NURS 6501 – Advanced Pathophysiology week 1  Initial post  The Role of Genetics in the Disease Process

NURS 6501 – Advanced Pathophysiology week 1  Initial post  The Role of Genetics in the Disease Process

According to the Centers for Disease Control and Prevention (CDC, n. d.), Viruses are the most common cause of a sore throat. However, strep throat is an infection in the throat and tonsils caused by bacteria called group A Streptococcus (group A strep). Sore throat, swallowing pain, fever, red and swollen tonsils, tiny red spots on the roof of the mouth, or swollen lymph nodes in the front of the neck are common symptoms. It is spread by coming into contact with droplets from an infected person’s cough or sneezing. It is most common in children aged 5 to 15 years old. To prevent the spread of the infection, practice good hand hygiene and cover your mouth and nose when coughing or sneezing. Antibiotics such as penicillin or amoxicillin are frequently used to treat it. Other serious infections caused by Group A streptococci (GAS) in humans include necrotizing fasciitis, rheumatic fever, and glomerulonephritis (CDC, n. d.).

DNA, the most important component of genes, serves as the blueprint for all proteins in the body, allowing genes to influence all aspects of body structure and function. Any change or error in a gene sequence can result in a genetic disease (McCance & Huether, 2019). Differences in host genes give different susceptibility and result in invasive group A Streptococcus (GAS) patients. According to a recent study, children with frequent tonsillitis have a genetically poor immune response to group A strep bacteria (Citroner, 2019). According to the study, it shows two specific form genes which reduced one’s ability to fight strep throat and resulted in recurrent tonsillitis, and one gene variation protected against group A strep infection. According to Galloway-Pena et al. (2018), GAS strains tend to change the sequence of the M protein, which prevents phagocytosis and weakens the host’s immune response, allowing infections to spread to humans. Vaccines against GAS infections target M proteins

The Reasons for Patient’ Presentation with the Specific Symptoms

The body’s immune response to invading microorganisms results in the above-mentioned symptoms. The soreness and white exudate on the tonsils in the throat, redness of the pharynx, and swelling of the cervical adenopathy are all inflammatory responses of innate immunity symptoms caused by Streptococcus bacteria. According to McCance and Huether (2019), “Inflammation is a rapid and nonspecific protective response to cellular injury”. The goal is to prevent further damage to tissue, limit infections, and begin healing. Inflammation manifestations result in redness, heat, swelling, pain, and loss of function and releases fluids like serous and purulent. Fever of 99.6F is an early sign of inflammation. Because many microorganisms that cause infections are sensitive to slight increases in body temperature, a febrile response can be beneficial to the body. Mast cells, endothelial cells, platelets, neutrophils, eosinophils, monocytes, macrophages, dendritic cells, natural killer cells, and lymphocytes are all types of cells that participate in the inflammatory process (McCance & Huether, 2019).

The Reason for Physiologic Response to the Stimulus 

Allergies are reactions caused by the immune system as it responds to environmental substances such as amoxicillin in this case study, where the patient is experiencing systemic anaphylaxis symptoms such as tongue swelling, difficulty breathing, and wheezing. The immune system defends the body from foreign antigens. Hypersensitivity or an altered immune response, such as an allergy to an antigen, can, on the other hand, cause disease or damage to the host cell (McCance & Huether, 2019).

The Cells Involved in the Process

Amoxicillin allergy reactions occur when the drugs bind to proteins on target cell plasma membranes and become immunogenic or function as targets of type II reactions. The immune system fights the allergen on the plasma membrane, destroying the cell in the process. The antigen antibiotics in this case study produce type II hypersensitivities in which allergic haptens bind to the surface of the specific cells and elicit an IgG and IgM response (McCance & Huether, 2019). Type II hypersensitivity reactions occur via five distinct mechanisms, with the antigen being destroyed via complement-mediated lysis. Second, antibodies kill cells via phagocytosis by macrophages. The third process is immune destruction mediated by neutrophils. The fourth process involves natural killer cells inducing apoptosis in target cells. The fifth process causes target cells to malfunction. It entails the modulation or obstructing of a receptor’s normal cellular function by an anti-receptor antibody. Endothelial cells, macrop