GI Pathology: UC + Crohn's Flashcards
Ulcerative collitis and Crohn’s disease are the two major forms of chronic idiopathic inflammatory bowel disease (CIBD). When do both diseases show a peak in terms of age?
- late adolescence and early adulthood
- little gender difference
- more common in white people
Why are both diseases considered idiopathic?
- underlying aeitology + pathogenesis poorly understood
- different aetiologies between two
- although clinical and pathological findings can overlap
What do most investigators believe CIBD results from?
a combination of:
- intestinal epithelial dysfunction
- aberrant mucosal responses in a genetically susceptible host
- altered composition of intestinal flora
Mutations in which gene are thought to be important in the development of Crohn’s?
- NOD2 gene
- product of which is involved in macrophage activation
What is a significant predisposing factor in Crohn’s disease that appears to be protective against UC?
Smoking
What is the diagnostic test for Crohn’s disease and UC?
- there is no single diagnostic test for crohn’s + UC
- accurate diagnosis depends on integration of clinical, endoscopic, microbiological, radiological and histopathological features
- it is important that infective causes of inflammation are considered and excluded
What is the gross appearance of ulcerative collitis?
- only the large bowel (colon + rectum) is affected
- rectum is almost always affected
- disease extends proximally in a continuous distribution to involve a variable amount of colon
- most severely affected mucosa is usually present distally
- proctitis (30%) and distal colitis (30%) are most common
What are microscopic features of ulcerative collitis?
- inflammation generally involves mucosal layer only
- there is extensive, diffuse mucosal ulceration w/ inflammation
- crypt abscesses are a typical feature - crypts full of neutrophils
- granulomas are not seen
What might patients with long-standing UC develop?
- inflammatory polyps (‘pseudopolyps’) - composed of inflammatory tissue - typically granulation tissue permeated by inflammatory cells, they are not dysplastic ie. they are not premalignant
- inc risk of developing colorectal carcinoma - those w greatest risk have extensive collitis + a long history (>8rs) of disease, pts are therefore offered colonoscopic surveillance, aim is to detect + treat dysplasia (ie pre-malignancy) before the development of an invasive adenocarcinoma
What is the clinical presentation of UC?
- bloody diarrhoea (pooing many times a day)
- lower abdo pain + cramps
- can be classified as mild/moderate/severe
- fever in moderate/severe cases
- inc HR in severe cases
- may present with anaemia
What are some extra-intestinal manifestations of ulcerative collitis?
- overlap with those of Crohn’s disease
- include uveitis
- migratory polyarthritis
- sacroilitis
- ankylosing spondylitis
- skin lesions
about 5% of pts with UC also have primary sclerosing chalngitis, these pts are at an increased risk of developing cholangiocarcinoma
What are gross features of Crohn’s disease?
- may affect any part of GI tract from mouth to anus
- preferentially involves the terminal ileum + proximal colon
- distribution is typically patchy + discontinuous (diseased segments are separated by normal areas)
What are the microscopic features of Crohn’s disease?
- deep fissuring ulcers, often in form of penetrating knife-like clefts through bowel wall
- transmural inflammation (ie. all layers of the bowel wall may be involved)
- non-caseating granulomas are often present (but not in every case)
What is a granuloma?
An aggregate of activated (epithelioid) histiocytes (activated macrophages resembling epithelial cells)
How is there a ‘cobblestone’ appearance in Crohn’s?
- linear fissuring ulcers may coalesce (join)
- cobblestones correspond to areas of surviving mucosa
- surrounded by fissuring ulceration
The inflammation in Crohn’s disease is transmural in nature. The inflammation may extend to the serosal surface and cause well recognised problems.
Name 3 of these problems and what are they are
- adhesions to other loops of bowel + intra-abdominal organs - adhesion = band of fibrous (scar) tissue that binds together normally separate anatomical structures
- fistula formation (an abnormal connection between two epithelial surfaces): enteroenteric (bowel to bowel), enterovaginal (bowel to vagina), entercutaneous (bowel to skin), enterovesical (bowel to bladder)
- stricture formation as transmural inflammation heals by fibrosis -> present as bowel obstruction
What is the clinical presentation of Crohn’s disease?
- more varied than UC
- chronic diarrhoea (most common)
- abdo pain and weight loss also common
Why might Crohn’s disease present with a right iliac fossa mass?
- subacute small bowel disease
- inflammatory
- associated with fistulae or abscess formation
What are more common clinical features of Crohn’s disease over UC?
- non-bloody diarrhoea (compared to bloody in UC)
- weight loss more prominent
- more abdominal pain
Give 5 major pathological differences between UC and Crohn’s
What is calprotectin?
- protein
- occurs in large amounts in neutrophils
- antimicrobial (antibacterial + antifungal) properties
- released during inflammation when neutrophils degranulated
When the bowel is inflammed, increased levels of calprotectin may be detected in the faeces. What does the faecal assay tell us in comparison to serum/plasma calprotectin?
- provides direct information about inflammation site
- whereas serum/plasma - inflammation might be anywhere
When is faecal calprotectin investigation reccommended?
- by NICE
- to distinguish between inflammatory and non-inflammatory bowel disorders
- in those with lower GI symptoms of recent onset
- where cancer is not suspected
