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Case 1

  • 30yo Lebanese man
  • Presents with bloody diarrhoea
    • 2 weeks duration
    • 10/12 motions per day
      • marker of severity, dehydration, loss of K+ through stool
    • blood and mucous present = inflammation (could be autoimmune or infective)
    • Mild LIF abdo pain
    • Should also ask about nocturnal diarrhoea as this is specific for bowel disease
    • gastroenteritis is short-lived but common. Once it gets after 2-4 weeks we think about other causes. The number 1 diagnosis is still an infection, but after 2-4 weeks, we start to think about other possibilities
  • O/E
    • BP 110/70
    • Pulse 105, Temp. 37.4
    • Soft abdo, LIF tenderness, no rebound or peritonism
  • Investigations
    • FBC: Hb 115g/L,WCC 9.5,Platelets 500
      • anaemia from bleeding
    • EUC: Normal
    • can show loss of fluid and electrolyte balance
    • Inflammatory Markers: CRP 60 mg/L,ESR 30mm/hr
      • not that WCC and platelets can go up in both infection and IBD - not specific
    • Stool Microbio: WBC +++,RBC +++, Enteric bacterial pathogen PCR: negative
    • AXR
      • Mucosal thickening: thicker wall of the bowel
      • Thumbprinting indicates mucosal inflammation: they become short and fat rather than long and thin
      • Lead piping - loss of haustra - thumbprint has become just a clean tube. In this case, this is present in the sigmoid colon
        • NB: haustra in large bowel don't cross the whole diameter of the lumen


    • Colonoscopy

Colo1.PNG Red, angry, inflamed, mucus visible, can't see blood vessel pattern under the mucosa. Hard to tell if it's infection or colitis.

  • DDx
    • Infection (should always be first ddx on first, acute presentation)
      • Bacterial
        • Campylobacter (primary cause), Salmonella, Shigella, E. Coli
        • Clostridium difficile (but no pseudomembranes on scope)
          • Mucus will wash away with the use of a foot pump that pumps water
      • Viral
        • Usually non-bloody, profuse, watery diarrhoea
        • Much more common
      • Protozoan
        • Giardia and cryptosporidia (usually longer Hx of crampy abdo pain and non-bloody diarrhoea)
        • Less common unless immunosuppressed
    • IBD
      • Ulcerative colitis
      • Crohn's colitis: chronic changes histologically - subclinically festering, and only symptoms for the past 2 weeks


  • Incidence
    • UC: 6-14 / 100,000
    • Crohn’s: 3-14 / 100,000 ; rising rapidly
  • Bimodal
    • Main peak: 15-30 years old
    • 2nd peak: 60-70 years old
  • Male=Female
  • Geography
    • Northern (and Southern) latitudes
    • Developed world


Don't really know what causes IBD

  • Genetics
    • Crohn’s > Ulcerative colitis
    • 10x increased risk in 1st degree family members
    • Twins: higher concordance in monozygotic twins than dizygotic twins
    • Genetic loci eg. IBD 1 = NOD2/CARD15
  • Environment
    • Smoking: increases risk of Crohn's, but ulcerative colitis is higher in ex-smokers or recently-quit smokers; smoking is protective
    • Geographic variations
  • Bacteria
    • disease in bacteria rich areas
    • no bacteria = no disease (in animal models)
    • antibiotics can help
  • IBD results from an inappropriate inflammatory response to intestinal bacteria in a genetically susceptible host

Intestinal Immune System

  • Bacteria
    • tolerance vs inflammation
    • homeostasis = constant state of low inflammation
  • Epithelium
    • Intercellular junctions
    • specialised cells (goblet and paneth)
  • Innate
    • sampling of lumen
    • epithelial cells, dendritic cells, macrophages
  • Adaptive
    • CD4+ Tcells (Th1, Th2, Th17, Threg)
    • B cells
    • migrations from vasculature

The normal mucosa is homeostatically producing a low-grade inflammation - ready to go when infection occurs.

