Gastroenterology (Free)

Gastroenterology (Free)

💩 Gastroenterology

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🥩 Hepatopancreatobiliary (HPB)
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Hepato - Liver
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How can the features of liver disease be classified?

What are the features of each?

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Compensated liver disease? (7)
  1. Fatigue
  2. Anorexia
  3. Nausea
  4. Abdominal pain
  5. Spider naevi
  6. Palmar erythema
  7. Gynaecomastia
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Decompensated liver disease? (4)
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Jaundice
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What are the differentials for a jaundiced patient?
  • Pre-hepatic
    1. Haemolysis e.g. G6PD deficiency
    2. Neonatal jaundice: Rhesus haemolytic disease, ABO haemolytic disease, hereditary spherocytosis
  • Intra-hepatic
    1. Damage: ALD, NAFLD, hepatitis, etc.
    2. Gilbert's syndrome
    3. Crigler-Najjar syndrome
  • Post-hepatic
    1. Gallstones: Mirizzi syndrome
    2. PBC/PSC
    3. Cholangitis
    4. Pancreatic cancer
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How do the stools and urine vary depending on the 3 classifications of jaundice?
  • Pre-hepatic: Normal urine and stools
  • Hepatic: Dark urine, normal/pale stools
  • Post-hepatic: Dark urine, pale stools
    • ‣
    Why pattern of symptoms occur in this case?
    1. Conjugated bilirubin is soluble, unconjugated is not.
      • Pre/intrahepatic → ↑ unconjugated
      • Post-hepatic → ↑ conjugated
    2. Soluble conjugated bilirubin dissolves in the urine (urobilinogen) as it cannot be excreted through the GI tract, giving urine a dark colour.
    3. Lack of bilirubin in the stools (due to biliary tract obstruction) make them pale.
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Ascites
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How is it investigated to determine cause?
  • Diagnostic tap to analyse the fluid contents
    • SAAG (Serum albumin:ascitic albumin ratio = SAAG)
      • High (transudate): Suggests low albumin
        • Raised portal pressure → Fluid shift
      • Low (exudate): Suggests high albumin
        • Cancer of abdomen
        • Infection → ↑ Vascular permeability (e.g. TB, SBP or pancreatitis)
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How is ascites managed?
  1. Low sodium diet
  2. Diuretic eg Spironolactone (Spiro better than Furosemide in ascites)
  3. Prophylactic antibiotics eg Ciprofloxacin
  4. Therapeutic paracentesis (ascitic drainage)
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If the disease is still present despite all of the management above, what is considered?
  • Transjugular intrahepatic portosystemic shunt (TIPSS)
  • Indicated in refractory ascites & secondary prophylaxis of variceal haemorrhage
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If there is a low SAAG & high neutrophils, what is the likely pathology?
  • Spontaneous bacterial peritonitis
    • ‣
    What pathogen is likely to be causing this?
    1. E. coli
    2. Klebsiella
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    What features make you suspect SBP?
    • Temperature
    • Distended tender abdomen
    • Can be asymptomatic, always consider in patients who deteriorate suddenly with no obvious cause
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    How can this be prevented?
    • Prophylactic PO ciprofloxacin
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    How is it managed?
    • Take ascitic culture
    • IV cefotaxime
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Varices
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How do these present?
  • Either asymptomatic and found incidentally, or as an acute upper GI bleed.
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What are the two scoring systems for an upper GI bleed?

What are each of them used for?

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Glasgow-Blatchford score
  • Pre-endoscopy score
  • Decides timing of intervention, if the score is high the patient must go straight for treatment rather than endoscopy first
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Rockall score
  • Post-endoscopy score
  • Stratifies based on mortality risk: Risk of rebleed after endoscopy
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What is given in the acute management? (4)
  1. ABCDE: Fluid / blood, FFP, Plts
  2. Terlipressin: Splanchnic vasoconstriction → Lower portal venous pressure going through varices and decreases bleeding risk.
  3. Broad spectrum prophylactic antibiotics eg 7 days Ceftriaxone (dec infection risk and risk of rebleed)
  4. Urgent endoscopy within 24h for band ligation
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What is the post-endoscopy protocol management?

