Chronic obstructive pulmonary disease (COPD) refers to two lung diseases, chronic bronchitis and emphysema, that are typically caused by smoking. In COPD, airflow to the lungs is limited by inflammation and damage to airways and lung tissue. Symptoms include cough, sputum production, wheezing, shortness of breath, and weight loss. Treatment focuses on smoking cessation, bronchodilators, oxygen therapy, and managing exacerbations. Nursing care aims to improve ventilation and gas exchange, manage anxiety, and ensure effective airway clearance and rest.

1. Mr. Yahye Sheikh Abdulle
Msc Nursing 1st year
Kle college of Nursing
Chronic obstructive
pulmonary diseases

2. Chronic obstructive pulmonary
diseases
COPD is also known as chronic obstructive
lung disease (COLD), chronic obstructive
airway disease (COAD), chronic airflow
limitation (CAL) and chronic obstructive
respiratory disease (CORD)
Chronic obstructive pulmonary disease
(COPD) refers to chronic bronchitis and
emphysema, a pair of two commonly co-
existing diseases of the lungs in which the
airways become narrowed.

3. This leads to a limitation of the flow of air to and from the
lungs causing shortness of breath.

4. In COPD, less air flows in and out of the
airways because of one or more of the
following:
 The airways and air sacs lose their elastic
quality.
 The walls between many of the air sacs are
destroyed.
 The walls of the airways become thick and
inflamed.
 The airways make more mucus than usual,
which tends to clog them.

6. Incidence
 It is the 4th leading cause of mortality
and 12th leading cause of disability in the
united states.
 In 2020 COPD is the 3rd leading cause
of death.

7. CAUSES
Smoking. Smoking is primary risk factors for
COPD. The numerous irritants found in cigarette
smoke stimulate excess mucus production and
coughing, destroy ciliary function and lead to
inflammation and damage of bronchiolar and
alveolar walls.

9. Air pollution high levels of urban air
pollution are harmful to persons with
existing lung disease. However, the
effect of outdoor air pollution as a risk
factor for COPD. Another risk factor
for COPD development is fossil fuels
that used for indoor heating and
cooking.

10. Occupational exposures- exposure
to workplace dusts found in coal
mining, gold mining, and the cotton
textile industry and chemicals such as
cadmium, and fumes from welding
have been implicated in the
development of airflow obstruction.
Exposure of these irritants causes the
airway to be hyper responsive.

11. Infection :infections is risk factor for
developing COPD. Severe recurring
respiratory tract infection in childhood
have been associated with reduced
lung function and increased
respiratory symptoms in adulthood.
Recurring infections impair normal
defense mechanisms, making
bronchioles and alveoli more
susceptible to injury.

12.  Genetics-Alpha 1-antitrypsin deficiency
is a genetic condition that is responsible for
about 2% of cases of COPD. In this
condition, the body does not make enough
of a protein, alpha 1-antitrypsin. Alpha 1-
antitrypsin protects the lungs from damage
caused by protease enzymes, such as
elastase and trypsin, that can be released
as a result of an inflammatory response to
tobacco smoke

13. RISK FACTORS FOR COPD

14. Pathophysiology

15. pathophysiology
COPD is characterized by airflow limitation that
is poorly reversible. chronic exposure to
cigarette smoking is the number one cause of
the disease, but repeated exposure to
secondhand smoke, air pollution and
occupational exposure (to coal, cotton, grain)
are also important risk factors.

16. Smoking and other airway irritants cause
neutrophils, T-lymphocytes, and other
inflammatory cells to accumulate in the
airways. Once activated, they trigger an
inflammatory response in which an influx of
molecules, known as inflammatory
mediators, navigate to the site in an
attempt to destroy and remove inhaled
foreign debris.

17. Under normal circumstances, the
inflammatory response is useful and leads
to healing. In fact, without it, the body
would never recover from injury. In COPD,
repeated exposure to airway irritants
perpetuates an ongoing inflammatory
response that never seems to shut itself
off. Over time, this process causes
structural and physiological lung changes
that get progressively worse.

18. As inflammation continues, the airways
constrict, becoming excessively narrow
and swollen. This leads to excess mucus
production and poorly functioning cilia, a
combination that makes airway clearance
especially difficult. When people with
COPD cannot clear their secretions, they
develop the hallmark symptoms of COPD,
including a chronic, productive cough,
wheezing and dyspnea.

19. Finally, the build-up of mucus attracts a host of
bacteria that thrive and multiply in the warm, moist
environment of the airway and lungs.
The end result is further inflammation, the formation of
diverticula in the bronchial tree, and bacterial lung
infection, a common cause of COPD exacerbation.

20. CLINICAL FEATURES
 Chronic cough
 Sputum production
 Wheezing
 Chest tightness
 Dyspnoea on exertion
 Wt.loss
 Respiratory insufficiency
 Respiratory infections
 Barrel chest- chronic hyperinflation leads to
loss of lung elasticity.

