohol misuse

(but can be after binge)

Insulin resistance, diabetes, obesity, lack of XS alcohol

A&E: travel to endemic area/

faeco

-oral (contaminated water)

B: Unprotected sex/MSM/verticalC: blood products (IVDU needle sharing)FEVERMany drugs, important one is paracetamol (

 acute liver failure)

Others: NSAIDs, GCs, isoniazid,

fluclox, erythromycinOther AI disease (T1DM, hashimoto’s, coeliac) F>MIxAST:ALT >2↑GGTAST:ALT <1AST/ALT (in 1000s)Viral serologyAST/ALT (in 1000s)Serum paracetamol concentrationAST/ALTANA, ASMA (Biopsy: interface hepatitis + plasma cells)Mx

Alcohol abstinence, nutrition, (steroids)

Diet + exercise + RF control

See viral hepatitis table

Paracetemol

overdose- N-acetyl cysteine

Not required for year 3

Slide26

Haemochromatosis

Definition: condition leading to abnormal iron deposition in certain organs

(liver

,

pancreas

, skin, pituitary, heart, joints)

Primary haemochromatosis

Hereditary- autosomal recessive.

Cannot stop iron absorption from GI tract

Secondary haemochromatosis

Iron overload e.g., multiple transfusions,

Clinical features:

75% asymptomatic.

Key symptoms are hepatomegaly,

diabetes mellitus onset

,

bronze skin

, arthralgia, male impotence

M experience before F

May progress to cirrhosis and HCC

Investigations:

1

st-

Transferrin saturation (raised) and serum ferritin (raised,

non-specific as acute phase protein

)

Gene typing of HFE

Liver biopsy (gold standard)

Hereditary (AR) or multiple transfusions

Bronze skin

Onset of diabetes

Arthralgia, heart disease

Slide27

Wilson’s disease

Definition: Impaired copper

excretion, copper accumulates in liver and brain

Clinical features:

Hepatitis + dementia + parkinsonism in young person

Hepatosplenomegaly,

abdo

pain, jaundice, ascites, portal HTN

Kayser-Fleischer rings

Epidemiology:

Autosomal recessive genetic disorder. Age of onset 5-35 years

Investigations

1

st-

LFTs (raised transaminases/bilirubin), 24-hr urinary copper, slit lamp examination

↓ serum ceruloplasmin (copper transport protein), ↑ serum free copper and urinary copper excretion

Genetic testing/liver biopsy and measurement of copper content (gold standard)

Slide28

Cirrhosis

AetiologyAlcohol misuse, viral hepatitis (B/C), autoimmune hepatitis, haemochromatosis, NASH, chronic biliary disease

(Macronodular- viral Micronodular- alcoholic)

Normal liver replaced with

fibrosis

and

nodules

of regenerating hepatocytes

Can be stable or decompensated (liver failure)

Slide29

Stigmata of chronic liver disease

Slide30

Portal hypertension

↑ pressure in portal vein due to cirrhosis (of any cause)

Blood flows from portal to systemic circulation (

porto

-systemic

anastamosis

)

Lower

eosophagus

Anal canal

Umbilicus

Splenorenal

This leads to:

Distended veins (varices)

Ascites

Splenomegaly

Slide31

Signs of portal hypertension

Slide32

Cirrhosis

ManagementTreat cause + avoid hepatotoxic drugs (alcohol, sedative, opiates, NSAIDs etc.)

Monitor risk of complications (MELD score, 6-monthly USS, endoscopy upon diagnosis and every 3 years)

Manage complications:

Encephalopathy

Treat precipitating event (GI bleed, infection etc.) + short term protein restriction

Oral l

actulose, phosphate enema

Avoid sedatives

Slide33

Encephalopathy

Key RFs:

GI bleed, infection

Slide34

Cirrhosis

ManagementTreat cause + avoid hepatotoxic drugs (alcohol, sedative, opiates, NSAIDs etc.)

