NURS 530 Discussion chronic relapsing inflammatory bowel diseases
NURS 530 Discussion chronic relapsing inflammatory bowel diseases
NURS 530 Discussion chronic relapsing inflammatory bowel diseases
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DQ1 according to NURS 530 Discussion chronic relapsing inflammatory bowel diseases, Select one of the following discussion prompts to address:
Describe the pathophysiology of celiac disease, clinical manifestations, evaluation, and treatment. What are the differences between non-celiac gluten sensitivity and celiac disease?
What trends, if any, have you noticed among the following conditions? Describe the pathophysiology, clinical manifestations, evaluation, and treatment of gastroesophageal reflux disease (GERD), peptic ulcer disease, and gastritis.
Describe the chronic relapsing inflammatory bowel diseases (ulcerative colitis and Crohn disease), and summarize the pathophysiology, clinical manifestations, evaluation, and treatment recommendations for each.
DQ2 Select one of the following discussion prompts to address:
Review this Mayo Clinic interview. Define fibromyalgia and describe the pathophysiology, clinical manifestations, evaluation, and treatment. Comment on advances in diagnosis and management of this disorder that debunk the idea that the disorder is “in the patient’s head.”
Define osteoporosis and describe the risk factors, pathophysiology, clinical manifestations, evaluation, prevention, and treatment.
Describe osteoarthritis (OA) and rheumatoid arthritis (RA), and discuss the pathophysiology, clinical manifestations, evaluation, and treatment for each.
according to NURS 530 Discussion chronic relapsing inflammatory bowel diseases Inflammatory bowel disease (IBD), comprising Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic, relapsing-remitting inflammatory disorder of the gastrointestinal (GI) tract. CD and UC vary in the region of the GI tract they affect; the extent of inflammation and resulting tissue damage; and their associated symptoms. UC tends to exhibit continuous superficial inflammation which spreads from the rectum and is limited to the colon (large intestine), with bloody diarrhoea as the most common symptom. Inflammation associated with CD is transmural (affects all layers of GI tract tissue), patchy (areas of inflammation are interspersed with healthy unaffected tissue) and can present anywhere along the entire GI tract and, in some cases, in the skin and joints. The symptoms of CD are more diverse than for UC, including diarrhoea, abdominal pain and weight loss.
The exact cause of IBD is unclear. There appear to be four main factors which influence the disease: host genetic susceptibility, a dysregulated immune response and impairment of intestinal epithelial barrier function, and environmental factors (Figure 1).
Figure 1. Factors internal and external to the host that influence inflammatory bowel disease (IBD).
Genetic susceptibility
Genome-wide association studies (GWASs) have identified a number of genetic loci associated with IBD, including genes specific to either CD or UC, and some which are common to both (Figure 2). The risk of developing IBD conferred by variants at each locus is small for all but a few genes (e.g. IL10RA and IL10RB). It may be the case that IBD only occurs when multiple genetic variations associated with the disease are present. Another possibility is that environmental factors are required to trigger the onset of disease in genetically susceptible individuals.
Figure 2. Genes associated with Crohn’s disease (CD), ulcerative colitis (UC) or both forms of IBD, from recent genome-wide association studies and their meta-analyses.
Environmental factors
Environmental factors such as the commensal microflora, pathogenic infections and metabolic factors are thought to play a role in the development and perpetuation of IBD. The intestinal microbiota, which is dominated by bacteria, but also includes viruses, fungi and protozoa, is crucial for development of the host immune system but also appears to be the target of the inflammatory response during IBD. The composition of the intestinal microbiota appears to be altered during disease, although whether this causes, or results from, intestinal inflammation is unclear. The effects of antibiotics, pathogenic infections and diet on IBD might be explained by their impact on the commensal microflora.