21. Bronchitis
 Bronchitis results from inflammation of bronchi
leading to increased musus production, cough
and eventual scaring of the bronchial lining.
 acute (short term) Infections or lung irritants
cause acute bronchitis.
 chronic is an ongoing, serious condition. It
occurs if the lining of the bronchial tubes is
constantly irritated and inflamed, causing a
long-term cough with mucus
 It is defined as the presence of cough and
sputum production for atleast 3 months.

22. Chronic bronchitis is characterized by
the following :
 A increased in size and number of
submucus glands in the large bronchi,
which increase mucus production.
 An increased number of goblet cells which
also secrete mucus.
 Impaired cillary function which reduce
mucus clearance.

24. PATHOPHYSOPLOGY
 Irritants irrritate the airway
 Excess mucus production
 Inflammation
 Cause the mucus secreting glands and goblet cells to
increase in number.
 Ciliary function is reduced

25.  More mucus production
 Bronchial walls become thickened and lumen
narrows and mucus plug the airway
 Alveoli adjacent tto the bronchioles may become
damaged and fibrosed.
 Alter function of alveolar macrophages.
 Infection

26. Signs and symptoms-Acute
 sore throat,
 fatigue (tiredness),
 fever, body aches,
 stuffy or runny nose,
 vomiting, and
 Diarrhea
 persistent cough
 cough may produce clear mucus
 shortness of breath

27. Chronic symptoms
 coughing,
 wheezing, and
 chest discomfort.
 The coughing may produce large amounts of
mucus. This type of cough often is called a
smoker's cough.

28. EMPHYSEMA
Definition:-
Emphysema is defined as enlargement of
the air spaces distal to the terminal
bronchioles, with destruction of their walls
of the alveoli.
As the alveoli are destroyed the alveolar
surface area in contact with the capillaries
decreases.
Causing dead spaces (no gas exchange
takes place) Leads to hypoxia.

29. In later stages:
CO2 elimination is disturbed and increase in CO2
tension in arterial blood causing respiratory
acidosis

30. There are three types of emphysema
1. Centriacinar
2. Panacinar
3. Paraseptal

31. Centriacinar(centrilobular) emphysema the most
common type produce destruction in bronchioles
usually in the upper lung region. Inflammation
begins in the bronchioles and spread peripherally
but usually the alveolar sac remains intact. This
form of emphysema occurs most often in
smokers.

32. Panicar emphysema destroys the entire
alveolus and most commonly involves the
lower portion of the lung. This form of
disease is generally observed in
individuals with ATT deficiency.

33. Paraseptal or distal acinar emphysema primarily
involves the distal airway structures alveolar
ducts and alveolar sacs. The process is localized
around the septa of the lung or pleura. It is
believed to be the likely cause of spontaneous
pneumothorax

34. DIAGNOSIS
Blood Test
Blood tests can help determine if symptoms are
being caused by an infection.
An arterial blood gas test will measure the
amount of oxygen in blood. This is one
indication of how well lungs are working. This
can help doctor determine how severe COPD
is and whether need oxygen therapy.

35. . Chest X-ray or CT scan
A CT scan is a type of X-ray that creates a more
detailed image than a standard X-ray. Whichever
type doctor chooses, an X-ray will give a picture
of the structures inside chest. These include your
heart, lungs, and blood vessels. Your doctor will
be able to see if client has evidence of COPD. If
symptoms are being caused by another condition
such as heart failure, the doctor will be able
identify that as well

36. Sputum Examination
Doctor may order a sputum examination,
especially if the client has a productive cough.
Sputum is the mucus the client cough up.
Analyzing sputum can help identify the cause
of breathing difficulties and may rule out some
lung cancers. If there is a bacterial infection,
it can be identified and treated.
ECG
The doctor might request an ECG to determine
if your shortness of breath is being caused by
a heart condition.

37. Pulmonary Function Test
 pulmonary function tests (PFTs) measure
how well the lungs are moving air in and
out. They also measure how well the lungs
are moving oxygen to the blood.
 Spirometry (meaning the measuring of
breath) is the most common of the
pulmonary function tests (PFTs). It
measures lung function, specifically the
amount (volume) and/or speed (flow) of air
that can be inhaled and exhaled.

39. MANAGEMENT
MEDICAL MANAGEMENT
SURGICAL MANAGEMENT
NURSING MANAGEMENT

40. MEDICAL MANAGEMENT
The treatment goal for the client with COPD
are:
To improve ventilation
To facilitate the removal of bronchial
secretions
To promote health maintenance
To reduce complications, and
To slow progression of the disease

41. Smoking cessation
Cessation of cigarette smoking is single
most effective and cost effective
intervention to reduce the risk of
developing COPD and stop the
progression of the disease. After
discontinuation of smoking, the
accelerated decline in pulmonary function
slows and pulmonary function usually
improves.