Monitor risk of complications (MELD score, 6-monthly USS, endoscopy upon diagnosis and every 3 years)

Manage complications:

Encephalopathy

Treat precipitating event (GI bleed, infection etc.) + short term protein restriction

Oral l

actulose, phosphate enema

Avoid sedatives

Ascites

Sodium restriction ±

Diuretics (

fures+spir

) ±

Large volume paracentesis

Spontaneous bacterial peritonitis*

Abx (cefuroxime+

metronidazole)

*(>

250 neutrophils per mm

3

 ascitic fluid)

E.Coli

Varices

Primary prophylaxis

Non-selective

β

-blocker (if small), EVL (if big)

Ruptured (

haematemesis)

ABCDE, IV fluids/blood (when Hb<7g/dL)

Terlipressin

+ Abx

EVL (after resuscitation, when

haemody

stable)

Secondary prophylaxis

Non-selective

β

-blocker (to replace

terlipressin

after 2-5 days)

TIPS procedure (EVL +

β

-blocker fails to prevent)

*uncontrollable bleeding use balloon tamponade/metal mesh stent

Slide35

SBA 3

A 59 year old man with a history of long-standing alcoholism and previous episodes of hepatic encephalopathy presents to ED with altered mental status

, fever

and

worsening abdominal distension and tenderness

. An ascitic tap shows neutrophil concentration of

345 cells/mm3

Given the most likely diagnosis, how would you manage this patient?

Reassure and discharge

IM chlordiazepoxide and IV rifaximin

Large volume paracentesis

IV Cefotaxime and oral lactulose

IV vancomycin and IV albumin

Slide36

Liver failure

Definition: severe liver dysfunction leading to jaundice, encephalopathy and coagulopathyAcute: paracetamol overdose

(transaminitis +++) (50% of ALF)/ viral hepatitis

Acute-on-chronic

: acute

decompensation

in patients with chronic liver disease

Ix

Identify cause (viral serology, paracetamol levels, etc.)

Mx

See acute med for paracetamol overdose

Treat complications

Liver transplant

Slide37

Liver abscesses/cyst

Pyogenic abscess

S. Aureus (kids), E. Coli (adults)

60% related to biliary disease

e.g., gallstones, strictures

Amoebic abscess

Entamoeba histolytica

infection (

faeco

-oral spread)

Amoebic dysentery (profuse bloody diarrhoea)

Hydatid cyst

Tapeworm

Echinococcus granulosis

infection

Can be massive. Sheep-rearing countries

Definition:

Liver infection

 walled off collection pus/cyst fluid

Hx:

Fever, malaise, weight loss, RUQ pain (

shoulder pain), jaundice. Foreign travel.

Ex:

Jaunice, tender hepatomegaly, dullness to percussion/↓ breath sounds at right

lung base

Ix

: Bloods (FBC- mild anaemia,

leukocytosis

,

eosinophilia for hydatid cyst

Stool microscopy: For

Entamoeba histolytica

or

Echinococcus granulosis

Aspiration and culture of abscess: pyogenic (most polymicrobial), amoebic (anchovy sauce with necrotic hepatocytes/trophozoites)

TB

Extrapulmonary manifestation!

Slide38

Slide39

SBA 4

A 38 year old lady attends the A&E department with jaundice, itchy skin and dark urine for the last few days. On examination, there were no signs of liver disease, but scratch marks on her arms. Her past medical history includes a benign breast lump which was removed 3 years ago, and a UTI treated one week ago at the GP. She has only ever drunk 14 units of alcohol per week and smokes 15 cigarettes per week.

Investigations

Albumin 38 g/L (35-51)

ALT 65 IU/L (<40)

AST 55 U/L (<40)

ALP 1024 U/L (35-51)

GGT 59 U/L (11-42)

Bilirubin 245

umol

/L (<17)

What is the most likely diagnosis?

