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COPD Case Study

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COPD Case Study

Introduction

Chronic and obstructive pulmonary disease is a common condition in the respiratory

system that is incurable but highly preventable and manageable, both pharmacologically and

non-pharmacologically. COPD includes permanent damage to the lungs, crusading

breathlessness, wheezing, coughing, and sputum production. Early discovery of the disease

offers patients symptom-relieving treatments that enhance their life quality. COPD is

characterized by airflow blockage and an inflammatory response to the lungs. The answer is

caused by prolonged exposure to foreign particles and gases, especially cigarette smoke. COPD

is common to smokers and individuals over the age of 40. The disease's prevalence increases

with age and is ranked the third cause of morbidity and mortality globally. In 2015, COPD had a

prevalence of 174 million and caused about 3.2 million deaths worldwide. COPD is common in

adulthood and the winter months. COPD is suspected and assessed in patients with the relevant

symptoms and risk factors.

Pathophysiology

COPD occurs from the critical processes of airway inflammation and narrowing. The

abnormal response stimulated after inhaling toxic agents leads to hypersecretion (chronic

bronchitis), airflow inflammation (asthma), and tissue damages (emphysema). Mucous

hypersecretion leads to a chronic productive cough. Chronic bronchitis is not necessarily linked

to an airflow blockage, and not all patients with COPD experience symptomatic mucous

hypersecretion (Madison & Irwin, 2020). The hypersecretion is caused by squamous metaplasia,

additional goblet cells, and the enlarged size of the bronchial submucosal glands as a response to

the chronic irritation by foreign particles and gases. Ciliary dysfunction results from squamous
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metaplasia of the epithelial cells and leads to abnormal mucociliary escalator and difficulties in

breathing.

Airflow obstruction occurs in the small airways that are less than 2mm in diameter.

Notably, this is due to the inflammation and airway reformation, and inflammatory excretions in

the small tracheas. Additional factors are loss of lung elasticity which results from damage of the

alveolar walls, and deterioration of the alveolar support, which is offered by the alveolar

attachments (Owen et al., 2017). Airway obstruction holds air during exhalation leading to

hyperinflation during the exercises. Hyperinflation decreases the aspiratory capacity, hence the

resulting residual power in the movement. These conditions result in breathlessness and reduced

exercises capacity. The airflow obstruction was examined by spirometry.

Emphysema develops in the late stages of COPD during severe gas exchange abnormalities and

leads to the destruction of the lung tissues. The damage leads to the rupture of alveoli creating

big air pockets. The leading factors include pulmonary arterial reduction caused by hypoxia,

change of the pulmonary arteries, damage of pulmonary capillary layer, and endothelial

dysfunction (Jonatahan et al., 2019). Pulmonary arterioles change structurally, resulting in

persistent hypertension, dysfunction, and enlargement of the pulmonale. The constriction makes

breathing difficult since it hinders the oxygen from moving through the bloodstream.

Objective and Subjective Data Analysis

Objective Data

Nancy had a temperature of 38.30C, which indicates she had a fever. The fever in Nancy

is a sign of respiratory infection like chronic bronchitis and pneumonia, which is the

inflammation of alveoli. Chronic bronchitis occurs due to the hypersecretion of mucus by the

goblet cells, and the epithelial cells in the airway respond to the infection by releasing the
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inflammatory exudates. The immune response leads to prolonged hyperreactivity. B.

pertussis expression of toxins in the airway leads to fever through a response of the body to the

reaction of bacteria (Zhao et al., 2018).

Nancy had an oxygen saturation rate of 88% and 90%, which is abnormal. COPD causes

changes in the lung structures, which affect a patient's breathing. Damage to the lung tissues

(emphysema) limits the alveoli from getting sufficient oxygen, a situation referred to as alveolar

hypoxia. Hypoxia initiates a chain reaction that results in low oxygen in the blood; thus, the

oxygen saturation level is below 95. Once the patient exhales, the damaged alveoli fill to work

correctly, and the old air gets trapped, limiting room for fresh oxygen to circulate (Brat et al.,

2018).

