Hepatology + Pancreatobilliary Disease Flashcards
What are 4 functions of the liver?
Detoxification of xenobiotics
Synthesis of plasma proteins and clotting factors
Site of gluconeogenesis
Production of bile
Clinical presentation of acute liver injury
Malaise
Nausea
Anorexia
Jaundice (occasionally)
Clinical presentation of chronic liver injury
Ascites, Oedema
Haematemesis (varices)
Malaise, anorexia,
Bruising, itching
Palmar erythema, spider naevi, clubbing
Hepatomegaly
Fetor hepaticus - patient breath smells like rotten eggs and garlic
What are examples of liver function tests?
Serum bilirubin
Serum albumin
Prothrombin time
Liver enzymes:
Serum alkaline phosphatase (ALP)
Serum aspartate aminotransferase (AST)
Serum alanine aminotransferase (ALT)
Gamma glutamyl transpeptidase (GGT)
What is the relevance of checking aminotransferase (ALT/AST) levels?
These enzymes are contained in hepatocytes and leak into the blood with liver cell damage.
What is a consequence of chronic liver disease?
Can lead to liver fibrosis and eventually cirrhosis.
What can be calculated using ALT and ALP as a clinical indicator?
ALT:AST ratio
What would the ALT:AST ratio be like in viral hepatitis?
ALT>AST (>1)
What would the ALT:AST ratio be like in alcoholic liver disease/steatohepatitis?
AST>ALT (<1)
What is an indicator of liver cirrhosis in viral hepatitis?
ALT:AST ratio <1 (AST higher than ALT)
What would cause raised serum ALP levels?
Intrahepatic and extrahepatic cholestatic disease of any cause, due to increased synthesis.
What is jaundice?
Yellowing discolouration of the skin and eyes due to hyperbilirubinaemia causing bilirubin deposition.
Aetiology of pre-hepatic jaundice
Gilbert’s syndrome (underactivy in UDP glucoronyltransferase enzyme)
Crigler-Najjar syndrome - deficiency in UDP glucoronyltransferase.
Haemolysis
What can cholestatic jaundice be classified into?
Hepatic and post-hepatic jaundice.
Aetiology of hepatic/intrahepatic jaundice
Viral hepatitis (ABCD, EBV)
Alcoholic hepatitis
Hepatocellular carcinoma
Congestive heart failure
Aetiology of post-hepatic/extrahepatic jaundice
Gall stone in bile duct
Cholangitis (bile duct inflammation)
Bile duct carcinoma
Which type of jaundice is caused by high levels of uncongugated bilirubin?
Pre-hepatic jaundice
Which type of jaundice is caused by high levels of conjugated bilirubin?
Cholestatic (intra + extrahepatic) jaundice.
Clinical presentation of pre-hepatic jaundice
Normal urine
Normal stools
No itching
Normal LFTs
Clinical presentation of cholestatic jaundice
Dark urine
Pale stools
Itching - gets worse when feeling hot.
Abnormal LFTs
Upper abdomen pain radiating to shoulder.
Investigation of jaundice
Abdominal ultrasound to check for biliary obstruction
Check for viral markers
Liver enzymes (ALT, ALP, AST)
Aetiology/risk factors for cholelithiasis (hepatobilliary stones)
Female, fat (obesity), fertile (multiparity), forty, fair.
Haemolytic anaemia
Clinical presentation of hepatobilliary stones
Epigastric/right hypochondriac colic
Despite colic name, severe, constant crescendo-ing pain.
Can increase after a fatty meal.
Can radiate to shoulder due to diaphragmatic irritation.
Can be accompanied by nausea/vomiting.
Can cause jaundice + associated symptoms if in billiary tree.
What conditions can be caused by gallbladder stones?
Cholecystis
Obstructive jaundice (Mirrizi syndrome)
What conditions can be caused by intra and extrahepatic stones?
Primary sclerosing cholangitis
Pancreatitis
Obstructive jaundice
Management of hepatobilliary stones
Gall bladder stones;
Laparoscopic cholecystectomy
Bile acid dissolution therapy (<1/3 success)
Bile duct stones:
ERCP with stent placement
Aetiology of acute cholecystitis
Cholelithiasis
Pathophysiology of cholecystitis
Obstruction causes distension of gall bladder due to increased bile storage.