Hong kong protocol:

  • Omeprazole STAT then continuous infusion to reduce the rebleeding risk
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What is given as secondary prophylaxis to prevent re-bleeding?
  • Propranolol: Reduces azygos blood flow and variceal pressure
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Hepatic encephalopathy (HE)
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What is it?
  • Ammonia build-up causing cerebral oedema
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What are the features- early and late?
  • Early: Confusion (suspect in anyone with liver failure and altered consciousness)
  • Late: Fetor hepaticus, coma
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How is it graded?
  • 0 - Normal mental status
  • I - Mild confusion (also slurred speech)
  • II - Moderate confusion (Lethargic & drowsy)
  • III - Disorientated to time & place, but rousable. Stupor, incoherent speech
  • IV - Coma, unresponsive
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How is it managed?

First-line:

  1. PO lactulose: Reduces nitrogenous waste
    • ↑ faecal flow through the GI tract → ↓ time for proteins to be broken down → ↓ amino acid absorption → ↓ ammonia
  2. IV mannitol: Reduces cerebral oedema

Second line:

  1. Rifaximin: Specialist treatment to decrease activity of ammonia-producing gut flora
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What pain management should be avoided?
  • Morphine
    • ‣
    Why does this increase risk of HE?
    • Slowed gut motility → ↑ amino acid absorption → ↑ ammonia
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Liver function tests (LFTs)
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Which LFTs are raised in liver damage?
  1. ALT > 10-fold rise
  2. AST
  3. Unconjugated bilirubin
  4. GGT
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Which LFTs are raised in cholestatic damage?
  • ALP > 3-fold rise
    • Isolated rise in ALP is suggestive of increased bone breakdown: Mets, vitamin D deficiency, fractures, renal osteodystrophy
  • GGT
    • Suggests biliary epithelial damage and bile flow obstruction
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How do you test the synthetic function of the liver?
  • Albumin
  • Bilirubin
  • Clotting
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Why must you be cautious when interpreting a raised ALP?
  • ALP can be raised due to both liver and bone problems, and high in pregnancy.
    • ‣
    What tests are useful to differentiate them?
    • Liver: Abnormal GGT & other LFTs
    • Bone: Abnormal calcium +/- vitamin D
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Name the differentials for liver disease.
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Acute liver failure
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How does this present?
  • Non-specific: Fatigue
  • Liver-specific: Decompensated liver features discussed above
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What investigation is most useful in determining if they have this?
  • INR > 1.5
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What are the common causes of this? (5)
  1. Hepatitis
  2. Alcohol
  3. Drugs
  4. Autoimmune hepatitis
  5. Budd-chiari syndrome
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Alcoholic liver disease
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What is used to assess alcohol dependence?
  1. AUDIT questionnaire
  2. SADQ questionnaire
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What is the advice around weekly alcoholic intake?
  • Drink up to 14 units per week, spread this evenly over 3 days or more
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How is chronic alcoholism managed?
  1. Mild dependence: < 15 U/day / ≤ 20 on AUDIT
    • CBT first-line
  2. Moderate dependence: > 15 U/day OR > 20 on AUDIT
    • Assisted withdrawal with chlordiazepoxide
  3. Severe: > 30 U/day OR > 30 on SADQ OR high risk of seizures/delirium tremens
    • Inpatient withdrawal
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How is acute alcohol withdrawal managed?
  1. IV pabrinex OD
  2. Chlordiazepoxide reducing regime
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What liver function test can give you an indication alcohol is the cause?
  • GGT: Although not specific and so must be accompanied by other LFTs
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NAFLD
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What features are suggestive of NAFLD? (5)
  1. Obesity
  2. Type 2 diabetes
  3. High triglycerides
  4. Hypertension
  5. Smoking
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How is this investigated?
  1. Bloods: LFT and lipids
  2. Liver USS: Fatty changes
  3. Enhanced liver fibrosis (ELF) blood test
    • Combination of hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase → Algorithm creates a score
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How do you get a definitive diagnosis?
  • Biopsy (rarely done)
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What is severe NAFLD called?
  • Non-alcoholic steatohepatitis (NASH): Fat has caused chronic inflammation and cell death
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How is this managed?
  • Conservative: Weight loss (even 10% improves LFTs), stop smoking, avoid alcohol
  • Statins (as NAFLD and metabolic syndrome are RF for CVD)
  • If NASH: Consider pioglitazoes and vitamin E (under specialist)
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Hepatitis
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Viral
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How are the types transmitted?
  • A&E: Faeco-oral
  • B&C: Blood & baby
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Which ones can only be acute, never chronic?
  • Hepatitis A & E
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Which ones have vaccines available?
  • Hepatitis A & B
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Which type of Hepatitis doesn't exist without the presence of HepB first?
  • Hepatitis D
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Which of the hepatitis' is a DNA virus?
  • Hepatitis B is a DNA virus
  • The rest are RNA viruses
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If there is a 'ground glass appearance' on light microscopy of hepatic tissue, what does this suggest?
  • Chronic HepB infection
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A nurse has a needlestick from a known HepB patient, she hasn't finished her HepB course. How is this managed?
  1. HepB immunoglobulin
  2. Accelerated HepB vaccine course
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Autoimmune
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Who commonly presents in an exam history?
  • Young females
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What antibodies would you look for?
  1. Anti-smooth muscle antibodies
  2. ANA (anti-nuclear antibodies)
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How are they managed?
  1. Immunosuppression: Steroids / azathioprine
  2. Liver transplant
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Cirrhosis
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What scoring system measures the severity of cirrhosis?
  • CHILD-PUGH score
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    What factors does it consider?
    1. Encephalopathy
    2. Ascites
    3. Bilirubin
    4. Albumin
    5. Prothrombin time
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How do you monitor management?
  • MELD score (6 monthly): Gives mortality rate and guides referral for transplant
  • USS & AFP (6 monthly): Screens for hepatocellular carcinoma
  • Endoscopy (3 yearly): Looking for varices
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How do you manage cirrhosis?
  1. Treat underlying cause
  2. Manage complications (e.g. ascites)
  3. Definitive management: Liver transplant
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What are the complications of cirrhosis?
  • Increased mortality
  • Ascites & SBP
  • Liver failure
  • Hepatocellular carcinoma
  • Renal failure/Hepatorenal syndrome
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Hepatocellular carcinoma
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Who is at high risk of this?
  1. All patients with cirrhosis
  2. HepB / HepC: Particularly high risk
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What is the screening test for this?
  • Alpha-feto protein (AFP)
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Drug-induced liver injury (DILI)
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Paracetamol overdose

