My Gastroenterology

  1. What questions should be asked in a history investigating suspected IBD?
    • Stool frequency, consistency, urgency and blood
    • Abdominal pain,
    • Malaise, fever or weight loss
    • Extraintestinal symptoms
    • Travel
    • Family history
    • Smoking
  2. What lab investigations are useful when diagnosing IBD?
    • FBC (Anaemia, WBC, platelets)
    • ESR, CRP
    • U+Es (dehydration)
    • LFTs
    • Stool cultures + C.Diff toxin
    • Faecal calprotectin (stool WCCs)
  3. What is seen on colonoscopy in Crohn's and ulcerative colitis?
    • Crohn's: Ulceration and inflammation
    • Ulcerative colitis: Granular mucosa, reduced blood vessels
  4. What criteria define an acute exacerbation of an IBD?
    • Bowel movements >6 daily
    • PR blood frequent
    • Raised temperature
    • HR >90
    • Haemoglobin <10
    • ESR >30
  5. What treatments are used in acute exacerbation of an IBD?
    • Prophylactic LMW heparin
    • IV hydrocortisone
    • If no improvement >72hrs, infliximab > ciclosporin
    • Surgery if immunosuppression contraindicated/refractory
  6. Outline the use of steroids in controlling an IBD
    • Indicated if severe systemic symptoms
    • IV hydrocortisone/methylprednisolone
    • Allow remission, but not maintenance (maximum course 1 week)
  7. What immunosuppressive drugs can be used in the management of IBDs
    • Methotrexate/thiopurines
    • Effective in active and maintenance therapy of both IBDs
  8. What is the biologic treatment of IBD and when is it used?
    • Infliximab
    • Anti-TNF monoclonal antibody
    • Used in very severe UC or fistulating Crohn's
    • Allergy common/Expensive
  9. Outline the use of surgery in the management of the IBDs
    • Ulcerative colitis: Surgery curative; ileo-anal pouch or ileostomy
    • Crohn's: Indicated in strictures, perforations or fistulations. Remission can still occur, so used sparingly
  10. What is the cause of Whipple's disease, and what are its clinical features?
    • Tropheryma whipplei infection when patient has a lack of immunity
    • Weight loss, arthralgia, diarrhoea, abdominal pain
  11. Describe some complications of acute appendicitis
    • Acute inflammation of mucosa = ulceration and transmural inflammation
    • Gangrene can cause perforation, generalised peritonitis or abscess
  12. Define ulcerative colitis, its presentation and complications
    • Chronic inflammation of the mucosa and submucosa of the large intestine and rectum (no granulomas)
    • Onset 15-25, with gradual onset of chronic bloody diarrhoea
  13. Define Crohn's disease, its presentation and complications
    • Chronic transmural inflammation in any part of gut (usually ileum and anus) causing garnulomas and 'fissuring ulcers'
    • Common in smokers, 15-25yoa, with cramps, abdominal pain, vomiting, mouth ulcers, weight loss and bleeding
    • Fistulas, stenosis, abscess and inflammation cause 'knots' in bowel. Greatly increased cancer risk.
  14. What is 'indeterminate colitis'?
    When a diagnosis of colitis is between Crohn's and UC
  15. What is 'microscopic colitis'?
    • Profuse watery diarrhoea
    • Colonoscopy normal
    • Abnormal histology; either collagenous or lymphocytic (relates to inflammatory cells in lamina propria)
    • May be associated with drug treatment, e.g. PPIs, statins
  16. Outline the pathophysiology of ischaemia affecting the gut
    • Extreme problem, with certain death if not operated upon
    • Mucosal/transmural infarction, coagulative necrosis and gangrene
  17. Outline the presentation of acute and chronic gut ischaemia
    • Acute: abdominal pain and bloody stool
    • Chronic: Pain when eating, with weight loss (abdominal angina)
  18. Outline some causes of gut ischaemia
    • Hypotension (watershed infarction)
    • Strangulated hernia
    • Mesenteric artery/vein thromboembolism
    • Volvulus (sigmoid colon twisting)
  19. Outline the pathogenesis of cholesterol stones
    • Excessive secretion of cholesterol or decrease secretion of bile salts
    • Precipitation occurs
    • Example is Crohn's, reducing bile salt recycling
  20. Outline how Crohn's is different from UC
    • Crohn's:
    • Usually involves terminal ileum and anus, but not the rectum.
    • The areas of inflammation are patchy, not continuous.
    • Deep ulceration, may even be transmural
    • Stenosis is common
    • Granulomas
  21. Outline the pathogenesis of bile stones
    • Excessive bile secretion (e.g. haemolytic anaemia)
    • Causes bile precipitation after concentration in the gall bladder
  22. Describe chronic cholecystitis, its pathogenesis and its clinical features
    • May be a progression from acute cholecystitis, with gallstones virtually always present
    • Inflammation due to chemical damage from supersaturated bile, not bacterial infection
    • Ulceration, fibrosis and macrophage/lymphocyte infiltration
  23. How does a bladder mucocoele occur?
    • Gallstone becomes stuck in Hartmann's pouch of gallbladder
    • Reduces bile entry, but mucin still secreted
    • No inflammation, but distension
  24. How does a gallstone ileus occur?
    • Fistula develops between gallbladder and duodenum from inflammation/necrosis
    • Allows entry of a large stone into terminal ileum, and air into biliary tree
  25. What is the link between painless obstructive jaundice and carcinoma of bile ducts/pancreas?
    • Cancer growth compresses bile duct
    • Back up of bile prevents excretion from liver
    • Bilirubin builds up in blood, causing jaundice
  26. How does cystic fibrosis affect the GI tract?
    • Mucous can block the bile ducts, preventing bile salt transportation to the GI
    • Bile salts needed by some pancreatic enzymes = reduction in digestions efficiency
    • Hepatic cirrhosis can occur, causing ascites, varicosities and splenomegaly
    • Pancreatic scarring can also occur
  27. Describe an insulinoma
    • Commonest functional tumour of the pancreas
    • Presents with hypoglycaemia
    • Usually benign, but even malignant have much better prognosis
  28. What important points should be remembered about the bilirubin cycle when assessing plasma bilirubin?
    • Increased unconjugated bilirubin = increased haemolysis OR liver damage (produced more or conjugated less)
    • Bile duct obstruction leads to conjugated biliruin in plasma
    • Urobilinogen created in GI tract - if bilirubin transport obstructed, urine doesn't contain urobilinogen
  29. Briefly outline the anatomy of teeth
    • Central chamber of tooth has stroma and vessels
    • Surrounded by dentine (tubular connective tisuse) with enamel surface (calcium)
    • Attached by ligaments to mandible and by connective tissue fibres to gums.
  30. What is oral leukoplakia?
    • Treated as pre-malignant squamous dysplasia, with keratosis
    • Change in histology, with mild cytological atypia
    • Behaves like any dysplasia; may become more atypical, then carcinoma in situ
    • Usually found on floor of mouth (chemical pooling) or soft palate
    • HPV and smoking common causes
Card Set
My Gastroenterology
Liver, GI, pancreas pathology