Can result in ischaemia, progressive inflammation, and infection.
Clinical presentation of cholecystitis
Biliary colic
Can progress to right upper quadrant pain due to peritoneal involvement.
Fever
Murphy’s sign - pain during inspiration when examiner’s hands are on the gall bladder.
Investigation of acute cholecystitis
First line: Abdominal ultrasound
LFTs: Normal-High ALP, ALT, bilirubin
Raised CRP, ESR
Management of acute cholecystis
IV fluids
Opiate analgesia
IV antibiotics
Laparoscopic cholecystectomy
What bacteria are associated with cholecystitis?
Klebsiella
Escherichia coli
Enterococcus
Pseudomonas species
Bacteroides fragilis,
Clinical presentation of acute/ascending cholangitis
Reynold’s pentad:
Biliary colic (RUQ pain)
Fever
Cholestatic jaundice - dark urine, pale stools and skin may itch
Confusion/altered mental state
Hypotension
Investigation of acute/ascending cholangitis
Abdominal ultrasound - FL
MRCP - GS
FBC: Elevated neutrophil count
Raised ESR, CRP
LFTs:
Raised serum bilirubin - bile duct obstruction if very high
Raised serum ALP
High ALT + AST, (ALT>AST)
Management of acute/ascending cholangitis
ERCP or laporoscopic cholesystectomy
IV antibiotics - cefotaxime, metronizadole
Aetiology of drug induced liver injury
Antibiotics
CNS drugs
Analgesics
Examples of antibioitics that can cause drug induced liver injury
Rifampicin
Flucloxacillin
Co-amoxiclav (augmentin)
How does paracetamol get metabolised by the liver normally?
Normally, mostly P2 metabolism.
Some levelof PI metabolism via oxidation which causes toxic NAPQI production
It is conjugated with glutathione and subsequently excreted.
Hepatic pathphysiology of paracetamol overdose induced liver injury
Large amounts of paracetamol causes shunting to P1 metabolism, causing increased NAPQI production.
Glutathione depletion occurs, causing NAPQI buildup.
Can lead to kidney tubular necrosis and hepatic failure if left untreated.
Clinical presentation of paracetamol induced liver injury
Anorexia, nausea and vomiting
Acute RUQ pain
Jaundice, confusion.
Investigation of paracetamol induced liver injury
Raised ALT, PTT (>70 sec)
Metabolic acidosis (pH <7.3)
Raised creatinine
Management of paracetamol induced liver injury
Activated charcoal
IV N-Acetylcysteine - replenishes glutathione stores
What is ascites?
Ascites is the accumulation of free fluid within the peritoneal cavity.
Aetiology of ascites
Liver cirrhosis
Portal hypertension
Peritonitis, TB
Nephrotic syndrome
Hypoalbuminemia (low oncotic pressure)
Ovarian, uterine, neoplasia
Pathophysiology of ascites
Portal hypertension = splanchnic vasodilation causing fluid leakage and activation of RAAS = fluid retention.
Hypoalbuminaemia = low oncotic pressure = fluid leakage.
Clinical presentation of ascites
Abdominal swelling, distended abdomen.
Shifting dullness - muffled sound upon abdominal percussion.
Peripheral oedema
Management of ascites
Fluid and salt restriction
Diuretics - spironolactone, furosemide
Fluid drainage - paracentesis
Trans-jugular intrahepatic portosystemic shunt (TIPS)
What parameter after ascites paracentesis can be used to asses the cause of ascites?
Serum–ascites albumin gradient
(Serum albumin - ascities fluid albumin)
> 1.1 g/dl indicates portal hypertension.
Pathophysiology of alcohol-induced hepatic steatosis.
Ethanol metabolisation causes altered redox potential in liver.
Causes increased fatty acid synthesis and decreased fatty acid oxidation.
Can lead to fat-laden swelling of cells (steatosis)
Clinical presentantation of alcohol-induced hepatic steatosis
Vomiting, nausea, diarrhoea - due to general GI effects of alcohol
Maybe hepatosplenomegaly.
