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1. NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample
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Disease sample essaysPathophysiology of Inflammatory Bowel DiseaseInflammatory bowel
disease (IBD) is a term given to chronic and recurring conditions that affect the
gastrointestinal tract (Centers for Disease Control & Prevention (CDC), 2017). Irritable
bowel syndrome (IBS) is a condition that affects the movement of the intestine (CDC,
2017). Ulcerative colitis and Crohn’s disease are the two most common IBD. In ulcerative
colitis lesions are mostly contained in the large intestine especially on the left side. With
ulcerative colitis, the crypt of Lieberkuhn in the large bowel becomes infiltrated with T cells
that damage the epithelium. Immunoglublin E and G, along with B cells and plasma cells
increase at the site of inflammation and goblet cells release mucus (Basson,
2017). Ulceration occurs in the mucosa with rare narrowing of the lumen of the large
intestine; polyps form throughout the large intestine (Dudley-Brown & Huether,
2012). Crohn disease lesions may range from the mouth to the anus called skip lesions. The
inflammation of Crohn disease is thought to be triggered by cell-mediated response and
increased levels of interferon-gamma and tumor necrosis factor alpha. In IBD, Crohn
disease, the increase in interferon-gamma and tumor necrosis factor-alpha, along with
stimulation of Th1 cells, produces inflammation throughout the small and large intestine
mucosa and serosa layers. NURS 6501 – Pathophysiology of Inflammatory Bowel Disease
sample essays. Injury to bowel tissue occurs as neutrophils and macrophages infiltrate the
site of inflammation. Granuloma ulcerations occur in some areas of the bowel and skip
other areas (Dudley-Brown & Huether, 2012).Pathophysiology of Irritable Bowel
SyndromeIrritable bowel syndrome is a functional gastrointestinal bowel disorder causing
increased contractions of the colon. IBS is diagnosed by characteristic cluster of symptoms
without detectable structural abnormalities. The pathophysiology of IBS is complex and
involves a number of factors. Hypersensitivity to pain in the visceral gut occurs by either
malfunctioning of the central nervous system or receptors in the wall of the gut; known as
the brain-gut axis. Malfunction of the brain-gut axis can increase gastrointestinal motility
causing diarrhea or decease gastrointestinal motility causing constipation. A decreased
transit time is, also, associated with normal intestinal flora overgrowth. Individuals with

2. IBS have minimal intestinal inflammation, permeability alterations, and decreased immune
response in the gut. Intolerance or allergy to certain foods stimulate an immune response
in the mucosa, change the normal gut flora and increase visceral
hypersensitivity. Furthermore, changes in the brain-gut axis and pain perception increase
with psychosocial issues such as stress (Dudley-Brown & Huether,
2012). Similarities/Differences with Inflammatory Bowel Disorder and Irritable Bowel
SyndromeSimilarities and differences between IBS and IBD can be addressed by the
interactions of the gut immune system and the central nervous system. Both inflammatory
bowel diseases (IBD) and irritable bowel syndrome (IBS) have similar symptoms of altered
bowel patterns associated with abdominal pain or discomfort. Both diseases share
pathophysiologic mechanisms include altered mucosal permeability; the mucosal immune
system alters the interaction of luminal flora, mucosal immune triggering, gut motility
alterations, and severe, prolonged life stressors in symptom alteration. IBD is characterized
by inflammation or ulcerations in the small or large intestine; thus these changes are not
linked with IBS. Classic signs and symptoms of the inflammatory process in the
gastrointestinal tract are diarrhea, rectal bleeding, weight loss, and fever, sometimes related
with extra intestinal signs. Usually, abdominal pain is not the most obvious symptom in
IBD, whereas, the main symptom in IBS is abdominal pain. Unlike IBS, the cause of IBD is
caused by genetic predisposition, environmental factors, infectious agents, altered gut
epithelial permeability, and impaired immune responses. NURS 6501 – Pathophysiology of