How are the following managed:

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Ingestion < 1 hr ago
  • Activated charcoal
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Staggered overdose > 15 hrs ago
  • Start N-acetylcysteine
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Ingestion < 4 hrs ago
  • Wait until 4 hrs to take a level, treat if high
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Ingestion 4-15 hrs ago
  • Take immediate level, treat if high
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What other drugs can damage the liver?
  • Methotrexate
  • Amiodarone
  • Isoniazid
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Budd-Chiari syndrome
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What is this?
  • Obstruction of venous outflow from the liver into the inferior vena cava (IVC)
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What triad of features indicates this?
  1. Hepatomegaly
  2. Abdominal pain
  3. Ascites
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Inherited
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Wilson's disease
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What features suggest this?
  1. Hepatic: Hepatitis, cirrhosis,
  2. Neurological: Ataxia, tremor, dystonia
  3. Psychiatric: Change in personality
  4. Other: Kayser-Fleischer rings, Coombs negative haemolytic anaemia
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How would you investigate?
  1. Serum caeruloplasmin
  2. 24 hour urinary copper (screening test)
  3. Genetic analysis for ATP7B gene
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How is it managed?
  • Copper chelators: Penicillamine, trientine
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Haemochromatosis
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How is this inherited?
  • Autosomal recessive: Mutations in the HFE gene
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How can this present? (6)
  1. Pseudogout
  2. Dilated cardiomyopathy
  3. Cirrhosis
  4. Diabetes - Pancreatic deposition of Fe
  5. Grey skin discolouration
  6. Hypogonadism
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What is seen on routine bloods? (3)
  1. FBC: ↑ Hb
  2. LFT: ↑ transaminases
  3. BM: High
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What is a typical picture on iron studies? (3)
  • ↑ transferrin saturation (M > 55%, F > 50%)
  • ↓ TIBC
  • ↑ Ferritin & Fe
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What is seen on liver biopsy?
  • Perl's stain
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How are they managed?
  1. Lifelong venesection & aspirin
  2. Desferrioxamine (Fe-chelating agent)
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A1AT deficiency
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What features suggest this?
  1. Liver: Cirrhosis (clubbing, palmar erythema, spider naevi)
  2. Respiratory: Emphysema (inhalers)
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Pancreato - Pancreas
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What are the two functions of the pancreas?
  1. Exocrine: Production of enzymes that are released into the small intestine to help digest food.
    1. Amylase → breaks down carbohydrates
    2. Lipase → breaks down fats
    3. Proteases → break down proteins
  2. Endocrine: Production of hormones, including insulin and glucagon.
    1. Alpha cells → Glucagon → Signals the liver to convert stored glycogen into glucose.
    2. Beta cells → Insulin → Signals cells to take up glucose from the bloodstream and store it for energy.

