Ulcerative Colitis and other IBD have become common among the population due to a stressful lifestyle and improper diet. Before we start getting into the pathophysiology of Ulcerative Colitis, let’s understand what pathophysiology is.
What is Pathophysiology?
Pathophysiology is an intersection of physiology with pathology. It is the study of disordered physiological processes that are associated with a disease or injury. Physiology is the study of the operating mechanism of a living organism. Pathology is a discipline that describes the condition observed during an undesired state. Thus pathophysiology of Ulcerative colitis is the study of functional changes that occur when a body is affected by IBD and goes through an undesirable state.
It is one of the main forms of IBD, which arises in the colonic mucosa most often characterized by blood in stools. The other common symptoms usually include diarrhea, rectal pain & bleeding, weight loss, fever, fatigue, an urgency to defecate, etc. The symptoms and the intensity can vary depending on the inflammation and UC pathophysiology.
Pathogenesis of Ulcerative Colitis
Ulcerative Colitis usually begins in the rectum and extends nearby or sometimes it also involves the entire colon. The rectum is involved in the majority of the cases, while the degree of proximal extension varies. The inflammation can also affect the mucosa and submucosa. In the initial stage of the disease, the mucous membrane is finely granular with a loss of the normal vascular pattern. When the severity increases the muscularis is involved. Even though the inflammation is limited to the mucosa, the continuous involvement can go along the length of the colon in severe cases.
The epithelial barrier is covered by the mucinous layer which is the first-line defense of the mucosal immune system. It provides a physical separation between the host immune cells and the luminal microbes. In UC, synthesis and alteration of sulphation of colonic mucin subtypes are decreased. Damage to this barrier leads to the increase in permeability which is due to the defective regulation of tight junctions. This damage results in increased uptake of luminal antigens. However, if these dysfunctions precede ulcerative colitis is still unclear.
The intestine’s immune system is to maintain the equilibrium of tolerance to commensal flora and dietary antigens, along with the responsiveness to enteric pathogens. The primary role of non-pathogenic enteric bacteria in UC pathogenesis has been evidently proven from genetically engineered models. It develops chronic intestinal inflammation after colonization with commensal gut bacteria. But it remained void of disease in the bacteria-free conditions.
This study when held in human beings supported the importance of enteric microflora, in disease pathogenesis as well as the potential severity of inflammation and disease phenotype. Ulcerative Colitis results from a breakdown of the homeostatic balance between the host’s mucosal immunity and enteric microflora. This usually results in an aberrant immune response against commensal non-pathogenic bacteria.
Antigens activate the immune response by interacting with macrophages and dendritic cells. Dendritic cells are antigen-presenting cells of the mammalian immune system, with the main function of processing antigen material and presenting it on the cell surface. They act as a messenger between the innate and the adaptive immune system. In the case of UC, the number of activated and dendritic cells is increased, with an increased stimulatory capacity. This suggests an important role of these cells in the perpetuation of inflammation.
Toxic Colitis occurs when transmural extension of ulceration in localized ileus and peritonitis. The colon starts losing muscular tone and begins to dilate, within days. Chances for colonic perforation are high which might increase the mortality rate significantly. The terms of toxic megacolon and dilation are discouraged as the toxic inflammatory state and its complication can happen without frank megacolon.
Ulcerative Colitis isn’t life-threatening by itself, but it can be debilitating and can lead to life-threatening complications. Due to the pathophysiology of Ulcerative colitis, the risk of colon cancer is elevated along with other complications such as anemia.
While there is no known cure, lifestyle change can greatly reduce the signs and symptoms and also bring in long-term remission.
This is why at High Carb Health we recommend the people with UC to give the sabbatical rest that their body demands. This rest will aid the body and mind to get the maximum effect of self-healing. However, keeping in mind the busy lifestyle of people, we understand that a long sabbatical period is not possible. But it is mandatory to give the body as much rest and extra sleep as possible. By cooperating with nature and changing your injurious lifestyle habits, you will be able to enjoy a blossoming of health and spirit.
- What is the pathophysiological process of ulcerative colitis?
Ulcerative Colitis is characterized by rectal bleeding and diarrhea. The pathogenic mechanism is an aberrant immune response in which antibodies are formed against colonic epithelial proteins.
- What is the pathophysiology of IBD?
The pathophysiology of Ulcerative Colitis and Crohn’s includes factors like abnormal gut microbiota, environmental changes, gene variants, and immune dysregulation.
- What are the main causes of Ulcerative Colitis?
The pathogenesis of Ulcerative Colitis is still unknown, though it is known to be the result of a poor immune system. The other major causes are- genetics, poor diet, lifestyle, environmental factors, etc.
- What is the most important factor for IBD pathogenesis?
The adaptive immune system has been considered to be an important factor in the IBD pathogenesis. Recent research in genetics and immunology confirms that the innate immune system maintains great importance in inducing gut inflammation.