Alcoholic hepatitis

Pancreatic cancer

Drug induced cholestasis

Choledocholithiasis

Acute cholangitis

Slide40

SBA 5

A 35-year-old obese woman with a history of gallstones presents to the emergency department with severe, constant right upper quadrant (RUQ) pain for around 16 hours. She has been vomiting and still feels nauseous. O/E the tympanic temperature was 39.8°C, murphy’s sign was positive, but no evidence of jaundice.

FBC

WBC 22 x 10^9/L (4-11)

LFTs

No significant abnormalities

Given the likely diagnosis, how would you initially manage this patient?

Oral paracetamol and fluids

Nil by mouth and urgent laparoscopic cholecystectomy

Nil by mouth and urgent ERCP

Clear fluids only, IM diclofenac, IV fluids and antibiotics

Clear fluids only, IM diclofenac, IV fluids and antibiotics and percutaneous cholecystostomy

Slide41

SBA 6

A 43-year-old man with a history of mild ulcerative colitis is noted to have markedly elevated serum alkaline phosphatase, slightly elevated aminotransferases, and normal bilirubin on routine laboratory testing. He complains of fatigue and upper abdominal pain.

Which investigative finding fits the likely diagnosis?

Presence of antimitochondrial antibodies

Presence of anti-smooth muscle antibodies

Beads on a string appearance on MRCP

Raised CA19-9 tumour marker

Presence of

antihepatitis

B surface antigen antibody (anti-HBsAg)

Slide42

Jaundice- raised bilirubin

Pre-hepatic

Haemolysis/Gilbert’s

Hepatocellular

Hepatitis

Cirrhosis

Liver mass

Haemochromatosis

Normal LFTs

Raised ALP/GGT

Hepatocyte damage

Bile duct damage

Raised AST/ALT

Post-hepatic

Gallstone

Pancreatic cancer/(bile duct cancer)

PSC/PBS

Drugs

Slide43

SBA 4

A 38 year old lady attends the A&E department with jaundice, itchy skin and dark urine for the last few days. On examination, there were no signs of liver disease

, but scratch marks on her arms. Her past medical history includes a benign breast lump which was removed 3 years ago, and a

UTI treated one week

ago at the GP. She has only ever drunk

14 units of alcohol per week

and smokes

15 cigarettes per week

.

Investigations

Albumin 38 g/L (35-51)

ALT 65 IU/L (<40)

AST 55 U/L (<40)

ALP 1024 U/L (35-51)

GGT 59 U/L (11-42)

Bilirubin 245

umol

/L (<17)

What is the most likely diagnosis?Alcoholic hepatitisPancreatic cancer

Drug induced cholestasis

Choledocholithiasis

Acute cholangitis

Slide44

Post-hepatic jaundice

Diagnosis

Typical features

Pathogenesis

Gallstones

Hx biliary colic or cholecystitis

Small gallstones get through the cystic duct into biliary tree

Cholangitis

Charcot’s triad:

Pain, fever, jaundice

Ascending infection of bile ducts by

E. Coli

in stagnant bile

Pancreatic cancer

Painless jaundice + palpable gall bladder (Courvoisier’s)Tumour (usually in) head of pancreas occludes distal bile ductBile duct cancer (aka cholangiocarcinoma)Gradual onset obstructive pattern

Direct occlusion by disease

PBC/PSC

PBC: Hx of AI condition

PSC: Hx of UCChronic inflammation of bile ducts

Slide45

Gallstones- easy

Gallstone in gallbladder=

Cholelithiasis

Cholelithiasis + pain=

Biliary colic

Cholelithiasis + inflammation ±secondary infection=

Acute cholecystitis

No jaundice

!

