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A white female, 22 years of age, presents with frequent upset stomachs accompanied with severe abdominal pain, leading to frequent and constant diarrhea, about five to six times a day. She states that it began about a year ago after eating a very spicy meal. It is noted that her mother has also been experiencing similar problems for many years and has seen a doctor to confirm the presence of Chron disease.
Chron disease (CD) has been stated to result from constant and timely activation of the mucosal immune system and falls under the category of inflammatory bowel disease (IBD) (Kumar). Here homeostasis is disrupted causing intense immune reactions against normal flora as well as defects to the epithelial barrier function (Kumar). It is believed that unregulated and intense immune responses to commensal microbes in the gut are the cause of CD and therefore there is an inability of the immunity regulation, genetic susceptibility, and environment triggers (Kumar). Genetically, 15% of patients are affected by their first degree relatives and many genes contribute to the development of CD, such as HLA- DR1/ DR1/ DQw5 allelic combination, specific to North American white patients (Kumar). Another genetic factor cause is NOD2, an encoded protein with a nucleotide- binding oligomerization domain, is expressed in many types of leukocytes and may trigger the NF-kB pathway, a transcription factor that triggers the production of cytokines and other innate immunity proteins (Kumar). NOD2 may reduce the activity of proteins and activate intracellular microbes and uncontrolled immune response (Kumar).
Intestinal flora and abnormal T- cell responses also play a role in CD. Intestinal flora could flourish and obtain mucosal lymphoid tissue and trigger immune response if defects in the barrier function of intestinal epithelium are activated, or T- cells producing a hyperactive local immune response with either an increase or decrease in control over T- lymphocytes (Kumar). Within the T- cell category it has been noted that CD appears to be the result of delayed- type hypersensitivity reaction due to IFN- gamma- producing TH1 cells (Kumar).
When fully developed there is delimited and transmural involvement of the bowel due to the inflammatory process with mucosal damage, noncaseating granulomas, and fissuring with formation of fistulas (Kumar). CD is 40% involved in the small intestine and 30% of cases in the colon (Kumar). The serosa of the diseased bowl becomes granular and gray, and mesenteric fat can wrap around the bowl surface (Kumar). The intestinal wall will become rubbery and thick and the lumen becomes narrowed (Kumar). The small intestine will narrow and strictures in the colon are usually less severe with demarcations at infected site (Kumar). Fissures appear and develop between the fold of the mucosa and can lead to formation of fistuals (Kumar). All of these will then lead to structural changes of the small intestine and glandular distortion on the colon (chronic mucosal damage due to neutrophil infiltrates in isolated crypts) where the mucosal cells may undergo metaplasia forming gastric antral type glands or Paneth cells (Kumar). Ulceration usually appears with severe active disease followed by transmural inflammation affecting all layers, where chronic inflammatory cells attack the mucosal layer and much of the underlying tissue with accompaniment of lymphoid aggregates (Kumar). Diseased segments present with muscularis mucosa that has been reduplicated, thickened, and irregular causing fibrosis of the submucosa, muscularis propria, and mucosa eventually leading to strictures (Kumar).
The patient will usually present with infrequent attacks of mild diarrhea, fever, and abdominal pain at the beginning followed by physical or emotional stress that may contribute flare ups; and if there is colonic involvement, there can be fecal blood loss due to anemia over time (Kumar). As the chronic disease progresses the fibrosing strictures at the terminal ileum and fistulas at the loops of the bowels, urinary bladder, vagina, or perianal skin with cause complications like extensive loss of albumin, generalized malabsorption, specific malabsorption of Vitamin B12 (resulting in anemia), or malabsorption of bile salts leading to steatorehha (Kumar). Extraintestinal manifestations include migratory polyarthritis, sarcoiliitis, ankylosing spondylitis, erythema nodosum, and clubbing of finger tips (Kumar). With all of these factors affecting the intestinal tract there is an increase in chance of cancer with long standing progressive CD (Kumar).
Chrons disease has no single test which the diagnosis is made (Kumar). Microscopic and macroscopic appearances are essential in a definitve diagnosis, where a clinical history, radiographic examination, laboratory findings and pathologic examinations are all needed of tissue samples (Kumar). Certain tests such as pANCA and another that detects an antibody against the cell wall mannan polysaccharide of Saccharomyces cervisiae (ASCA) is used to determine if the individual possesses CD (Kumar). Also barium can be passed through for x- ray readings to confirm narrowing of the lumen (Kumar). Other treatments include supportive care for the patient if stress is present or just to aid in providing knowledge of proper diet to ease or maintain the symtoms of the disease, corticosteroids, immunomodulating drugs, and sometimes even antibiotics are given (Mercks).
With my patientâ€™s presentations above and her genetic involvement, I would prescribe a treatment of a barium infused x- ray to show the presence of a constricted lumen in the gastrointestinal tract, along with a tissue sample to confirm the presence of CD. Prescription of some sort of drug to ease the pain along with dietary and lifestyle changes would also be taught to insure the least amount of flare ups.