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Nursing And Adaptive Response Research Paper

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Introduction Adaptive response refers to how the human body protects itself from injury or infection. It is the third line of defense after inflammatory response and innate immunity (Huether & McCance, 2017). Advanced practice nurses should understand patient’s adaptive responses to alterations caused by disease processes. This paper explains the pathophysiology of tonsillitis, irritant contact dermatitis (ICD), and stress responses as determined from scenario 1, 2 and 3 (see Appendix A). In addition, it presents the mind map of tonsillitis that shows epidemiology, pathophysiology, risk factors, clinical presentation, diagnosis, and adaptive responses.

Scenario 1: Acute Tonsillitis

The conclusion from scenario 1 (see Appendix A) is a 2-years-old female patient suffering from on and off fever, sore throat, and swallowing pain for three days. Physical examination shows the patient’s throat is red with 4 tonsils, diffuse exudates, and palpable tender anterior cervical nodes. Patient's vital signs reveal a heart rate of 128 beats per minute, respiratory rate of 24 beats per minute, and temperature of 102.30F. These symptoms and signs are clinical presentations of acute tonsillitis.

Tonsillitis is the inflammation of the palatine tonsil (part of the waldeyer ring) by viral or bacterial infections (Skovbjerg et al., 2015). The waldeyer ring consists of a few lymph nodes that produce lymphocytes and antibodies. So, it acts as a defensive wall that attacks pathogens in food, drink, or air respiration. Common viruses that cause tonsillitis include Epstein-Barr virus (EBV), rhinovirus, adenovirus, coronavirus, and influenza. The most common bacterial cause of tonsillitis is Group A Streptococcus. In reality, distinguishing between viral and bacterial acute tonsillitis is difficult (Skovbjerg et al., 2015).

Acute tonsillitis begins with the infiltration of Group A Streptococcus to the epithelial layer of palatine tonsils. Once the invasion has occurred, the mast cells are triggered and inflammatory mediators (cytokines)...

Cytokines then recruit polymorphonuclear leukocytes and its infiltration causes sore throat, fever, and tonsillitis. This process can be clinically seen as the tonsils are red with enlarged diffuse exudates (Skovbjerg et al., 2015). Other symptoms of acute tonsillitis include dysphagia (difficulty in swallowing), odynophagia (pain when swallowing), and tender cervical nodes.
The inflammation of the tonsils demonstrates the actions of the inflammatory response, the second line of defense in the human body (Huether & McCance, 2017). Inflammation is an adaptive response that promotes healing by protecting the body from further injury and preventing infection of the injured tissue. Other adaptive responses include tender cervical nodes, enlarge tonsils with exudates, and fever.

Scenario 2: Irritant contact dermatitis (ICD)

In scenario 2 (See Appendix A), Jack, a 27-year-old male, is a maintenance engineer and often works with abrasive solvents and chemicals. He has noticed that both his hands are red and flaky after exposure to cleaning fluids. These symptoms are clinical presentations of irritant contact dermatitis (ICD). ICD is an “inflammatory response of the skin due to various external stimuli” (Lee, Stieger, Yawalkar, & Kakeda, 2013). It occurs when a chemical agent causes direct injury to the skin leading to skin barrier disruption, cellular changes, and release of various proin?ammatory mediators (Eberting, 2014).

The pathogenesis of ICD is multifactorial (Hammer & McPhee, 2019). If chemical irritants such as acetone come into contact with the skin, it damages the epidermal cells by extracting lipids from the stratum corneum (the outermost layer of the skin). Chemical irritants can also damage protein structures such as, involucrin, keratin, proflaggrin and loricrin, thereby exposing new water binding sites and causing transepidermal water loss (TEWL) and disorganization of the lipid bilayers (Lee et al., 2013). The end result of this damage to the epidermal skin barrier is the activation of…

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