Pathophysiology Inflammatory Bowel Disease (IBD)Ulcerative colitis (UC) and Crohn disease (CD) are known as chronic relapsing inflammatory bowel diseases (IBDs) that is more prevalent in white populations in which causes are thought to include; genetics, environmental factors, alterations in epithelial cell barrier functions, and altered immune intestinal microflora (Huether & McCance, 2017). “Inflammatorybowel diseases (IBD) are related to an immunological imbalance of the intestinal mucosa, mainlyassociated with cells of the adaptive immune system, which respond against self-antigens producing chronic inflammatory conditions in these patients” (de Mattos et al., 2015). The intestinal epithelium prevents bacteria or antigen entry into the circulation by sealed intracellular junctions, these junctions are defective from either barrier function failure or as a result of severeinflammation. The intestinal immune system is the key component in the pathophysiological process of IBD (McDowell & Bhimji, 2018). It is known that genetic and environmental factors are two major components of IBD. The genome-wide associated with IBD is the nucleotide polymorphisms (SNPs) which included mediators of immune function, autophagy, and epithelial function that creates the interaction of host and microorganisms (Hammer & McPhee, 2014). The other environmental factors effecting CD include; bacteria, viruses, indigenous microbes, dietary factors, smoking, defective immune responses, and psychosocial interactions. The recentdata suggests that certain activity during neonatal period influences the immune response in the adult, stemming from microbiota transmitted from mother to child. This early exposure of intestinal microbiota may play an important component to the pathogenesis of IBD (Hammer & McPhee, 2014). The intestinal loss of tolerance or weakening activates dendritic cells, triggeringtheir transport to mesenteric lymph nodes, where they promote differentiation of naïve T cells to Th1, Th2, and Th17 cells, or T-regulatory cells. Next is the production of proinflammatory
cytokines and chemokines, including tumor necrosis factor, interleukins, toxic oxygen free radicals, and interferon-gamma (IFN-y), damages the intestinal epithelium. This pathophysiolically changes increases the risk of colon cancer significantly after 30 to 35 years of IBD, especially if untreated (Huether & McCance, 2017). Pathophysiology Irritable Bowel Syndrome (IBS)“According to the updated ROME III criteria, IBS is a clinical diagnosis and presents as one of three predominant subtypes: (1) IBS with constipation (IBS-C), (2) IBS with diarrhea (IBS-D), and (3) mixed IBS (IBS-M)” (Saha, 2014). The role of irritable bowel syndrome (IBS) has traditionally been conceptualized as a chronic and debilitating functional gastrointestinal condition of visceral hypersensitivity (leading to abdominal discomfort or pain) and gastrointestinal motor disturbances (leading to diarrhea or constipation). Evidence is beginning
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- Irritable bowel syndrome, IBS, inflammatory bowel, Rani et al.