Investigation of alcohol-induced hepatic steatosis
FBC: Macrocytic anaemia indicates heavy drinking.
Liver biochem: Raised ALT and AST
FL: Abdominal ultrasound
GS: Liver biopsy - fatty infiltration
Management of alcohol-induced hepatic steatosis
Drinking cessation
Pathophysiology of alcohol-induced hepatitis
Excessive alcohol can cause infiltration by neutrophils & cause hepatocyte necrosis
Investigation of alcohol-induced hepatitis
Liver biopsy: Mallory bodies, large mitochondria.
FBC: Leucocytosis
Raised serum bilirubin, AST, ALT, ALP, PT
Clinical presentation of alcohol induced hepatitis
Jaundice
Ascites
Fever
Hepatomegaly
Management of alcohol induced hepatitis
Enteral feeding to maintain nutrition.
Antibiotics, antifungal prophylaxis.
Aetiology of portal hypertension
Pre-hepatic: Portal vein thrombosis
Intra-hepatic: Liver cirrhosis, schistosomiasis
Post-hepatic: Budd-Chiari syndrome (hepatic vein thrombosis)
Pathophysiology of portal hypertension
Increased intrahepatic resistance due to injury causes portal hypertension.
Results in splanchnic vasodilation and lowered BP.
Complications of portal hypertension
Gastroesophageal varices, splenomegaly.
What is a varice?
Pathologically enlarged veins.
Aetiolology of oesophageal varices
Portal hypertension
Cirrhosis
Schistosomiasis infection
Alcoholism
Pathophysiology of oesophageal varices
Drop in systemic BP due to portal hypertension causes RAAS activation and increased CO.
Results in high circulating volume which can cause oesophageal varice formation.
Can start bleeding if portal pressure above 12mmHg.
Clinical presentation of oesophageal varices.
Haematemesis
Melaena
Abdominal pain
Hypotension and tachycardia
Splenomegaly
Investigation of oesophageal varices
Endoscopy to find source of bleeding.
Management of oesophageal varices.
IV terlipressin to increase systemic BP
Endoscopic variceal banding.
Propanolol prophylaxis.
Aetiology of non-alcoholic fatty liver disease
Obesity
Hypertension
Type 2 diabetes
Hyperlipidaemia
Pathophysiology of non-alcoholic fatty liver disease
Oxidative stress injury and other factors lead to lipid peroxidation in the presence of fatty infiltration and inflammation.
Fibrosis is caused by insulin resistance which can induce connective tissue growth factor.
Investigation of non-alcoholic fatty liver disease
Abdominal ultrasound - shows steatosis.
Liver biopsy - Mallory bodies.
Management of non-alcoholic fatty liver disease
Lifestyle advice - weight loss, low cholesterol diet, exercise
Pioglitazone
What can cause coma in patients with liver disease?
Hepatic encephalopathy
Hyponatraemia
Hypoglycaemia
Aetiology of liver cirrhosis
Hepatocellular carcinoma
Hepatitis B,C,D
Non-alcoholic fatty liver disease
Chronic alcoholism - most common cause.
What is liver cirrhosis?
End stage, irreversible liver damage characterized by loss of lobular architecture.
Pathophysiology of liver cirrhosis
Liver injury causes necrosis and apoptosis, releasing cell contents and
reactive oxygen species (ROS).
Activation of Kupffer cells causes myofibroblast proliferation.
Myofibroblasts cause collagen deposition and fibrosis.
What are the types of liver cirrhosis?
Micronodular and macronodular cirrhosis
Characteristics of micronodular liver cirrhosis
Regenerating nodules are usually
<3mm in size with uniform involvement of the liver;
Characteristics of macronodular liver cirrhosis
The nodules are of variable size with non-uniform distribution - can be caused by infection.
Aetiology of macronodular liver cirrhosis
Viral hepatitis
Aeitology of micronodular liver cirrhosis
Alcohol or biliary tract disease.
What state can the liver be left in upon cirrhosis?
Compensated - still some liver function left
Decompensated - end stage liver failure
What score can be used to determine the prognosis of liver cirrhosis?
Child-Pugh score.
Risk factors for primary billiary cholangitis
Female, smoking, 40-50 age.
