Respond to Stacy and Sonia
Advanced patho
Respond to Stacy and Sonia
1 day ago
Stacy Adam
Wk 1 Discussion
COLLAPSE
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Wk1 Discussion 6501
The 16-year-old boy in the discussion scenario presented to the clinic with specific complaints that are common in Strep Throat infection. He complained of a sore throat for 3 days. He denied recent cold, influenza, ear infections, or allergies. Redness, +3 tonsil edema, positive anterior and posterior cervical adenopathy, low-grade temperature, and pharyngeal exudate were noted by the practitioner on the exam. A diagnosis of Strep Throat was confirmed by a positive rapid strep throat culture. Penicillin was prescribed.
Strep Throat is not a genetic disorder, but an infectious one caused by A. Streptococcus bacteria. It is not gender-specific. Strep throat most commonly occurs during the late winter or early spring months as a direct result of people being grouped closely together indoors allowing it to spread easily via direct contact (American Academy of Family Physicians, 2016).
The patient’s symptomology and positive culture confirm that he was infected by A. Streptococcus bacteria. His body’s response to A. Streptococcus bacteria is the body’s initial inflammatory response to this bacteria; redness, swelling, heat, and pain (Kahn Academy, 2010). The patient’s anaphylactic response to penicillin was mediated by ‘IgE antibodies that are produced by the immune system in response to an environmental allergen’ (Justiz-Vaillant & Zito, 2019). These allergens include pollens, animal dander, dust mites or fungi (Justiz-Vaillant & Zito, 2019). The patient’s anaphylactic response to penicillin, a fungus, was unknown prior to its administration.
When a bacterial infection occurs, the body releases mast cells that are activated by chemokines to attack the infection (Kahn Academy, 2010). Histamine is released causing vasodilation (Kahn Academy, 2010). Endothelial cells are pushed apart and capillaries become larger and dilated, causing swelling to occur (Kahn Academy, 2010). The capillary walls become more porous allowing more cells to pass through them (Kahn Academy, 2010). Neutrophils act as the first responders and are attracted to the chemokines (Kahn Academy, 2010). They roll along the endothelial wall, squeezing through to eat up bacteria and damaged cells (Kahn Academy, 2010). Specific action via B and T cells are also activated to attack and destroy the bacteria (Kahn Academy, 2010).
The patient’s anaphylactic response, Type I hypersensitivity reaction, to IgE antibodies is produced by the ‘immune system in response to environmental allergens’ (Justiz-Vaillant & Zito, 2019). If left untreated, it can result in a life-threatening or irreversible injury that includes death (Justiz-Vaillant & Zito, 2019). While the patient did not have a known allergy and it was disclosed that he had none, Type I hypersensitivity reactions occur after a previous sensitization (Justiz-Vaillant & Zito, 2019). In a Type I hypersensitivity reaction, mast cells quickly release a large amount of ‘histamine and later on leukotrienes’ after encountering an allergen (Justiz-Vaillant & Zito, 2019). This reaction can lead to ‘bronchospasm, laryngeal edema, cyanosis, hypotension, and shock’ in the most severe cases (Justiz-Vaillant & Zito, 2019).
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