Hepatobiliary Flashcards
Define acute liver failure
Liver loses its ability to repair and regenerate leading to decompensation. Decompensation is characterised by jaundice, coagulopathy, and hepatic encephalopathy.
Describe the epidemiology of acute liver failure
ALF is the primary indication for liver transplantation in around 8% of cases within Europe.
Describe the aetiology of acute liver failure
Drugs: paracetamol, alcohol.
Viral infection: hepatitis, Epstein Barr virus. Autoimmune hepatitis.
Neoplastic: hepatocellular or metastatic carcinoma.
Metabolic: Wilson’s disease, alpha 1 antitrypsin.
Vascular: Budd Chiari
What are risk factors for acute liver failure
Chronic alcohol abuse, female, chronic hepatitis
Describe the pathophysiology of acute liver failure
Destruction of hepatocytes leads to inflammation and fibrosis. The destruction of the architecture of the nodules of the liver means it cannot perform its functions properly, repair or regenerate.
What are the key presentations for acute liver failure
Jaundice, abnormal bleeding, hepatic encephalopathy (confusion, altered mood, asterixis (liver flap), comatose)
What are the signs and symptoms for acute liver failure
Malaise, nausea, vomiting, confusion, abdominal pain
What is the gold standard investigation for acute liver failure
LFTs: bilirubin, PT/INR, serum AST + ALT, NH3 all raised. Albumin and glucose decreased.
What are the first line investigations for acute liver failure
LFTs: bilirubin, PT/INR, serum AST + ALT, NH3 all raised. Albumin and glucose decreased.
FBC: anaemia, thrombocytopenia, leukopenia. U&E (urea and creatinine raised, deranged electrolytes)
What are further investigations for acute liver failure
Toxicology screen, abdominal USS, blood cultures, EEG for HE
What is the differential diagnosis for acute liver failure
Acute hepatitis, drug or alcohol intoxication, viral infection
What is the management for acute liver failure
1st line – intensive care management, ABCDE, fluids analgesia. Assessment for liver transplant.
Treat underlying causes and complications, e.g., paracetamol overdose
What monitoring is done for acute liver failure
Fluids - urinary and central venous cannulas
Bloods - daily FBC, U&E, LFT and INR
Glucose - 1-4hr + administer IV glucose if needed
What are complications for acute liver failure
Hepatic encephalopathy (lactulose), ascites (diuretics), cerebral oedema (IV mannitol), bleeding (vitamin K), sepsis (sepsis 6, antibiotics)
What is the prognosis for acute liver failure
Survival from ALF is greater than 60% and around 55% of patients will have spontaneous recovery without need for liver transplantation.
The overall one year survival following emergency liver transplantation is around 80%.
Worst prognosis if grade III-IV encephalopathy, age >40 years, low albumin, high INR, DILI. Late onset hepatic failure worse than fulminant failure.
What is the role of the liver
- Storage(i.e. glycogen, iron, vitamins)
- Breakdown(i.e. drugs, toxins, ammonia, bilirubin)
- Synthesis(i.e. bile, cholesterol, coagulation factors, growth factors)
- Immune function(i.e. innate immune protein production, resident immune cells)
Define chronic liver disease
Chronic liver disease is caused by repeated insults to the liver, which can result in inflammation, fibrosis and ultimately cirrhosis.
CLD is generally defined as progressive liver dysfunction for six months or longer. The end result of chronic liver disease is cirrhosis, which describes irreversible liver remodelling.
Describe the epidemiology of chronic liver disease
- CLD represents the fourth commonest cause of years of life lost in those aged under 75.
- In England and Wales an estimated 600,000 patients have CLD.
Describe the aetiology of CLD
Acute liver disease is most common cause, non-alcoholic fatty liver disease.
Acute causes which progress to chronic:
Drugs: paracetamol, alcohol.
Viral infection: hepatitis, Epstein Barr virus. Autoimmune hepatitis. Neoplastic: hepatocellular or metastatic carcinoma.
Metabolic: Wilson’s disease, alpha 1 antitrypsin.
Vascular: Budd Chiar
Describe the risk factors of CLD
Alcohol, obesity, T2DM, drugs, metabolic disease
Describe the pathophysiology of CLD
Destruction of hepatocytes leads to inflammation (hepatitis) which leads to fibrosis (reversible damage). This can progress to cirrhosis - scarring of liver caused by long term liver damage which is irreversible. Cirrhosis can be compensated, with some preserved liver function, or decompensated which causes end-stage liver failure.
What are the key presentations of CLD
Jaundice, ascites, abnormal bleeding, hepatic encephalopathy (confusion, altered mood, asterixis (liver flap), comatose), low serum albumin
Describe the clinical manifestations of CLD
Signs
Portal hypertension, oesophageal varices (enlarged veins), caput medusae (cluster of swollen veins in abdomen), spider naevi, palmar erythema, gynecomastia, clubbing, fetor hepatis (sweet musty rotten egg garlic breath), Dupuytren’s contracture, hepatomegaly
Symptoms
Malaise, nausea, vomiting, abdominal pain, pruritis, bleeding
What is the gold standard investigation for CLD
Liver biopsy (distortion of liver parenchyma)
What are the first line investigations of CLD
1st line LFTs: bilirubin, PT/INR, serum AST + ALT, NH3, GGT all raised. Serum albumin and glucose decreased.
FBC: anaemia, thrombocytopenia, leukopenia. U&E (urea and creatinine raised, deranged electrolytes)
What are other investigations for CLD
Abdominal ultrasound, ascites tap
What are the differential diagnosis for CLD
Budd Chiari, portal vein thrombosis, constrictive pericarditis
What is the management for CLD
1st line – prevent progression, lifestyle monitoring (less alcohol, reduce BMI), liver transplant (MELD score – model for end-stage liver disease. Assesses severity and transplant likelihood).
Manage complications: hepatic encephalopathy, ascites, etc.
What monitoring may be done for CLD
-
Hepatocellular Carcinoma -
- Six monthly surveillance with ultrasound +/- AFP (tumour marker) as patients with cirrhosis are at high risk of HCC
What are potential complications with CLD
- Hepatic encephalopathy
- Ascites
- Gastrointestinal bleeding(i.e. variceal bleed)
- Bacterial infections(i.e. SBP)
- Acute kidney injury
- Hepatorenal syndrome
- Hepatopulmonary syndrome
- Hepatocellular carcinoma
- Acute-on-chronic liver failure
What is the prognosis for CLD
2 years without transplant
Describe the breakdown of RBCs
- Red blood cells are broken down, releasing haemoglobin.
- Haemoglobin is broken down into haem and globin, with haem being further broken down into unconjugated bilirubin and iron. Globin and iron from haem is recycled for erythropoiesis.
Describe the properties of unconjugated bilirubin
- Unconjugated bilirubin is abreakdown product of haemfrom senescent red blood cells
- Unconjugated bilirubin isnot water-solubleand requiresconjugationfor excretion in bile
How is unconjugated bilirubin conjugated
-
UGT (UDP-glucuronosyltransferase)in the liver converts unconjugated bilirubin into conjugated bilirubin, making it water-soluble
- Conjugation involves the addition of glucuronic acid to bilirubin
- Conjugated bilirubin is secreted into the bile canaliculi andstored in the gallbladderas a component of bile
What happens to conjugated bilirubin
- When it is released into the intestinal tract, conjugated bilirubin is broken down intourobilinogenand thenstercobilinby bacteria
- Stercobilin is excreted infaeces, giving it a brown colour
- Some urobilinogen is reabsorbed and is either directed back into making bile (enterohepatic circulation) or transported to the kidney and excreted in theurine, giving it a yellow colour
Define cholelithiasis (gallstones)
Cholelithiasis (gallstones) refers to the development of a solid deposit or ‘stone’ within the gallbladder.
Describe the epidemiology of gallstones
- Gallstones affect up to 20% of the population.
- F>M
- Prevalence increases with age, before levelling off in the sixth - seventh decade of life.
- More common in caucasians, Native American’s and Hispanics.
- The vast majority of people with gallstones will remain asymptomatic (80%).
Describe the aetiology of gallstones
Bile is secreted by hepatocytes into the biliary circulation. It is stored in the gallbladder. Bile is composed of bile acids (or salts), phospholipid, bilirubin, cholesterol and water. Imbalance in composition and stasis leads to stone formation.
What are the risk factors for gallstones
5 Fs: Fat, Fertile, Forty, Female, Fair
Family history, rapid weight loss, diabetes and medications
Describe the clinical manifestations of gallstones
Gallstones: biliary colic severe colicky RUQ pain, comes and goes (>30 minutes), worse after eating a fatty meal. Nausea and vomiting.
What is the gold standard investigation for gallstones
Gallstones: abdominal USS (1. Identify stones, 2. Gallbladder wall thickness – inflammation, 3. Duct dilation)
What are the primary investigations for gallstones
Gallstones: raised ALP, normal FBC and CRP, raised bilirubin if gallstone is blocking bile duct
What are the differential diagnosis for gallstones
Pancreatitis, peptic ulcer disease, gallbladder cancer
What is the management for gallstones
Gallstones: NSAIDs/analgesia. Elective cholecystectomy (surgical removal of gallbladder) Bile duct clearance if gallstones in bile ducts (ERCP).
What are the complications of gallstones
Gallstones > cholecystitis > cholangitis. Sepsis
What is the prognosis for gallstones
The majority of patients with gallstones will be asymptomatic. 1-4% of patients develop gallstone-related complications, the most common being biliary colic. 10-20% of those who have had an attack of biliary colic will go on to develop a more serious complication, such as acute cholecystitis.
Define biliary colic
Biliary colic refers to a pain in the RUQ/epigastrium caused by gallstones.
Though termed a ‘colic’ the pain is normally constant lasting from 30 minutes to 6 hours.
Describe the epidemiology of biliary colic
- It is the most common symptomatic manifestation of cholelithiasis (gallstones) affecting around 10-20% of patients.
- Prevalence increases with age
- F>M
- More common in caucasians, Native American’s and Hispanics.
What are risk factors for biliary colic
Risk factors for gallstones:
5 Fs: Fat, Fertile, Forty, Female, Fair
Describe the pathophysiology of biliary colic
The pain occurs when a stone impacts against the cystic duct during contraction of the gallbladder with increased pressures in the gallbladder itself.
