Symptoms Of Gastrointestinal Inflammatory Diseases Health And Social Care Essay

Symptoms Of Gastrointestinal Inflammatory Diseases Health And Social Care EssayInflammation is a type of defence mechanism that the body exhibits in response to damage to part or all of its tissues. Depending on the severity of the insult and consequent damage to cells, the incendiary response involves recruitment of varying proportions of neutrophils, eosinophils, basophils, lymphocytes (both T and B cells), natural killer cells and cells of the monocyte macrophage lineage. Inflammation normally seeks to eliminate the cause of the insult and repair the damage caused. However, if the damage persists, lasting recruitment of inflammatory cells to the injured knowledge base will lead to further damage leading to degenerative inflammation. 9 The GI (GI) tract is a hollow muscular tube running from the mouth to the anus. It is to the highest degree 7 to 9 meters long in adult. The enormous mucosal surface, which is the innermost layer of the GI tract, is constantly exposed to a pl ethora of antigenic, mitogenic, mutagenic, and toxic stimuli therefore clearly making the gastrointestinal tract vulnerable to such inflammatory responses. 10Gastrointestinal inflammatory diseasesInflammation can affect any part of the gastrointestinal tract.Inflammatory Bowel DiseaseThe inflammatory bowel diseases (IBD) are chronic inflammatory diseases affecting the gastrointestinal tract. IBD encompasses two forms of intestinal inflammation, namely ulcerative inflammatory bowel disease and Crohns disease. Crohns Disease whitethorn affect all parts of the gastrointestinal tract, but more commonly it involves the distal part of the small intestine and the colon. On the otherwise hand, ulcerative colitis results in colonic inflammation which can affect only the rectum, or can progress proximally to involve the colon, either partly or entirely 11. Currently, the etiology of IBD is unknown, but recent investigations shake off identified contribution of genetic, environmental as well as immunological factors underlying the disease 12. allergicness to disease is thereby determined by genes encoding immune responses which are triggered by environmental stimuli 13. Figure 1.1 shows a combination of genetic and environmental culprits triggering activating of intestinal immune and non-immune systems which culminate in inflammation and tissue damage. 14Figure 1.1 Etiology and pathogenesis of IBD.Current medical therapy of IBD consists of salicylates, corticosteroids, immunosuppressants and immunomodulators. However, their use is associated with severe side effects and complications, such as an increased rate of malignancies or infectious diseases. 15Gastritis (Inflammation of stomach lining)Gastritis represents a group of disorders characterized by gastric epithelial cell injury and regeneration unneurotic with the induction of inflammatory changes in the gastric mucosa 16. Inflammation of the gastric mucosa occurs as a result of an imbalance between mucosal antitank and aggressive factors. It is now well established that H. pylori infection is the cause of the most common form of chronic gastritis 17. Studies mystify established that H.pylori directly contributes to abundant inflammatory response and cause injury to gastric epithelial cells through elaboration of cytotoxic factors and it may also make gastric epithelial cells more susceptible to carcinogenic conversion 18. There is also evidence that drugs and alcohol may cause gastritis. Iron therapy has also been implicated as a cause of gastritis. Iron-pill gastritis involves mucosal erosion which is accompanied by acute and chronic inflammation and marked regenerative epithelial changes 19. Autoimmune and hypersensitivity reactions may also be culprits in gastritis. 20Esophagitis (Inflammation of the oesophagus)eosinophilic esophagitis is a chronic inflammatory condition whereby presence of dense eosinophilic inflammation of esophageal mucosa contributes to esophageal dysfunctio n. Eosinophilic esophagitis is a newly acknowledged disease whose incidence and prevalence is rapidly increasing in developed and developing countries 21. The disease is a major cause of gastrointestinal morbidity among children and adults. It is thought to be immune mediated, whereby food or environmental antigens trigger a T-helper (Th)-2 inflammatory response. 22PancreatitisChronic pancreatitis is well-known as a persistent inflammatory disorder of the pancreas, characterized by destruction of the pancreatic parenchyma, maldigestion, chronic pain and diabetes mellitus. Susceptibility to chronic pancreatitis is inherited in a complex manner, involving mutations in several(prenominal) genes conferring various degrees of risk. 23 Although the exact etiology of acute and chronic pancreatitis is unknown, studies have revealed that they are most customaryly caused by a high consumption of alcohol and tobacco 24. Other common causes include gallstones, hypertriglyceridemia, hyperparat hyroidism, trauma, pancreatic tumors, and intra-abdominal and non-abdominal surgery. Drugs constitute a relatively infrequent cause of acute pancreatitis and account for 1.4 to 2% of the cases in the general population. 