Inflammatory Bowel Disease sample essays.Treatments for Inflammatory Bowel Disorder
and Irritable Bowel SyndromeDiagnosis and treatment of Irritable Bowel Disease is based
on clinical presentation, history, physical and exclusion of other causes of symptoms
(Huether & McCance, 2017). To rule out other causes of the symptoms, endoscopies, CT
scans, blood tests, abdominal ultrasounds and tests to rule out illnesses such as lactose
intolerance and celiac disease could be done (Huether & McCance, 2017). The patient is
diagnosed using the Rome III criteria which basically says that the patient has abdominal
pain or discomfort for at least 3 days per month for the past 3 months with at least two
incidences if improvement with bowel movement, change in frequency of stool or change in
appearance of stool (Huether & McCance, 2017). Mesalamine products are often prescribed;
steroids and aminosalicylates are used to suppress the inflammatory response and help to
alleviate cramping pain. Immunosuppressants and immunomodulatory agents may induce
and maintain remission. For severe cases, hospital admission for the administration of
intravenous fluids and steroids may be needed. Surgical intervention to manage
complications may also be necessary. There is no cure for IBS and the treatment is not
specific, but based on each patient symptoms and is often started with incorporation of
fiber in the diet. Laxatives, anti-diarrheals, antispasmodics and analgesics are often a part of
the treatment plan (Huether & McCance, 2017). Evaluations for food allergies, parasites,
and bacterial infections are also performed. Alternative therapies may include: probiotics,
hypnosis, acupuncture, and psychotherapy. The treatment of IBD and IBS are very different
and cannot be used interchangeably. Genetics Impact on Inflammatory Bowel Disorder and
Irritable Bowel SyndromeThere is a strong genetic factor with IBD with a positive family
history. UC is more predominate in the white population and is associated with other auto

3. immune disorders. CD includes genetic factor with positive family history and altered
immune responses (Huether & McCance, 2017). According to McPhee & Hammer (2014), “a
combination of genetic risk and environmental factors are recognized key elements in the
pathogenesis of inflammatory bowel disease. There are many newly recognizable genes that
are susceptible for both Crohn’s disease and ulcerative colitis. It is postulated that the
stigma associated with IBS led to relatives not sharing information with others, resulting in
underestimates of familial aggregation of IBS (Saito, et al., 2008). An estimated 33 percent
of individuals with IBS have a positive family history of the disorder (p. 790). A positive
family history of any of these disorders can alarm the examining practitioner and can lead
to early diagnosis and treatment.ReferencesBasson, M. (2017). Ulcerative colitis. Retrieved
from http://emedicine.medscape.com/ article/183084-overview# aw2aab6b2b4aa.Centers
for Disease Control and Prevention. (2017). Inflammatory bowel disease. Retrieved
from www.cdc.gov/ibd/ Dudley-Brown, S. & Huether, S. (2012). Alterations of digestive
function. In S.J. Huether & K.L. McCance (Eds.). Understanding pathophysiology (5th ed, p.
894-937). St. Louis, MO: Mosby.Heitkemper, M., Kohen, R., Jun, S., & Jarrett, M. (2011).
Genetics and gastrointestinal symptoms. Annual Review Of Nursing Research, 29261-280.
doi:10.1891/0739-6686.29.261Huether, S. E., & McCance, K. L. (2017). Understanding
pathophysiology (6th ed.). St. Louis, MO: Mosby.Hammer, G. G. , & McPhee, S.
(2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.) New
York, NY: McGraw-Hill Education.Saito, Y., Zimmerman, J., Harmsen, W., De Andrade, M.,
Locke, G., Petersen, G., & Talley, N. (2008). Irritable bowel syndrome aggregates strongly in
families: a family-based case-control study. Neurogastroenterology And Motility, 20, 790-
797. NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample
essays. Pathophysiology of Inflammatory Bowel Disease (IBD) and Irritable Bowel
Syndrome (IBS)WEEK 8 DISCUSSIONAs we know all know, our gastrointestinal tract which
extends from the mouth to anus is a hallow organ (Huether &Re McCance, 2017, p.