Associated with other autoimmune disorders - hashimoto’s, Sjorgen’s, Keratoconjunctivitis.
Pathophysiology of primary billiary cholangitis
T-cell mediated autoimmune reaction causing bile duct damage.
Chronic granulomatous inflammation which can result in cholestasis.
Clinical presentation of primary billiary cholangitis.
Itching
Fatigue
Jaundice
Abdominal pain
Hepatomegaly
Investigation of primary biliary cholangitis
LFTs: Raised ALP, conj bilirubin, GGT
Low albumin
Serology - antimitochondrial antibodies.
Liver biopsy: Portal tract infilitration with leukocytes
Management of primary biliary cholangitis
Ursodeoxycholic acid - bile acid analogue
Vitamin ADEK supplements
Aetiology/risk factors of primary sclerosing cholangitis
Male gender
Association with ulcerative colitis and cholangiocarcinoma.
Pathophysiology of primary sclerosing cholangitis
Progressive fibrosis, stricturing and scarring of the bile ducts.
Investigation of primary sclerosing cholangitis
Raised ALP and GGT
MRCP - gold standard, beading” of intra/extrahepatic bile ducts
Serology - pANCA
Clinical presentation of primary sclerosing cholangitis
Itching, pain, chills jaundice, inflammatory bowel disease
Management of primary sclerosing cholangitis
Symptomatic management:
- Colestyramine for pruritus (itching)
- Vitamin ADEK supplements
- Liver transplant
What does ERCP and MRCP stand for?
Endoscopic retrograde cholangiopancreatography
Magnetic resonance cholangiopancreatography
How would primary sclerosing cholangitis appear histologically?
Periductal oedema, onion skin appearance.
What is haemochromatosis?
Inherited metal storage disorder causing iron deposition in organs.
Aetiology of haemochromatosis
Autosomal recessive mutation on HFE gene (chromosome 6)
Male gender
Pathophysiology of haemochromatosis
The HFE gene protein interacts with transferrin receptor 1 causing intestinal uptake of iron exceeding transferrin binding capacity.
Disrupts hepcidin expression which does not allow for iron release from cells.
Causes uptake by liver and other organs over a long period and cause fibrosis.
Clinical presentation of haemochromatosis
Men are more symptomatic.
Triad of grey/bronze skin pigmentation (due to melanin deposition), hepatomegaly and diabetes mellitus
Fatigue
Joint pain - arthropathy, especially MCPs.
Hypogonadism
Arrythmias - palpitations
Why are men more symptomatic in haemochromatosis?
Women lose iron through menstruation and have lower dietary iron intake.
Investigation of haemochromatosis
Serum iron - elevated (>30)
Serum ferritin - elevated
Genetic testing for HFE gene
Liver biopsy
Management of haemochromatosis
Venesection
Low iron diet
Avoid fruits
Aetiology of Wilson’s disease
ATP7B gene mutation (autosomal recessive)
How is copper normally metabolized?
Goes from GI tract to liver bound to albumin.
Binds to apoceruloplasmin in the liver, forming ceruloplasmin and secreted into the blood.
Remaining copper excreted into the bile and faeces.
Pathophysiology of Wilson’s disease
Failure of copper excretion from bile due to defective ceruloplasmin transport causes copper deposition into tissues.
Clinical presentation of Wilson’s disease
Acute/chronic hepatitis symptoms e.g jaundice
Tremor, dysarthria, involuntary movements and eventually dementia
Kayser–Fleischer ring, - green brown pigment at corneoscleral junction.
Investigation of Wilson’s disease
Total serum copper - reduced since deposition in tissue.
Ceruloplasmin - decreased
Free copper - increased since less ceruloplasmin for it to be bound to
24 hr Urinary copper - elevated
Liver biopsy
Management of Wilson’s disease
Lifelong penicillamine - copper chelating agent
Trientine & zinc acetate for maintenance in asymptomatic.
Low copper diet (e.g no choc, peanuts)
What is the function of alpha-1-antitrypsin?
Prevents tissue damage by inhibits the proteolytic enzyme neutrophil elastase.
Aetiology for alpha-1-antitrypsin deficiency?
SERPINA1 protein mutation - autosomal recessive.
