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Help needed with pathophysiology
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Patricia was called at work by a woman at the local day care center. She told Patricia to come and pick up her son because he was not feeling well. Her son, 3½- year-old Marshall, had been feeling tired and achy when he woke up. While at day care, his cheeks had become red, and he was warm to touch. He did not want to play with his friends, and by the time Patricia arrived, he was crying. Later that afternoon, Marshall’s condition worsened. He had fever, chills, a sore throat, runny nose, and a dry hacking cough. Suspecting Marshall had influenza, Patricia wrapped him up and took him to the community health care clinic.
1. Why did Marshall’s presentation lead Patricia to think he had influenza and not a cold? Why is it important to medically evaluate and diagnose a potential influenza infection? 1. Marshall's rapid symptom onset, particularly malaise, suggests influenza rather than the common cold, which typically presents less aggressively. A medical evaluation is crucial to prevent inappropriate antibiotic use, as these are ineffective against influenza.
The influenza A virus damages the epithelial cells of the respiratory tract. They undergo necrosis and shed away to leave gaps between underlying basal cells. Extracellular fluid escapes through the basal membrane and contributes to fluid accumulation in the respiratory passages. Damaged ciliated cells are unable to move mucous within the airways, so mucous accumulation and congestion become an additional component to the infection. Surface antigen HA facilitates the movement of the influenza A virus into the epithelial cells of the respiratory tract. The NA glycoprotein promotes viral replication and release from the host cell. Viruses damage the protective mucous membranes in the nasopharynx. Because they also encourage mucous secretions, macrophage activity on pneumococci is inhibited while bacterial adhesion to the epithelium is enhanced. Pneumonia is a condition that causes inflammation of the alveoli. Cyanosis occurs as a result of the decrease in gas exchange through the inflamed alveolar membrane and subsequent decline in hemoglobin saturation.