Describe the clinical manifestations of biliary colic
- Nausea and vomiting
- Right upper quadrant pain
- Epigastric pain
- Pain may radiate to right shoulder or interscapular region
Episodes typically last 30 minutes - 6 hours. Often worse after ingestion of fatty foods.
Note: there are no signs on abdominal examination. Murphy’s sign negative.
What are the first line investigations for biliary colic
Abdominal ultrasound - can identify gallstones as well as looking for dilation of the CBD and presence of stones in CBD.
LFTs - may show derangement of LFTs - indicative of stones within the biliary system (which can be asymptomatic). It is essential to identify patients with CBD stones prior to any cholecystectomy.
What are the differential diagnosis for biliary colic
- Cholecystitis
- Ascending cholangitis
- Common bile duct stone
- Gastritis
- Peptic ulcer disease
- IBS
- Carcinoma on right side of colon
- Renal colic
- Pancreatitis
Describe the management for biliary colic
NSAIDs/analgesia. Elective cholecystectomy (surgical removal of gallbladder) Bile duct clearance if gallstones in bile ducts (ERCP).
Describe the complications of biliary colic
- Obstructive jaundice:due to**a stone that obstructs the common bile duct; presents with jaundice, pale stools and dark urine
- Cholecystitis:inflammation of the gallbladder results infever,rightupperquadrantpain(usually > 6 hours) and positiveMurphy’s sign
- Ascending cholangitis:infection of the biliary tree results in ‘Charcot’s triad’ (rightupperquadrantpain,feverandjaundice)
- Acute pancreatitis:gallstones are the most common cause
- Gallbladder empyema
- Gallstone ileus:a rare form of small bowel obstruction due to impaction of a gallstone within the lumen of the small intestine via a cholecysto-duodenal fistula
- Gallbladder cancer: gallstones are thought to increase the risk by up to 5-fold
Define acute cholecystitis
Acute cholecystitis refers to inflammation of the gallbladder most commonly occurring due to impacted gallstones (calculous cholecystitis)
Relatively rarely acute cholecystitis occurs in the absence of gallstones (acalculous cholecystitis).
Describe the epidemiology of acute cholecystitis
Acute cholecystitis occurs in 10% of patients with symptomatic gallstones
What are the risk factors for acute cholecystitis
5 Fs: Fat, Fertile, Forty, Female, Fair
Describe the pathophysiology of acute cholecystitis
Cholecystitis: gallstones block the cystic duct, preventing the gallbladder from draining. Bile builds up and distends the gallbladder which can reduce vascular supply and leads to inflammation.
What are the clinical manifestations for acute cholecystitis
Cholecystitis: RUQ pain, may radiate to right shoulder, fever, fatigue, RUQ tenderness. Murphy’s sign: press on GB and inhale, patient will wince in pain and stop inspiration. Nausea and vomiting.
What is the gold standard investigation for acute cholecystitis
Cholecystitis: abdominal USS (gallstones, thick gallbladder walls from inflammation, fluid around gallbladder)
Describe the first line investigations for acute cholecystitis
Cholecystitis: positive murphy’s sign, FBC: raised WCC and CRP, LFTs may be elevated (ALP, bilirubin, AST and ALT)
What are the differential diagnosis for acute cholecystitis
- Pancreatitis
- Peptic ulcer disease
- Cholangitis
- Appendicitis
- Basal pneumonia
Describe the management for acute cholecystitis
Cholecystitis: IV fluids, antibiotics, analgesia. Cholecystectomy surgery within 72 hours of symptoms. ERCP if gallstones in bile ducts.
What are the complications of acute cholecystitis
- Gallbladder empyema:acute inflammation results in the gallbladder filling with pus and can lead to perforation
- Gallstone ileus:when a gallstone passes from the biliary tract into the intestine via a fistula resulting in small bowel obstruction
- Acute cholangitis: infection of the biliary tree commonly caused by gallstones which move into the common bile duct
- Obstructive jaundice: if stone moves to CBD
- Procedure-related: bile duct injury
What is the prognosis for acute cholecystitis
Prompt medical management with intravenous antibiotics and identification of sepsis alongside an early laparoscopic cholecystectomy is associated with a very good prognosis. In patients with biliary colic without cholecystitis, early laparoscopic cholecystectomy reduces the risk of future episodes and the risk of cholecystitis. Gallbladder perforation has a mortality of over 30%, whilst untreated acute acalculous cholecystitis has a mortality of up to 50%
What does positive Murphy’s sign mean
Murphy’s sign is indicative of cholecystitis. As the patient breathes out, place your hand below the right costal margin. As the patient breathes in an inflamed gallbladder moves inferiorly, the patient catches their breath. To be considered positive, it should be absent on the left side.
Describe chronic cholecystitis
Chronic inflammation of the gallbladder +/- colic
Describe the pathophysiology of chronic cholecystitis
- Repeated lodging and dislodging of gallstone in CBD, causing inflammation and fibrosis of the gallbladder
- In some cases, there may not be lodging and dislodging of gallstones. Instead, gallstones within the gallbladder can cause irritation to the gallbladder and causes damage this way.
- Overtime, this leads to inflammation, fibrosis and maybe even calcification. This is known as porcelain gallbladder. This makes the gallbladder visible on x-ray
Describe the clinical manifestations of chronic cholecystitis
- Flatulent dyspepsia
- Abdominal discomfort - RUQ pain (esp after meal)
- Distension
- Nausea
- Fat intolerance (fat stimulates cholecystokinin release and gallbladder contraction)
Describe the investigations for chronic cholecystitis
- Ultrasound - to image stone and assess CBD diameter
- MRCP - used to find CBD stones
- X-ray - may show porcelain gallbladder
What are the differential diagnosis of chronic cholecystitis
- If symptoms persist post-treatment, consider:
- Hiatus hernia
- IBS
- Peptic ulcer
- Chronic pancreatitis
- Tumour
Describe the management for chronic cholecystitis
- Cholecystectomy
- ERCP + sphincterectomy prior to surgery
What are the complications for chronic cholecystitis
Increased risk of gallbladder cancer
Define acute cholangitis
Acute ascending cholangitis refers to infection of the biliary tree characteristically resulting in pain, jaundice and fevers.
Describe the epidemiology of acute ascending cholangitis
- Acute cholangitis is relatively uncommon and presents as a complication of gallstones in about 1% of patients.
- Age > 50 years
- Affects men and women equally
- There appears to be greater incidence in caucasians, hispanics and Native Americans - following the distribution of gallstones.
- It occurs following ERCP in around 0.5 - 3%.
- Recurrent pyogenic cholangitis is seen in southeast Asian populations.
Describe the aetiology of acute ascending cholangitis
- Choledocholithiasis
- Benign stricture
- Malignant stricture
What are the risk factors for acute cholangitis
- Gallstones:the most common predisposing factor
- Stricture of the biliary tree:benign or malignant
- Post-procedure injuryof the bile ducts e.g. post-ERCP
Describe the pathophysiology of ascending cholangitis
Ascending cholangitis: infection and inflammation of the bile ducts due to prolonged bile duct blockage from gallstones, or bacterial infection from ERCP procedure (E. coli, klebsiella, enterococcus). Bile isn’t ‘flushing out’ the ducts so bacteria migrate from GI tract and cause biliary tree infection. Bile is prevented from entering the GI tract causing jaundice
What are the key presentations of ascending cholangitis
Ascending cholangitis: Charcot’s triad: RUQ pain, fever, jaundice. Patient may have sepsis.
What is the gold standard investigation for ascending cholangitis
Cholangitis: ERCP endoscopic retrograde cholangio-pancreatography (direct observation of bile duct and stones)
What are the first line investigations for ascending cholangitis
Cholangitis: FBC: raised WCC and CRP, leucocytosis. LFTs: raised ALP, aminotransferases, and bilirubin. Blood cultures. Abdominal USS: bile duct dilation and gallstones
What are the differential diagnosis for ascending cholangitis
- Acute cholecystitis
- Peptic ulcer disease
- Pancreatitis
- Hepatic abscess
- Appendicitis
- Biliary colic
Describe the management for ascending cholangitis
Cholangitis: IV antibiotics (cefuroxime and metronidazole), fluids, blood cultures (sepsis risk). ERCP (bile duct clearance) then cholecystectomy.
What are the complications for ascending cholangitis
- Biliary sepsis:the commonest complication and typically presents with Reynolds’ pentad
- Acute pancreatitis:CBD stones can obstruct the pancreatic duct
- Hepatic abscess
- Risks of ERCP: duodenal perforation, pancreatitis, biliary sepsis, intra-abdominal bleeding
What is the prognosis for ascending cholangitis
The majority of patients recover quickly with effective resuscitation, initiation of antibiotics and adequate biliary drainage. The prognosis is worse if decompression is delayed or emergency surgical drainage is required (rather than non-surgical). Factors that predict a poor prognosis include high fever, hyperbilirubinaemia, hypoalbuminaemia, and older age.
Define primary biliary cholangitis
Autoimmune disease where T cells attack cells of small bile ducts in the liver causing inflammation. Leads to cholestasis and subsequent leakage of bile into the circulation
Describe the epidemiology of primary biliary cholangitis
- Rare disease with a prevalence of < 0.05%
- Middle-aged:peak incidence between 45 and 60 years old
- Female gender: ten times more common in females
Describe the aetiology of primary biliary cholangitis
Unknown. Genetic predisposition and environmental factors
Describe the risk factors for primary biliary cholangitis
Female, age 45-60, smoking, other autoimmune disease, rheumatoid diseases, past pregnancy, chronic UTI
Describe the pathophysiology of primary biliary cholangitis
Immune system attacks small intralobular bile ducts in the liver which obstructs bile outflow causing cholestasis. Bile acids, bilirubin and cholesterol build up in the blood as they aren’t being excreted in bile. Bile acids cause itching, bilirubin cause jaundice and cholesterol causes deposits in the skin (xanthelasma) and blood vessels. The back-pressure of the bile obstruction and overall disease process leads to fibrosis, cirrhosis, and liver failure.