Pathophysiology of alpha-1-antitrypsin deficiency
Causes panacinar emphesyma in the lungs through alveolar duct collapse.
Liver tissue damage leads to cirrhosis and hepatocellular carcinoma.
Clinical presentation of alpha-1-antitrypsin deficiency
Children: Liver disease, like cirrhosis, jaundice, hepatitis, etc.
Adutls: COPD, emphysema etc with no smoking history.
Investigation of alpha-1antitrypsin deficiency
Low serum α1-antritrypsin
Liver biopsy: PAS positive globules containing misfolded a1 antitrypsin
CXR - Barrel chest
CT chest shows emphysema
Spirometry shows obstruction (FEV:FVC <0.7)
Management of alpha-1 antitrypsin deficiency
Smoking cessation
Management of complications.
Pathophysiology of Budd-Chiari syndrme
Obstruction to the venous outflow of the liver owing to occlusion of the hepatic vein.
Aetiology of Budd-Chiari syndrome
Hepatocellular carcinoma, polycythaemia, thrombus formation, renal tumours.
Clinical presentation of acute Budd-Chiari syndrome
Abdominal pain
Nausea
Vomiting
Tender hepatomegaly
Ascites
Clinical presentation of chronic Budd-Chiari syndrome
Hepatosplenomegaly
Mild jaundice
Ascites
Negative hepatojugular reflux
Portal hypertension.
Investigation of Budd-Chiari syndrome
Early: Hypoalbuminuric ascites fluid
Late: Hyperalbuminuric ascites fluid
Histology - centrilobular compression and necrosis
Ultrasound/CT/MRI - hepatic vein occlusion
Management of acute Budd-Chiari syndrome
Transjugular intrahepatic portosystemic shunt (TIPS)
Anticoagulant prophylaxis
Management of chronic Budd-Chiari syndrome
Liver transplant
Anticoagulant prophylaxis.
Pathophysiology of hepatic encephalopathy
In cirrhosis, portal blood bypasses the liver via collaterals.
Lack of detoxification can cause toxic metabolites like ammonia to build up in the brain.
Clinical presentation of hepatic encephalopathy
Confusion
Liver flap (asterixes - flapping tremor with wrist extended)
Drowsiness
Coma
Investigation of hepatic encephalopathy
EEG
Arterial blood ammonia
Check visual evoked responses
Management of hepatic encephalopathy
Lactulose - reduces colon pH to inhibit NH3 absorption.
Rifaximin - antibiotic that reduces NH3 producing gut bacteria.
What is acute liver failure?
Acute liver failure (ALF) is defined as acute liver injury with encephalopathy and deranged coagulation (INR >1.5) in a patient with a previously normal liver.
Aetiology of acute liver failure
Hepatitis ABDE, Cytomegalovirus
Autoimmune hepatitis
Paracetamol overdose, alcoholism
Hepatocellular carcinoma
Clinical presentation of acute liver failure
Jaundice
Confusion, drowsiness - HE
Spasticity and hyper-reflexia
Cerebral oedema
Fetor hepaticus - patient breath smells like rotten eggs and garlic
Bruising
Investigation of acute liver failure
Hyperbilirubinaemia
ALT, AST - elevated
Low levels of coagulation factors
High ammonia, low glucose
EEG - encephalopathy
Abdominal ultrasound - liver size, hepatic vein patency.
Management of acute liver failure
Treat causative problem.
Coagulopathy - IV Vit K
Raised ICP - IV Mannitol
Encephalopathy - Lactulose
Antibiotic prophylaxis
Aetiology of chronic liver disease
Alcohol
Non alcoholic steatohepatitis (NASH)
Viral hepatitis (B, C)
Immune:
autoimmune hepatitis
primary biliary cholangitis
sclerosing cholangitis
Metabolic:
haemochromatosis
Wilsons
a1 antitrypsin deficiency
Vascular :
Budd-Chiari
Viral aetiology of hepatitis
Hepatitis ABCDE viruses
EBV, CMV, VZV
Organismal aetiology of hepatitis
Protozoa -Toxoplasmis gondii
Bacteria - Syphilis, M.tuberculosis
Non-infective causes of hepatitis
Alcohol
Autoimmune hepatitis
NAFLD
What hepatitis viruses usually cause acute hepatitis?
