Week 13 - GI and liver Flashcards
Describe the duct system of the liver and gallbladder which leads to the duodenum.
You have the left and the right hepatic ducts coming from the liver to form the common hepatic duct which joins with the cystic duct from the gallbladder to form the common bile duct which joins with the pancreatic duct and enter the duodenum through the ampulla of vater.
What are gall stones typically made of? How are gallstones usually diagnosed?
Cholesterol, bile pigment or mixed.
Ultrasound.
How does bile become lithogenic for cholesterol?
How does bile become lithogenic for bilirubin?
- If there is excessive secretion of cholesterol or decreased secretion of bile salts.
- If there is excessive secretion of bilirubin i.e. haemolytic anaemia.
What is acute cholecystitis? What are the clinical features of acute cholecystitis? What are the potential complications?
Acute gallbladder inflammation usually due to gallstones in the cystic duct which causes supersaturation of bile and chemical irritation.
Severe right upper quadrant pain, tenderness and fever and leucocytosis normal serum amylase.
Empyema, gangrene and rupture.
What are the main causes of acute pancreatitis?
Secondary to gallstones.
Secondary to alcohol.
Post ERCP, hypercalcaemia, drugs (azothioprine), mumps.
How does acute pancreatitis present?
Severe upper abdominal pain, fever, leucocytosis, raised serum amylase.
What are the potential complications of acute pancreatitis?
Fat necrosis, haemorrhage, pancreatic abscess, pseudocyst, chronic pancreatitis.
What is the most common subtype of pancreatic carcinoma? What is survival rate 1 year after diagnosis?
Ductal adenocarcinoma.
1 in 8
What are the risk factors for pancreatic cancer?
Germline mutations (e.g. BRCA) accounts for small proportion of patients.
SMOKING is the biggest risk factor.
Alcohol.
What are the signs and symptoms of pancreatic cancer?
Painless obstructive jaundice.
New onset diabetes.
Abdominal pain due to pancreatic insufficiency or nerve invasion.
What are the treatment options of pancreatic carcinoma?
Whipple’s resection - only for some tumours of the head of the pancreas.
- (Neo)adjuvant therapy - folfirinox
What is the blood supply and drainage of the liver?
Supply - hepatic artery and portal vein
Drainage - hepatic veins.
List the broad causes of injury to the liver.
Drugs/toxins i.e. alcohol Abnormal nutrition or metabolism Infection Obstruction to bile or blood flow Autoimmune liver disease Genetic/deposition syndrome Neoplasia
What is cirrhosis and what is its three stage definition?
Cirrhosis = end stage liver disease.
- Diffuse process with
- Fibrosis
- Nodule formation
What common investigations are done in diagosing liver disease?
Blood tests: LFTs, haematol, viral and autoimmune serology, metabolic tests.
Radiology: usually at least ultrasound.
What are some of the common histological patterns of acute liver disease?
- acute hepatitis
- acute cholestasis/cholestatic hepatitis
- fatty liver disease
- chronic hepatitis
- chronic biliary disease
- hepatic vascular disease
- genetic/deposition disease
What is the histological appearance of acute hepatitis?
Diffuse hepatocyte injury and swelling. Spotty necrosis, inflammatory cell infiltrate.
What are the causes and the histological appearance of cholestatic hepatitis?
Causes:
- extrahepatic biliary obstruction
- drug injury e.g. antibiotics
Histology: brown bile (bilirubin) pigment +/- acute hepatitis.
What does hepatitis B histology look like?
Acute hepatitis plus fibrosis. Ground glass cytoplasm in hepatocytes.
What are the causes and histology of chronic biliary cholestatic disease?
Causes - primary biliary cirrhosis, primary sclerosing cholangitis.
Histology - focal, portal predominant inflammation and fibrosis with bile duct injury, granulomas in PBC
What is the most common type of liver cyst?
Von Meyenberg complex
What is the pathophysiology behind primary biliary cirrhosis?
Autoimmune disease with serum anti-mitochondrial antibodies (AMA) and high IgM.
What are some signs of chronic liver disease and portal hypertension?
Chronic liver disease: spider naevi, foeter hepaticus, encephalopathy, synthetic dysfunction: prolonged PT, hypoalbuminaemia.
Portal hypertension: caput medusa, hypersplenism, thrombocytopenia.
How is ascites managed?
Low salt diet Spironolactone Furosemide Paracentesis Transjugular intrahepatic portosystemic shunt Liver transplant Aim for weight loss 0.5-1 kg/day
What scoring system is used to assess encephalopathy? How is it treated?