Not obstructing biliary flow*

Ix

 USS liver and biliary tree

Slide46

Gallstones- easy

Gallstone in gallbladder=

Cholelithiasis

Cholelithiasis + pain=

Biliary colic

Cholelithiasis + inflammation ±secondary infection=

Acute cholecystitis

Mx

Incidental finding… no Mx

Analgesia + elective lap chole

Initial:

Clear fluids only. Analgesics, fluid resus,

broad IV Abx if infection.

Definitive: Lap chole

(within 1 week if uncomplicated)

Slide47

Gallstones- easy

Gallstone in CBD=

Choledocholithiasis

Choledocholithiasis + infection=

Ascending cholangitis

May be jaundice/raised

ALP/GGT

Obstruction to biliary flow

Choledocholithiasis + pain=

Biliary colic

Ix

:

USS liver and biliary tree

ERCP if suspect acute cholangitis

Slide48

Gallstones- easy

Gallstone in CBD=Choledocholithiasis

Choledocholithiasis + infection=

Ascending cholangitis

Choledocholithiasis + pain=

Biliary colic

Mx

(Analgesia) + ERCP

+ lap chole

Slide49

Endoscopic Retrograde Cholangio

-Pancreatography (ERCP)

Slide50

Gallstones- easy

Gallstone in CBD=Choledocholithiasis

Choledocholithiasis + infection=

Ascending cholangitis

Choledocholithiasis + pain=

Biliary colic

Mx

(Analgesia) + ERCP

+ lap chole

Initial:

Clear fluids only.

Analgesics, fluid

resus, broad IV Abx

+ ERCP

Lap chole

Slide51

Gallstones- all in 1 slide

Symptomatic cholelithiasis

Choledocholithiasis

Acute cholecystitis

Acute cholangitis

Sx

RUQ pain

Jaundice

Fever

X/✓

(post-prandial)

X

X

X/

X

(Murphy’s +ve)X (NOTE!)

Bloods WCC

LFTs

-

-

-

-/slightly ↑

-/slightly ↑

Take cultures

Imaging(diagnostic)US: stones in GB (acoustic shadow)

US: stones in CBD +/-dilated CBDUS: stones in GB + GB wall thickening + GB lumen dilation(USS)ERCP if charcot’s triadInitial managementIF SYMPTOMATIC

AnalgesiaAnalgesia+ERCP (regardless of symptoms)

Clear fluids only. Analgesics, fluid resus, broad IV Abx if infection.

Clear fluids only. Analgesics, fluid

resus, broad IV Abx +

ERCP Definitive managementElective lap chole

Elective lap choleEarly lap chole within a week of onset. Otherwise, delayed to let inflammation settle.Elective lap chole

ComplicationsBiliary colic, acute cholecysitis

, choledocholithiasisObstructive jaundice, acute cholangitis, pancreatitisGallbladder empyema, porcelain gallbladder, risk of GB cancer, gallstone ileus

Bile duct perforation/bile peritonitis/sepsis

Charcot’s triad

Slide52

Gallstones

Pigment stones (5%)

Calcium bilirubinate

HAEMOLYSIS!

(liver fluke)

Risk factors: 5 Fs

Fair

Fat

Fertile (1 or more kids)

Female

Forty

+OCC, Crohn’s

Mixed stones (80%)

Cholesterol stones (10%)

>50% cholesterol

Slide53

SBA 5

A 35-year-old obese woman with a history of gallstones presents to the emergency department with severe, constant right upper quadrant (RUQ)

pain for around 16 hours. She has been vomiting and still feels nauseous

. O/E the tympanic temperature was

39.8°C

,

murphy’s sign was positive

, but

no evidence of jaundice.

FBC

WBC 22 x 10^9/L (4-11)

LFTs

No significant abnormalities

Given the likely diagnosis, how would you initially manage this patient?

