inflammatory bowel disease Flashcards
inflammation ….. infection
IS NOT
What are the two major forms of IBD
- Crohn’s disease
- Ulcerative colitis
epidemiology of IBD
o Peak between the ages of 15-30 and second peak between the ages of 60-80.
oMore frequent in“rich” countries/places such as north America, Scandinavia, andEurope.
Where does UC begin
Colon and rectum
Where does CD begin
Any part of the GI tract
describe the development of UC
Continuous pattern of inflammation
describe the development of CD
Skips lesions
describe the onset of UC
Acute (sudden/rapid) onset
describe the onset of CD
Gradual onset
What happens within patients with UC
»Ulcers, ulcerations, (pseudo)polyps, bulges in mucosa
»Normal architecture damaged
»Microbiome affected.
» BLOOD IN STOOL
»Can cause colon cancer
What happens within patients with CD
» Entire intestinal wall affected.
» Granulomas (inflammations)
» Thicker wall, smaller lumen
» Cobble stones
» Perforations – stool leaks into abdominal cavity
What are the symptoms of UC
» Rectal bleeding
» Having to go to the toilet very often
» Loose stools
» Abdominal pain on the lower left side
»Tenesmus: urge to defecate
» Blood in stool
WHat are the symptoms of CD
» Chronic and nocturnal diarhhea OR constipated
» Pain in lower right abdomen
» Weight loss
» Mild fever
» Increases in severity with age = progressive disease
» absecces and fistulae
What are the extra intestinal symptoms of UC
»Joint pain
»Canker sore(aften) in mouth
»Spinal deformation due to inflammation
»Slow healing wounds
»Erythema nodosum
»Eye bleeding
WHat are the extra-intestinal symptoms of CD
» Inflammated joints
» Same as ulcerative colitis
» Kidney problems
» Galstones
» Liver problems
Crohn’s disease clinical features
(1) Inflammation -> small intestine (abdominal pain, diarrhea, and fever) & large intestine (diarrhea, blood loss, weight loss and fever)
(2) Stricturing -> Bowel obstructions due to wall thickening
(3) Penetration -> abscesses and fistulae (abnormal passages get formed)
describe the pathogenesis of IBD
- Genetic susceptibility: some kind of genetic predisposition – variants that cause an exaggerated inflammatory response.
- Immune response: the overreactive immune response – people with IBD react worse to inflammations.
- Environmental triggers: we see that IBD is more common inn wealthy countries so environmental factors do play a role HOWEVER we’re not really sure which ones.
- Microbiome (more recently added): the collection of all bacteria that live inside our intestines – people with IBD have distinctively different microbiomes than their family members without IBD.
Risk factors that can cause IBD
» Diet
» Infection – if people with a genetic predisposition get certain infections, their body will react with an exaggerated inflammatory
response = the start of IBD
o Crohn’s – mycobacterium paratuberculosis
o Ulcerative colitis - after episodes of infective diarrhea
» Appendectomy (ONLY UC)
» Stress – stress triggers a relapse of IBD (NOT THE CAUSE BUT CAN TRIGGER RELAPSE)
What actually happens within the body during the overreactive immune response? (IBD)
= it’s an abnormal reaction of the T-cells that cause an exaggerated inflammatory response
o (Causative agents+luminal factors+modifying factors)–cause an inflammation.
But HOW?
o Lymphatic T-cells get sent to the affected zone.
o These T-cells cause the exaggerated inflammatory response.
o If the response is not transmural then it’s UC, if it is then it’s Crohn’s disease.
Explain the diagnosis of IBD
- Blood tests – check for c-reactive protein which gets released in blood during an inflammatory reaction
- Stool studies
- Colonoscopy (=most frequently done) and endoscopy
a. Ileo-colonoscopy with biopsies (sometimes with small intestine as well)
b. Upper endoscopy with biopsies
(Capsule endoscopy - capsule with camera = still in development)
Explain the treatment of IBD
= the main goal of the treatment is to minimize the intestinal inflammation + improve general health + repair/heal the mucosa
Pharmacological management
o Anti-inflammatory agents: 5-amino salicylic acid (5-ASA)
o Steroids, cortisone they suppress the immune system HOWEVER can only be given for acertain number of days.
o Anti-tumor necrosis factor(anti-TNF) agents–TNF is a protein in your body that causes inflammation (everything that can be given ends with …mab)
o Probiotics – they strengthen the microbiome daily.
Is UC transmural or not
no, NOT transmural
Is CD transmural or not
yes, transmural
Tenesmus
urge to defecate
abscesses
localized collections of pus that result from an infection
fistulae
abnormal connections or tunnels that form between two organs or between an organ and the outside of the body
- the transmural inflammation can lead to the formation of fistulae
Erythema nodosum
red spots on legs
explain the role of appendectomy in UC
people that get an appendectomy are less likely to develop UC, and people who developed UC after appendectomy were less likely to develop recurrent disease. = less severe course