NURS6501- Maladaptive Responses to Immune Disorders

Discussion 1: Maladaptive Responses to Immune Disorders

Maladaptive responses to disorders are compensatory mechanisms that ultimately have adverse health effects for patients. For instance, a patient’s allergic reaction to peanuts might lead to anaphylactic shock, or a patient struggling with depression might develop a substance abuse problem. To properly diagnose and treat patients, advanced practice nurses must understand both the pathophysiology of disorders and potential maladaptive responses that some disorders cause.

Consider immune disorders such as HIV, psoriasis, inflammatory bowel disease, and systemic lupus E. What are resulting maladaptive responses for patients with these disorders?

To Prepare

Review Chapter 6 and Chapter 8 in the Huether and McCance text. Reflect on the concept of maladaptive responses to disorders.
Select two of the following immune disorders: HIV, psoriasis, inflammatory bowel disease, or systemic lupus E (SLE).
Identify the pathophysiology of each disorder you selected. Consider the compensatory mechanisms that the disorders trigger. Then compare the resulting maladaptive and physiological responses of the two disorders.
Select one of the following factors: genetics, gender, ethnicity, age, or behavior. Reflect on how the factor might impact your selected immune disorders.

By Day 3

Post a brief description of the pathophysiology of your selected immune disorders. Explain how the maladaptive and physiological responses of the two disorders differ. Finally, explain how the factor you selected might impact the pathophysiology of each disorder.

Read a selection of your colleagues’ responses.

By Day 5

NURS6501- Maladaptive Responses to Immune Disorders

INITIAL POST

NURS 6501 Week Two Discussion #1

Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) is an autoimmune process characterized by chronic inflammation of all or sections the small intestine, colon or both, and is differentiated into Crohn disease (CD) or Ulcerative Colitis (UC), with periods of exacerbations and remission (Hammer, and McPhee, 2014). The inflammatory process causing IBD is from the loss of immune tolerance to normal intestinal antigens triggering T cell activation. With T cell activation proinflammatory cytokines such as tumor necrosis factor and interleukins cause inflammation and damage the intestinal epithelium (Huether, and McCance, 2017). IBD signs and symptoms include GI upset, abdominal pain, diarrhea, vomiting, rectal bleeding, and malabsorption (Hammer, and McPhee, 2014). UC presents itself as a continuous lesion of superficial inflammation and pseudopolyps from the distal colon to the proximal colon, CD presents itself with skip lesions or patchy areas of transmural inflammation in the ileocecal area, colon, and perianal inflammation can be present (Hammer, and McPhee, 2014)

Psoriasis

Psoriasis is a type of Papulosquamous disorder, is due to an inflammatory response involving skin, scalp, and nails (Huether and McCance 2017). In psoriasis, the inflammatory response of immune cells such as macrophages, dendritic, T, and natural killer cells secrete inflammatory mediators (Huether and McCance 2017). Interferon, Tumor necrosis factor, cytokines, and interleukins are the inflammatory mediators that increase dermal vasculature, cell metabolism causing hyperproliferation of skin cells (Huether and McCance 2017). Normally the regeneration of the epidermis is over a two to three-week period, and in psoriasis, regeneration decreases to three to four days omitting cell maturation and keratinization causing the skin to thicken and to form a scaly, silvery plaque (Huether and McCance 2017). Erythrodermic, guttate, inverse, plaque, and pustular are the several varieties of psoriasis, and manifestations can be from mild to severe (Huether and McCance 2017).

Differences of the Maladaptive and Physiological Responses

Both psoriasis and IBD are autoimmune inflammatory diseases with relapsing and remitting courses. In psoriasis T cell activation of proinflammatory cytokines cause damage to normal epidermis cells (Huether and McCance 2017). The inflammatory response in IBD is from the loss of immune tolerance to normal intestinal antigens triggering T cell activation triggering destruction to the intestinal epithelium (Huether and McCance 2017). The difference is the end organ affected

Genetics

Documented in both IBD and psoriasis is a low level familial linked presence. In countries north of the equator psoriasis affects one to four percent of the population (Huether and McCance 2017). Psoriasis development later in life is due more to a behavioral factor as opposed to it being familial when developed earlier. Behavioral factors are related to smoking, alcohol consumption, obesity, diabetes and hypertension (Huether and McCance 2017). The risk for genetically inheriting genes for IBD is low at 20-30% (Hammer, and McPhee, 2014). However, abnormalities in immune function modulators, impaired epithelial functions, and autophagy are present in all cases of IBD (Hammer, and McPhee, 2014).

References

Huether, 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.

NURS6501- Maladaptive Responses to Immune Disorders

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NURS6501- Maladaptive Responses to Immune Disorders