Scenario 1: Pathophysiology
Jennifer may be suffering from the Pharyngitis disease, an acute form of infection present in children. The condition is associated with various signs and symptoms that include sore throats that may reveal nasopharyngitis, tonsillopharyngitis, and tonsillitis. Multiple entities have capabilities of causing inflammation or pharynx irritation(Irlam et al., 2013). In young children, pathogenic fungi, bacteria, and viruses such as Epstein –Barr Virus, enterovirus or adenovirus infection may cause the condition. The infection of the virus requires supportive therapy as a method of managing the condition. The condition can also be caused by pathogenic bacteria such as GABHS. The bacteria treatment requires antibiotic therapy. The supportive care is required in all the pediatric pharyngitis cases either caused by viral or bacterial infection with the aim of prevention adverse symptoms such as diarrhea. All the cases involving pharyngitis in children, primary pathogenic bacteria accounts for approximate 30% (Cattalini et al., 2015). The most common pathogenic bacteria responsible for infection include GABHS bacteria, Group G and C streptococci among others. The GABHS are responsible for most pediatric cases involving pharyngitis.
The innate immune system attaches the pathogenic bacteria or fungi. The infection agentsmicropinocytosis results in exudates formation. The throat is erythematous is as a result of diffuse exudates and tonsil inflammation. As a result, the anterior nodes on the left side is tender to touch and palpable. The mediators of the phalangeal inflammation include interleukins and the arachidonic acid metabolites. This causes the fever to elevate as a result of abnormal set point activity in the hypothalamus temperature regulatory center. The rheumatic fever of Jennifer is as a result of the severe form of tonsillopharyngitis.
The adaptive response to alteration of the patients
The activation of the adaptive and innate immune system in children will occur in response to pharyngitis/tonsillitis infection in Jennifer case. The autonomous nervous system of Jennifer will trigger the heart chronographic effects or simply the heart rate to the normal or homeostatic condition. Jennifer temperature will be brought to normal through the action of her hypothalamus triggering the control of the homeostatic temperature. The immunological factors responsible for Jennifer tonsils swelling are as follows. The activation of the Toll-Like Receptors (TLR), in macrophages triggers the adaptive immune response. The activation causes the neutrophils and the macrophages to enhance the antimicrobial activity thereby releasing the cytokines at the infection site as well as the presentation of the antigen to naïve T cells (Kumar et al., 2014). The microbial engulfment process takes place through the dendritic cell maturation process induction by the TLRs. The process also causes the migration of the cells to the tonsils. The cells activate and defend the specific T cells to produce cluster differentiation molecules such as CD 80 and 40 as well as the acting against the infection through the endosomal pathway.
The inflammation alterations in the tonsils include increased capillary and vasodilation which present clinically as sore throat, fever and tonsillar exudates (McPhee & Hammer, 2010) Enlarged and Tender lymph nodes takes place as a result of these nodes trap or filter foreign particles entering the body (Yildizoglu, 2015)
Scenario 2: pathophysiology
Jack may be suffering from contact dermatitis. This is based on the fact that he is a maintenance engineer at a building involved in newspaper production. Based on this scenario, it is quite clear that sometimes Jack uses bare hands while touching some chemicals and solvents when touching various chemical and solvents. He has therefore exposed his hands to some of the cleaning agents.
When developing irritant contact dermatitis (ICD), the initial step is hapten binding (Ale &Maibach, 2014). The contact allergens can be classified as chemicals of low molecular weight, usually less than 500 Daltons. These chemicals are known as haptens. The haptens have the capability of stratum corneum skill barrier penetration. The can be the substance that occurs naturally such as the resin of poison ivy urushiol. Additionally, they can be from synthetic dies or cleaning agents. Jack may have contact with some of the haptens in the cleaning agents he handled without using gloves. The skin proteins binding with the haptens occurs through the formation of the covalent bond between a nucleophillic side of the amino acid of the skin protein and the electrophilic side of the haptens (Becker, 2013). The binding protein at as carrier to the haptens, thereby providing them with the ability to be recognized by the components of the immune system. The T-cell mediated delayed hypersensitivity is triggered and causes the redness and the irritation in the areas of the skin responsible for the infection.
The adaptive response to alteration of the patients
The haptens are responsible for activation of the innate immunity through Toll-like receptors activation (TLRs). The inflammation observed in the skin is as a result of the innate mediated immune response. Keratinocytes play an essential role in the perpetuation and the initiation of the inflammation of the skin. The keratinocytes accomplish this through response to the cytokines and the release of the cytokines(McGuckin&Govednik, 2015). The cytokines are also consistently produced by the resting keratinocytes. Some of the cytokines produced by keratinocytes upon interaction with keratinocytes include the tumor necrosis factors and the interleukin 1, and this falls under the category of the inflammatory cytokines. Other cytokines released include the chemotactic cytokines such as the interleukin 10 and 8. Others include the growth promoting cytokines such as the interleukin 15, 7 and 6. The inflammation of the leucocytes into the epidermis is promoted by the intercellular adhesion molecule 1.
Chemical exposure cause the epidermis damage thereby causing the triggering of interleukin 1, 6,8. Additionally, the tumor necrosis factors are also released (Simmon, Aeberhard. Erdemoglu & Simon, 2014). The release is associated with the process of inflammation which is presented clinically as reddened, cracked and irritated dermis (Huether & McCance, 2012)
Pathophysiology, the adaptive response to alteration of the patients and associated alterations
According to this case, an experience of an individual with stress that results from high levels of glucocorticoids secretions by the hypothalamic pituitary adrenal axis (Huether & McCance, 2012). The HPA acts as an adaptive framework for maintenance of equilibrium of a changing environment. Glucocorticoids control many elements of the focal sensory system such as excitement, discernment, rest, temperament, and cardiovascular tone (Wolkow, Ferguson, Aisbett, & Main, 2015). In this manner increment in glucocorticoids during the stress responses causes variety of adaptive changes to facilitate response by the body to the environmental changes (Huether & McCance, 2012). The adaptive responses that are noted in this given situation comprises of the changes in the appetite levels, mood swings, racing heart, as well as alteration of sleep.
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Federation of Oto-Rhino-Laryngological Societies (EUFOS): Affiliated With The
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Irlam, J., Mayosi, B. M., Engel, M., &Gaziano, T. A. (2013). Primary Prevention of Acute Rheumatic Fever and Rheumatic Heart Disease With Penicillin in South African Children With Pharyngitis. Circulation: Cardiovascular Quality and Outcomes, 6(3), 343-351.
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Yildizoglu, U., Polat, B., Gumral, R., Kilic, A., Tosun, F., &Gerek, M. (2015). Effect of antibiotic use on bacterial flora of tonsil core in patients with recurrent tonsillitis. European Archives of Oto-Rhino-Laryngology: Official Journal of The European