ICL 14.4: Inflammatory Bowel Disease Flashcards
what is IBD?
chronic or relapsing immune mediated
inflammation of the GI tract
chronic and relapsing inflammation; must see it in the CT or scope –> IBS doesn’t have inflammation!
what are the 2 major forms of IBD?
- Crohn’s disease
- ulcerative colitis
a less common form is microscopic colitis, which has 2 subdivisions: collagenous colitis and lymphocytic colitis
there’s also indeterminate colitis (about 10%)
what are the potential causes of IBD?
- genetic predisposition
- environmental factors = infections, antibiotics, NSAIDs, diet, smoking*
- immune system abnormalities; inappropriate reaction by the body’s immune system
what is the pathophysiology of IBD?
an inappropriate, immune-mediated, chronic, inflammatory response to intestinal bacteria in a genetically susceptible person following exposure to an environmental agent
what parts of the colon are effected in Crohn’s vs. ulcerative colitis?
Crohn’s = skipping regions of the colon and small bowel; segmental involvement of ischemic regions; deeper involvement into the wall of the bowel
ulcerative colitis = starts at the rectum and moves proximally as it gets worse; continuous inflammation that’s superficial
what is the onset, extension, rectal involvement, distribution of disease, skip lesions, cobblestone appearance and depth of inflammation of ulcerative colitis?
onset = acute or subacute
extension = affects only the colon
rectal involvement = always
distribution of disease = continuous area of inflammation
skip lesions = absent
cobblestone appearance = absent
depth of inflammation = shallow, mucosal
what is the onset, extension, rectal involvement, distribution of disease, skip lesions, cobblestone appearance and depth of inflammation of Crohn’s disease?
onset = insidious
extension = can affect any part of the GIT from the mouth to the anus
rectal involvement = rare (terminal ileum most commonly involved)
distribution of disease = patchy areas of inflammation
skip lesions = present
cobblestone appearance = present
depth of inflammation = may be transmural; deep into tissues
what does a biopsy from Crohn’s show?
granuloma
if there isn’t a granuloma that doesn’t mean it’s not Crohn’s though
what does a biopsy from ulcerative colitis show?
crypt abscess
what are the clinical manifestations of ulcerative colitis?
- acute course
- marked diarrhea
- frequent blood in stool
- occasional abdominal pain
- perianal disease is rare
- intestinal obstruction is rare
- small bowel involvement is rare
- rectum is always involved!!
what are the clinical manifestations of Crohn’s disease?
- indolent onset
- watery diarrhea is present
- infrequent blood in the stool
- frequent abdominal pain
- frequent perianal diseases like abscess and fistulas
- frequent intestinal obstruction and strictures due to transmural inflammation
- small bowel involvement is common = terminal ileum specifically
- rectum is spared 50% of the time
what are the extraintestinal complications associated with IBD?
- episcleritis/uveitis*
- kidney stones*, hydropnephrosis, fistulae, UTIs
- erythema nodosum*, pyoderma grangrenosum (not as common)
- stomatitis or aphthous ulcers in the mouth
- gallstones
- ankylosing spondylitis, sacroilitis or peripheral arthritis in the joints
- phlebitis (circulation)
when do you see extraintestinal complications of IBD present?
if you have a patient with IBD and it’s under control, you dont expect the person to have extra-intestinal symptoms
they only happen when they person stops taking medications or are exposed to an environmental triggers
why are kidney stones an extra-intestinal symptoms of IBD?
oxalate kidney stones are common in Crohn’s disease!!
you absorb fatty acids in the small bowel and calcium and oxalate combine and get excreted together – but in Crohn’s where the terminal ileum is involved (this is where you reabsorb bile salts) you lose the bile salts and therefore the ability to absorb the fatty acids – so instead they’re left in the lumen and they combine with the calcium via saponification and the calcium is no longer free to combine with oxalate so oxalate is reabsorbed and goes to the kidney and you get kidney stones!
what is primary sclerosis cholangitis?
this is a condition in the liver and bile duct that is STRONGLY associated with iBD, specifically ulcerative colitis! so if someone has PSC, most of them also tend to have IBD! it’s an 80% chance; but if you have someone with ulcerative colitis only 10-15% have PSC
it causes inflammation and fibrosis leading to stricture of the bile ducts
patients present with fevers, chills, abnormal LFT, RUQ abdominal pain, jaundice, dark urine, pruritus
it’s slowly progressive leading to cirrhosis, portal HTN, and liver transplantation
may lead to cholangiocarcinoma and a higher risk of colon cancer*
which extra-intestinal manifestations may not be associated with the IBD disease activity?
- ankylosing spondylitis, sacroiliitis, type 2 peripheral arthritis (polyarticular)
- anterior uveitis
- primary sclerosing cholangitis (PSC)
- pyoderma gangrenosum (controversy exists)
what diarrhea results from a terminal ileum resection less than 100 cm?
bile acid diarrhea
this is because ↓ bile acid absorption in the ileum leads to water/chloride secretion in the colon
treatment: bile acid sequestration (cholestyramine)
what diarrhea results from a terminal ileum resection greater than 100 cm?
steatorrhea
bile salt depletion leads to fat malabsorption because you need bile salts to absorb fats
treatment = low fat diet, medium-chain triglyceride replacement
do you do colon cancer surveillance for people with IBD?
yes!! they have increased risk for colon cancer!!
for long standing colitis you should do surveillance in patients with:
1. UC involving more than the rectum
- Crohns colitis in at least 1/3 of the colon
do a colonoscopy every 1-2 years after 8-10 years of a standing diagnosis of IBD
the only exception is people with colitis and PSC, PSC dramatically increases the risk for colon cancer so you need to do a colonoscopy every 1-2 years immediately following the diagnosis of colitis in PSC patients
how do you diagnose IBD?
- initial labs (CBC, CMP, CRP).
- stool studies –> rule out infection “including C. diff” because it presents similarly to UC –> also do a fecal calprotectin test because this directly correlates to inflammation in the gut! calprotectin is in leukocytes which means there’s activity if levels are elevated
- imaging
- endoscopy
what is a mayo endoscopy score of 0-3 for iBD?
0 = normal/inactive disease, no friability or granularity, intact vascular pattern
1 = mild disease, erythema, decreased vascular pattern, mild friability
2 = moderate disease = marked erythema, absent vascular pattern, friability, erosions
3 = severe disease, moderate signs, spontaneous bleeding, ulceration
how do you do a CT enterography for iBD? when is it indicated?
new standard in CT imaging of small bowel in Crohn’s
what you do is give neutral/low-density oral contrast which distends the small bowel which allows you to see the bowel wall and do CT imaging during the enteric phase –> you’ll see extra contrast in the walls due to wall thickening from chronic inflammation; you might also see prominent vasa recta = comb sign; indicative of inflammation
you can also do MR enterography which is similar to CTE but just with MR
what are the serologic results in IBD?
ASCA and pANCA aren’t good tests for diagnosis because sensitivity is low and they’re not that accurate
so they’re ordered as an add on sometimes but they’re not super important
but in general, ASCA is more associated with Crohn’s while pANCA is more associated with UC
what are the goals of treatment of IBD?
we are treating the result of IBD, not the cause!! we dont even really understand the cause to even treat it…
treating earlier is better
- achieve mucosal healing and induce remission
- maintain steroid-free remission
- prevent/treat complications of disease
- avoid short and long term toxicity of therapy
- enhance quality of life