906). Sometimes, it may often be challenging to come up with a diagnosis of irritable bowel
syndrome (IBS) and inflammatory bowel disease (IBD) due to the presence of overlapping
mechanism which still makes both as separate conditions. IBD is divided into two types of
condition namely ulcerative colitis and Crohn disease. NURS 6501 – Pathophysiology of
Inflammatory Bowel Disease sample essays. According to rectum (Dudley-Brown and
Huether, ulcerative colitis is a chronic inflammatory disease that causes an ulceration of the
colon and rectum. It is characterized with a period of remission followed with
relapse. According to (Hammer & McPhee, 2014, p. 372). It is unknown what triggers
inflammatory bowel disease. Ulcerative colitis is superficial and most likely developed in
the colonic mucosa While crohn diseases granulomatous and is located throughout the
gastrointestinal tract (Hammer & McPhee, 2014). Patient with crohn disease may exhibit
symptoms such as diarrhea, rectal bleeding, weight loss and abdominal pain along with
vitamin b12 and vitamin D malabsorption, while those patients with ulcerative colitis may
present with fever, tachycardia, dehydration, weight loss, bleeding and inflammation
(Huether & McCance, 2017).Pathophysiology of IBD(Huether & McCance,
2017).Pathophysiological Mechanisms of Inflammatory Bowel Disorder and Irritable Bowel
SyndromeIt is unclear what the triggers are for inflammatory bowel disease (IBD), but what

4. we do know is that there are two forms; Crohn disease and ulcerative colitis (Hammer &
McPhee, 2014, p. 372). Crohn disease (CD) is transmural and granulomatous which can be
found throughout the GI track, whereas ulcerative colitis (UC) is superficial and limited to
the colonic mucosa (Hammer & McPhee, 2014). CD symptoms include diarrhea, rectal
bleeding, weight loss and abdominal pain along with vitamin b12 and vitamin D
malabsorption (Huether & McCance, 2017). In UC a patient may experience fever,
tachycardia, dehydration, weight loss, bleeding and inflammation (Huether & McCance,
2017) NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample
essays.Pathophysiology of IBD There are two forms of IBD. Crohn disease “is
transmural and granulomatous in character, occurring anywhere along the GI tract while
ulcerative colitis is superficial and limited to the colonic mucosa” (Hammer & McPhee, 2014,
p. 372). Under normal circumstances, the intestine is able to control mucosal epithelieum
inflammatory responses to dietary and microbial antigens. In IBD, this process is defective,
resulting in uncontrolled inflammation. Common symptoms for both CD and UC are
diarrhea and abdominal pain though it is important to note that constipation may
associated with UC. The diarrhea can be quite severe, resulting in dehydration,
malnutrition, and weight loss. Diarrheal blood loss can result in anemia. Pathophysiology of
Inflammatory Bowel Disease (IBD) and Irritable Bowel Syndrome (IBS)IBD is categorized
into two sections: ulcerative colitis and Crohn disease. Ulcerative colitis is a chronic
inflammatory disease that causes an ulceration of the colon and rectum (Dudley-Brown and
Huether, 2017). Ulcerative colitis is characterized by remition and relapse. According to
Stratton (2017), ulcerative colitis results from aberrant immune response to gut luminal
antigen in a genetically susceptible individual. Phagocyte’s response to gut flora and
secretion of proinflammatory cytokines activates the T cells, causing mucosal inflammation
and damage NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample essays. It
is also believed that an abnormal or deficient interleukin (IL)-25 that controls some T
helper cell responses is involved in the mechanism of ulcerative colitis. In Crohn disease, the
inflammation results from the activation of cell-mediated responses, elevated interferon-
gamma, and tumor necrosis factor-alpha. The inflammation originates from the intestinal
submucosa and proliferates to the mucosa and serosa. The inflammation and tissue injury
seen in this disorder is associated with the activation of neutrophils and marcophages
(Dudley-Brown and Huether, 2017) NURS 6501 – Pathophysiology of Inflammatory Bowel
Disease sample essays. ReferencesHammer, G. G., & McPhee, S. (2014). Pathophysiology of
disease: An introduction to clinical medicine. (7th ed.) New York, NY: McGraw-Hill
EducationHuether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.).
St. Louis, MO: Mosby.Dudley-Brown, S., & Huether, S. E. (2017). Alterations of digestive
function. In Huether, S. E., & McCance, K. L. (2017). Understanding
pathophysiology (6th ed.). St. Louis, MO: Mosby NURS 6501 – Pathophysiology of
Inflammatory Bowel Disease sample essays