Main interaction: between dendritic cells and CD4 T cells. TH1 and TH17 = Crohns. TH2 and TH17 = Ulcerative colitis. Treg play a role in damping down inflammation. IBD - there is an imbalance here.

Colitis macro: Granular, mucus, loss of haustration. Colitis micro: intestinal crypts branch, and chronic inflammatory cells, and fibrosis.

Ulcerative Colitis


Pathology - memorise

  • Only affects colon
  • Always involves rectum
  • Continuous disease - no skip lesions; it's always a continuous distribution of disease
  • Superficial lesions
    • Mucosal inflammation
  • Macroscopic
    • Loss of vascular lesions
    • granular, erythematous
    • mucopurulent exudate
  • Histology
    • acute inflammation oedema
    • chronic inflammatory changes
    • Mediated by Th2 and Th17
    • Crypt branching
    • Fibrosis
    • Distortion of normal architecture

Clinical Features

  • Hx
    • Bloody diarrhoea
      • 2-4 motions/day in mild, >10/day in severe disease
    • usually duration of >2 weeks
    • Pain and fevers --> usually mild unless severe disease. Unlike Crohn's, pain is rare.
    • weight loss in severe disease
    • rectal disease
      • tenesmus (constant need to pass stools), urgency, frequency, per-rectal bleeding or mucous
        • this is because inflammation keeps the nerve endings firing
  • O/E
    • Mild tenderness (no rebound)
    • Severe tenderness or peritonism concerning
  • Blood tests
    • FBC
      • anaemia, leukocytosis, thrombocytosis
    • EUC
      • dehydration, electrolyte losses
    • Inflammatory markers
      • CRP,ESR
    • Nutriontional markers
      • low iron levels
    • Stool microbiology
      • critically important
      • Infectious diarrhoea is an important differential
    • Radiology
      • Abdominal X-ray (monitor for toxic megacolon)
      • CT scan (only useful if Dx in doubt) - real risk of multiple CTs causing cancer
        • CT findings: Thick bowel wall, hyperaemia, fat stranding off the edge of the bowel
    • Endoscopy
      • important to assess macroscopic appearance
      • important to get histology


  • Toxic megacolon; bowel dilated >8cm, surgical emergency, need a colectom
    • Fulminant colitis
    • Bowel increases in size
    • lots of microperforations
  • Malnutrition
  • Colorectal cancer
    • Disease greater than 8 years duration
    • risk also exists in crohns colitis
    • chronic inflammation & ongoing mitosis due to ongoing injury --> dysplasia --> carcinoma
    • regular surveillance colonoscopy (every 2 years) for dysplasia once disease >8 years (NB: it's not diagnosis duration, it's symptom duration)
      • if they get dysplasia, you need a colectomy, because there are actually multiple areas of high grade dysplasia
  • Thromboembolic disease
    • PE, needs DVT prophylaxis

Case 1 cont.

  • Same pt 48hrs later
  • Febrile 39 degrees, and tachycardic 110/min
  • stools culture -ve
  • diarrhoea persists at >10 motions per day
  • more abdo pain
  • distended tender abdomen
  • Toxic megacolon is an important complication of UC

Case 2

  • 30 yo lady
  • back at uni doing grad course
  • non-smoker
  • presents to ED w/ abdo pain and vomiting
  • PMH
    • appendicectomy
    • episodes of pain since 20
  • O/E
    • afebrile, BP 11/70, pulse 100
    • mild dehydration
    • abdomen distended, generalised tenderness, tinkling bowel sounds, no peritonsim or rebound
  • investigations
    • AXR
      • look for air-fluid levels(erect) and distended bowel (supine)
    • CT shows terminal ileum inflammation
    • Colonoscopy reveals inflammed ileocaecal valve and strictured ileum

Stacked coins = plicae circularis = valvulae conniventes = X-ray indicator of small vowel

  • Supine film = dilated loops of small bowel. Lack of gas in large bowel.
  • Erect film = air fluid levels (see menisci). In gastroenteritis you're allowed about 3; but she has probably 20.
    • These menisci indicate a lot of fluid in the small bowel
  • Radiological hallmark - Dilate small bowel on supine film, lack of gas in the large bowel, and air fluid levels on an erect film.
  • Complication of Crohns = terminal ileal stricture causing obstruction


