GI/Liver Flashcards
Describe the presentation, investigation and management of chronic pancreatitis
‘a progressive inflammatory condition of the pancreas marked by replacement of the normal parenchyma with fibrous tissue’
Aetiology - TIGAR-O
Toxic/Metabolic, Idiopathic, Genetic, Autoimmune, RAP/SAP Associated, Obstructive
Presents with epigastric pain, weight loss, malabsorption, diabetes, jaundice
Investigations include elevated serum amylase and lipase, serum Ig4, abnormal faecal elastase, calcification on CT, MRCP, EUS, biopsy and labelled carbon breath test for exocrine insufficiency
Manage with lifestyle modification (smoking and alcohol cessation), analgesia, management of exocrine needs (e.g. pancreatic enzyme supplements) and endocrine needs (e.g. diabetes)
May require surgical intervention, such as duct drainage or distal pancreatectomy
Describe the clinical and histological appearance of acute cholestasis and its most common causes
Histological hallmarks include brown bile pigments and features of acute hepatitis
May present with jaundice, signs of gallstones etc.
Causes include extrahepatic biliary obstruction or drug injury (e.g. by antibiotics)
Describe the clinical and histological appearance of Fatty Liver Disease and its common causes
Risk factors include obesity, HTN, T2DM and hyperlipidaemia
May present with hepatomegaly, nausea, vomiting, diarrhoea, jaundice, ascites, ankle oedema
Histological features include steatosis, alcoholic hepatitis (infiltration by polymorphonuclear leucocytes and hepatocyte necrosis, with giant mitochondria and Mallory bodies)
Mallory bodies are suggestive of alcoholic damage
Alcoholic cirrhosis may also be seen (classically micronodular)
Most common cause is alcohol, however, fatty liver disease may be independent of alcohol
Describe the clinical and histological appearance of chronic hepatitis and its most common causes
Characterised by inflammatory cell infiltrate, lobular change, focal lytic necrosis, apoptosis, focal inflammation and fibrosis
Specific causes have specific appearances (e.g. ground glass appearance in hepatitis B)
Specific clinical features will reflect the underlying disease process
Causes include hepatitis B/C, autoimmune disease, Wilson’s disease and haemochromatosis
Describe the features of acute and chronic cholecystitis
Arises due to obstruction of gallbladder emptying, usually due to gallstones, resulting in distention, compromised blood supply and inflammation
Presents with severe RUQ pain, tenderness and fever
Chronic cholecystitis may be a sequel to repeated attacks of acute cholecystitis
Inflammation in chronic is secondary to chemical damage
Gallstones are virtually always present in chronic cholecystitis
Describe the causes of upper GI bleeding
Varices - Oesophageal varices arise due to cirrhosis of the liver, which leads to portal hypertension and shunting of blood to the porto-systemic circulation. This causes distention of the blood vessels in the oesophagus, which may become prone to rupture and severe bleeding
Peptic Ulcers - Commonly associated with h. pylori infection and increased gastric acid secretion
Gastritis/Duodenitis/Oesophagitis
Malignancy
Mallory-Weiss Tear
Describe common hepatic neoplasms
Haemangioma - Benign blood vessel tumour
Hepatic Adenoma - Mainly affects young women and is often associated with hormonal therapy
Hepatocellular Carcinoma - Most common primary liver tumour, usually arising in cirrhosis and associated with elevated serum alpha feto-protein
The most common origin of secondary liver malignancy is the GI tract (50%), followed by breast, ovaries, bronchus and kidneys
Describe the pathophysiology of Inflammatory Bowel Disease
- Ulcerative Colitis
- ‘relapsing and remitting inflammatory disorder of the colonic mucosa which may affect just the rectum or extend to involve part of the colon’
- Caused by an inappropriate immune response to colonic flora in genetically susceptible individuals
- Pathological features include hyperaemia, haemorrhagic colonic mucosa with/without pseudopolyps
- Continuous inflammation is limited to the mucosa
- Crohn’s
- ‘a chronic inflammatory disease characterised by transmural granulomatous inflammation affecting any part of the gut from mouth to anus’
- Unlike UC, there is unaffected bowel between areas of active disease (skip lesions)
Describe the management of Inflammatory Bowel Disease
- Common Treatments
- Corticosteroids
- IV Hydrocortisone/Methylprednisolone or Oral Prednisolone
- Rapid induction of remission
- Poor evidence for maintaining remission
- Thiopurines
- Azathioprine and Mercaptopurine are unlicensed for IBD therapy
- Effective maintenance therapy
- Steroid-sparing agent for those requiring 2+ courses a year or relapse on <15mg prednisolone
- Prevents T-cell clonal expansion in response to antigenic stimuli
- Biologics
- Infliximab
- Murine Anti-TNF Alpha
- Severe or fistulating Crohn’s or rescue acute severe UC
- Adalimumab or Golimumab
- Infliximab
- Corticosteroids
- For UC Alone
- Aminosalicylates
- Anti-inflammatory
- Mesalazine most widely used
- Can cause renal impairment
- Aminosalicylates
- For Crohn’s Alone
- Methotrexate
- Anti-inflammatory immunosuppressant
- Anti-metabolite
- Side effects include GI upset, hepatotoxicity, immunosuppression, sepsis
- Methotrexate
Describe the features of liver cysts
Usually developmental or degenerative in origin
Most common is the Von Meyenberg complex (a simple biliary hamartoma)
Usually no treatment required
State the constituents of gallstones and risk factors for their development
