Pathophysiology & Clinical Findings of the Disease
1. Are the spirometry results consistent with an obstructive or restrictive pulmonary
disease? What
... [Show More] is the most likely pulmonary diagnosis for this patient?
In this case study for week 3, I believe the patient has an obstructive pulmonary
disease. The patient's FVC (Forced Vital Capacity) and FEV1 (Forced Expiratory Volume
in 1 second) ratio is 56%, less than the normal pulmonary function of 80% (Langan &
Goodbred, 2020, p. 365). The patient's FVC also remained normal, suggesting an
obstructive defect (Langan & Goobred, 2020, p. 365). I think the patient is suffering
from COPD.
2. Explain the pathophysiology associated with the chosen pulmonary disease.
I believe the patient has Chronic Obstructive Pulmonary Disease. COPD can have
two types of clinical manifestations. Chronic Bronchitis is an example defined as an
elevated secretion of mucus and chronic productive cough for at least three months of the
year for at least two years (Huether & McCance, 2017, p. 701). Huether & McCance state
that inhaled irritants result in inflammation with infiltration of neutrophils, macrophages,
and lymphocytes into the bronchial wall (2017, p. 701). Continual inflammation will lead
to bronchial edema with an increase in mucous glands and goblet cells, leading to an
increase in thick tenacious mucus that is not merely cleared because of impaired ciliary
function (Heuther & McCance, 2017, p.701). The lung's defenses are compromised,
which leads to increased susceptibility to infection, and damaged airways complicated by
bronchospasms (Huether & McCance, 2017, p. 701). Increased mucous production leads
to obstruction, ventilation-perfusion mismatch, hypoxemia, and air trapping (Huether &
McCance, 2017, p.701).
Another manifestation of COPD is Emphysema. Huether and McCance define
emphysema as an abnormal permanent enlargement of gas-exchange airways
accompanied by the destruction of alveolar walls without prominent fibrosis (2017, p.
701). According to Huether and McCance, emphysema is characterized by the collapse of
alveoli through elastin breakdown within the septa by an imbalance between proteases
and antiproteases, oxidative stress, and apoptosis of lung structural cells (2017, p. 702).
Alveolar destruction produces large air spaces within the lung parenchyma (bullae) and
air spaces adjacent to pleurae (blebs), which are neither effective in gas exchange
(Huether & McCance, 2017, p. 702). Huether and McCance state the expiration becomes
more difficult because of loss of elastic recoil reduces the volume of air that can be
expired passively, and the air is trapped in the lungs (2017, p. 702). Air trapping will
cause hyperexpansion of the chest, causing a barrel-like appearance over time. According
to Huether and McCance, the destruction of alveolar walls and pulmonary capillaries
causes pulmonary artery hypertension and cor pulmonale (2017, p.702). [Show Less]