Please respond to Gayla post in one of the following ways :Share insights on how the factor you selected impacts the pathophysiology of the immune disorder your colleague selected.
Expand on your colleague’s posting by providing additional insights or contrasting perspectives based on readings and evidence.
I did HIV and Psoriasis

5 minutes ago Gayla Cragg
DB week 2 Psoriasis & Inflammatory Bowel Disease
COLLAPSE
Psoriasis

Pathophysiology

Psoriasis is a “common chronic, persistent or relapsing, scaling skin condition” (Meier & McCalmont, 2014, p. 190). In this condition, the epidermis is thickened due to a shortened duration of the keratinocyte cell cycle while the proliferative cells double (Meier & McCalmont, 2014). This pattern of cell growth results in plaques with distinct, erythematous margins which have white or silvery scales (Meier & McCalmont, 2014). Lesions often develop “on the face, scalp, elbows, and knees…” (McCann, Nicol, and Huether, 2017, p. 1062). Individuals with psoriasis may also develop psoriatic arthritis and nail disease (Meier & McCalmont, 2014).

Maladaptive Response

Individuals who develop psoriasis are at risk for developing a variety of comorbid conditions such as inflammatory bowel disease and metabolic syndrome (McCann, Nicol, and Huether, 2017). Diseases such as “hypertension, insulin resistance, dyslipidemias, abdominal obesity, nonalcoholic fatty liver disease” are potential risks of metabolic syndrome (McCann, Nicol, and Huether, 2017, p. 1063). The pathogenesis of psoriasis, as well as treatment regimens, can lead to the increased risk of cancer (McCann, Nicol, and Huether, 2017).

Physiological Response

The immune response of the body is initiated which results in “production of cytokines, such as interferon, tumor necrosis factor (TNF), interleukin-23 (IL-23), and IL-12, by macrophages, dendritic cells, and neutrophils” (Meier & McCalmont, 2014, p.191). This process results in “attraction, activation, and differentiation of T cells” (Meier & McCalmont, 2014, p. 191). The T helper 1 and T helper 17 cells produce additional cytokines, which lead to further growth of the epidermis. This growth of inflammatory cells results in “a positive feedback loop that perpetuates the pathologic process” (Meier & McCalmont, 2014, p.191).

Effect of Age

Psoriasis is most often noted to develop in the third decade of life; however, can occur from birth to late in life (Meier & McCalmont, 2014). Development of psoriasis later in life may be related to other chronic conditions such as “obesity, smoking, hypertension, and diabetes” (McCann, Nicol, and Huether, 2017, p. 1062).

Inflammatory Bowel Disease

Pathophysiology

Inflammatory bowel disease involves recurrent episodes of diarrhea which contains blood, mucus and white cells (Mills & Stappenbeck, 2014). The presence of microbial infectious disease process has been excluded by negative stool cultures (Mills & Stappenbeck, 2014). Inflammatory bowel disease can be noted in two forms, Crohn disease, and ulcerative colitis, both of which the etiology of the disease is unknown (Mills & Stappenbeck, 2014).

Maladaptive Response

Patients who have Crohn disease have been noted to have inflammatory disorders of areas outside the gastrointestinal tract, such as joints, eyes, skin, bile duct, mucous membranes, and liver (Mills & Stappenbeck, 2014). Other complications can include kidney stones and blood clots, which are related to the enduring impact of the stress of the disease on the body (Mills & Stappenbeck, 2014).

Ulcerative colitis is found in “the mucosa of the colon and rectum” (Mills & Stappenbeck, 2014, p. 376). There is a risk of adenocarcinoma which increases as the duration of the disease progresses (Mills & Stappenbeck, 2014). Another complication is megacolon, which results in poor motility and the risk of rupture (Mills & Stappenbeck, 2014).

Physiological Response

Risk factors may include genetic, environmental, and altered immune response (Huether, 2017). The intestines may not be able to discriminate between harmful and complementary bacteria (Huether, 2017). This lack of discrimination may activate dendritic cells, which triggers transport to mesenteric lymph nodes, where T cells are differentiated “to Th1, Th2, and Th17 cells, or T-regulatory cells” (Huether, 2017, p. 921). Huether (2017) notes “proinflammatory cytokines and chemokines,…damages the intestinal epithelium” (p. 921).

Effect of Age

There has been a link between early exposure to intestinal microbes from the mother (Mills & Stappenbeck, 2014). This contributing factor which should be discussed when obtaining the family history.

Conclusion

Both psoriasis and inflammatory bowel disease have inflammation of epithelial cells and mucosa in common. A genetic overlap has been noted between Crohn disease and psoriasis (McCann, Nicol, and Huether, 2017). Sundarrajan & Arumugam (2016) noted that “the biological processes involved in inflammatory response and cell signaling formed a common basis between psoriasis and its associated comorbidities” (p. 1). Screening of comorbidities should be considered when treating immune disorders such as psoriasis and inflammatory bowel disease.

References

Huether, S.E. (2017). Alterations of digestive function. In Huether, S. E., & McCance, K. L. Understanding pathophysiology (6th ed., pp. 906-949). St. Louis, MO: Mosby

McCann, S.A., Nicol, N.H., & Huether, S.E. (2017). Structure, function, and disorders of the integument. In Huether, S. E., & McCance, K. L. Understanding pathophysiology (6th ed., pp. 1053-1083). St. Louis, MO: Mosby

Meier, M.M., & McCalmont, T.H. (2014). Diseases of the skin. In Hammer, G. G., & McPhee, S. Pathophysiology of disease: An introduction to clinical medicine (7th ed., pp. 187- 212) New York, NY: McGraw-Hill Education.

Mills, J.C. & Stappenbeck, T.S. (2014). Gastrointestinal disease. In Hammer, G. G., & McPhee, S. Pathophysiology of disease: An introduction to clinical medicine (7th ed., pp. 333-383) New York, NY: McGraw-Hill Education.

Sundarrajan, S., & Arumugam, M. (2016). Comorbidities of Psoriasis – Exploring the Links by Network Approach. Plos One, 11(3), e0149175. doi:10.1371/journal.pone.014917

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