Stones may be pure cholesterol or bile pigment, but most are mixed
Bile becomes lithogenic for cholesterol if there is excessive secretion of cholesterol or decreased secretion of bile salts
Excessive secretion of bilirubin can cause its precipitation in concentrated bile
Risk factors include increased BMI, increased age, female sex, multiparity and Caucasian race (5 F’s)
Describe the presentation, investigation and management of pancreatic cancer
3% five year survival rate
Risk factors include smoking, male, alcohol, history of chronic pancreatitis, high BMI, family history
Presents with jaundice, abdominal/back pain, weight loss, acute pancreatitis, double duct sign, recent diagnosis of diabetes
Investigate with CT or MRI
Management may be surgical (Whipple’s resection or duct stenting or gastrojejunostomy) or medical (chemotherapy, pancreatic enzyme replacement therapy)
Describe the clinical and histological appearance of acute hepatitis and its most common causes
Signs and symptoms may be specific to the underlying disease process
Jaundice, malaise, nausea, vomiting, diarrhoea
Appearances include diffuse hepatocyte injury characterised by swelling, cytoplasmic granularity, vacuolation and necrosis
Causes include viruses (Hepatitis A-E and EBV), drugs, alcohol and Wilson’s Disease
Describe the presentation, investigation and management of exocrine pancreatic insufficiency
May arise due to pancreatitis, CF, pancreatectomy
Main presenting feature is malnutrition
Investigate with direct pancreatic function test or indirect (faecal elastase/fat)
Aim of management is to ensure a normal nutritional stats and avoid steatorrhea, weight loss and maldigestion-related symptoms
Treat with pancreatic enzyme supplementation (enteric coated pancreatin) and a PPI
Describe the presentation, investigation and management of acute pancreatitis
Aetiology - I GET SMASHED:
Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps/Malignancy, Autoimmune, Scorpion Sting, Hyperlipidaemia, Hypercalcaemia, ERCP/EUS, Drugs (e.g. Azathioprine)
Presents with acute, severe upper abdominal pain (may radiate to back, partially relieved by sitting/bending forward), jaundice, or signs of severe pancreatitis (multi-organ failure, pleural effusions, ascites)
Investigate with serum amylase (3x ULN), serum lipase (remains elevated for longer than serum amylase), AXR, contrast CT and MRCP
Manage with fluid replacement, analgesia, PO/enteral nutrition and antibiotics if septic for mild cases
Treat underlying cause (e.g. abstinence from alcohol or cholecystectomy)
Symptomatic fluid collections may need draining
Describe the diagnosis of Inflammatory Bowel Disease
FBC, CRP, ESR, U&Es, LFTs
Blood Cultures
Stool Cultures
Faecal Calprotectin
AXR
Colonoscopy and Biopsy
Crohn’s - MRI, Endoscopy
State the LFT pattern expected in obstructive jaundice
Marked elevation in ALP
Mild elevation in ALT/AST
Raised Bilirubin
Describe the clinical presentation, investigation and management of cholelithiasis/acute cholecystitis
Jaundice, severe RUQ pain, tenderness and fever
USS, X-Ray (only detects 10%), and Bloods (high bilirubin/CSR/ESR, leucocytosis and obstructive LFTs)
Manage with cholecystectomy if does not resolve spontaneously
Describe the management of acute upper GI bleed
Resuscitation (fluids, oxygen, check bloods)
IV PPIs (reduces re-bleed risk and mortality if given post-endoscopy)
Endoscopic Therapy (adrenaline injection, heater probe and endoscopic clips)
Restrictive Transfusion if Hb <7-8g/dL
Platelets if active bleeding and platelet count <50x109/L
FFP if INR>1.5
Prothrombin Complex Concentrate if on Warfarin and active bleeding
Describe the clinical presentation of Inflammatory Bowel Disease
Diarrhoea
Abdominal Pain
Weight Loss
Fever, Malaise, Anorexia, Fatigue
Tenesmus
Crohns - Fistulae, Obstruction
UC - Distended Abdomen, Clubbing, Erythema Nodosum, Pyoderma Gangrenosum
Describe drug-induced liver disease
Common
Drugs can cause almost any pattern of liver disease
Most drug hepatotoxicity is idiosyncratic (rare but usually a single clinical pattern) thus difficult to investigate, e.g. Augmentin
Occasionally there is predictable liver damage, e.g. Paracetamol or Methotrexate
Non-prescribed drugs are important too, e.g. over the internet, illicit or herbal
Describe the investigation of upper GI bleeding
Risk assessment with Admission Rockall or Glasgow Blatchford score
High Risk - Emergency Endoscopy
Moderate Risk - Admit and Next Day Endoscopy
Low Risk - Consider Out-Patient Management
Describe the presentation, investigation and management of biliary sepsis (ascending cholangitis)
‘infection of the biliary tree, usually originating at the junction with the duodenum and ascending to the gall bladder, which usually contains gallstones’
Charcot’s Triad (Fever, Jaundice and RUQ Pain)
Reynolds Pentad (Fever, Jaundice, RUQ Pain, Mental Confusion and Septic Shock)
Investigate with raised amylase, obstructive LFTs, raised bilirubin and positive blood cultures
Manage with broad-spectrum antibiotics and ERCP
Describe the presentation, investigation and management of Primary Sclerosing Cholangitis
‘chronic progressive cholestatic liver disease, characterised by inflammation and fibrosis of the intrahepatic and/or extrahepatic bile ducts, resulting in diffuse, multi-focal stricture formation’
Presents with RUQ pain, pruritis, fever, jaundice, weight loss and fatigue
Investigate with obstructive LFTs, low albumin, prolonged PT, positive ANCA, abdominal USS, MRCP and ERCP
Manage with pruritis relief, immunosuppression, ERCP with stenting of strictures