Describe the key presentations of primary biliary cholangitis
Pruritis, fatigue, Jaundice, xanthelasma
Describe the clinical manifestations of primary biliary cholangitis
Signs:
Pale stools, signs of cirrhosis (hepatomegaly, ascites, spider naevi)
Symptoms:
Abdominal pain, joint pain
What is the gold standard investigation for primary biliary cholangitis
Anti-microbial antibodies (AMA) present
What are the first line investigations for primary biliary cholangitis
LFTs: raised bilirubin, alkaline phosphatase, aminotransferases, GGT. Decreased albumin. Abdominal USS (excludes extrahepatic cholestasis)
What are further investigations for primary biliary cholangitis
Liver biopsy (bile duct lesions and granuloma formation)
What are the differential diagnosis for primary biliary cholangitis
Primary sclerosis cholangitis (AMA would not be found), obstructive bile duct lesion, cholestasis (pregnancy, drug-induced)
Describe the management for primary biliary cholangitis
1st line – Ursodeoxycholic acid (bile acid analogue reduces intestinal absorption of cholesterol and dampens the inflammatory response).
Cholestyramine (bile acid analogue) for pruritis. Liver transplant if severe
What monitoring needs to be done for primary biliary cholangitis
Regular LFT; ultrasound +/- AFP if cirrhotic (with chronic liver diseases, such as hepatitis and cirrhosis, AFP may be chronically elevated).
What are the complications with primary biliary cholangitis
Liver cirrhosis, portal hypertension, steatorrhea, osteoporosis, hypercholesterolaemia, malabsorption
What is the prognosis for primary biliary cholangitis
Portal hypertension, advanced histological stage, and failure to respond to ursodeoxycholic acid are poor prognostic factors. Median survival is approximately 9 years, however, in patients diagnosed at an asymptomatic stage, survival is twice as high compared to those diagnosed at a symptomatic stage.
Define primary sclerosing cholangitis
Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts, resulting in strictured ‘beaded’ appearance of bile ducts.
Describe the epidemiology of primary sclerosing cholangitis
Male, heavily associated with IBD especially ulcerative colitis, less common than PBC, more common in northern europe and NA. Mean diagnosis is 40
Describe the risk factors for primary sclerosing cholangitis
Male sex, aged 40-50, inflammatory bowel disease (UC and Crohn’s), family history
Describe the pathophsyiology of primary sclerosing cholangitis
Inflammation of intrahepatic and extrahepatic bile ducts leads to fibrosis and stricturing. This obstructs bile flow causing cholestasis. The biliary strictures lead to build up of bile acids and bilirubin in the blood causing pruritis and jaundice. Ongoing strictures eventually leads to fibrosis, cirrhosis, and liver failure.
Describe the key presentations for primary sclerosing cholangitis
Pruritis, fatigue, Charcot’s triad: RUQ abdominal pain, fever, jaundice, hepatomegaly, IBD signs and symptoms
What is the gold standard investigation for primary sclerosing cholangitis
MRCP (magnetic resonance cholangiopancreatography) – bile duct strictures or lesions
What are the first line investigations for primary sclerosing cholangitis
1st line LFTs: raised bilirubin, ALP, AST and ALT, GGT. Decreased albumin.
Serology: no antimicrobial antibodies (AMA), maybe pANCA antibodies
What are the differential diagnosis for primary sclerosing cholangitis
Primary biliary cholangitis/cirrhosis, secondary sclerosing cholangitis, hepatitis
What is the management for primary sclerosing cholangitis
1st line – symptomatic treatment. Ursdeoxycholic acid doesn’t work. Cholestyramine for pruritis (bile acid analogue). Consider liver transplant. Encourage a health lifestyle
What are potential complications for primary sclerosing cholangitis
Portal hypertension, cirrhosis, cholangiocarcinoma, colorectal cancer, hepatic encephalopathy
Describe the prognosis for primary sclerosing cholangitis
Theaverage survivalof patients newly diagnosed with PSC is9.3 to 18 years. Despite the rare nature of this disease, PSC is the5thleading indication for liver transplantationin the USA. For those who receive aliver transplantation, the 5-year survival rate is approximately85%.
Define acute pancreatitis
Sudden and rapid onset inflammation of the pancreas
Describe the epidemiology of acute pancreatitis
- In the UK there are an estimated 30 per 100,000 cases each year and the incidence is increasing globally
- The overall mortality rate in the UK is reported as around 5%, rising to 25% for patients with severe disease.
- In the UK, around 50% of cases are caused by gallstones, 25% by alcohol, and 25% by other factors.
- Increases with advancing age
- Afro-Caribbean ethnicity: risk is 2-3 fold higher in black populations than white
- Sex: alcohol-related pancreatitis is more common in males, whilst gallstone-related pancreatitis is more common in females
- Gallstone pancreatitis is more common in white women >60 years of age, especially among patients with microlithiasis.
Describe the aetiology of acute pancreatitis
I GET SMASHED: Idiopathic, Gallstones, Ethanol (alcohol), Trauma, Steroids, Mumps, Autoimmune, Scorpion sting, Hyperlipidaemia, ERCP, Drugs (diuretics)
Describe the risk factors for acute pancreatitis
Middle-age woman, young/middle-age man, gallstones (MC women), alcohol (MC men), ERCP, diet, obesity, T2DM, family history
Describe the pathophysiology of acute pancreatitis
Gallstones block flow of bile and pancreatic juices into the duodenum. Reflux of bile into pancreatic duct and prevention of pancreatic juice containing enzymes from being secreted results in inflammation. Cascade of zymogen/enzyme activation which triggers the recruitment of inflammatory cells and the release of inflammatory mediators.
Alcohol is directly toxic to pancreatic cells causing inflammation.
Autoimmune: pancreas releases exocrine enzymes which auto digest the pancreas.
What are the key presentations for acute pancreatitis
Severe epigastric pain radiating to the back, vomiting, abdominal tenderness, hypocalcaemia
What are the clinical manifestations for acute pancreatitis
Signs:
Jaundice, tachycardia, Chvostek sign, grey turner (flank bruising) and Cullen sign (periumbilical bruising), signs of hypovolemia and pleural effusion
Symptoms:
Dyspnoea, fever, nausea and vomiting
What is the gold standard investigation for acute pancreatitis
Serum lipase raised (3 times the upper limit level)
What are the first line investigations for acute pancreatitis
Serum amylase raised (3 times the upper limit level), FBC: leucocytosis with left shift (increase in immature:mature WBCs), raised haematocrit, raised CRP. Raised urea, low calcium.
Imaging: chest x-ray, abdominal USS (gallstones), CT scan (inflammation, necrosis, effusions)
Diagnosis needs 2 of 3: acute abdominal pain, elevated pancreatic enzymes (amylase/lipase), abnormal imaging
What are the further investigations for acute pancreatitis
Glasgow score (severity of pancreatitis): Pao2 low, Age >55, Neutrophils raised, Calcium low, uRea raised, Enzymes raised, Albumin low, Sugar raised (PANCREAS)
What are the differential diagnosis for acute pancreatitis
Abdominal aortic aneurysm, peptic ulcer disease, cholangitis, oesophageal spasm
Describe the management for acute pancreatitis
1st line – ABCDE, IV fluids, analgesia, nil by mouth, oxygen, antibiotics, electrolyte replacement.
ERCP for gallstones, treat complications
What are the complications for acute pancreatitis
Renal failure, ARDS, sepsis, pancreatic abscess, pseudocysts, pancreatic necrosis
Describe the prognosis for acute pancreatitis
25% of acute pancreatitis cases are severe and associated with complications. Severe cases often require critical care input, and are associated with prolonged hospital stay and an increased mortality rate (25%), compared to the overall mortality rate (5%).
What is necrotising pancreatitis
A severe subtype of acute pancreatitis
- Necrosis presents within thefirst 24-48 hoursresulting in the death of portions of the pancreas
- It should be suspected in those who continue to haveabdominal pain, nausea and feverdespite supportive management of acute pancreatitis
- Thekey diagnostic factoris non-enhancing low attenuating pancreatic tissue onCT imaging, which signifies necrosis
- Some hospitals performfine-needle aspirationto determine if necrotic tissue is infected, but false negatives are possible
- Walled-off necrosis(WON) occurs after 4 weeks, at which point percutaneous drainage or open necrosectomy may be indicated;earlynecrosectomy has ahigh mortality rate
- Despite the above, the presence of sepsis and multi-organ dysfunction may warrantearly surgery
- It carries apoor prognosisand has a high risk of becoming infected
Define chronic pancreatitis
Chronic pancreatitis refers to inflammation of the pancreas. Unlike acute pancreatitis, chronic pancreatitis is irreversible. It is characterised by structural changes e.g. fibrosis, calcification and atrophy which leads to a decline in function of the pancreas.
Describe the epidemiology of chronic pancreatitis
- Alcohol is the primary risk factor accounting for 80% of cases, whilst 20% of cases have an unknown cause
- The age at presentation varies with aetiology. Hereditary pancreatitis has a peak age at 10 to 14 years, juvenile idiopathic chronic pancreatitis at 19 to 23 years, alcoholic chronic pancreatitis at 36 to 44 years, and senile idiopathic chronic pancreatitis at 56 to 62 years.
- M>F
- Worldwide prevalence is around 4-5%
Describe the aetiology of chronic pancreatitis
Alcohol consumption, progression from acute pancreatitis, trauma, chronic kidney disease, cystic fibrosis
What are risk factors for chronic pancreatitis
- Alcohol excess
- Smoking
- Family history
- Ductal obstruction e.g. gallstones, tumours, structural abnormalities
- Genetic - cystic fibrosis and haemochromatosis
Describe the pathophysiology of chronic pancreatitis
Repeated bouts of acute pancreatitis can progress to chronic pancreatitis. With each bout of acute pancreatitis, there is ductal dilatation and damage to pancreatic tissue. Fibrotic tissue forms causing narrowing of ducts leading to stenosis.
