GI Flashcards
(169 cards)
What 2 conditions make up the inflammatory bowel diseases
Crohns and Ulcerative Colitis
Define Crohn’s disease with epidemiology
Inflammatory bowel disease characterised by transmural inflammation of the ENTIRE GI tract (mouth to anus). Terminal ileum and colon most commonly affected.
North Europe, UK, North America, 20-40 years
Risk factors for Crohns
- Family history
- Smoking
- White people (particularly Jewish origin)
- Oral contraceptive pill
- Diet low in fibre
- NSAID
Causes of Crohns
Genetic: NOD2/CARD15 gene mutation
Environmental:
- Smoking
- Oral contraceptive pill
- NSAIDs
Bacterial: Mycobacterium paratuberculosis, Pseudomonas and Listeria
Pathophysiology of Crohns
Chronic inflammation of the GI tract. Pathogen is presented to GI immune cells causing T helper cells to bind to it. This causes the release of inflammatory cytokines such as Interferon Gamma and TNF-a, which further stimulate immune response and inflammation
It is thought that genetic abnormalities leads to a dysfunction, causing inflammation to be unregulated.
This causes transmural inflammation with areas of healthy bowel in between, known as skip lesions, providing a cobblestone appearance of the bowel. Inflammation of the bowels can lead to malabsorption.
Signs and symptoms of Crohns
Signs
- Aphthous mouth ulcers
- Abdominal tenderness
- Perianal lesions - Skin tags, fistulae, fissures, abscesses, ulcers
Symptoms
- Diarrhoea (prolonged and often)
- Abdominal pain
- Weight loss and failure to thrive
- Several extra-intestinal manifestations affecting skin, joints, eyes (next card)
Extra-intestinal manifestations of Crohns
Skin:
- Perianal/mouth ulcers
- Erythema nodosum (swollen fat under skin, looks red, usually on shins)
- Pyoderma gangrenosum (rapidly enlarging, very painful ulcer)
Musculoskeletal:
- Arthritis of the large joints
- Seronegative spondyloarthropathies
- Clubbing
Eyes:
- Conjunctivitis
- Iritis
Investigations in Crohn’s
Faecal calprotectin (inflammatory marker in GI tract) - Raised
Serum antibodies
- pANCA negative (more in UC)
- ASCA positive (more in Crohn’s)
Endoscopy/Colonoscopy + Biopsy GOLD
- Endoscopy: Skip lesions, cobblestoning, strictures
- Biopsy: Transmural inflammation, non caseating granulomas, goblet cells present
CT/MRI can be used to find skip lesions, fistulas, abscesses
Histology of Crohn’s
Transmural inflammation, non caseating granulomas, goblet cells present
Treatment of Crohn’s
Cease NSAID, smoking
Induce remission
- Elemental diet
- Glucocorticoids: Budenoside (mild), prednisolone (moderate), IV Hydrocortisone (very severe)
- Immunosuppressants (Azathioprine or methotrexate)
- Anti TNF antibodies (infliximab)
Maintain remission
- Azathioprine
Complications of Crohn’s (6)
- Peri anal abscesses
- Anal fissure/fistula
- Small bowel obstruction
- Colorectal cancer
- Osteoporosis
- Anaemia/malnutrition
Crohns vs UC mnemonic
NESTS (Crohn’s)
N - No blood (rarer but still possible!)
E - Entire GI tract
S - Skip lesions
T - Terminal ileum and transmural inflammation
S - Smoking Risk factor
CLOSEUP (UC)
C - Continuous inflammation
L - Limited to colon and rectum
O - Only mucosa affected
S - Smoking protective
E - Excrete blood and mucus
U - Use aminosalicylates
P - Primary Sclerosing Cholangitis
Define Ulcerative Colitis with important epidemiology
Relapsing and remitting inflammatory bowel disease that characteristically involves rectum, and can extend up large bowel, up to ileocaecal valve. Doesn’t affect anus
Similar epidemiology to Crohns but 3x more common in NON SMOKERS (smoking is protective)
Risk factors for Ulcerative Colitis (6)
- Family History
- HLA-B27
- NSAIDs
- Infections
- Not smoking
- Chronic stress/depression
Pathophysiology of Ulcerative Colitis (4)
- IBD involving continuous inflammation, affecting only the colon on its mucosal layers. Usually starts at the rectum, working its way proximally to the caecum but never going past the ileocaecal valve.
- Relapsing, remitting course (Flares with new damage to bowel wall, followed by tissue healing).
- Can affect rectum only (proctitis), extend up to splenic flexure (left-sided colitis) or entire colon (pancolitis)
- Pseudopolyps develop due to regenerating mucosa that forms a kind of scar that looks like a polyp.
Signs and symptoms of UC
Signs
- LLQ pain and tenesmus (Rectal pain, feeling like you need to poo when you dont)
- Bloody, mucusy diarrhoea
- Weight loss/malnutrition
- Relapsing, remitting course
Symptoms
- Abdominal pain
- Cramping
- Diarrhoea
- Fever,malaise during attacks
Extra intestinal manifestations of UC
- Erythema nodosum
- Pyoderma gangrenosum
- Uveitis
- Colorectal cancer
- Ankylosing spondylitis
Investigations in UC
Faecal calprotectin - high
Xray, CT may be used for imaging
Check for C.diff cause of diarrhoea
Antibodies
pANCA positive
ASCA negative (Crohns)
Colonoscopy and biopsy GOLD
- Colonoscopy - Continuous mucosal ulcers and goblet cell depletion
- Biopsy - Psuedopolyps, crypt abscesses, goblet cell depletion. Inflammation limited to mucosa + submucosa
Histology in UC
Psuedopolyps, crypt abscesses, goblet cell/mucin depletion. Inflammation limited to mucosa + submucosa
What severity scoring system is used in UC
Truelove + Witts
Treatment of UC
1st (induce remission) - aminosalicylate (mesalazine/sulfasalazine) Rectal in proctitis, oral otherwise
if moderate/not responding prednisolone first.
In severe, IV hydrocortisone.
Cyclosporin (immunosuppressant) and Infliximab (TNF-a inhibitor) can also be given.
Next (Maintain remission)
- Aminosalicylate + azathioprine
If severe or non responsive,
Colectomy can be done (Curative)
Complications of UC (6)
PRIMARY SCLEROSING CHOLANGITIS!
Toxic megacolon
Bowel perforation
Colonic adenocarcinoma
Strictures or bowel obstruction
Extra intestinal manifestations
Define fulminant UC with symptoms and treatment
Sudden onset acute, severe flareup of UC.
> 10 bowel movements a day
Continuous bleeding
Abdominal tenderness
Toxicity
Colonic dilation
Hospital IV corticosteroid (hydrocortisone)
IV Ciclosporin or infliximab
Consider colectomy
Define Coeliac disease
Systemic autoimmune type 4 hypersensitivity reaction affecting the small intestine, triggered by dietary gluten peptides such as those found in rye, barley, wheat. Malabsorption is hallmark of the disease.