The patient had elevated blood pressure of 148/78 and 140/80. High blood pressure is a

result of pulmonary hypertension. The leading factors for pulmonary hypertension are

remodeling of arteries, vasoconstriction, and thrombosis of pulmonary arteries. The

physiological effects of these obstructions are partial blockage of the small pulmonary arteries

resulting in increased blood pressure (Brat et al., 2018). COPD also leads to gas exchange

abnormalities in advanced stages and is characterized by hypoxemia leading to limited oxygen

inhalation and carbon dioxide exhalation. Notably, this shows a fall in blood oxygen levels, and

the arteries narrow, thus increasing blood pressure.

Nancy had an elevated heart rate of 169 and 95. The high heart rate during exercises and

rests is due to the damage of the nerve fibres by the COPD. COPD leads to low blood oxygen

levels, which cause narrowed arteries band, thus higher blood pressure in the arteries that run

from the heart and lungs. Notably, this stresses the heart and makes it beat harder than in normal
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conditions. The right side of the heart may also undergo dysfunctionally and enlargement

causing changes in the pulmonary arterioles, thus elevated and irregular heartbeats in the patient.

Nancy showed an elevated respiratory rate of 27 and 25 upon physical examination. COPD

infection causes the airways to trap air during the exhalation process due to the airflow

obstruction. The blockage causes inflammation of the airway, and the lung alveoli are destroyed.

The running of air and outside the lungs reduces. The oxygen getting into the body becomes

limited and complicated to exhale the carbon dioxide out of the respiratory tissues. Notably, this

causes shortness of breath which in turn leads to tachypnea (elevated respiration rate).

Subjective Data

Nancy complains of a painful cough to the nurses. The cough is a result of mucous hype

secretion (Song & Chung, 2020). The hypersecretion is caused by the squamous metaphases,

additional goblet cells, and enlarged bronchial submucosal glands due to the irritation of foreign

gases and particles. COPD leads to mucus hypersecretion in the lungs and leads to frequent

coughing to clear the mucus from the lung's surface. Nancy talks of a lack of appetite after

admission. Emphysema theta develops in the later stages of COPD damages the lung alveoli

causing the lungs to have complications in taking oxygen and exhaling carbon dioxide. The lung

tissue damage expands the lung Colum e in size, hence flattening the diaphragm, which reduces

the amount of space between the lungs and stomach (Seronsen et al., 2020). Once this occurs, the

lungs and stomach push against each other, causing discomfort while eating, thus loss of

appetite.

Nancy also complained of sleeplessness during the admission. Sleepiness occurs in

COPD patients due to the obstructions in both gas exchange and ventilation during sleep. COPD

damages the lung alveoli causing hypoxemia in patients with COPD. The respiratory
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insufficiencies result in enlarged physiological dead space in COPD, which causes a more

significant reduction in alveolar ventilation with low tidal volumes than healthy persons. Most

patients experience hypoxemia while awake, and they are likely to have nocturnal oxygen

desaturation due to lying on the steep part of the oxyhemoglobin dissociation curve. Nocturnal

oxygen desaturation in COPD patients damages the sleep quality since they experience the

desaturation either during the day or night, causing sleep apnea during the day or night (Vukoja

et al., 2018). The nocturnal cough might obstruct sleep in COPD patients, causing sleepiness.

Nancy had audible wheezing and complained of tiredness on her second day in the hospital.

COPD leads to airflow obstruction due to the inflammation and narrowing of the airways. Once

the patient exhales, the air is forced through the obstructed airway and traps air, causing a

whistling sound (wheezing). COPD causes abnormal gas exchange abnormalities, which are

characterized by arterial hypoxemia. A peculiar exchange of gases occurs due to the abnormal

ventilation flow, which is caused by the anatomical changes in COPD patients. Abnormal gas

exchanges make it hard for COPD patients to inhale oxygen and exhale carbon dioxide in the

lungs. The shortage of oxygen and accumulation of carbon dioxide leads to tiredness.