Crohn's Disease

  • Sites
    • Anywhere in GI tract
      • Most common: terminal ileum or cecum). Crohn's can have only colonic involvement. Hallmark is the Crohn's has skip lesions - doesn't just start at the rectum and be continuous.
  • Lesions are transmural - can affect all layers of bowel wall. Disease can go all the way through and fistulate out into the peritoneum
    • NB: small bowel has villi not crypts
    • Can stick another bit of bowel to it, or bladder, or skin. Can cause fistulae - connection between two mucosal surfaces, or an enterovesical/enterocutaneous/enterovaginal fistula
    • If nothing gets stuck, it can cause a peritoneal abscess
    • Penetrating, transmural disease
  • Separate, discrete (apthous) ulcers in Crohn's
  • Commonly inflamed ileocecal valve

Feature: deep ulcers that are criss-crossing, with islands of relatively normal mucosa, forming a cobblestone appearance.

Inflammation - loss of villi

Granulomas can occur - histiocytes surrounded by lymphocytes

Pathology - memorise

  • Can affect any part of GI tract
    • mouth to anus
    • mostly ileum and caecum
  • Discontinuous
    • skip lesions
  • transmural inflammation
  • deep, linear ulcers
    • cobblestoning
  • strictures, fistulae, and fissures
    • strictures: chronic inflammation --> fibrosis --> narrowing/obstruction --> proximal dilatation
  • granulomas on histo
    • not always
  • mediated by Th1 and Th17
  • can cause perianal disease - perianal fistulae (multiple opening around the rectum where poo can seep out), or perianal abscess

Clinical Features

  • Hx
    • abdo pain; cramping
    • diarrhoea
    • weight loss
    • symptoms of complications
      • bowel obstruction --> pain, vomiting, no bowel movement
      • abscess --> pain, fever, unwll
      • fistula --> anal discharge, pneumoturia
  • O/E
    • nutritional
    • abdo tenderness
    • perianal disease
    • weight, BMI, nutrition
  • Blood Tests
    • FBC
      • nutritional
      • anaemia, leukocytosis, thrombocytosis
    • EUC
      • dehydration, electrolyte losses
    • Inflammatory markers
      • CRP, ESR
    • Nutritional markers
      • iron levels, B12, folate
  • Investigations
    • Stool Microbiology
    • Radiology
      • CT/MRI enterogram (superseded SB series)
      • Abdo Xray (if clinical features of obstruction)
      • Standard CT scan (useful if abscess suspected)
    • Endoscopy
      • colonoscopy with ileoscopy
      • important to get tissue for histology
    • should probably have gastroscopy to document UGI dx

Note that colonoscopy not so useful as it's hard to get to the jejunum. Small bowel series (old fashioned) - drink dye, scan. Lumen becomes very narrow --> obstruction (string-like). Also look for rose-thorn ulcers and abscesses. Colo2.PNG

Extraintestinal Disease associated with IBD

  • Primary Sclerosing Cholangitis
    • Associated with colitis
    • 10% of IBD get PSC at some time in their life
    • 90% of PSC patients get IBD at some point
    • increases risk of colorectal cancer above colitis risk
  • Arthritis
    • asymmetrical, large joint
    • often back, sacrolitis
  • Skin
    • erythema nodusum - raised, red, tender lumps
    • pyoderma gangrenosum
  • eyes
    • episcleritis
    • uveitis
  • NB: Bowel cancer
    • PR bleeding, iron deficiency anemia and a change in bowel habit. Usually doesn't come on suddenly
    • Ulcerative colitis increases risk for cancer


  • IBD has complex aetiology - likely combination of genetics, environment and bactera
  • Pathophysiology - interaction between APC and CD4 T-cell the key
  • Clinical manifestations - depend on pathology
  • Investigations - histology very important
  • Complications
    • High morbidity condition with complications
      • DVT! - prophylaxis