What are the key presentations for chronic pancreatitis
Severe pain in epigastric region which can radiate to back, steatorrhea, jaundice, loss of exocrine function (no pancreatic enzymes secreted in GI tract, especially lipase), loss of endocrine function (lack of insulin causing diabetes),
What are other symptoms of chronic pancreatitis
Weight loss, nausea and vomiting
What is the gold standard investigation for chronic pancreatitis
X-ray/CT/MRI scan shows calcification of pancreas and dilated ducts
What are the first line investigations for chronic pancreatitis
1st line Faecal-elastase 1 (low), faecal fat (high), pancreatic function tests (decreased function), ERCP for visualisation of ducts, bloods (low/no amylase and lipase)
What are the differential diagnosis for chronic pancreatitis
Pancreatic cancer, acute pancreatitis, abdominal aorta aneurysm, peptide ulcer disease
What is the management for chronic pancreatitis
1st line – control pain (analgesia, NSAIDs) and risk factors (less alcohol, less smoking, obesity)
Replace pancreatic enzymes in deficiency (lipase), nutritional supplements. Insulin for diabetes. ECRP with stenting. Surgery to drain bile ducts
What monitoring is done for chronic pancreatitis
Patients are recommended to be seen yearly for non-invasive testing, to include laboratory blood work and perhaps stool tests to monitor for specific complications, including:
- Cholestasis and biliary obstruction (LFTs)
- Malnutrition
- Baseline bone densitometry in high-risk patients
- Steatorrhoea (qualitative faecal fat)
- Diabetes (glucose).
What complications occur with chronic pancreatitis
Pancreatic exocrine insufficiency, diabetes mellitus, pancreatic calcification, steatorrhea, pancreatic pseudocysts, pancreatic cancer, malabsorption, gastric varices, metabolic bone disease
What is the prognosis for chronic pancreatitis
Almost all patients will develop exocrine insufficiency, and up to 75% will develop endocrine insufficiency. Survival is dependent upon the underlying cause, with a life expectancy of 55-72% in chronic pancreatitis due to alcohol excess.
Define alcoholic liver disease
Effects of long-term alcohol consumption on the liver. Fatty liver > alcoholic hepatitis > liver cirrhosis
Describe the epidemiology of alcoholic liver disease
- The prevalence of alcohol-use disorders among men and women in the European region was 14.8% and 3.5%, respectively, in 2016. In the UK, it is estimated that 24% to 28% of adults drink in a hazardous or harmful way.
- M>F prevalence
- Main cause of liver disease and failure
Describe the aetiology of alcoholic liver disease
Chronic heavy alcohol consumption
Describe the pathophysiology of alcoholic liver disease
Progression of alcoholic liver disease.
1. Fatty liver (steatosis): drinking leads to build up of fat in the liver. Treatment: stop drinking alcohol.
2. Alcoholic hepatitis: long term alcohol drinking causes inflammation in liver sites. Damaged intermediate fibres = bundles of Mallory bodies. Treatment: permanent alcohol abstinence.
3. Cirrhosis: liver is made up of scar tissue instead of healthy liver tissue. Irreversible.
Describe the key presentations for alcoholic liver disease
Early stages (asymptomatic). Later: abdominal pain, hepatomegaly, jaundice, spider naevi (cluster of minute blood vessels under skin), alcohol dependency
Describe the clinical manifestations for alcoholic liver disease
Signs:
Palmar erythema, dupuytren’s contracture (fingers bend towards palm of hand), ascites, hepatic encephalopathy, caput medusae (enlarged superficial epigastric veins), bruising, asterixis (flapping tremor), gynecomastia
Symptoms:
Abdominal pain, fatigue, weight loss, confusion, fever, N+V
What is the gold standard investigation for alcoholic liver disease
Liver biopsy: steatosis, inflammation, Mallory bodies
What are the first line investigations for alcoholic liver disease
LFTS: Gamma-glutamyl transferase (raised), AST and ALT (transaminases - raised), AST:ALT (ratio>2), ALP (alkaline phosphatase - raised), bilirubin (raised), albumin (low),
FBC: anaemia, thrombocytosis, high MCV
What are other investigations for alcoholic liver disease
Ultrasound, CT, alcohol dependence (CAGE and AUDIT)
What are the differential diagnosis for alcoholic liver disease
Hepatitis A B C, acute liver failure
What is the management for alcoholic liver disease
1st line - Completely stopping alcohol consumption. Give chlordiazepoxide for delirium tremens – alcohol withdrawal (tremors, agitation, ataxia, disorientation)
Also: weight loss, stop smoking, corticosteroids for alcoholic hepatitis (prednisolone), liver transplant if severe (must abstain from alcohol for 3 months first)
What are complications for alcoholic liver disease
Wernicke-Korsakoff syndrome (thiamine deficiency), hepatic encephalopathy, renal failure, hepatocellular carcinoma, portal hypertension
What is the prognosis for alcoholic liver disease
Good if you stop alcohol
Define non-alcoholic fatty liver disease
Chronic liver disease with evidence of hepatic steatosis (fat build up) which is not a secondary cause of alcohol consumption. Stages: non-alcoholic steatosis, non-alcoholic steatohepatitis, fibrosis, cirrhosis
What is the epidemiology of non-alcoholic fatty liver disease
- Commonest liver disorder in industrialised western countries
- Affects around 3/4’s of all obese individuals
- Individuals with metabolic syndrome
Describe the aetiology of non-alcoholic fatty liver disease
Metabolic syndrome: obesity, hypertension, diabetes, hypertriglyceridemia, hyperlipidaemia
What are the risk factors for non-alcoholic fatty liver disease
Metabolic syndrome: obesity, hypertension, diabetes, hypertriglyceridemia, hyperlipidaemia. Drugs (NSAIDs, amiodarone)
Describe the pathophysiology of non-alcoholic fatty liver disease
Stages of NAFLD:
1. Non-alcoholic steatosis (fat build up in hepatocytes)
2. Non-alcoholic steatohepatitis (steatosis and inflammation)
3. Fibrosis
4. Cirrhosis
Insulin resistance plays a role. Overtime, insulin receptors are less responsive to insulin so liver increases fat storage and decreases fatty acid oxidation. This means there is less secretion of fatty acids into the blood stream. There is also increased synthesis and uptake of free fatty acids from the blood (known as steatosis).
This ultimately damages lipid membrane, leading to mitochondrial dysfunction and cell death. This generates inflammation. Inflammation + steatosis = steatohepatitis.
Damage also attracts neutrophils to the liver. Chronic steatoheptitis can trigger stellate cells to lay down fibrotic tissue (fibrosis).
The architecture then changes to the point where disease is now classed as cirrhosis
Describe the key presentations for non-alcoholic fatty liver disease
Asymptomatic. Very severe = liver failure signs: Hepatomegaly, jaundice, ascites, pain in upper right quadrant. Absence of chronic alcohol consumption
What are the symptoms of non-alcoholic fatty liver disease
Fatigue, malaise, nausea, vomiting
What is the gold standard investigation for non-alcoholic fatty liver disease
Liver biopsy (steatosis, inflammation, fibrosis)
What are the first line investigations of non-alcoholic fatty liver disease
Deranged LFTs: increased PT/INR, low albumin, increased bilirubin, increased AST and ALT, increased GGT
FBC: anaemia, thrombocytopenia. Lipid profile (raised LDL, cholesterol, triglyceride)
Liver ultrasound (fatty infiltrates)
What are the other investigations for non-alcoholic fatty liver disease
Assess risk of fibrosis with fibrosis score
What are the differential diagnosis for non-alcoholic fatty liver disease
Alcoholic liver disease, hepatitis BC, Wilson’s disease
What is the management for non-alcoholic fatty liver disease
1st line – treat underlying cause and reduce risks (lose weight, exercise, smoking, control diabetes, LDL). Medication: pioglitazone, vitamin E, statins, ACEi.
End stage (cirrhosis irreversible): liver transplant
What are the complications for non-alcoholic fatty liver disease
Ascites, variceal haemorrhage, portal hypertension, hepatocellular carcinoma, hepatic encephalopathy
What is the prognosis for non-alcoholic fatty liver disease
The overall prognosis in patients with steatosis (fatty liver without evidence of active inflammation) is considered to be good and a majority of patients will remain stable throughout their lifetime. The same cannot be said of non-alcoholic steatohepatitis (NASH), which is considered the progressive form of NAFLD.
Patients who have NASH progress to cirrhosis 9% to 20% of the time. Up to one third of these patients will die from complications from liver failure or require liver transplantation.
Recurrent NAFLD following liver transplantation is now a well-recognised phenomenon. The incidence of the development of post-liver transplantation steatosis ranges anywhere from 25% to 100%, and the incidence of NASH ranges from a low of 10% to as high as 37.5%.
Hepatic steatosis affects up to 80% of patients with chronic hepatitis C infection. Concurrent fatty liver disease with hepatitis C includes increased disease progression, elevated risk of primary liver cancer, and a decreased response to antiviral therapy.
Define liver cirrhosis
Result chronic inflammation and damage to liver cells. When the liver cells are damaged, they are replaced with scar tissue (fibrosis) and nodules of scar tissue within the liver (regenerative nodules)
Describe the epidemiology of liver cirrhosis
- Liver disease is the third biggest cause of premature mortality in the UK with 62,000 working life years lost.
- In Europe, cirrhosis related to either viral infection (21% with 13% of HCV infection and 7% of hepatitis B virus infection), or alcohol abuse (19%) are the main indications of liver transplant.
Describe the aetiology of liver cirrhosis
Most common: Alcoholic liver disease, non-alcoholic fatty liver disease, hepatitis B, hepatitis C
Rarer: haemochromatosis, Wilson’s disease, alpha 1 trypsin deficiency
Describe the risk factors for liver cirrhosis
Alcohol misuse, IV drug use, unprotected sex, obesity
Describe the pathophysiology of liver cirrhosis
Fibrosis of liver leads to irreversible chronic scarring and damage – cirrhosis. “End-stage liver damage”. Injured liver cells form regenerative nodules with fibrotic tissue in between. Regenerative nodules make the liver bumpier compared to a normal liver.
Describe the key presentations for liver cirrhosis
Hepatomegaly, jaundice, ascites, regenerative nodules, splenomegaly, hepatic encephalopathy (asterixis), palmar erythema, spider naevi, xanthelasma (yellow growths on eyelids), caput medusae, hepatic fetor
Describe the clinical manifestations of liver cirrhosis
Signs: Gynecomastia, haemoptysis, melaena (black stools due to GI bleeding), bruising, peripheral oedema, altered mental state, bleeding
Symptoms: Abdominal pain, nausea, vomiting, confusion, pruritis, bleeding
What is the gold standard investigation for liver cirrhosis
Liver biopsy (distortion of liver parenchyma – regenerative nodules)Hat
What are the first line investigations for liver cirrhosis
LFTs: bilirubin, PT/INR, serum AST + ALT, NH3, GGT all raised. Serum albumin and glucose decreased.