Pharmacological Management

The doctor prescribed 250mg of amoxicillin. Amoxicillin is an antibiotic and plays a vital

role in reducing exacerbations. Exacerbations can be a result of bacterial or viral infections.

Antibiotics help fight respiratory infections like acute bronchitis, which is part of COPD (Basgge

et al., 2021). Acute bronchitis is the first stage of COPD caused by bacteria B.pertusis; thus,

amoxicillin is prescribed to fight acute bronchitis exacerbation. In addition to the antibacterial

effects, amoxicillin has anti-inflammatory effects that fight airway inflammation, which is likely

to contribute to COPD management.

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The doctor also administered 5mg of perindopril dosage. Perindopril is highly effective in

reducing diastolic and systolic pressure (Calencea et al., 2020). COPD develops pulmonary

hyperextension at the late stages of the condition. Pulmonary hypertension is associated with

partial blockage of pulmonary arterioles leading to high blood pressure. Perindopril was used to

stimulate smooth blood flow by preventing the remodeling of pulmonary arterioles, which

tighten the blood vessels, lowering the blood pressure in COPD patients. 40 mg of furosemide

was prescribed to correct the abnormal gas exchange abnormalities (Fernandes et al., 2017).

Furosemide causes metabolic alkalosis, a diminished chemoreceptor that leads to decreased

alveolar ventilation in COPD patients.

The doctor administered 10mg of Metoclopramide to control in the patient. The patient

was suffering from nausea due to the chronic cough. Metoclopramide works by stopping the

signaling between the CTZ and the vomiting centre. This blocks the substance dopamine and

reduces the feeling of nausea and vomiting. The medical officer also offered panadol oste to

control osteoarthritis. Osteoarthritis is a comorbidity of COPD that causes chronic pain in COPD

patients. Panadol oste will relive chronic pain for about eight hours by inhibiting prostaglandin in

the central nervous system.

The medical officer prescribed 100mg of coloxyl for constipation. COPD causes

inflammation of the respiratory lung tissues. The inflammation directly leads to inflammation of

digestive tract hence abdominal distention and constipation. Coloxy contains poloxamer which

draws water into the stool, making it soft and easy to pass; thus relieving constipation.

The officer also prescribed 18 mcg of spirivia for treatment of COPD exacerbations.

Spirivia will help treat bronchopasm and dyspnea which occur due to the narrowing and

obstruction of airflow in COPD patients. Spirvia relaxes airways’ muscles and improves air flow
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to the lungs. Additionally, the medical officer prescribed 500mcg of ipratopium to treat

respiratory obstruction. Ipratopium prevents, wheezing, coughing and shortness of breathe in

COPD patients. Ipratopium would control airflow obstruction in Nancy by relaxing and opening

the airflow to make inhalation and exhalation easier. To make the breathing easier the doctor also

prescribed 5mg of salbutamol. Sulbutamol functions by relaxing air flow muscles in the lungs.

The drug would help Nancy by relieving symptoms such as coughing and wheezing.

The medical officer prescribed 40mg of prednisolone to treat respiratory inflammation.

COPD is characterized by lung inflammation of the lung tissues and cells. The drug would help

reducing inflammation in the lungs by the amount of inflammatory compounds in the lungs.

Conclusion

Although COPD is incurable, it is highly treatable and manageable. The medical officer

prescribes drugs that will control each symptom that Nancy is experiencing. The main

underlying causes for Nancy’s symptoms and signs are to hypersecretion, airflow inflammation

and tissue damages. Inflammation of the airflow and tissue damages contributed to high blood

pressure , elevated heart and oxygen saturation levels in Nancy. Hypersecretion contributed to

coughing and pain. The drugs prescribed were meant to correct all this symptoms to manage the

COPD condition in Nancy.

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