25 intestinal fluGastroenteritis refers to inflammation of the gastrointestinal tract, involving the stomach and intestines. Acute gastroenteritis is a common disease occurring worldwide, which affects all age groups and leading to an estimated three million deaths annually. In many patients the causal agent cannot be identified, but research has implicated bacteria and parasites as well as viruses such as rotavirus, adenovirus, and caliciviruses as major culprits in causing gastroenteritis. 26Symptoms of gastrointestinal inflammatory diseasesTable 1.1 Symptoms of GI inflammationGastrointestinal Inflammatory DiseaseSymptomsInflammatory Bowel DiseasesDiarrhoeaBlood in stoolsGastrointestinal bleedingAbdominal painFistulas (usually around the rectal area, may cause drai ning of pus, mucus, or stools)ConstipationWeight loss 11Gastritisunwellness nauseant (possibly with blood)Abdominal pain and bloatingIndigestionLoss of appetiteBlood in the stools. 27EsophagitisFood impactionsDysphagia (difficulty swallowing)NauseaVomitingHeartburnchest pain or abdominal pain 28PancreatitisAbdominal painNauseaVomitingWeight lossMild yellowing of skin (jaundice)Fatty stools 29GastroenteritisAbdominal painNausea and vomitingDiarrhoeaJoint stiffness or muscle painPoor feeding and weight loss 30Biomarkers of Gastrointestinal inflammationInflammatory activities occurring at bottom the gastrointestinal tract can be assessed using a variety of techniques. Presently, the most reliable means to assess intestinal inflammation is endoscopy with mucosal biopsy. However, this technique is expensive, invasive, time-consuming and is not popular with patients 31. Moreover, this technique requires a skilled operator and an uncomfortable preparatory regimen. Other techniques consti tute measurement of conventional non-invasive acute-phase inflammatory markers in plasma and faeces. 32Blood inflammatory biomarkersSerological biomarkers are principally produced when the intestine is exposed to the normal commensal bacteria and their increased levels might be indicatory of an impaired or wrongly regulated inflammatory response. Erythrocyte sedimentation rate (ESR), white blood cell count (WBC) and C-reactive protein (CRP) are well-established indicators of inflammatory conditions at heart the intestine. 33C-reactive protein (CRP)CRP is one of the vital acute phase proteins in humans, which is normally produced in low quantities by hepatocytes (/= 30 kg/m2. However, this method has been subjected to criticism because it does not separate plonk from fat-free mass such as muscle and bone 76. In addition, it has also been observed that for the same value of BMI, women are, on average, fatter than men, and Asians are, on average, fatter than Caucasians 77. diffusi on of body fat is highly important in evaluating obesity-related health risks. It has been well-established that accumulation of intra-abdominal fat, that is central obesity, shows stronger correlation with disease states in comparison with total body fat 78. According to a recent conceive, waist circumference, and not BMI, explains obesity-related health risk. 79Obesity is associated with low-grade inflammation. The inflammatory process originates and resides mainly in adipose tissue, as it is trusty for production and secretion of various proteins involved in development of obesity related adverse health effects 80 . Through this mechanism, increasing obesity leads to decrement of adiponectin levels, which has anti-inflammatory properties, and to designate levels of C-reactive protein (CRP) and results in systemic inflammation, including gastrointestinal inflammations. Intestinal inflammation is a key feature in severe obesity 81. A study has established diet-induced intestina l inflammation as an early biomarker and mediator of obesity 82. Findings in adult humans and in animals have suggested that the inflammatory status at mucosal surfaces of various organs including the adipose tissue, ooesophagus, pancreas, colon, which are associated with the increase of fat mass, may be involved in the pathogenetic pathship canal of obesity complications 81. In addition, animal studies showed that round mice display enhanced intestinal permeability 83. Recent epidemiological studies have demonstrated that obesity is associated functional bowel disorders, which may have resulted from a low-grade inflammation 81. Furthermore, obesity has been establish to increase the severity of acute pancreatitis through amplification of the immune response to injury 84. Obesity, especially abdominal obesity, was also found to be a significant risk factor for erosive esophagitis 85. Very recently, an association of obesity with endoscopic gastritis was demonstrated. 