The pathophysiology irritable bowel syndrome
The pathophysiology irritable bowel syndrome The pathophysiology irritable bowel syndrome Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder characterized by chronic abdominal pain, bloating, and altered bowel habits such as diarrhea, constipation, or a combination of both. Despite its prevalence, the precise pathophysiology of IBS remains complex and not fully understood, involving an interplay of multiple factors that disrupt normal bowel function and sensation.
One central aspect of IBS pathophysiology is dysregulation of the brain-gut axis, which refers to the bidirectional communication network between the central nervous system and the gastrointestinal tract. This axis involves neural pathways, hormonal signals, and immune mediators that coordinate gut motility, secretion, and sensation. In individuals with IBS, this communication is often altered, leading to heightened visceral sensitivity and abnormal motility patterns. Patients frequently report a lower threshold for pain and discomfort in response to normal intestinal stimuli, suggesting increased visceral hypersensitivity. The pathophysiology irritable bowel syndrome
Altered gastrointestinal motility is another hallmark of IBS. Instead of smooth, coordinated movements, the intestines may exhibit hypermotility or hypomotility depending on the subtype of IBS. For example, diarrhea-predominant IBS (IBS-D) is associated with increased intestinal transit, while constipation-predominant IBS (IBS-C) features delayed transit. These motility disturbances can be influenced by abnormalities in enteric nervous system signaling, neurotransmitter imbalances—such as serotonin dysregulation—and smooth muscle dysfunction. The pathophysiology irritable bowel syndrome
Visceral hypersensitivity plays a significant role in the symptomatology of IBS. It refers to an increased sensitivity of the intestinal walls to distension and other stimuli. This heightened sensitivity can be due to peripheral mechanisms, such as sensitization of pain receptors on afferent nerve fibers in the gut, and central mechanisms involving altered processing of pain signals within the brain. Factors like stress, psychological comorbidities, and previous infections can exacerbate visceral hypersensitivity, perpetuating the cycle of pain and discomfort.
Immune activation and low-grade inflammation are also implicated in IBS pathogenesis. Although IBS is not an inflammatory disease like Crohn’s or ulcerative colitis, some patients exhibit increased numbers of immune cells such as mast cells and T lymphocytes in the gut mucosa. These immune cells release mediators like histamine, cytokines, and prostaglandins, which can influence nerve activity and motility, further contributing to symptoms. The pathophysiology irritable bowel syndrome
The pathophysiology irritable bowel syndrome Alterations in the gut microbiota, or dysbiosis, are increasingly recognized as an important factor. Changes in the composition and diversity of intestinal bacteria may impact gut barrier function, immune responses, and fermentation processes, leading to gas production and bloating. These microbiota changes can also influence serotonin levels and other neurochemical pathways, linking microbiota to the brain-gut axis.
The pathophysiology irritable bowel syndrome In summary, the pathophysiology of IBS involves a multifaceted interplay among neural, hormonal, immune, and microbial factors. Dysregulation of the brain-gut axis, abnormal motility, visceral hypersensitivity, low-grade inflammation, and microbiota alterations collectively contribute to the development and persistence of symptoms. Understanding these mechanisms not only aids in diagnosis but also guides targeted therapies aimed at modulating these pathways for symptom relief.
