Chronic Obstructive

Pulmonary Disease

NATIONAL UNIVERSITY
College of Allied of Health
Department of Pharmacy

Presented by:

Mamon, Mawia
Bevera, Venus Polatrix G.
Cruz, Mark John A.
Case

History of Present Illness:

A 65 year-old male was brought to the hospital because of dyspnea.

His condition started 4 years ago with a cough that is usually worse in the morning. The
cough was productive of white to sometimes yellowish sputum. His cough usually lasts for
weeks but usually goes away on its own. He did not seek consult because he thought that this
was just an allergic cough as this recurs every year so he just drinks a glass of water in the
morning in an attempt to relieve this. Three months ago, he started to experience occasional
shortness of breath and worsening of cough. He also noticed that it is easier for him to inhale
than to exhale. He self-medicated with Robitussin because he thought that he was just having a
usual cough. His condition even progressed that about a week ago, he already finds it tiring to
walk short distances because he easily experiences shortness of breath. When looked at himself
at the mirror, he noticed significant weight loss and muscle wasting.

On physical examination, the patient was noted to be tachypneic (RR= 28) with
prolonged expiration. His chest was noticed to be wide like a barrel. Wheezing and crackles were
heard on auscultation which become less after coughing. Chest X-ray was requested revealing
hyperlucent lungs and flattened diaphragm.

Past Medical History:

- No known chronic diseases
- No bronchial asthma
- No allergies
- No previous surgical operations and hospitalization
- Immunization is unknown

Family History:
- Both parents have HTN, both are deceased
- No history of cancer or any pulmonary disease

Social History:
- 40 pack-years
- Non-alcoholic beverage drinker
 Table of Contents

Case of the Patient…………………………………………………………………

Chronic Obstructive Pulmonary Disease as a Disease…………………………….

Information Relevant to the Case………………………………………………….

Concept Map………………………………………………………………………

Treatment Options…………………………………………………………………
Chronic Obstructive Pulmonary Disease as Disease

COPD has both pulmonary and systemic component; chronic inflammation of the
airways, lung tissue and pulmonary blood vessels as result of exposure to inhaled irritants such
as tobacco smoke. The more a person smokes, the more likely that person will develop COPD.
This is frequently related to cigarette smoking and mainly involves two related diseases chronic
bronchitis and emphysema. Both are frequently present and cause chronic obstruction of airflow
and obstruction of the lungs. The obstruction is generally permanent and progresses (becomes
worse) over time. There are two main forms of COPD:

The Chronic Bronchitis is defined as a cough that occurs every day with sputum
production that lasts for at least 3 months, 2 years in a row. Includes an inflammatory
mononuclear cell infiltrate in the airway wall and a neutrophil influx into the airway lumen. The
molecular events that produce the inflammation and its pathogenetic role in causing mucus
hypersecretion are beginning to be elucidated. Bronchitis is an inflammation of the bronchial
tubes, the airways that carry air to your lungs. It causes a cough that often brings up mucus. It
can also cause shortness of breath, wheezing, a low fever, and chest tightness. There are two
main types of bronchitis: acute and chronic. Chronic bronchitis is one type of COPD (chronic
obstructive pulmonary disease). The inflamed bronchial tubes produce a lot of mucus. This leads
to coughing and difficulty breathing. Cigarette smoking is the most common cause. Breathing in
air pollution, fumes, or dust over a long period of time may also cause it.

Signs and Symptoms:

 Cough
 Production of mucus (sputum) yellowish, it may be streaked with blood.
 Fatigue
 Shortness of breath
 Slight fever and chills
 Chest discomfort

Emphysema is defined as an abnormal permanent enlargement of air spaces distal to

the terminal bronchioles, accompanied by the destruction of alveolar walls and without obvious
fibrosis. It is used interchangeably with chronic obstructive pulmonary disease, or COPD. In
emphysema, the lungs are over-inflated so that they lose their elasticity and elastic recoil. There
are balloon-like bullae or blisters in the lung tissues. Because carbon dioxide is trapped in the
bullae, the body is deprived of fresh air flowing into the lungs.

You get emphysema when the linings of the tiny air sacs in your lungs become damaged beyond
repair. Over time, your lung damage gets worse.
 The fragile tissues between air sacs are destroyed and air pockets form in the lungs.
 Air gets trapped in these pouches of damaged tissue.
 The lungs slowly get larger, and you find it harder to breathe.

Signs and Symptoms:

 Mild to severe
 Shortness of breath (dyspnea)
 Cough
 Difficulty of breathing
Information Relevant to the Case

Pertinent Positives:

60 year old
Male
40 pack-years
Worsening of cough
Prolonged expiration
Shortness of breath
Weight loss
Muscle wasting
Barrel chest
Wheezing and Crackles
Hyperlucent lungs
Flattened diaphragm

Pertinent Negative:

No allergies
No known chronic disease
No bronchial asthma
No family history of cancer or any pulmonary disease
Narration of Concept Map:

The Toxins in Tobacco Smoke will lead to elastic fiber breakdown and
The Elastic in connective tissue in the lungs will decrease. Leads to decrease
of the Alveolar Recoil and it will cause Air trapping, that increases end
respiratory volume and because of that the lungs is hyperinflated that’s why
you have Flattened Diaphragm and Hyperlucent lung in Chest X-ray.
Hyperinflated lungs will caused widening of Antero Posterior diameter width
that’s why you have Barrel Chest. Toxins in Tobacco Smoke will damage the
air sacs because of that the surface area for gas exchange decreases. So, it
increases need for CO2 leads to Pro-longed Expiration. The decrease in
surface area for gas exchange the 02 decreases and it stimulates Muscles of
Respiration that increases the Respiratory Rate leads to Tachypnea. Because
of the decrease in 02 it will decrease the blood flow to multiple body parts
that buildup of metabolites and it increase the Metabolism leading to weight
loss. Decrease in 02 also resulting in decrease of 02 ending muscles so that
the muscle will be weaken leading to Muscle Wasting. Toxins in tobacco will
damage the ciliated epithelium lining causing paralysis or dead cilia because
of that Mucociliary clearance will decrease lead to accumulation to mucus
and irritants that stimulate cough reflex that’s why you have productive
cough. Toxin in Tobacco Smoke can cause inflammation due to irritants to
smooth muscle leads to obstruction of smooth muscle leading to
bronchoconstriction that can cause narrowing airways so that the patient
experience Progressive dyspnea and Wheezes. And also, inflammation due to
irritants that can cause enlargement of mucus gland in the lining of smooth
muscle that can cause increase in goblet cell secretion that leads excessive
mucus production, so it leads also to accumulation to mucus and irritants that
stimulates cough reflex so that the patient experience productive cough.
Excessive mucus production can result in fluid and air interaction leading to
Crackles.
Treatment Options:

 Steroids
 Anti-Inflammatory Drugs
 Bronchodilators
 Oxygen Therapy