Disease:

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Acute pancreatitis
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What are the causes?

I GET SMASHED

  1. Idiopathic
  2. Gallstones
  3. Ethanol (alcohol)
  4. Trauma
  5. Steroids
  6. Metabolic
  7. Autoimmune
  8. Scorpion sting
  9. Hypercalcaemia
  10. ERCP
  11. Drugs: Azathioprine, sulfasalazine, valproate, diuretics (loop/thiazide), steroids, tetracyclines
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What are the classic symptoms and signs?
  • Nausea & vomiting
  • Severe epigastric pain radiating to back
  • Low grade fever
  • Tachycardic
  • Hypotensive
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What markers are used to test for pancreatitis?
  • Amylase
  • Lipase (more sensitive, more expensive): Remains high for 12 days
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What are the signs of poor prognosis according to Glasgow scoring system?
  • PaO2 < 8kPa (60mmHg): ARDS
  • Age > 55 years
  • Neutrophils - WBC > 15 x109/l
  • Calcium < 2
  • Renal: Urea > 16mmol/l
  • Enzymes: AST/ALT > 200 iu/L or LDH > 600 iu/L
  • Albumin < 32g/l
  • Sugar: Glucose >10mmol/L
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Chronic pancreatitis
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What are the classic symptoms and signs?
  • Recurrent abdominal pain
  • Weight loss (malabsorption, exocrine insufficiency)
  • Jaundice
  • Can suffer episodes of acute-on chronic pancreatitis
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What is the importance of serum amylase with chronic pancreatitis?
  • It is often normal
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What are the common causes of chronic pancreatitis? (3)
  • Alcohol
  • Cystic fibrosis
  • Hereditary
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Pancreatic cancer
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What are the RFs?
  1. Smoking
  2. FH of pancreatic cancer
  3. Lynch syndrome or BRCA 1/2
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How might it present?
  1. Courvoisier's sign: Painless palpable GB & jaundice
  2. Trousseau's sign: Migratory thrombophlebitis
    • Recurrent episodes of blood clots causing vessel inflammation in different locations across the body
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What tumour marker is raised in this?
  • CA 19-9
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What are the most accurate imaging methods for staging?
  1. Endoscopic USS w/ biopsy
  2. CT TAP
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Biliary - Biliary Tree and Gallbladder
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Biliary anatomy
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Exercise: Labelling the biliary tree
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Answers
  1. Bile ducts
  2. Intrahepatic bile ducts
  3. Left and right hepatic ducts
  4. Common hepatic duct
  5. Cystic duct
  6. Common bile duct
  7. Sphincter of Oddi
  8. Major duodenal papilla
  9. Gallbladder
  10. Right lobe of liver
  11. Left lobe of liver
  12. Spleen
  13. Esophagus
  14. Stomach
  15. Pancreas
  16. Accessory pancreatic duct
  17. Pancreatic duct
  18. Small intestine
  19. Duodenum
  20. Jejunum
Jmarchn, CC BY-SA 3.0
Jmarchn, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
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Simplified Key Anatomy
Boumphreyfr, CC BY-SA 3.0
Boumphreyfr, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
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Biliary tree
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Autoimmune
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Primary biliary cholangitis
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Where does this affect the biliary tract?
  • Intrahepatic ducts: Bile ducts within the liver
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How can this present?
  • Fatigue, jaundice, pruritus, RUQ pain
  • Xanthoma, xanthelasma
  • Signs of cirrhosis and liver failure, e.g. ascites, splenomegaly
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Can you explain the pathophysiology and why those symptoms occur?
  • Inflammation of bile ducts → Bile outflow obstruction → Bile acid, bilirubin & cholesterol buildup → Pruritus, jaundice and xathelasma
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What antibodies are present in this?
  • Anti-mitochondrial IgM antibodies
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What other blood test is often raised in PBC?
  • ESR
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What diseases are associated with PBC often?
  • Other autoimmune diseases:
    • Thyroid
    • Coeliac
    • Rheumatoid conditions, e.g. Systemic sclerosis, RA
      • ‣
      Why may a patient with PBC have xerostomia (dry mouth)?
      • Sjogren's syndrome
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What is seen on biopsy?
  • Granulomas
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What two drugs can be used in the management?
  • Ursodeoxycholic acid: Reduces absorption of cholesterol
  • Colestyramine: Binds to bile acid to prevent absorption and help with pruritus
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Primary sclerosing cholangitis
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What location does it affect?
  • Intrahepatic and extrahepatic ducts
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What is this associated with in 70% of cases?
  • Ulcerative colitis
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How can this present?
  • Fatigue, jaundice, pruritus, RUQ pain, hepatomegaly, cirrhosis
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What is the gold standard investigation?
  • MRCP
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What antibodies are present in this?
  • There are no antibodies helpful in diagnosing PSC, none are sensitive or specific enough
  • p-ANCA is present the majority of the time
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What two drugs can be used in the management?
  • Ursodeoxycholic acid: Reduces absorption of cholesterol
  • Colestyramine: Binds to bile acid to prevent absorption and help with pruritus
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Cholangiocarcinoma
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What is it?
  • Cancer of the bile duct
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What are the three types?
  1. Intrahepatic: Affects bile ducts inside the liver.
  2. Perihilar (Klatskin): Occurs where the right and left hepatic ducts exit the liver and join to form the common hepatic duct. Also called a Klatskin tumor or perihilar cholangiocarcinoma.
  3. Extrahepatic (Distal): Occurs below the area where the common hepatic duct and cystic duct join to form the common bile duct.
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What’s the most common known predisposing factor?
  • Primary sclerosing cholangitis
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What tumour marker may be raised?
  • CA 19-9 (carbohydrate antigen)
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How do you manage?
  1. Curative surgery combined with radiotherapy and chemotherapy (only in early cases).
  2. Biliary stenting
  3. Palliative chemotherapy
  4. Palliative radiotherapy
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Acute cholangitis
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What is it?
  • Inflammation or infection of the common bile duct
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What are the features?
  • Charcot’s triad:
    1. Fever
    2. RUQ pain
    3. Jaundice
  • Reynolds pentad:
    1. Fever
    2. Hypotension
    3. Confusion
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What organisms commonly cause these infections?
  • Escherichia coli (27%)
  • Klebsiella (16%)
  • Enterococci (15%)