Oral paracetamol and fluids

Nil by mouth and urgent laparoscopic cholecystectomy

Nil by mouth and urgent ERCP

Clear fluids only, IM diclofenac, IV fluids and antibiotics Clear fluids only, IM diclofenac, IV fluids and antibiotics and percutaneous cholecystostomy

Slide54

PBC and PSC

Both inflammatory conditions of the bile ducts causing cholestasis

Primary biliary cirrhosis

Intrahepatic ducts only

F>M

Histology- ‘florid duct lesion’

Assoc. with

Sjorgen’s

, RA

Raised

antimitochondrial antibodies

usually diagnostic

Cirrhosis, HCC,

granulomas

Primary sclerosing cholangitis

Intra and extra-hepatic ducts

M>F

Histology- ‘

concentric onion skin fibrosis

Assoc. with

ulcerative colitis

Diagnose with MRCP (

beaded appearance

)- segmental fibrosis with saccular dilation

Many antibodies including

pANCA

may be raised

Complications include

cirrhosis

, HCC,

cholangiocarcinoma

PBC- “b

i

liary”-

intrahepaticPSC- “scleros

ing” – intra- and

extra- hepatic

Slide55

Pancreatic cancer

Pancreatic cancer- painless jaundice,

palpable gallbladder*

Mostly adenocarcinoma from exocrine tissue- 75% in

head

of pancreas

RFs: Smoking, obesity, TD2M, chronic pancreatitis

S+S. Commonly

delayed

presentation due to non-specific signs (malaise, weight loss,

abdo

pain). Jaundice is later sign.

Hepatomegaly if hepatic metastasis

Ix

1st- Can do USS but

pancreatic protocol CT

more sensitive and

shows

the extent of local or distant spread

Gold standard- biopsy (via ERCP/EUS)

Tumour marker: CA19-9

Slide56

Malignant liver tumours

Primary tumoursHepatocellular carcinoma (90%)

Cholangiocarcinoma

SECONDARY TUMOURS

(most common)

Metastasised commonly from bowel, breast,

eosophagus

, stomach, pancreas

Slide57

Hepatocellular carcinoma (aka hepatoma)

Primary malignancy of hepatocytes usually in cirrhotic liver

RF: hep C, hep B, alcoholic liver disease, AIH, haemochromatosis, NAFLD, aflatoxin, PBC. Smoking, obesity

S+S: Malaise, weight loss, anorexia, (RUQ pain). Jaundice, ascites (due to chronic liver disease) cachexia, hepatomegaly

Ix

LFTs, viral serology

Tumour marker: AFP

6 monthly

USS

for those at high risk of HCC/ 2

wk

wait if liver mass

Liver CT to confirm

Liver biopsy (gold standard)

Slide58

Bile duct cancer (cholangiocarcinoma)

Usually adenocarcinomas of bile duct epithelium

RFs:

PSC

, worm infections and cirrhosis

Can arise from intra-, extra-hepatic ducts or the gallbladder

S+S and

Ix

same as pancreatic cancer

-these diseases are distinguished by imaging/histology

Pancreatic cancer more common

Ix

1st- Abdo USS (dilated intrahepatic ducts, mass lesion)

Gold standard- biopsy (using ERCP)

Slide59

Before reviewing last SBA….

Took me: 21hrs

Takes you: 30 seconds

Feedback

Pleaseeeee

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Even if viewing slides later!

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robliver

Slide60

SBA 6

A 43-year-old man with a history of mild ulcerative colitis is noted to have markedly elevated serum alkaline phosphatase

, slightly elevated aminotransferases, and normal bilirubin on routine laboratory testing. He complains of fatigue and upper abdominal pain.

Which investigative finding fits the likely diagnosis?

Presence of antimitochondrial antibodies

Presence of anti-smooth muscle antibodies

Beads on a string appearance on MRCP

Raised CA19-9 tumour marker

Presence of

antihepatitis

B surface antigen antibody (anti-HBsAg)

Slide61

Slide62

Thank you

tinyurl.com/

robliver

Questions to:

Rob Grogan

rjg17@ic.ac.uk