86Results of a recent study pointed that circulate neutrophils are greatly activated in severely obese subjects, thereby indicating the association between obesity and activation of the innate immune response. In addition, elevated levels of faecal calprotectin, which is a non-invasive biomarker of intestinal inflammation, have been reported in individuals with high BMI 87. Another study demonstrated a strong correlation between circulate calprotectin levels with abdominal adiposity in Japanese men, and also showed that weight loss in the subjects led to decreased circulating calprotectin. 88GeneticsGastrointestinal inflammatory diseases may also be influenced by genetic components. Family studies have revealed strong familial association and high sibling risk ratio in etiology of eosinophilic esophagitis. 89 Genetic factors also play a role in pancreatitis. 90 In addition, increased familial risk has also revealed a genetic basis in Inflammatory Bowel Disease 91, and an increased faecal calpr otectin concentration has also been demonstrated in asymptomatic first-degree relatives of IBD patients, thus indicating a high prevalence of subclinical intestinal inflammation in them. 92GenderGender may play a role in gastrointestinal inflammatory diseases. Animal studies in mice have demonstratedthat femalesdevelop more severe intestinal inflammation than do males 93. On the other hand, a study has shown that bile reflux gastritis was more frequent to male gender 94. Another study found a positive correlation between the male sex and pancreatitis 95. Additional studies found that there is a slight preponderance of colitis ulcerosa in men and of Crohns disease in women 96.Lifestyle factorsSmokingCigarette smoking affects ulcerative colitis (UC) and Crohns disease (CD) in very antithetic ways. According to recent studies, smoking cigarettes has a negative effect on the course of CD, and that smoking cigarettes may have a protective effect in some patients with UC 97. Conversely, smoking cessation aggravates ulcerative colitis and improves CD 98. Furthermore, studies showed that smoking conferred a strong, independent and dose-dependent risk of pancreatitis that may be running(a) or multiplicative when combined with alcohol. 99.AlcoholMost cases of chronic pancreatitis are alcohol-related. 100 However, a recent study showed that faecal calprotectin concentrations in active-drinking alcoholics were not significantly different from the healthy controls thereby indicating the absence of a subclinical intestinal inflammation involving activation of neutrophils in the alcoholics. 101DietPro- or prebiotics will directly influence the microbial flora, while immunonutrition, including omega-3 fatty acids and certain polyphenols, including green tea polyphenols, may reduce the symptoms of gut inflammation 102. Studies have shown that lycopene, an antioxidant which is abundantly found in foods that have a natural red color such as tomato and watermelon, may play a role in attenuating the inflammatory process 103. A study showed that intestinal bacteria and high fat diet interact to promote proinflammatory changes in the small intestine 104. Certain studies suggested that refined net income consumption might be a risk factor for Crohns Disease, but not Ulcerative Colitis. Fat intake is reportedly positively associated with ulcerative colitis 105, whereas vegetables and fiber consumption seem to decrease GI inflammatory process as shown by decreased faecal calprotectin 106.StressPsychological stress reportedly increases disease activity in inflammatory bowel disease by both direct and indirect mechanisms as shown below. 107Figure 1.2 Direct and indirect ways by which stress can aggravate Inflammatory Bowel DiseasesSocioeconomic statusEpidemiological studies have demonstrated Inflammatory Bowel Diseases to be more prevalent among people of high socioeconomic status. Such an occurrence was explained by the hyegiene hypothesis, according to which individuals with higher standards of living may be living in clean environments and thus are more protected from childhood infections, but however exposure to infectious agents later in life makes them more vulnerable to chronic intestinal inflammation in adulthood 108. A study in China demonstrated that levels of faecal calprotectin were significantly increased in the rural infants as compared to urban ones. 5Gastric surgeryPartial gastrectomy increases the risk for chronic pancreatitis in male alcoholics 109. Appendectomy has possibly protective effects in ulcerative colitis but it is suggested as a risk factor in Crohns disease. Tonsillectomy is a risk factor for developing Crohns disease. 110