Investigations & Management:

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What bloods would you want?

Key bloods (but not all):

  • FBC: Leucocytosis is found in the vast majority of patients
  • CRP
  • LFT: Raised ALP ± GGT + raised bilirubin
  • U&E: Septic patients may have reduced renal function due to hypoperfusion
  • Procalcitonin: Bacterial infection
  • Blood culture
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What imaging would you consider?
  • USS: Bile duct dilation
  • MRCP for more detailed imaging
  • ERCP (diagnostic & therapeutic): Identify and remove the cause of the blocked biliary tree.
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Gallbladder: Cholecystitis
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Identifying & Classifying
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What is it?
  • Inflammation of the gallbladder usually occuring when a gallstone completely obstructs the neck of the gallbladder or cystic duct.
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What’s the typical presentation?
  • Sudden-onset, severe RUQ pain lasting several hours.
  • Tenderness in the right upper quadrant (with or without guarding).
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Name the two types.
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Calculous (90–95%)
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Partial: What do we call it when the obstruction is partial?
  • Biliary colic
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Complete: Why does the gallbladder become inflamed when outflow is completely obstructed?
  1. Trauma from the gallstone causes prostalandin release which stimulates an inflammatory response.
  2. Gallbladder then becomes more distended and inflamed causing compromise of blood flow and lymphatic drainage, leading to mucosal ischemia.
  3. Bacterial infection of the bile may then occur.
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Acalculous (5%)

Exact cause is poorly understood, but often in critically ill patients, associated with bile stasis or thickening.

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What are the risk factors?
  • Bile stasis: Trauma, severe systemic illness, and prolonged total parenteral nutrition use
  • Bile thickening: Fever and dehydration
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Name the key investigation.
  • Abdominal USS to identify presence of gallstones.
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Managing & Complications
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How do you manage them?
  1. Support: IV fluids, antibiotics & analgesia
  2. Definitive: Laparoscopic cholecystectomy
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Name 5 complications.
  1. Necrosis of the gallbladder wall (gangrenous cholecystitis).
  2. Gallbladder perforation.
  3. Biliary peritonitis.
  4. Pericholecystic abscess.
  5. Fistula between the gallbladder and duodenum.
  6. Jaundice due to inflammation of adjoining biliary ducts.
    7. ‣
    What is this called?
    • Mirizzi syndrome
  7. Sepsis.
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🌯 Luminal
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Upper GI (Mouth → Duodenum)

Anatomy:

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Oesophagus
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Gastro-oesophaegeal reflux disease (GORD)
‣
What is the best investigation for a hiatus hernia?
  • Barium swallow
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When going for an endoscopy, how is omeprazole management approached?
  • Stop 2 weeks before endoscopy as it could mask serious pathology, e.g. gastric cancer
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What drugs are associated with dyspepsia?
  1. NSAIDs/steroids
  2. Bisphosphonates
  3. CCBs
  4. Nitrates
  5. Macrolides
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Oesophageal varices

Dilated collateral blood vessels that develop as a result of portal hypertension, usually with a background of cirrhosis.