A & E
Clinical presentation of acute hepatitis
Jaundice
Fever (pyrexia)
RUQ abdominal pain
Tender hepatomegaly
Ascites
Clinical presentation of chronic hepatitis
Palmar erythema
Spider naevi
Dupuytren’s contracture (one or more fingers bending into palm of hand)
Investigation of acute hepatitis
Raised transaminases (ALT/ALP)
With/without raised bilirubin
What can be seen on serology for an acute hepatitis infection?
Anti-Hepatitis X Virus core IgM (e.g Anti-HBc IgM)
Hepatitis X Virus Surface Antigen (e.g HBsAg) - indicates ongoing infection
Hepatitis X e Antigen (e.g HBeAg) - indicates active viral replication and high transmissibility.
What can be seen on serology for a chronic hepatitis infection?
Anti-Hepatitis X Virus core IgG
(e.g Anti-HBc IgG, or HBcAb IgG)
Hepatitis X Virus Surface Antigen (e.g HBsAg) - indicates ongoing infection
If high transmissibility - Hepatitis X e Antigen
(e.g HBeAg)
What can be seen on serology for a patient who is vaccinated against hepatitis?
Antibody to Hepatitis B Virus Surface Antigen
(e.g Anti-HBs)
What can be seen on serology for a patient who has hepatitis immunity through a past infection?
Antibody to Hepatitis B Virus Surface Antigen
(e.g Anti-HBs)
Anti Hepatitis X Virus Core IgG (e.g HBcAb IgG)
Mode of transmission of hepatitis A and E
Faecal-oral route
Aetiology/risk factors for hepatitis A & E
Contaminated food + water
Immunocompromised patients
Prevention of hepatitis A
Active immunisation
Management of hepatitis E
If chronic infection (viral RNA > 6 months), treat with rivabarin.
Which hepatitis viruses have vaccinations?
Hepatitis B & C
Aetiology/risk factors of hepatitis B, C, D
IV drug users
Tatoos
Infected mothers
Unprotected sex
Mode of transmission of hepatitis B, C, D
Blood borne + body fluids
Unprotected sex
Mother to child
Management of chronic hepatitis B
If chronic or severely ill, DNA polymerase inhibitors tenofovir, entecavir + pegylated interferon alpha.
Complications of chronic hepatitis C
Liver cirrhosis and failure
Hepatocellular carcinoma
Prevention of hepatitis B, C, D
Antenatal viral screening
Childhood and healthcare worker immunisation - B
Screening of blood products
Barrier contraceptives
Pathophysiology of hepatitis D
Defective RNA requiring HBsAg for viral replication.
Can be co-infection or superinfection post hepatitis B
Investigation of hepatitis D
Serology:
Co-infection: Anti HBV IgM and Anti HDV IgM
Superinfection: Anti HBV IgG and Anti HDV IgM
Management of hepatitis D
Pegylated interferon-a
Management of hepatitis C
Direct acting antiviral therapy
Ex. Elbasvir/Grazoprevir + ribavarin
Pathophysiology of T1 autoimmune hepatitis
Associated with HLA-DR4 and DR3.
Can have anti-nuclear antibodies (ANA)
Anti smooth muscle antibodies (ASMA)
Anti soluble liver antigen/liver pancreas antibody (ASLA/LP)
Affects middle aged women mainly.
Pathophysiology of T2 autoimmune hepatitis
Associated with HLA DQB1, DRB1
Can have anti-liver kidney microsome antobodies (LKM1), anti-liver cytosol 1 antibody (LC1).
Affects children and young adults mainly.
Investigation of autoimmune hepatitis
Raised immunoglobulins
Serology: Relevant antibodies
Liver biopsy: Piecemeal necrosis (interface hepatitis).
Investigation of hepatobilliary stones
First line: Abdominal ultrasound.
Can also do MRCP - esp if in billiary tree.
