Pathophysiology of Inflammatory Bowel Disease
Inflammatory bowel disease (IBD) is a term given to chronic and recurring conditions that affect
the gastrointestinal tract (Centers for Disease Control & Prevention (CDC)
...
Pathophysiology of Inflammatory Bowel Disease
Inflammatory bowel disease (IBD) is a term given to chronic and recurring conditions that affect
the gastrointestinal tract (Centers for Disease Control & Prevention (CDC), 2017). Irritable
bowel syndrome (IBS) is a condition that affects the movement of the intestine (CDC,
2017). Ulcerative colitis and Crohn’s disease are the two most common IBD. In ulcerative colitis
lesions are mostly contained in the large intestine especially on the left side. With ulcerative
colitis, the crypt of Lieberkuhn in the large bowel becomes infiltrated with T cells that damage
the epithelium. Immunoglublin E and G, along with B cells and plasma cells increase at the site
of inflammation and goblet cells release mucus (Basson, 2017). Ulceration occurs in the mucosa
with rare narrowing of the lumen of the large intestine; polyps form throughout the large
intestine (Dudley-Brown & Huether, 2012). Crohn disease lesions may range from the mouth to
the anus called skip lesions. The inflammation of Crohn disease is thought to be triggered by
cell-mediated response and increased levels of interferon-gamma and tumor necrosis factor
alpha. In IBD, Crohn disease, the increase in interferon-gamma and tumor necrosis factor-
alpha, along with stimulation of Th1 cells, produces inflammation throughout the small and large
intestine mucosa and serosa layers. Injury to bowel tissue occurs as neutrophils and
macrophages infiltrate the site of inflammation. Granuloma ulcerations occur in some areas of
the bowel and skip other areas (Dudley-Brown & Huether, 2012).
Pathophysiology of Irritable Bowel Syndrome
Irritable bowel syndrome is a functional gastrointestinal bowel disorder causing increased
contractions of the colon. IBS is diagnosed by characteristic cluster of symptoms without
detectable structural abnormalities. The pathophysiology of IBS is complex and involves a
number of factors. Hypersensitivity to pain in the visceral gut occurs by either malfunctioning of
the central nervous system or receptors in the wall of the gut; known as the brain-gut axis.
Malfunction of the brain-gut axis can increase gastrointestinal motility causing diarrhea or
decease gastrointestinal motility causing constipation. A decreased transit time is, also,
associated with normal intestinal flora overgrowth. Individuals with IBS have minimal intestinal
inflammation, permeability alterations, and decreased immune response in the gut. Intolerance
or allergy to certain foods stimulate an immune response in the mucosa, change the normal gut
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