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What are the key features?
  1. Haematemesis
  2. Melaena
  3. Severe liver disease
  4. Cirrhosis (50% have varices)
  5. Spider nevi
  6. Jaundice
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What are differentials for haematemesis?
  1. Gastric varices
  2. Mallory-Weiss tear
  3. Peptic ulcer
  4. Upper GI malignancy
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What scoring systems may be useful?
  1. Rockall score: Estimate the risk of rebleeding or death in patients with upper GI bleed.
  2. Glasgow-Blatchford score: Stratifies upper GI bleeding patients who are "low-risk" and candidates for outpatient management.
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How would you investigate?
  1. Bloods: FBC, U&E, LFT, coagulation, HepB serology, G&S and cross match.
  2. Gastroscopy: Diagnostic of varices and allows assessment of their size.
  3. Consider:
    1. Capsule endoscopy
    2. Liver USS
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How do you manage them?
  1. ABCDE
  2. Consider, if appropriate:
    1. Transfusion
    2. Terlipressin / somatostatin analogue (e.g. octreotide)
    3. Prophylactic antibiotics (e.g. IV ceftriaxone)
  3. When stabilised, endoscopy & endoscopic variceal band ligation
    1. If endoscopy not immediately available, balloon tamponade or Danis stent
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Oesophageal cancer
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What are the common features?
  1. Dysphagia
  2. WL
  3. Retrosternal chest pain
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If a patient has Barrett's oesophagus, how are they managed if they have low-grade or high grade dysplasia, respectively?
  1. Low grade: High dose omeprazole & 6 monthly endoscopy
  2. High grade: Endoscopic ablation
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What cell types can they be?
  1. Squamous cell
  2. Adenocarcinoma (if Barrett's) - Lower 1/3
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Achalasia
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What is it?
  • Degeneration of the myenteric plexus around the LOS causing it to always contract
  • Difficulty swallowing both solids & liquids
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How is it investigated?
  1. Manometry: Tube into oesophagus that measures pressures
    • High pressure in the LOS, incomplete relaxation, absence of peristalsis
  2. Barium swallow: 'Bird's beak appearance'
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How is it managed?
  1. Medical: Nifedipine & omeprazole
  2. Definitive:
    1. Unfit for surgery: Balloon dilation of the LOS
    2. Fit for surgery: Heller's cardiomyotomy
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Stomach
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Peptic ulcer disease
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What are the two areas this can affect & the features of each?
  1. Stomach: Worse after meals
  2. Duodenum: Improves after meals
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What is Zollinger-Ellison syndrome?
  • Gastrinoma of the stomach → Excessive acid secretion → Ulcers
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How is H. pylori negative disease managed?
  • 4-8 weeks full dose PPI
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How are they followed up?
  • Repeat endoscopy 6-8 weeks after being discharged
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How are they managed if the ulcer perforates?
  1. NBM, IV fluids
  2. Laparotomy
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How are they managed if the ulcer causes a severe bleed?
  • Endoscopic clipping or thermal coagulation
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H. pylori
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How is this confirmed?
  • Faecal antigen
  • Urea breath test
‣
How is it managed initially?

Triple therapy (BD for 7 days):