Conn score
Non-absorbable disaccharides (i.e. lactulose) - get bowels moving
Non (minimally)-absorbable antibiotics - gut decontamination
What are some of the symptoms of hepatitis?
Malaise, fever, headaches, nausea, vomiting, anorexia, RUQ pain, dark urine, jaundice.
What lab results would you expect to see in hepatitis?
Raised ALT/AST/bilirubin, clotting derangement
How long does the hepatitis virus need to be present for it to be classed as chronic hepatitis? Is chronic hepatitis usually symptomatic or asymptomatic?
6 months
Asymptomatic
What are some of the other infectious causes of acute hepatitis apart from Hepatitis A-E?
EBV, CMV, Toxo Leptospirosis Q fever Syphilis Malaria Viral haemorrhagic fevers
How is viral hepatitis diagnosed in the laboratory?
Detection of specific immune responses (IgM or IgG)
Viral nucleic acid detection (RNA or DNA), or antigen detection (HBV, HCV) using PCR.
Give a summary of hepatitis A.
RNA virus Faeco-oral spread 1 month incubation Diagnosed by IgM to Hep A, and deranged Liver Tests Very low death rate No specific treatment No chronic carriage Travel related, rare in UK, though recent increase Excellent vaccine
Give a summary of hepatitis E.
RNA virus Faeco-oral spread + pork products Death rate 1-3% Only supportive treatment Chronic carriage in some Some neurological complications No immunity No vaccine
What are the different ways that hepatitis B can spread?
Mother to baby (vertical) Contaminated needles + syringes Child to child Organs and tissue transplant Sexually Blood transfusion
What percent of people with chronic HBV infection go on to develop chronic liver disease? What are the complications of this?
25% Cirrhosis Decompensation Hepatocellular carcinoma Death
These things are measured in hepatitis B lab tests: - sAg - surface antigen - sAb - surface antibody - cAb - core antibody - eAg - e antigen - eAb - e antibody - HBV DNA What does the presence of these markers indicate?
sAg - marker of infection sAb - marker of immunity cAg - marker of previous infection eAg - marker of high infectivity eAb - marker of low infectivity HBV DNA - marker of infection
What are the treatments for acute HBV and chronic HBV? Which chronic HBV patients would you treat? What is the aim of treatment?
Acute - no treatments
Chronic - interferon, tenofovir or entecavir
Only those with liver inflammation or fibrosis.
Aim is to suppress viral replication and prevent further liver damage.
How is HBV prevented?
Education - i.e. safe sex, needles
Immunisation - at risk groups
Prevention of transmission from mother to child - HBV immunoglobulin or vaccination or tenofovir in pregnancy.
Hepatitis D can only replicate with co infection with hepatitis…
How is treated?
How does it spread? What does it increase risk of?
B
Peg IFN
Spreads in the same way as hep B.
Chronic liver disease
Give a summary of hepatitis C.
- Hep C is most common Hepatitis Virus in UK
•Needle / Blood Transmission
•Infection is usually asymptomatic and not notices
•70% develop Chronic infection and at risk of cirrhosis
•Treatment aim is to cure
•Direct acting antiviral drugs (DAAs) cure nearly all
•No Vaccine and no reliable immunity after infection
What is the exocrine and endocrine function of the pancreas?
Exocrine - synthesis and secretion of enzymes for digestion of food.
Endocrine - synthesis and secretion of hormones for glucose control.
How do you make a diagnosis of acute pancreatitis?
2/3 of:
- pain in keeping with pancreatitis
- amylase 3x the upper limit of normal
- characteristic CT appearance
What causes pancreatitis?
Gallstones Alcohol Trauma/ ERCP Other drugs/ high lipids/ autoimmune/ viral Scorpion venom
What investigations would be done when assessing acute pancreatitis?
Blood tests - serum amylase, FBC, CRP, U&E, LFTs, plasma calcum, ABGs.
US to assess for gallstones.
MRCP to assess for CBD stones.
CT if diagnostic doubt or concern about complications.
What is the further management of acute pancreatitis?
Treat cause: ERCP Laparoscopic cholecystectomy (gallbladder removal) Alcohol addictions advice Stop medication
How would infected necrosis of the pancreas be managed?
Open necrosectomy, percutaneous necrosectomy, radiological drainage.
What are the 4 layers of the oesophagus? (include epithelium type).
Mucosa (non-keratinising stratified squamous epithelium) + muscularis mucosae
Submucosa
Muscularis propria
Adventitia
What are the two main type of oesophageal cancer and what risk factors are they associated with?
Squamous carcinoma - associated with smoking and drinking.
Adenocarcinoma - associated with GORD and obesity.
In barrett’s oesophagus what change does the epithelium undergo?