FBC: anaemia, thrombocytopenia, leukopenia. U&E (urea and creatinine raised, deranged electrolytes)
What are other investigations for liver cirrhosis
Abdominal ultrasound (nodules, hepatomegaly). Child-Pugh score: severity and prognosis of cirrhosis. Involves - bilirubin, albumin, INR, ascites, encephalopathy. MELD score: model for end-stage liver disease. Gives 3 month mortality estimate and liver transplant advice
What are the differential diagnosis for liver cirrhosis
Budd Chiari, portal vein thrombosis, constrictive pericarditis
What is the management for liver cirrhosis
1st line – treatment of underlying cause (stop alcohol, antivirals for hepatitis C). Lifestyle modification (alcohol, low LDL, low salt). Treat complications
2nd – liver transplantation
What are the complications for liver cirrhosis
Development of hepatocellular carcinoma, spontaneous bacterial pericarditis, oesophageal varices ruptures, Hepatic encephalopathy (lactulose), hepato-renal syndrome, ascites (diuretics), bleeding (vitamin K)
What is the prognosis for liver cirrhosis
2 years without transplant
Define portal hypertension
Complication of cirrhosis. Increased blood pressure in hepatic portal venous system. (portal vein, splenic vein, mesenteric vein)
Describe the aetiology for portal hypertension
Pre-hepatic: portal vein obstruction (thrombus)
Intrahepatic: cirrhosis, sarcoidosis, schistosomiasis, myeloproliferative disease, congenital hepatic fibrosis
Post-hepatic: right heart failure, constrictive pericarditis, Budd Chiari syndrome (hepatic vein obstruction)
Describe the pathophysiology of portal hypertension
Venous blood accumulates in portal system, raising pressure to 5-10mmHg. This leads to the formation of portosystemic shunts where blood is directed away from portal system and into systemic veins. This means the liver receives less blood causing reduced liver function and blood detoxification, leading to increased toxic products in the blood, e.g., ammonia which can cross BBB and cause hepatic encephalopathy. One of the portosystemic shunts is at the oesophagus causing oesophageal varices which can rupture causing upper GI bleed.
Describe the key presentations of portal hypertension
Asymptomatic until complications occur: ascites, caput medusa, GI bleeding from oesophageal varices, haemoptysis, melaena/haematochezia, jaundice, hepatic encephalopathy (asterixis, altered consciousness, lethargy, seizure, coma)
What is the gold standard investigation for portal hypertension
Hepatic venous pressure gradient measurement (difference in pressure between IVC and portal vein)
What are the first line investigations for portal hypertension
Liver USS (nodules = cirrhosis), CT/MRI scan (ascites, cirrhosis, splenomegaly), endoscopy (oesophageal varices). Labs (FBC, LFT, serology may identify cause)
What is the management for portal hypertension
1st line – beta blockers to reduce portal venous pressure.
Treat complications: ascites (reduce salt, diuretics), prevent oesophageal varices bleeding etc.
What are the complications for portal hypertension
Hepatic encephalopathy, spontaneous bacterial peritonitis, Ascites, bleeding (oesophageal varices), caput medusae, diminished liver function, enlarged spleen
Define oesophageal varices
Dilated collateral blood vessels which are a direct complication of portal hypertension and liver cirrhosis
Describe the aetiology of oesophageal varices
Portal hypertension and cirrhosis
Describe the pathophysiology of oesophageal varices
Portal hypertension leads to formation of portosystemic shunts where blood is diverted away from portal venous system and into systemic system. One of the portosystemic shunts is at the oesophagus which causes oesophageal varices, which are enlarged oesophageal veins. They are very fragile and can easily rupture causing an upper GI bleed.
Describe the key presentations of oesophageal varices
Upper GI bleeding: Haematemesis, melaena, haematochezia, splenomegaly
What is the gold standard investigation for oesophageal varices
Gastroscopy (presence of varices)
What are other investigations for oesophageal varices
FBC: anaemia, thrombocytopenia. LFTs: raised AST, ALT, ALP, bilirubin. U&Es: hyponatraemia
What are the differential diagnosis for oesophageal varices
Mallory Weiss tear, hiatal hernia, gastric varices, peptide ulcer disease
What is the management for oesophageal varices
Stop bleeding: terlipressin/octreotide, endoscopic banding variceal ligation, balloon tamponade, TIPPS (trans-jugular intrahepatic portosystemic shunt – decrease portal pressure by diverting blood to other veins).
Prevent bleeding: non-selective beta blocker, endoscopic banding variceal ligation, TIPPS
What are the complications for oesophageal varices
Spontaneous bacterial peritonitis, oesophageal stricture, bleeding
Define haematesis
Haematemesis is simply defined as “vomiting blood”. It is caused by bleeding from part of the upper portion of the gastrointestinal tract. It may be bright red or look like coffee grounds.
(Upper GI tract bleeds may also present as malaena - dark sticky poo)
Describe the aetiology of haematamesis
Common:
- Peptic ulcers
- Mallory-Weiss tear
- Oesophageal varices
- Gastritis/gastric erosions
- Drugs
- Oesophagitis
- Duodenitis
- Malignancy
Rare:
- Bleeding disorders
- Portal hypertensive gastropathy
- Aorto-enteric fistula
- Angiodysplasia
- Haemobilia
- Dieulafoy lesion
- Meckel’s diverticulum
- Peutz-Jegher’s syndrome
- Osler-Weber-Rendu syndrome
What are the primary investigations for haematamesis
- FBCs
- LFTs
- U&Es
- OGD
- Chest X-ray
- CT abdomen
Describe the management for haematamesis
- Rapid ABCDE assessment
- High flow O2
- Fluid resus if needed
- Correct clotting abnormalities
For suspected varices:
- Terlipressin +IV antibiotics
Peptic ulcer bleeds:
- achieve endoscopic haemostasis. Start IV PPI. Treat if positive for H.Pylori.
Define hepatitis A
Inflammation of the liver due to viral infection. Hepatitis A is an RNA virus spread by the faecal-oral route (through contamination food or water). It is acute.
Describe the epidemiology of hepatitis A
Very common hepatitis worldwide but rare in UK, common in Africa. Common in travellers
Describe the aetiology of hepatitis A
RNA virus spread through faecal-oral route (via contaminated food and water)
Describe the risk factors for hepatitis A
Living in endemic region, travel to endemic region, overcrowding, shellfish
Describe the pathophysiology of hepatitis A
Virus infected cells undergo cytotoxic killing and apoptosis by the immune system. Hepatocytes undergoing apoptosis are called councilman bodies. Cytotoxic killing causes inflammation of the liver.
What are the key presentations for hepatitis A
Acute. Fever, malaise, nausea + vomiting, jaundice
What are the clinical manifestations of hepatitis A
Signs: Cholestasis (slowing of bile through biliary system), dark urine, pale stools, hepatomegaly
Symptoms: Fatigue, headache, muscle aches, pruritis, abdominal pain
What is the gold standard investigation for hepatitis A
Gold Standard HAV serology: HAV IgM = active. HAV IgG = recovery or vaccination
What are the first line investigations for hepatitis A
Serum ALT and AST raised, bilirubin raised, ESR raised
What are the differential diagnosis for hepatitis A
Differential diagnosis Acute hepatitis B, acute hepatitis C, hepatitis E, EBV, CMV
What is the management for hepatitis A
1st line – supportive therapy, resolves by itself. Incubation period 2 weeks then self-limiting for 1-3 months.
Vaccine available. It is a notifiable disease.
Describe the complications of hepatitis A
Acute liver failure, acute kidney injury, pancreatitis
Define hepatitis B
Hepatitis is inflammation of the liver caused by viral infection. Hepatitis B is an enveloped DNA virus transmitted by blood and bodily fluids. Acute and chronic.
Describe the epidemiology of hepatitis B
Most common liver infection globally. Only 20% of cases become chronic. 50% of chronic hepatitis B in children under 6y.o.
Describe the aetiology of hepatitis B
Viral transmission by blood and bodily fluid (needles – needlestick injury, IVDU, tattoo. Vertical transmission to child, unprotected sex, contaminated household products (toothbrush), contact of minor cuts or abrasions
Describe the risk factors for hepatitis B
Unprotected sex, MSM, IVDU, healthcare workers, infected mother to child
Describe the pathophysiology of hepatitis B
Virus infected cells undergo cytotoxic killing and apoptosis by the immune system. Hepatocytes undergoing apoptosis are called councilman bodies. Cytotoxic killing causes inflammation of the liver
What are the key presentations for hepatitis B
Fever, N+V, jaundice, ascites, hepatomegaly
What are the clinical manifestations for hepatitis B
Signs: Jaundice, dark urine and pale stools, ascites, hepatosplenomegaly, urticaria, arthralgia
Symptoms: Fever, fatigue, malaise, nausea + vomiting, muscle aches, abdominal pain, pruritis
What is the gold standard investigation for hepatitis B
HBV DNA (direct count of viral load) and Serology:
HBV surface antigen – HBsAg = active infection
Core antigen in core of HBV – HBcAg = active infection
E antigen – HBeAg. Secreted by infected cells = active acute infection and replication. Correlates with infectivity.
IgM antibodies to core antigen - HBcAb = current or past infection. IgM = active infection (high in acute, low in chronic). IgG = past infection where HBcAg is negative.
IgG antibodies to surface antigen - HBsAb = current or past infection, or vaccination
What are the first line investigations for hepatitis B
LFTs: AST and ALT raised, bilirubin raised, alkaline phosphatase raised
What are further investigations for hepatitis B
Liver imaging
What are the differential diagnosis for hepatitis B
Acute hepatitis A C E, chronic hepatitis C, EBV hepatitis, CMV hepatitis
What is the management for hepatitis B
1st line – peginterferon alpha 2a subcutaneous injection, or tenofovir (inhibits viral replication)
Vaccination with HBV surface antigen (HBsAg). HBV is a notifiable disease.