  1. Omeprazole
  2. Amoxicillin
  3. Clarithromycin
‣
When tested 4 weeks later, how does management change if still positive?
  • Triple therapy: Metronidazole replaces clarithromycin
  • Refer to gastroenterology if still + after this
‣
Cancer
‣
What cell type is it likely to be?
  • Glandular: Adenocarcinoma
‣
What associations increase susceptibility?
  1. H. pylori infection
  2. Smoking
  3. Obesity
‣
What is seen on endoscopy?
  • Signet ring cells
‣
Duodenum
‣
Duodenal ulcers
  • Managed the same as gastric ulcers
‣
Coeliac disease
‣
What is the pathophysiology?
  • Gluten is broken down to gliadin in the small intestine → Inflammatory response → Cell destruction (lost surface area) → Malabsorption
‣
Presentation:
‣
What is coeliac disease most commonly linked with? What else is it associated with?
  • Common: T1DM & thyroid - All of these patients are tested for coeliac disease
  • Other autoimmune: Autoimmune hepatitis, PBC, PSC
‣
What is the rash may they present with?
  • Dermatitis herpetiformis (pruritic vesicles on the extensor surfaces)
‣
Why may they be anaemic?
  • Malabsorption of B12/folate
‣
What bloods will confirm your suspicions?
  1. IgA anti-TTG antibodies
    2. ‣
    What else should you test for with this?
    • Total IgA because if there's an IgA deficiency then the test will be negative but the disease may still be present
    ‣
    How can you confirm the diagnosis in those patients?
    • IgG anti-TTG/anti-EMA
  2. Anti-EMA antibodies
‣
What features are seen on intestinal biopsy? (2)
  1. Villous atrophy
  2. Crypt hypertrophy
‣
How are they managed?
  • Lifelong gluten free diet
  • Dapsone antibiotic for dermatitis herpetiformis
‣
Lower GI (Jejunum → Anus)

Common:

‣
Inflammatory bowel disease (IBD)
‣
Features:
‣
What features would make you consider IBD?
  • Abdominal pain, blood diarrhoea, mouth ulcers, other autoimmune conditions, WL, anaemia
  • Systemically unwell during flares
‣
How do you differentiate the two types?
‣
Crohn's (NESTS)
  • No/less blood or mucus in stool
  • Entire bowel is affected
  • Skip lesions
  • Terminal ileum most affected & Transmural thickness inflammation
  • Smoking makes it worse
‣
UC (CLOSEUP)
  • Continuous inflammation
  • Limited to colon & rectum
  • Only superficial mucosa affected
  • Smoking protective
  • Excrete blood & mucus
  • Use aminosalicylates
  • Primary sclerosing cholangitis
‣
What extra-intestinal manifestations would you look for?
  • Finger clubbing
  • Erythema nodosum
  • Pyoderma gangrenosum
  • Episcleritis/iritis
  • PSC in UC
‣
What are the types?
‣
Ulcerative colitis
‣
What site is most commonly affected?
  • Rectum
‣
Name 5 extra-intestinal manifestations.
  1. Skin: Erythema nodosum, pyoderma gangrenosum
  2. Primary sclerosin cholangitis (independent of flares)
  3. Eyes: Episcleritis, scleritis, anterior uveitis
  4. Osteoporosis (malabsorption)
  5. Peripheral neuropathy (B12)
‣
What is seen on colonoscopy?

Disease is limited to the mucosa, showing:

  1. Crypt abscesses
  2. Goblet cell depletion
  3. Mucin depletion
  4. Mucosal ulcers
‣
What is seen on barium enema?
  • 'Lead pipe sign' - Loss of haustral markings on the bowel
‣
What are the complications?
  • Toxic megacolon: AXR to investigate
    • ACR (colon dilation), Temp > 38.6°C, HR > 120bpm, anaemia, ↑ neutrophils
Hellerhoff, CC BY-SA 3.0
Hellerhoff, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Crohn's disease
‣
What is the epidemiology?

Age of onset is bi-modal:

  • 15-40 years: Majority
  • 60-80 years: Small second peak
‣
Where does it commonly target?
  • Distal ileum
  • Proximal colon
‣
What features are you looking for?
  1. Abdominal pain (potentially colicky)
  2. Diarrhoea (often chronic)
  3. Oral aphthous ulcers (can be painful)
  4. Perianal disease
‣
How do you investigate it? (5)
  1. Bedside: Faecal calprotectin
  2. Bloods: FBC (macrocytic anaemia), LFT (PSC).
  3. Radiology: USS/CT/MRI (fistulae, abscesses, strictures)
  4. Endoscopy: OGD & colonoscopy
    • Take biopsies to look for microscopic features.
    • If active disease only do flexible sigmoidoscopy because of risk of perforation in colonoscopy.
    • If colonoscopy is negative in Crohn's, use MRI to assess the small bowel.
‣
What are the key principles of management? (2)
  1. Induce remission
    2. ‣
    What is used to induce remission in Crohn's? (3)
    1. Steroids - PO prednisolone (mild-moderate) / IV hydrocortisone (severe)
    2. Add azathioprine/mercaptopurine
    3. Refractory: Infliximab
    ‣
    What is used to induce remission in UC?
    1. Aminosalicylate - Mesalazine (mild-mod)
      1. Suppository/enema first
      2. PO if extensive disease
    2. Steroids - PO prednisolone (mild-mod) / IV hydrocortisone (severe)
    3. IV ciclosporin (severe)
  2. Maintain remission
    3. ‣
    What is used to maintain remission in Crohn's?

