Pathophysiology of Chronic Obstructive Pulmonary Disease

COPD 1
PATHOPHYSIOLOGY OF CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
Name:
Institutional affiliation:

COPD 2
DAY ONE
Audrey is diagnosed with chronic obstructive disease. According to (National Health
Institute,2014) the guidelines provided indicate Audrey is most likely to have chronic bronchitis
or emphysema. Audrey might be suffering from chronic bronchitis since she has severe dyspnea,
coughs a lot and excess mucus production. Audrey might also be suffering from emphysema
which is characterized by barrel chest due to the hyperinflation of the lungs, dyspnea and a high
respiratory rate.
PATHOPHYSIOLOGY LINKS WITH CLINICAL FEATURES
Pathophysiology of chronic bronchitis majorly involves inflammation of the airway due to
irritants, excess mucus production which further worsens the airway flow. According to
(Hogg,2014) chronic bronchitis results due to inflammation of the airway due to irritation mostly
by the chemicals in cigarettes. This leads to an increase in goblet cells which secrete mucus and a
decrease in ciliary action hence stasis of mucus. The bronchial walls are filled with mucus
further decreasing the airway flow. The alveoli in the bronchioles have undergone fibrosis and
the macrophages which play a role in phagocytosis of foreign material are unable to function.
This increases the chance of infection as defense mechanism are compromised. Audrey has a
history of smoking. Smoking is a risk factor in chronic bronchitis. The excess mucus production
is due to the inflammation of the airway. The coughing is a reflex to get rid of the secretions
while the high respiratory rate is a compensatory mechanism of excreting accumulating carbon
(IV)oxide.
Pathophysiology of emphysema involves hyperinflation and damage to the alveoli. According to
(Hinkle and Cheever,2013) emphysema is as a result of alveolar hyperinflation hence the alveoli

COPD 3
are damaged mostly due to smoking. This causes decreased air exchange as there is less surface
area in contact with pulmonary capillaries. The accumulation of carbon (IV)oxide leads to
respiratory acidosis. The expiration is forceful, the rib joints are fixed and chest is rigid hence
barrel chest. Audrey presents with a barrel chest, high respiratory rate due to hypercapnia,
labored breathing due to low levels of oxygen saturation and constant fatigue.
RESPIRATORY COMPENSATION
Audrey attempts to compensate for the imbalance in physiological state by hyperventilation and
hyperinflation. (Stephen, Mauricio and Atul,2013) states that in chronic obstructive disease
hyperinflation is necessary in maintaining perfusion severe airflow limitation hence the
formation of barrel chest in Audrey’s case. Also, tachypnea demonstrated by respiratory rate of
32 breaths per minute increases lung elasticity. The compensatory mechanism is due to the rising
levels of retained carbon (IV)oxide which changes plasma Ph then triggers the respiratory center
in the medulla to increase the respiratory rate. The rate is increased to eliminate the carbon
(IV)oxide and increase the oxygen levels in the blood.
RISK FOR RESPIRATORY INFECTION
Audrey is at a high risk of suffering from respiratory infection because her primary defense
mechanisms have been altered in the disease process. (Sethi,2013, p.1210) states that patients
with chronic obstructive pulmonary disease have increased frequency of acquiring lower
respiratory tract infections both viral and bacterial. Audrey being a heavy smoker, the
tracheobronchial tree is disrupted as there is slowed ciliary activity, increased mucus secretions,
therefore, microbial agents are able to attack. Macrophages which phagocytose foreign agents
are decreased hence a higher risk of infections. Smokers are at a greater risk of infections

COPD 4
compared to nonsmokers (Einarsson et al.,2016). The immune defense mechanisms in
nonsmokers such as increased ciliary activity is efficient compared to that of smokers hence
Audrey is at a high risk of contracting a respiratory infection.
PULMONARY EMBOLISM
Audrey is constantly tired and has labored breathing which means she is unable to conduct
activities of daily living hence immobile. Long states of immobility increase the chances of
pulmonary embolism. Audrey is overweight at 110 kilograms which increases risk of pulmonary
embolism. (Akpinar et al.,2014, p.44) states that patients with chronic obstructive pulmonary
disease who are immobile and obese were more likely to have pulmonary embolism. This is
attributed to poor blood circulation hence stasis leading to clot formation. Proper management
includes fitting Audrey with deep venous thrombosis stockings since most clots form from the
lower extremities. Audrey’s medication includes anticoagulants which counter any clots that may
have formed. Audrey should be taught how to perform leg exercises to encourage blood
circulation.
DAY TWO
MUSCULOSKELETAL CONDITIONS
Audrey has a body mass index of 40.4 which is obesity grade three according to (Australian
Heart Foundation,2018). (Cielen, Maes and Gayan-Ramirez,2014) states that osteoporosis is a
comorbidity in patients suffering from chronic obstructive pulmonary disease. This is majorly
because of decreased bone mineral density which causes pathological fractures such as in
Audrey’s case. Osteoporosis progresses to fractures, therefore, increasing the stay of