What are the complications for hepatitis B
Liver failure, cirrhosis, hepatocellular carcinoma, HBV reactivation
Define hepatitis C
Inflammation of the liver due to viral infection. Hepatitis C is an RNA and is transmitted through blood and bodily fluids. It is acute and chronic.
Describe the epidemiology of hepatitis C
¼ fight off virus. ¾ it becomes chronic.
Describe the aetiology of hepatitis C
Viral transmission through blood and bodily fluids – unprotected sex, vertical transmission in childbirth, needlestick injury, sharing needles
Describe the risk factors for hepatitis C
IVDU, unsafe medical practices, unprotected sex, blood transfusion or organ transplant
Describe the pathophysiology of hepatitis C
Virus infected cells undergo cytotoxic killing and apoptosis by the immune system. Hepatocytes undergoing apoptosis are called councilman bodies. Cytotoxic killing causes inflammation of the liver.
Describe the key presentations for hepatitis C
Asymptomatic in acute. Chronic = jaundice, ascites, hepatosplenomegaly,
What are the clinical manifestations for hepatitis C
Fever, malaise, nausea and vomiting, fatigue, pruritis, muscle aches, abdominal pain
What is the gold standard investigation for hepatitis C
HCV RNA test (PCR) – indicates current or past infection. Viral RNA decreasing = recovery. Viral level same = chronic
What are the first line investigations for hepatitis C
HCV antibody Enzyme immunoassay – HCV IgG (positive indicates current infection), aminotransferases elevated
What are the differential diagnosis for hepatitis C
Chronic hepatitis B, alcoholic liver disease, steatohepatitis
What is the management for hepatitis C
1st line – direct acting antivirals (ribavirin, sofosbuvir). It is a notifiable disease. No vaccine available.
What are the complications for hepatitis C
Liver cirrhosis, hepatocellular carcinoma, cardiovascular disease
Define hepatitis D
Hepatitis is inflammation of the liver caused by viral infection. Hepatitis D is an RNA which only survives in patients who also have Hepatitis B. It is spread via blood and bodily fluids. Hepatitis D attaches itself to the surface antigen of Hepatitis B and cannot survive without this protein.
Describe the epidemiology of hepatitis D
Hepatitis B patients. Hepatitis D increases the complications and severity of Hepatitis B.
Describe the aetiology of hepatitis D
Viral transmission via blood and bodily fluids.
Describe the risk factors for hepatitis D
Hepatitis B: needlestick injury, IVDU, MSM, unprotected sex, vertical transmission
Describe the pathophysiology of hepatitis D
Virus infected cells undergo cytotoxic killing and apoptosis by the immune system. Hepatocytes undergoing apoptosis are called councilman bodies. Cytotoxic killing causes inflammation of the liver. Hepatitis D attaches itself to the surface antigen of Hepatitis B and cannot survive without this protein.
What are the key presentations for hepatitis D
Fever, malaise, nausea and vomiting, jaundice, hepatomegaly
Describe the clinical manifestations for hepatitis D
Signs: Jaundice, dark urine and pale stools, ascites, hepatosplenomegaly, urticaria, arthralgia
Symptoms: Fever, fatigue, malaise, nausea + vomiting, muscle aches, abdominal pain, pruritis
What is the gold standard investigation for hepatitis D
Serology: HDV IgM or IgG = active infection. HVD RNA in serum
What are the first line investigations for hepatitis D
1st line LFTs: AST and ALT raised, bilirubin raised, alkaline phosphatase raised
What are further investigations for hepatitis D
Liver imaging
What are the differential diagnosis for hepatitis D
Acute hepatitis A C E, chronic hepatitis C, EBV hepatitis, CMV hepatitis
What is the management for hepatitis D
1st line – no specific treatment. Treat hepatitis B – SC pegylated interferon alpha 2a or tenofovir. It is a notifiable infection.
What are the complications for hepatitis D
Cirrhosis, hepatocellular carcinoma
Define hepatitis E
Hepatitis is inflammation of the liver caused by viral infection. Hepatitis E is an RNA virus spread by the faecal-oral route (via contaminated food and water, dogs, and pigs). It is acute
Describe the aetiology of hepatitis E
Viral transmission via faecal-oral route (food, contaminated water, undercooked seafood and pork)
Describe the risk factors for hepatitis E
Undercooked seafood and pork, contaminated water, pregnant
Describe the pathophysiology of hepatitis E
Virus infected cells undergo cytotoxic killing and apoptosis by the immune system. Hepatocytes undergoing apoptosis are called councilman bodies. Cytotoxic killing causes inflammation of the liver.
Describe the key presentations of hepatitis E
Acute. Fever, malaise, nausea + vomiting, jaundice, hepatomegaly
Describe the clinical manifestations of hepatitis E
Signs: Jaundice, dark urine, and pale stools
Symptoms: Pruritis, abdominal pain, muscle aches and pain
What is the gold standard investigation for hepatitis E
HEV serology: HEV IgM antibodies = active infection. HEV IgG antibodies = recovery. HEV RNA = current infection
Describe the first line investigations for hepatitis E
Serum ALT and AST raised, bilirubin raised, ESR raised
What are the differential diagnosis for hepatitis E
Acute hepatitis B, acute hepatitis C, EBV, CMV
Describe the management for hepatitis E
1st line – no treatment. Very mild illness which is self-limiting within a month. It is a notifiable disease. No vaccine available.
Describe the complications for hepatitis E
Chronic hepatitis, liver failure (especially in pregnant women), cirrhosis, hepatocellular carcinoma
Describe the prognosis for hepatitis E
25% mortality in pregnant women
Define autoimmune hepatitis
Inflammation of the liver due to it being attacked by the body’s own cells.
Describe the epidemiology of autoimmune hepatitis
Young women
Describe the aetiology of autoimmune hepatitis
Unknown
Describe the risk factors for autoimmune hepatitis
Female, genetic predisposition, immune dysfunction, other autoimmune conditions, HLA DR3/DR4
Describe the pathophysiology of autoimmune hepatitis
T cells recognise liver cells as harmful and alert the immune system to attack the liver.
Type 1: occurs in adults, typically women. Anti-nuclear antibodies, anti-smooth muscle antibodies, anti-soluble liver antigen
Type 2: occurs in children. Anti-liver kidney microsomes-1. Anti-liver cytosol antigen type-1.
Describe the key presentations for autoimmune hepatitis
Asymptomatic or Malaise, fatigue, jaundice, fever, hepatosplenomegaly
What is the gold standard investigation for autoimmune hepatitis
Liver biopsy
Describe the first line investigations for autoimmune hepatitis
Increased transaminases AST and ALT (higher ALT since it is more associated with the liver). Decreased albumin. Prolonged prothrombin time.
Serology: Type 1 - Anti-nuclear antibodies, anti-smooth muscle antibodies, anti-soluble liver antigen.
Type 2 - Anti-liver kidney microsomes-1. Anti-liver cytosol antigen type-1.
What are the differential diagnosis for autoimmune hepatitis
Chronic hepatitis B C D, systematic lupus erythematous
Describe the management for autoimmune hepatitis
1st line – corticosteroid (prednisolone). Plus, immunosuppressant (azathioprine)
Liver transplant if resistant to medication
Describe the complications for autoimmune hepatitis
Cirrhosis, acute liver failure, corticosteroid complications (hypertension, osteoporosis, diabetes mellitus, growth impairment)
Define jaundice
Also called icterus, jaundice is yellowing of skin and eyes due to accumulation of conjugated or unconjugated bilirubin. 3 types: pre-hepatic, intra-hepatic, post-hepatic
Describe the aetiology of pre-hepatic jaundice
Pre-hepatic: unconjugated hyperbilirubinemia due to excessive red blood cell breakdown which overwhelms the liver’s ability to conjugate bilirubin. Causes: Haemolytic anaemia, Gilbert’s syndrome, Criggler-Najjar syndrome.
Describe the aetiology of intrahepatic jaundice
Intrahepatic: dysfunction of hepatic cells, liver loses ability to conjugate bilirubin, both conjugated and unconjugated bilirubin in blood. Causes: alcoholic liver disease, hepatitis, hepatocellular carcinoma, hepatotoxic medication
Describe the aetiology of post-hepatic jaundice
Post-hepatic: obstruction of biliary drainage causing increase in conjugated bilirubin. Causes: gallstones, cholangiocarcinoma, pancreatic cancer,
Describe the pathophysiology of jaundice
RBCs are broken down by reticuloendothelial macrophages in spleen, haemoglobin is broken down to heme and globin. Heme is broken down to Fe2+ and biliverdin. Biliverdin reductase converts biliverdin to unconjugated bilirubin which is water insoluble. Unconjugated bilirubin travels in the blood bound to albumin, to the liver. In the liver, enzyme UGT conjugates bilirubin making it water soluble. Conjugated bilirubin is stored in gallbladder and excreted into small intestine as bile and converted to urobilinogen by colonic bacteria. Some urobilinogen is converted to stercobilin, giving faeces its brown colour. Some urobilinogen is recycled in the enterohepatic circulation, and some goes to the kidneys where it is oxidised to urobilin which makes urine yellow. Jaundice occurs when this pathway is disrupted.
What are the key presentations for jaundice
Yellow skin and sclera. Pre-hepatic (normal urine and stool). Intrahepatic (dark urine, normal stool). Post hepatic (dark urine, pale stool). Pruritis
What are the first line investigations for jaundice
Pre-hepatic: conjugated bilirubin normal, unconjugated bilirubin increased, urobilinogen increased, ALP AST and ALT normal, urine conjugated bilirubin not present
Intrahepatic: conjugated bilirubin increased, unconjugated bilirubin increased, urobilinogen decreased, ALP increased, AST and ALT very increased, urine conjugated bilirubin present
Post-hepatic: conjugated bilirubin increased, unconjugated bilirubin normal, urobilinogen decreased, ALP highly increased, AST and ALT increased, urine conjugated bilirubin present
What are the further investigations for jaundice
Abdominal USS
Describe the management for jaundice
Depends on underlying cause
Define Wernicke’s encephalopathy and korsakoff syndrome
Wernicke-Korsakoff syndrome is caused by thiamine deficiency (vitamin B1). Wernicke’s encephalopathy is the acute, medical emergency reversible stage before progressive to Korsakoff syndrome which is the chronic, irreversible stage.