    Medical:

    1. Azathioprine/Mercaptopurine
    2. Methotrexate
    3. Infliximab
    4. Adalimumab

    Surgical:

    1. If only affecting one area of bowel severely, surgery will be considered.
    ‣
    What is used to maintain remission in UC?

    Medical:

    1. Aminosalicylate - Mesalazine (PO/PR)
    2. Azathioprine
    3. Mercaptopurine

    Surgical:

    1. Panproctocolectomy: Surgery to remove the colon & rectum. May have hemicolectomy, depends on case.
      • Patient has either a permanent ileostomy or ileo-anal anastomosis (J-pouch).
‣
Appendicitis
‣
What are the features of appendicitis?
  • Abdominal plain: Classically central/periumbilical then moves to right iliac fossa
  • Nausea and vomiting
  • Loss of appetite
  • Mild fever
  • Can get rebound tenderness
‣
What is Rovsing's sign?
  • Palpation in left iliac fossa causes pain in right iliac fossa
‣
How do you diagnose it?
  • Mostly clinical presentation
  • Raised inflammatory markers & WCC
‣
What conditions can a urine dipstick rule out?
  • Pregnant female
  • UTI
  • Renal colic
‣
How is it managed?
‣
What is the definitive management?
  • Appendicectomy
‣
What needs to be given before surgery & why?
  • Prophylactic IV antibiotics - Reduces wound infection
‣
What are the 2 options for surgery?
  • Laparoscopic
  • Open
‣
Diverticular disease
‣
Definitions:
‣
Diverticulum
  • Herniation of colonic mucosa through muscularis causing outpouchings
‣
Diverticulosis
  • The presence of diverticula WITHOUT symptoms
‣
Diverticulitis
  • Inflamed/infected diverticula
‣
Who is it common in? What are the 2 main risk factors?
  • Very common in older people
  • RFs: Low fibre diet & obesity
‣
What are the features of diverticulitis?
  • Left iliac fossa colicky pain
  • Diarrhoea
  • PR blood or mucus
  • Fever
  • Can be septic and peritonitic if severe!
‣
What investigation is important if suspect diverticulitis and why?
  • Abdominal XR (or CT abdo)
  • Erect CXR to identify a perforation
‣
How do you manage diverticulosis?
  • Often an incidental finding on CT
  • No treatment necessary: Advise high fibre diet and weight loss if necessary
‣
How do you manage diverticulitis?
  • Analgesia
  • Fluid resuscitation
  • Antibiotics
  • Unwell → Consider hospital admission
  • Severe → May need surgical drainage or resection
‣
Cancer

See Colorectal Surgery

‣
Irritable bowel syndrome (IBS)
‣
How is IBS different to the majority of GI conditions?
  • There is no organic underlying disease. Many think it is linked to stress and the mind
‣
What features can you get?
  • Diarrhoea or constipation predominant- fluctuating bowel habit
  • Abdominal pain
  • Bloating
  • Worse after eating, improved by opening bowels
‣
What investigations can you do to exclude other pathology before diagnosing?
  • FBC, ESR and CRP
  • Faecal calprotectin
  • Anti-TTG antibodies
  • CA125
‣
What is the management of IBS?
  • Provide reassurance
  • Low FODMAP diet
  • Symptom dependent:
    • Cramping: peppermint oil, buscopan (hyoscine butylbromide)
    • Diarrhoea: Loperamide
    • Constipation: Laxatives

Less common:

‣
Clostridium dificile
‣
What is a typical history?
  • Patient in hospital on antibiotics (broad spectrum - e.g. cephalosporins) for an infection develops watery diarrhoea & feels generally unwell
‣
What is seen on colonoscopy?
  • Yellow plaques & mucosal inflammation
‣
How are they managed? (2)
  1. PO metronidazole (mild)
  2. PO vancomycin (mod-sev)
‣
Name 1 severe complication.
  • Toxic megacolon
‣
Re-feeding syndrome
‣
What metabolic abnormalities occur with this?
  • Hypophosphataemia
  • Hypokalaemia
  • Hypomagnesaemia
  • Abnormal fluid balance

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