Pathophysiology of Pneumonia

Pneumonia is a common pulmonary parenchyma infection which currently ranks high as a leading cause of hospitalization in the United States. According to Kasper et al. (2018), it is classified into community-acquired (CAP), ventilator-associated (VAP), hospital-acquired (HAP) and care-associated (HCAP) pneumonia categories. Specific fungi, bacteria and viruses are all capable of causing pneumonia whose onset is marked by septicity in lung alveoli. A typical mode of infection is the inhalation of these airborne microbes, although self-infection can also occur in healthy individuals.

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For instance, Hemophilus influenzae and pneumococcus are bacteria residing in the human airway, where they commonly proceed to cause community-acquired (CAP) pneumonia. However, it is essential to recognize that low immunity is a predisposing factor for pneumonia infections.  The opportunistic microbes mentioned above have been known to affect such individuals since weak immune cells allow them to grow unabated within the alveoli. Pneumonia aggravates the lungs’ air sacs by filling them with pus, which signals the inception of the symptomatic stage (Alpers, 2014, p. 4).

As a result, persons infected with pneumonia cough excessively and may produce blood-stained mucus. Shaking chills also become common and are occasioned by shallow breathing. Persons with pneumonia may also experience sharp chest pains that are further exacerbated by their coughing. Furthermore, those infected experience intermittent confusion and bouts of nausea. Several diagnostic studies can be conducted if a physician presumes pneumonia as the cause of the symptoms cited. A chest x-ray can aid in diagnosing pneumonia since it allows the physician to pinpoint the location of the infection. Doctors also recommend a sputum test which is then analyzed to determine the microbes responsible for causing pneumonia.  

Additionally, blood tests are also critical when seeking to diagnose pneumonia. The underlying pathophysiological process triggering the symptoms is as a result of the immune system’s reaction in the lungs. Lung capillaries become sieve-like, allowing fluid mucus to ooze into the air sacs. As a result, the overall surface area for an oxygen-carbon dioxide interchange reduces, resulting in faster shallow breathing in patients.

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