Describe the aetiology of Wernicke’s encephalopathy and Korsakoff syndrome
Excess alcohol (alcohol reduces thiamine levels), inadequate intake (malnutrition, anorexia), impaired absorption (stomach cancer, IBD)
Describe the pathophysiology of Wernicke’s encephalopathy and Korsakoff syndrome
Thiamine deficiency impairs glucose metabolism, decreasing cellular energy. Brain is vulnerable to impaired glucose.
Alcohol reduces thiamine by interfering with thiamine conversion to its active form, preventing absorption, causes cirrhosis which interferes with thiamine storage in liver
What are the key presentations for Wernicke’s encephalopathy and korsakoff syndrome
Wernicke’s: confusion, apathy, difficulty concentrating, ophthalmoplegia weakness and paralysis of eye muscles, ataxia – difficulty with coordinated movement.
Korsakoff: severe memory impairment (anterograde and retrograde), confabulation (creates stories to fill in memory gaps), behavioural changes
Describe the first line investigations for Wernicke’s encephalopathy and Korsakoff syndrome
Clinical diagnosis, thiamine levels decreased, LFTs deranged, MRI degeneration of mammillary bodies
What are the differential diagnosis for Wernicke’s encephalopathy and Korsakoff syndrome
Alcohol intoxication, alcohol withdrawal, viral encephalitis
What is the management for Wernicke’s encephalopathy and Korsakoff syndrome
1st line – IV thiamine infusion (pabrinex). Can be given with glucose, magnesium, and multivitamins
What are the complications with Wernicke’s encephalopathy and Korsakoff syndrome
Korsakoff’s syndrome, ataxia, ophthalmoplegia, hearing loss
Define ascites
Collection of fluid in the peritoneal cavity
Describe the aetiology of ascites
Cirrhosis, congestive heart failure, peritonitis, malignancy, nephrotic syndrome
Describe the pathophysiology of ascites
Excessive build-up of fluid in the peritoneal cavity. Poor liver function = low albumin = low blood oncotic pressure = fluid loss into the peritoneal cavity
Describe the key presentations for ascites
Distended large abdomen, shifting dullness: percuss abdomen and observe dullness over fluid and resonance over air. Supine = central abdomen resonant as bowel floats, flanks dull as fluid collects. Lying on side = flank resonant as fluid moves to other side
What is the gold standard investigation for ascites
Abdominal ultrasound (fluid in peritoneal cavity)
What are the differential diagnosis for ascites
Alcoholic liver disease, hepatitis C, congestive heart failure
What is the management for ascites
1st line – treat underlying cause. Diuretic (spironolactone and furosemide) to drain fluid. Low sodium diet. Paracentesis.
What are the complications with ascites
Dyspnoea, abdominal infections (SBP), kidney failure
Define alpha 1 antitrypsin deficiency
Metabolic disease caused by genetic abnormality of protein alpha 1 antitrypsin
Describe the aetiology of alpha 1 antitrypsin deficiency
Autosomal recessive mutation of protease inhibitor gene on chromosome 14
What are the risk factors for alpha 1 antitrypsin deficiency
Young/middle aged male, smoking
Describe the pathophysiology for alpha 1 antitrypsin deficiency
A1AT is a protease inhibitor which inactivates elastase, an enzyme which breaks down elastin. Deficiency of normal A1AT means elastase is not inactivated so it breaks down elastin unchecked.
Liver: A1AT is produced in liver. Mutated protein damages liver causing fibrosis, cirrhosis, HCC.
Lungs: protease enzymes attack connective tissue in lungs, damaging alveoli walls causing emphysema and bronchiectasis.
What are the key presentations for A1AT deficiency
Lung – shortness of breath, chronic cough, wheeze, mucus production, emphysema, COPD like symptoms
Liver – jaundice, cirrhosis (+ complications: HE, oesophageal varices), hepatitis, hepatomegaly
What is the gold standard investigation for A1AT deficiency
Serum alpha 1 antitrypsin low
What are the first line investigations for A1AT deficiency
Serum alpha 1 antitrypsin low,
reduced pulmonary function tests (spirometry obstruction FEV:FVC <0.7), #
chest x-ray/CT: hyperinflated chest, panacinar emphysema and bronchiectasis,
LFTs: elevated bilirubin, aminotransferase, ALP.
Liver biopsy (cirrhosis and periodic acid Schiff pink staining A1AT mutant globules
Other: genetic testing
What are the differential diagnosis for A1AT deficiency
Asthma, COPD, bronchiectasis, viral hepatitis
What is the management for A1AT deficiency
1st line - no curative treatment: stop smoking, A1AT infusions, standard COPD treatment (inhalers, oxygen), standard liver disease treatment (lactulose for HE)
Describe the complications of A1AT deficiency
Hepatocellular carcinoma, COPD, cirrhosis
Define haemochromatosis
Metabolic disorder where body absorbs too much iron leading to increase total body iron and iron deposition into tissues which can poison the tissues (liver, pancreas, heart, pituitary)
Describe the aetiology of haemochromatosis
Autosomal recessive mutation of human haemochromatosis protein (HFE) on chromosome 6
Describe the risk factors for haemochromatosis
Family history, male (because women lose iron in menstruation), age >50
Describe the pathophysiology of haemochromatosis
Mutation in HFE causes increased iron absorption. Iron is deposited into other tissues, process called hemosiderosis (liver, pancreas, heart, pituitary, joints, skin). Extra iron leads to organ damage through free radical production which cause cellular damage > cell death > fibrosis
What are the key presentations for haemochromatosis
Chronic tiredness, joint pain, pigmentation (bronze/slate-grey discolouration), hair loss, hypogonadism, erectile dysfunction, amenorrhoea, cognitive symptoms (memory and mood disturbance)
What are the clinical manifestations of haemochromatosis
Signs: Chronic liver disease, cirrhosis, heart failure, arrhythmias
Symptoms: Fatigue, weakness, lethargy, joint pain
What is the gold standard investigation for haemochromatosis
Liver biopsy (brown spots of iron deposited in hepatocytes. Prussian blue stain shows iron as blue)
What are the first line investigations for haemochromatosis
FBC: high transferrin saturation, high iron, high serum ferritin, decreased total iron binding capacity. LFTs: raised aminotransferases
Other: genetic testing, MRI
What are the differential diagnosis for haemochromatosis
Secondary haemochromatosis (from transfusions), hepatitis B and C, NAFLD
What is the management for haemochromatosis
1st line – phlebotomy/venesection to decrease serum iron, ferritin, and iron saturation. Done weekly.
2nd line – iron chelation (desferrioxamine). Lifestyle modification
What are the complications for haemochromatosis
Cirrhosis, diabetes mellitus, hepatocellular carcinoma, hypogonadism
Define Wilson’s disease
Metabolic disease which causes excessive accumulation of copper in body and tissues which can lead to tissue damage.
Describe the aetiology of Wilson’s disease
Autosomal recessive mutation of ATP7B gene on chromosome 13
What are the risk factors for Wilson’s disease
Young <20, family history
Describe the pathophysiology of Wilson’s disease
Autosomal recessive defect in ATP7B copper-binding protein which leads to copper building up in hepatocytes and production of free radicals. Excess copper and free radicals damage injures the hepatocytes and copper spills out into blood where it circulates to other tissues causing free radical damage (e.g., brain, basal ganglia, cornea, liver)
Describe the key presentations of Wilson’s disease
Liver: hepatitis, cirrhosis
Neurological: Parkinsonism (tremor, bradykinesia, rigidity), dysarthria (speech difficulties), dystonia (abnormal muscle tone,) concentration and coordination difficulties, dementia
Psychiatric: depression, psychosis
Eyes: Kayser-Fleischer rings in cornea (brown circles of copper deposits in Descemet’s membrane)
What are the signs of Wilson’s disease
Hepatosplenomegaly, renal disease, osteopenia, haemolytic anaemia
What is the gold standard investigation for Wilson’s disease
Liver biopsy (increased copper, hepatitis)
What are the first line investigations for Wilson’s disease
Serum copper and ceruloplasmin reduced (copper in tissues not blood), 24hour urinary copper excretion high, abnormal LFTs
What are further investigations for Wilson’s disease
Slit-lamp examination (Kayser-Fleischer rings), MRI brain, genetic testing
What are the differential diagnosis for Wilson’s disease
Hepatitis B and C, haemochromatosis, alpha 1 antitrypsin deficiency
Describe the management for Wilson’s disease
1st line – copper chelation with penicillamine (or trientene)
2nd – zinc salts, decrease copper diet (reduce liver, chocolate, nuts, mushrooms, shellfish), liver transplant if cirrhosis
What are the complications of Wilson’s disease
Cirrhosis
Define hepatic encephalopthy
Brain infection due to toxic metabolites (especially ammonia) not removed by the liver due to liver dysfunction.
Describe the aetiology of hepatic encephalopathy
Liver cirrhosis
Describe the pathophysiology of hepatic encephalopathy
Ammonia is produced by intestinal bacteria when they break down proteins and is absorbed in the gut. Ammonia builds up in the blood in patients with cirrhosis because liver impairment prevents hepatocytes from metabolising ammonia into harmless waste products, and collateral vessels between the portal and systemic circulation means that ammonia bypasses the liver and enters systemic circulation directly.
Describe the key presentations for hepatic encephalopathy
Reduced consciousness, confusion, stupor, coma, changes to personality mood and memory. Asterixis, rigidity, hypokinesia. Signs of chronic liver failure.
Describe the first line investigations for hepatic encephalopathy
Blood ammonia raised, abnormal LFTs, EEG (decrease in brain wave frequency and amplitude), U&E (maybe hyponatraemia or hypokalaemia)
Describe the management for hepatic encephalopathy
Laxatives (e.g., lactulose) promote excretion of ammonia from gut before it is absorbed.
Antibiotics (e.g., rifaximin) reduce the number of intestinal bacteria which produce ammonia.
Nutritional support, e.g., nasogastric feeding
Define spontaneous bacterial peritonitis
Infection of ascitic fluid caused by bacterial infection. Not attributed to any intra-abdominal, ongoing inflammatory or surgically correctable condition.