Metaplasia - from non-keratinising stratified squamous to collumnar glandular epithelium with goblet cells.
What is the Barrett’s oesophagus associated with progression to?
Adenocarcinoma.
What are the three causes of chronic gastritis?
A - autoimmune
B - bacterial (h. pylori)
C - chemical
What are some acute causes of gastritis?
Alcohol, medication i.. NSAIDs, severe trauma, burns, surgery.
In autoimmune gastritis, where are the autoantibodies directed against?
Parietal cells and intrinsic factor.
What are some of the causes of chemical gastritis?
Bile reflux, NSAIDs, ethanol, oral iron.
What three ways does upper GI bleeding present?
- haematemesis
- coffee ground vomit
- melaena
Bleeding from what parts of the GI tract would be classed as upper GI bleeding?
Oesophagus
Stomach
Duodenum
List some of the causes of upper GI bleeding?
Peptic ulcer Oesophagitis Gastritis Duodenitis Varices Malignancy Mallory Weiss tear
Describe the early assessment and triage of upper GI bleed?
Rescucitate - pulse and BP, IV access for fluids/bloods (check bloods, esp. Hb and urea) Lie flat and give oxygen.
Risk assessment and timing of endoscopy (using Rockall or Glasgow blatchford.) :
high risk - emergency endoscopy. Moderate risk - admit and next day endoscopy. Low risk - out patient management.
What types of therapy are performed endoscopically for treatment of upper GI bleed?
Adrenaline injection. Heater probe Endoscopic clips Hemostatic powders Thrombin, laser
What class of drug should be given IV post-endoscopy to high risk patients to reduce rebleeding and mortality from a peptic ulcer? What other treatment should be given once Hb reached <7-8g/dL?
Proton pump inhibitors. Blood transfusion Platelet transfusion FFP Prothrombin complex concentrate
What medications should be stopped after an upper GI bleed? What should be restarted?
NSAIDs should be stopped.
Aspirin should be continued at a low dose once haemostasis is achieved.
Clopidogrel, warfarin and DOACs. Once haemostasis achieved, assess risks/benefits but generally aim to restart to reduce CV mortality.
How are varices treated?
Endoscopic banding, transjugular, intrahepatic portosystemic shunt (TIPS), beta blockers, balloon tamponade
Name three things that can cause varices.
Alcohol, hep C, NAFLD
What is the response to acute variceal bleeding?
Resuscitation - restore circulating volume - transfuse once Hb<7 g/dL - consider airway protection
Diagnosis - endoscopy
Therapy - antibiotics early - vasopressors (Terlipressin) early - endoscopic band ligation - ….rescue TIPS
What is used in primay prophylaxis of variceal bleeding and prevention of rebleeding?
Beta blockers or band ligation
Describe some of the differences between ulcerative colitis and crohn’s disease.
UC - Mucosal inflammation, limited to the colon, slight male preponderance, more common.
Crohn’s disease - transmural, can affect any part of the GI tract, slight female preponderance.
What is the aetiology of IBD?
Mixture of genetic susceptibility and environmental triggers. Smoking increases risk of Crohn’s, decreases risk of ulcerative colitis.
What investigations would you for suspected IBD?
FBC, ESR U&E, LFT CRP Stool cultures + C diff. toxin Faecal calprotectin AXR Colonoscopy or flexible sigmoidoscopy Small bowel radiology - MRI or CT, labelled white cell scan.
List the treatments used for both UC and Crohn’s, just UC and just Cohn’s/
Both
Corticosteroids
Thiopurines i.e. azathioprine
Biologics i.e. infliximab, adalumimab
UC
Aminosalicylates i.e. mesalazine
Crohn’s
Methotrexate
Immune modulating diets
How would you treat acute severe colitis?
IV hydrocortisone or methylprednisolone.
If no improvement:
- rescue therapy:
Ciclosporin, infliximab.
What is the role of surgery in IBD?
UC - curative surgery. Remove colon and do ileostomy or ileo-anal pouch
Crohn’s - surgery indicated for stricturing, perforation, fistulizing disease. Sparing as it will come back.
What are the complications of cirrhosis?
Ascites
Variceal bleeding
Encephalopathy
Hepatocellular carcinoma
What is refractory ascites?
Fluid overload unresponsive sodium restriction, 400mg/day spironolactone, 160mg/day frusemide.
How is refractory hepatitis treated?
Large volume paracentesis
TIPS
Liver transplant
What is the immediate management of spontaneous bacterial peritonitis?
IV antibiotics and IV albumin
After resuscitation from variceal bleeding, what should you give?
Terlipressin and antibiotics and endoscopic band ligation
