Natural Tx of IBD Flashcards
what are the 4 forms of IBD?
Crohn’s
indeterminate colitis
UC
microscopic colitis
where does Crohn’s mostly affect the GI?
SI, ileocecal valve and surrounding area, splenic flexure of colon, just before sigmoid colon
what can be a tell-tale appearance for Crohn’s?
cobblestoning appearance of bowel wall
what will the bowel wall look like in UC?
pseudopolyps, ulceration, loss of haustra
microscopically what will Crohn’s look like?
crypts are non-existing
lamina propria is extremely thickened
microscopically what will UC look like?
severe crypt distortion and less organized
besides the distal ileum and the R colon, where else can Crohn’s appear? what percentages are associated with each spot?
besides the R colon and distal ileum (MC spots) Crohn’s can appear gastroduodenally 5% of the time, in the SI alone 5% of the time and in the colon alone 20% of the time
what is progression (complication) that can occur with Crohn’s?
stenosis or inflammation of the ileocecal valve both of which can lead to fistula formation of the SI directly with the colon
stenosis occurs 50% of the time, inflammation 30% of the time and fistula formation appears 20% of the time
what are some common sxs to see in the following organs/systems w/Crohn's? eyes? KD? skin? mouth? liver? biliary tract? joints? circulation?
eyes: episcleritis, uveitis
KDs: stones, hydronephrosis, fistulae, UTI
skin: erythema nodosum, pyroderma grangrenosum
mouth: stomatitis, apthous ulcers
liver: steatosis
biliary tract: gallstones, sclerosing cholangitis
joints: sponylitis, sarcoilitis, peripheral arthritis
circulation: phlebitis
4 step pathogenesis process of Crohn’s
2 factors that can impact the progression/end of the possible first step?
- causative agent (bacteria, virus, dietary)
- immune response
- inflammation
- tissue injury
modifying factors: environmental, genetic
luminal factors: luminal bacteria, digestive enzymes, bile acids
what kind of an immune response is Crohn’s? explain the immune cell cascade that happens
Th1 response
MOs activate T cells which generate a Th1 response
what demographic is most likely to be dx with Crohn’s?
caucasian jews
what are some hostile factors that could lead to a pt developing Crohn’s? what protective factors usually keep the GI healthy?
hostile: bacteria, bile acids, bacterial and dietary ags, digestive enzymes, Th1 lymphocytes
protective: impermeable mucosa, mucus, sIgA, PGE2, PGI2, UL-1ra, cortisol, IL-4, IL-10, TGF-b, VIP, somatostatin, glutamine, SCFA, Th2 lymphocytes
compare-contrast the depth to which Crohn’s affects the GI tract vs UC
Crohn’s: affects the mucosal and submucosal layers
UC: only affects the mucosal layer
in UC what happens to the normal intestinal crypts and what can form?
crypts get distorted and lost their goblets cells
abscesses can form
describe UC pathogenesis
microbial pathogens are introduced to the GI, there is an ineffective immune response
dietary ags or non-pathogenic microbes come into contact with the GI and we get an abn immune response
luminal ags are present which leads to an immune response to the luminal ag along with to the person’s own epithelium= auto-immune
3 forms of UC? where does each affect in the GI? which has the greatest risk of colon CA
proctitis: rectum
left-sided colitis: descending colon through the rectum
pancolitis: ascending, transverse, descending colon through the rectum
greatest risk of colon CA in pts w/pancolitis, even if they go/are in remission
what is the main complication in UC?
toxic megacolon b/c of the loss of haustra and ‘tubularization’ of the LI