Describe the epidemiology.
Approximately 600,000 adults in the US are affected by ulcerative colitis.
Higher in White populations than in Black, Hispanic, or Asian populations
Highest among individuals of Ashkenazi Jewish descent
15–35 years of age
Another smaller peak may be observed in individuals > 55 years of age.
Similar for men and women
List risk factors.
Genetic predisposition (e.g., HLA-B27 association)
Ethnicity (White populations, individuals of Ashkenazi Jewish descent)
Family history of inflammatory bowel disease
Episodes of previous intestinal infection
Increased fat intake (especially saturated fat and animal fat)
Oral contraceptive use
NSAIDs may exacerbate ulcerative colitis.
Describe the pathophysiology.
The exact mechanism is unknown but studies suggest that ulcerative colitis is caused by abnormal interactions between host immune cells and commensal bacteria. 
Dysregulation of intestinal epithelium: increased permeability for luminal bacteria → activation of macrophages and dendritic cells → antigen presentation to macrophages and naive CD4+ cells leads to:
Secretion of proinflammatory cytokines (IL-6, IL-12, TNF-α) and chemokines (CXCL1, CXCL3, and CXCL8) → recruitment of other immune cells (e.g., neutrophils) to the site
Differentiation of naive CD4+ cells to Th2 effector cells
Recruitment of natural killer cells
Dysregulation of the immune system: upregulation of lymphatic cell activity (T cells, B cells, plasma cells) in bowel walls → enhanced immune reaction and cytotoxic effect on colonic epithelium → inflammation with local tissue damage (ulcerations, erosions, necrosis) in the submucosa and mucosa
Autoantibodies (pANCA) against cells of the intestinal epithelium
Th2 cell-mediated response
Pattern of involvement
Ascending inflammation that begins in the rectum and spreads continuously proximally throughout the colon
Inflammation is limited to the mucosa and submucosa.
The rectum is always involved in ulcerative colitis.