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Diverticulosis and Angiodysplasia

Diverticulosis and Angiodysplasia: Pathogenesis and Clinical Features Diverticulosis Author: Yan Yu Reviewers: Jason Baserman, Jennifer Au Paige Shelemey, Tony Gu Kerri Novak* * MD at time of publication Abnormal Angiogenesis vWF Deficiency Older Ageà weakening the circular muscles strutting the colon High intracolonic pressure (i.e. from peristalsis pushing against colonic waste that’s low in fiber and harder to move) Angiodysplasia Autoimmune Diseases Unclear Mechanisms These patients tend to have “arterial-venous malformations” that rise up to the mucosa of the lower GI tract Irritation of these malformations leads to bleeding into the GI tract lumen Lower GI bleed (occult, slow, asymptomatic, large- volume blood loss, usually associated with iron deficiency anemia) Renal Failure Older Age Gradual expansion over time thins the diverticular wall Capillaries within diverticuli burst and leak blood into the colon lumen Lower GI bleed (usually stops by itself) Colon wall forms little outpouchings (diverticuli) Stretching of colonic serosa stimulates somatic sensory nerves innervating the colon Bloating, cramping (But most often PAINLESS) Trapping of feces in the colonic diverticuli Bacteria have more time to metabolize the undigested materials, producing gas Flautulence Irregular defecation Both conditions share similar features: • Both are common, and their prevalence increases with age • Are relatively benign and most are easy to treat (80% stop w/o intervention) • Both present without pain in a previously-well patient • Together, account for 50-80% of lower GI bleeds (diverticulosis > angiodysplasia) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Re-Published August 4, 2019 on www.thecalgaryguide.com