Describe the epidemiology of spontaneous bacterial peritonitis
E. coli most common causative organism. Most common infection in cirrhosis.
Describe the aetiology of spontaneous bacterial peritonitis
Gram negative: E. coli, klebsiella. Gram positive: staph aureus
Describe the risk factors of spontaneous bacterial peritonitis
Cirrhosis, liver failure, GI bleeding
Describe the key presentations of spontaneous bacterial peritonitis
Severe abdominal pain with shock and collapse, fever, ascites, guarding (rigidify helps pain, pain eased when pressing hands on abdomen, lying still)
Describe the clinical manifestations of spontaneous bacterial pericarditis
Signs: hypothermia, hypotension, tachycardia
Symptoms: Nausea and vomiting, confusion
What is the gold standard investigation of spontaneous bacterial peritonitis
Ascitic fluid absolute neutrophil count (ANC) raised >250cells/mm3
Describe the first line investigations for spontaneous bacterial peritonitis
1st line FBC: leucocytosis, anaemia. Raised CRP/ESR.
Blood cultures and ascitic tap (show causative microorganism)
hCG test (exclude pregnancy). Abdominal x-ray (exclude bowel obstruction). Chest x-ray (air below diaphragm)
What are the differential diagnosis for spontaneous bacterial peritonitis
Renal colic, secondary peritonitis, chemical peritonitis, tuberculosis peritonitis
Describe the management for spontaneous bacterial peritonitis
1st line – IV antibiotics: piperacillin/tazobactam. Cephalosporins (cefotaxime) are also used.
Consider vancomycin (better coverage), IV albumin, large volume paracentesis. Peritoneal lavage (surgical cleaning of peritoneal cavity)
What are the complications of spontaneous bacterial peritonitis
Sepsis, renal failure, death
Define paracetamol overdose
Excessive ingestion of paracetamol. Serious toxicity >150mg/kg in a 24-hour period. In adults the maximum dose in 24 hours if 4g.
Describe the epidemiology of paracetamol overdose
Most common cause of acute liver failure
Describe the pathophysiology of paracetamol overdose
In an overdose there are not enough glutathione stores in the liver so toxic NAPQI (toxic by-product of paracetamol) builds up and damages the liver.
What are the key presentations of paracetamol overdose
Nausea, vomiting, anorexia, right upper quadrant pain, jaundice, coma
Describe the first line investigations for paracetamol overdose
Serum paracetamol concentration (very high), LFTs (elevated ALT), prolonged prothrombin time, hypoglycaemia
Describe the management for paracetamol overdose
1st line – activated charcoal within 1 hour of ingestion. Plus, N-acetylcysteine (increases availability of glutathione)
Describe the complications for paracetamol overdose
Liver failure, multiorgan failure, death
Describe Gilbert’s syndrome
Genetic condition of mild unconjugated hyperbilirubinemia
Describe the aetiology of Gilbert’s syndrome
Autosomal recessive condition. Main cause of inherited jaundice
Describe the pathophysiology of Gilbert’s syndrome
Decreased UDPGT activity leads to decreased conjugation of bilirubin > unconjugated hyperbilirubinemia
What are the key presentations of Gilbert’s syndrome
Short episodes of jaundice. Asymptomatic between episodes.
Describe the first line investigations for Gilbert’s syndrome
Unconjugated bilirubin elevated. Exclude other causes of unconjugated hyperbilirubinemia.
Describe the management for Gilbert’s syndrome
No treatment
Define pancreatic cancers
Majority are adenocarcinoma of exocrine pancreas. Usually in head or neck of pancreas.
Describe the aetiology of pancreatic cancers
Genetic mutations in ductal epithelial cells
Describe the risk factors for pancreatic cancers
Smoking, alcohol, diabetes, chronic pancreatitis
Describe the key presentations for pancreatic cancer
Courvoisier sign (painless palpable gallbladder and jaundice) with pale stool and dark urine. Pruritis, weight loss. Trousseau sign of malignancy (blood clots felt as small lumps under skin)
What is the gold standard investigation for pancreatic cancer
Pancreatic CT protocol (pancreatic mass)
Describe the first line investigations for pancreatic cancer
Abdominal ultrasound (pancreatic mass, dilated bile ducts)
Describe the management for pancreatic cancer
1st line – surgical resection (Whipple)
Define hepatocellular carcinoma
Primary liver that originates in the liver, arising from hepatocytes in predominantly cirrhotic liver. 90% of primary liver cancers
Describe the risk factors for hepatocellular carcinoma
Viral hepatitis (B and C), alcoholic liver disease, NAFLD,
Describe the pathophysiology of hepatocellular carcinoma
Metastasises to lymph nodes, bones, and lungs through haematogenous spread (hepatic/portal vessels)
What are the key presentations for hepatocellular carcinoma
Chronic liver disease signs: jaundice, ascites, hepatic encephalopathy, hepatomegaly. Weight loss, tired all the time (TATT), RUQ pain
What are the first line investigations for hepatocellular carcinoma
Raised serum alpha-fetoprotein (HCC tumour marker). 1st line abdominal USS, GS = CT scan
Describe the management for hepatocellular carcinoma
1st line – surgical resection of tumour. Also: liver transplant
Define cholangiocarcinoma
Primary liver cancer which originates from bile ducts. Least common primary liver cancer after hepatocellular carcinoma
Describe the risk factors of cholangiocarcinoma
Age >50, parasitic flukeworms, primary sclerosing cholangitis
What are the key presentations of cholangiocarcinoma
Courvoisier’s sign (painless jaundice and palpable gallbladder), weight loss, abdominal pain, fever, malaise, pruritis
Describe the first line investigations of cholangiocarcinoma
CA19-9 raised (tumour marker for cholangiocarcinoma), CEA raised (carcinoembryonic antigen), LFTs: raised bilirubin, ALP
1st line – abdominal USS and CT. GS = ERCP (endoscopic retrograde cholangiopancreatography)
Describe the management for cholangiocarcinoma
1st line – surgical resection or ERCP can be used to stent in the bile duct that the cholangiocarcinoma is compressing, to drain bile and relieve symptoms
Define an epigastric hernia
Hernia: bowel protrusion through defect in wall of its cavity.
Epigastric: in upper abdomen epigastric area
What are the key presentations for an epigastric hernia
Painful swelling of upper abdomen
Describe the first line investigations for an epigastric hernia
Clinical diagnosis, ultrasound
Describe the management for an epigastric hernia
Surgical repairDes
Describe the complications for an epigastric hernia
Incarceration, obstruction and strangulation
Define a femoral hernia
Hernia: protrusion of bowel through a defect in the wall of its cavity
Femoral: bowel comes through femoral canal
Describe the pathophysiology of a femoral hernia
High risk of incarceration, obstruction, and strangulation due to narrow opening and rigid femoral canal borders. Femoral canal: potential space medial to femoral vein
What are the key presentations of a femoral hernia
Painful swelling in medial upper thigh, pointing down. Lateral and inferior to pubic tubercle. May be cough impulse
Describe the first line investigations for a femoral hernia
Clinical diagnosis, Ultrasound, CT, MRI
Describe the management for a femoral hernia
Surgical repair
Describe the complications of a femoral hernia
Incarceration, obstruction, strangulation
Define hiatal hernia
Hernia: bowel protrusion through defect in the wall of its cavity
Hiatal: herniation of stomach through the diaphragm hiatus
Describe the risk factors for hiatal hernias
Obesity, increasing age and pregnancy
Describe the pathophysiology of hiatal hernias
20% - rolling: gastroesophageal junction stays in abdomen, other parts of stomach, e.g., fundus folds around and up through diaphragm aperture, alongside the oesophagus.
80% - sliding: stomach slides up through the diaphragm with the gastroesophageal junction passing through the diaphragm.
Describe the key presentations of hiatal hernias
Heartburn/GORD, dyspepsia (indigestion), bowel sounds in chest, dysphagia,
Describe the first line investigations for hiatal hernias
Chest x-ray, barium swallowing, endoscopy, oesophageal manometry
Describe the management for hiatal hernias
1st line – surgical repair or conservative treatment of gastric acid reflux (proton pump inhibitor)
Define incisional hernia
Hernia: bowel protrusion due to defect in wall of its cavity
incisional: tissues protrude through surgical scar due to weakness of muscles and tissues following closure from surgery
What are the key presentations for incisional hernia
Painful swelling in area of incision
Describe the first line investigations for incisional hernia
Clinical diagnosis, ultrasound
Describe the management for incisional hernias
Surgical repair or left alone
Define inguinal hernia
Hernia: protrusion of organ through a defect in the wall of its containing cavity.
Inguinal: protrusion of abdominal contents through inguinal canal. spermatic cord herniates through inguinal canal in males.
Describe the aetiology of inguinal hernias
Male, heavy lifting, chronic coughing, past abdominal surgery
Describe the pathophysiology of inguinal hernias
Presents superior and medial to pubic tubercle.
Direct: 20%, directly through abdominal wall in Hesselbach’s triangle. RIP: rectus abdominis medial border, inferior epigastric arteries, Poupart’s (inguinal) inferior border ligament.
Indirect: 80%, bowel herniates through inguinal canal
Describe the key presentations of inguinal hernias
Painful swelling in groin, when an indirect hernia is reduced, and pressure applied to deep inguinal ring it will remain reduced. When pressure is applied to a direct hernia it will not stop the herniation.
Describe the first line investigations for inguinal hernias
Clinical diagnosis. Also: ultrasound, CT, MRI
Describe the management for inguinal hernias
1st line – surgical repair (laparoscopic, tension-free mesh repair)
Describe the complications for inguinal hernias
Incarceration (cannot be reduced, trapped in herniated position), obstruction (blocks faeces passage), strangulation (ischaemia)
Define umbilical hernias
Hernia: obstruction of bowel through a defect in the wall of its cavity. Umbilical hernias occur around the umbilicus
Describe the pathophysiology of umbilical hernias
Muscle weakness around umbilicus. Common in children
What are the key presentations for umbilical hernias
Asymptomatic, bulge at umbilicus, pain can occur on straining abdominal wall
Describe the first line investigations for umbilical hernias
Clinical diagnosis, Ultrasound
Describe the management for umbilical hernias
1st line – spontaneous resolution or surgical repair.
Describe the complications for umbilical hernias
Incarceration, obstruction, strangulation