High ALT if infection
Aetiology of cholangiocarcinoma
Primary sclerosing cholangitis
Fluke worm infection
Clinical presentation of cholangiocarcinoma
Abdominal pain +/- ascites
Malaise
Jaundice
Dark urine
Pale stools
Investigation of cholangiocarcinoma
First line: Abdominal ultrasound
Gold standard: MRCP
LFT - raised bilirubin and ALP
Management of cholangiocarcinoma
Surgical resection
ERCP with stenting
Aetiology of hepatocellular carcinoma
Liver cirrhosis, viral hepatitis (esp B and C), alcoholic liver disease, NAFLD
Clinical presentation of hepatocellular carcinoma
Weight loss
Hepatomegaly
Jaundice
Ascites
Hepatic encephalopathy
Pruritus
Investigation of hepatocellular carcinoma
First line - abdominal ultrasound
Gold standard - abdominal CT
Serum α-fetoprotein - tumour marker in HCC, will be raised.
Management of hepatocellular carcinoma
Surgical resection of tumour
Liver transplant
What other regions can a hepatocellular carcinoma metastisize to?
Lymph nodes, bones, lungs.
Aetiology of pancreatitis
I - Idiopathic
- G - Gallstones (majority - 60%)
- E - Ethanol (i.e. alcohol - 30%)
- T - Trauma
- S - Steroids
- M - Mumps
- A - Autoimmune
- S - Scorpion venom
- H - Hyperlipidaemia
- E - ERCP (endoscopic retrograde cholangiopancreatography)
- D - Drugs e.g. azathioprine, furosemide (diuretics), corticosteroids, NSAIDs, ACE inhibitors
- Also pregnancy and neoplasia
Pathophysiology of pancreatitis
Buildup of pancreatic enzymes can cause tissue autodigestion and haemhorrage.
Clinical presentation of pancreatitis
Acute epigastric pain radiating to the back.
Retroperitoneal haemhorrage - Cullen and Turner’s sign
Nausea/vomiting
Hypotension due to fluid oedema within gut
Pyrexia
What are Cullen’s and Grey Turner’s signs?
Cullens - periumbilical ecchymosis (skin discoloration)
Grey Turner’s - left flank discoloration
Investigation of pancreatitis
Serum amylase - elevated + diagnostic if combined with symptoms and 3x raised.
GS: Raised serum lipase - specific for pancreatitis
Urinalysis - raised urine amylase
CRP - elevated
Abdominal CT - best imaging if biochem not indicative.
What scoring system is used to assess the severity of pancreatitis?
Apache and Glasgow scoring system.
Complications of acute pancreatiits
Necrotizing pancreatitis
Pseudocyst formation
Progression into chronic pancreatitis
Management of pancreatitis
Nil by mouth to reduce pancreatic enzyme secretion.
Analgesia - tramadol
Antibiotic prophylaxis - cefuroxime, metronidazole.
Aetiology/risk factors of pancreatic cancer
Smoking
Alcohol
Excessive aspirin usage
Old age
Obesity
T2DM
Pathophysiology of pancreatic cancer
Mostly affects exocrine pancreas.
Mainly occurs in the head of the pancreas, but can be in body or tail.
Clinical presentation of pancreatic cancer
Abdominal pain radiating to the back - cancer of body/tail.
Painless jaundice + DUPS - cancer of head
Weight loss
Courvoisier’s sign - palpable pancreas/GB with painless jaundice
Steatorreah = obstruction of pancreatic duct
Investigation of pancreatic cancer
First line - abdominal ultrasound
Gold standard - Abdominal CT with contrast and pancreatic mass protocol.
Management of pancreatic cancer
Surgical removal of tumour - whipple procedure (pancreatoduodenectomy) for head tumors.
Pancreatectomy for body/tail tumours.
Chemotherapy
Differences in acute and chronic pancreatitis
Chronic causes irreversible pancreatic damage e.g fibrosis.
Longer duration of disease.
What vitamin supplementation is used in chronic pancreatitis?
ADEK vitamins because they are fat soluble.
Pancreatitis causes malabsorption of fat due to decreased lipase production.
What type of jaundice is raised ALP an indication of?
Post-hepatic jaundice
What type of jaundice is raised AST/ALT an indiciation of?
Intrahepatic jaundice
Mangement of alcohol withdrawal
Acamprosate/naltrexone - NMDA receptor antagonists.
2 causes of asterixis
Chronic liver disease
CO2 retention
