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Genetics
Extracolonic Manifestations
Tips & Tricks
G ranulomas
I leal involvement (ALWAYS)
F istulas
T ransmural lesions
S kip lesion
15% of IBD patients have an affected primary family member
References
Jostins L, Ripke S, Weersma RK, et al. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature. 2012;491(7422):119-24.
Friedman S, Blumberg RS. Inflammatory Bowel Disease. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 19e. New York, NY: McGraw-Hill; 2015. http://accessmedicine.mhmedical.com.ezproxy2.library.drexel.edu/content.aspx?bookid=1130&Sectionid=79747914. Accessed February 15, 2016.
Dr. Clearfield's lecture (IFM, 2015)
U lcers
L arge intestine
C ontinuous
C olorectal CA
C rypt abscesses
E xtends proximally
R ed diarrhea
S clerosing cholangitis
UC Genetics
Migratory polyarthritis
Erythema nodosum
Aphthous ulcers
Uveitis
Pyoderma gangrenosum
Ankylosing spondylitis
Primary sclerosing cholangitis
Parent with UC = child has 3-4% chance
Concordance rate for monozygotic twins = 15%
CD Genetics
NOD2/Card 15 locus on
chromosome 16
Parent with CD = child has 6-8% chance
Concordance rate for monozygotic twins = 60%
IBD
Ulcerative Colitis (UC)
Crohn Disease (CD)
Associations
Genetic Effects
RA
Ankylosing spondylitis
T1DM
Asthma
SLE
Pathophysiology
Genetically "prepared" intestinal tract
Cellular response genes
Tuberculosis response genes
Chronic state of dysregulated inflammation
Immune response to ________, with or without some component of ____________