Dysregulated immune response
IBD is an immune-mediated disease, but is not considered to involve autoimmunity. The intestine contains an enormous antigenic load derived from the food and microbial flora present. Of the approximately 1014 bacteria in the intestines, the majority are harmless commensals which are beneficial to our health in numerous ways such as aiding digestion and preventing the colonisation of pathogenic species. The intestinal immune system is separated from this luminal content by a single epithelial cell layer, and must initiate the appropriate response – tolerance or protective immunity – upon exposure to each antigen. IBD is thought to arise when an inappropriate immune response is mounted against commensal bacteria. GWASs and experimental results have indicated a number of facets to this dysregulation, for example pro-inflammatory pathways driven by IL-23, decreased immune regulatory mechanisms, and defective barrier function of the intestinal epithelium.NURS 530 Discussion chronic relapsing inflammatory bowel diseases shows some key cell populations and mediators thought to be involved in intestinal inflammation. Monoclonal antibody-mediated blockade of the pro-inflammatory cytokine TNFα is very effective at reducing disease in many cases of IBD, highlighting a key role for this molecule in intestinal inflammation. Patients with disease refractory to this treatment, which is only employed after the failure of other therapies such as non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids and immunosuppressants, necessitate the discovery and development of novel therapeutic strategies.
Figure 3. Key cellular populations and mediators in intestinal homeostasis and the pathogenesis of inflammatory bowel disease. DC, dendritic cell; IEC, intestinal epithelial cell; ILC, innate lymphoid cell; Mφ,macrophage; sIgA, secretory IgA; Th, helper T cell; TReg, regulatory T cell.
Clinical and Pathological Characteristics
A chest radiograph and a CT scan should be part of the diagnostic process. If at all possible, PFTs should be collected because they can serve as a baseline during treatment. Endoscopy aids in the discovery of upper airway obstruction or stenosis, as well as the collection of tissue for microbiological and histology examinations. A full blood count with differential should be performed, as well as a metabolic panel. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) can be used to monitor disease activity during treatment. Atypical antineutrophil cytoplasmic antibodies (ANCAs), characterized by a fine granular and perinuclear (“snowdrift”) pattern, are found in 50 percent to 70 percent of patients with ulcerative colitis and 10 percent to 30 percent of patients with Crohn disease (predominantly those with colonic involvement). In individuals with suspected underlying IBD, serologic testing for ANCAs may be beneficial. In individuals with serositis, ANAs can aid in the detection of drug-induced lupus syndrome. Because thromboembolic disease is a known source of morbidity and death in IBD patients, the clinician should keep a low threshold in mind while considering and ruling out pulmonary embolism in this group.
This section goes through the several compartments of the respiratory system that are affected by IBD, as well as the distinct aspects of the location, clinical presentation, and pathologic features of each (Table 79-1).
Inflammation of the airways
according to NURS 530 Discussion chronic relapsing inflammatory bowel diseases Inflammation of the tracheobronchial tree, encompassing the larynx, trachea, and large and small airways, is a symptom of inflammatory bowel disease. Inflammation in the major airways is the most frequent, affecting roughly 40% of IBD patients. Involvement of the upper respiratory tract or small airways is seen in about 10% of patients. The extent and location of involvement vary; some individuals have involvement limited to a small area, others have patchy illness affecting several anatomic levels of the conducting airways, and yet others have involvement of the entire tracheobronchial tree. Only 10% of people with airway illness have CD, while the great majority have UC. The majority of patients are female, with a median age of 42 years at presentation. About 5% of people have airway illness before being diagnosed with IBD, and these patients are typically significantly younger (median age, 13 years).
Inflammation of the glottis and epiglottis results in narrowing and stenosis in the larynx. A dry, deep-toned cough with stridor is one of the symptoms. Because severe cases of laryngeal inflammation in IBD can lead to hypoxia, it is one of the three disorders that need immediate medical attention. Tracheobronchitis, or inflammation of the large airways, causes a chronic, otherwise inexplicable cough that can be dry or produce copious volumes of mucopurulent sputum. The term “chronic bronchial suppuration” was used to describe this ailment because of the purulent substance. It’s also the condition that, in 1976, made the connection between IBD and lung disease. Bronchitis is caused by long-term chronic inflammation and suppuration, which often has a basilar distribution. Airflow obstruction with or without sputum production is a symptom of small airway disease. Microscopic involvement is frequently detected distally from affected major airways, despite the fact that it is unlikely to be the dominating feature.