42. Drug therapy
Medications for COPD:
Reduce symptoms
Increase the capacity of exercise,
Improve overall health and
Reduce the severity of exacerbations.

43. Bronchiodilator drug therapy are agents
that widen the air passages by relaxing the
bronchial smooth muscle and improve the
ventilation of lungs. They are usually
administered via inhalation route but in
rare occasions may be given orally or
administered intravenously. Regular
treatment with long acting bronchiodilators
is more effective and convenient than
treatment with short acting forms.

44. The principal bronchiodilator treatment are Beta2
agonists, anticholinergics, and
methylxanthines used singly or combination.
The choice of bronchioldilators depends on
availability and patient’s response.
Beta2 agonists are sympathomimetic drugs that
acts on the beta-adrenoceptors in the smooth
muscles of the airway and cause
bronchioldilation. These drugs may also enhance
mucus clearance and improve the endurance of
respiratory muscles.

45.  Short acting Beta2 agonists(e.g., albuterol)have
minimal adverse effects with rapid onset of
action, a peak effect in 60 to 90 minutes and
duration of 4 to 6 hour.
 Side effects that may develop with the use of
these drugs are tachycardia, tremor,
nervousness, and nausea.
 Anticholinergic agents offer greater
bronchiodilator effect and fewer side effect than
short acting inhaled beta2 agonists.
 These drugs work by blocking the cholinergic
receptors located in the larger airways, resulting
in bronchiodilation. Ipratropium(atrovent) is the
most commonly used drug in this category.

46. Oxygen therapy
O2 therapy is frequently used in the treatment of
COPD another problem associated with
hypoxemia. Long term o2 therapy improves
survival, exercise capacity, cognitive
performance and sleep in hypoxemic patients.O2
is colorless, odorless testless gas that
constitutes 20.95% of the atmosphere. O2 raises
the partial pressure of oxygen(PO2) in inspired
air.
Indications for use: goals for 02 therapy are
 To reduce the work of breathing,
 To maintain the PaO2
 To reduce the workload of heart
 To keep the SaO2 more than 90% during rest

47. Oxygen is usually administered to treat
hypoxemia caused by
 Respiratory disorders such as COPD
pulmonary hypertension pneumonia and
pulmonary emboli
 Cardiovascular disorders such as
myocardial infraction, angina pectoris and
cardiogenic shock
 Central nervous system disorders such as
overdose of opiods

48. SURGICAL MANAGEMENT
bullectomy
Bullae are enlarged airspaces that do not
contribute to ventillation but occupy space in
the thorax,these areas may be surgically
excised
lung volume reduction surgery
It involves the removal of a portion of the
diseased lung parenchyma.this allows the
functional tissue to expand.
lung transplantation

49. Nursing management
Nursing diagnosis
Impaired gas exchange related to decreased ventilation
Objectives
Improve ventilation
Intervention
a. Monitor lung sounds every 4 to 8 hours.
b. Perform chest physiotherapy
c. Advice the client to drink at least 8 to 10 glasses of
fluid per day unless contraindicated
d. Teach the client in coughing technique
e. Asses the condition of oral mucus membrane and
perform oral care

50. Nursing diagnosis
Disturbed sleep pattern related to dyspnea
Objectives
Getting adequate rest
Intervention
 Promote relaxation by providing a darkened,
quiet environment, ensure adequate room
ventilation.
 Avoid use of sleeping pills
 Schedule care activities to allow periods of
uninterrupted sleep.

51. Nursing diagnosis
Activity intolerance related to inadequate
oxygenation
Objective
Improve to perform daily activity
Intervention
 Monitor the severity of dyspnea
 Stop or slow any activity that leads to change in
respiratory rate
 Advice the client to avoid conditions that
increase oxygen demand

52. Nursing diagnosis
Anxiety related to acute breathing difficulties and fear
of suffocation
Objectives
Relieve fear of dying
Intervention
 Provide a quiet, calm environment.
 During acute episodes, open doors and curtains and
limit the number of people in the room.
 Encourage the use of breathing retraining and
relaxation technique
 Give sedative and tranquilizers with extreme caution.
 Nonpharmacological methods of anxiety reduction
are more useful

53. Nursing diagnosis
Ineffective airway clearance related to excessive
secretions and ineffective coughing
Objective
Effective airway clearance
Intervention
 Monitor lung sounds every 4 to 8 hours.
 Perform chest physiotherapy
 Advice the client to drink at least 8 to 10 glasses
of fluid per day unless contraindicated
 Teach the client in coughing technique
 Asses the condition of oral mucus membrane
and perform oral care

54. Complications
 More frequent lung infections, such as
pneumonia.
 An increased risk of thinning bones
(osteoporosis), especially if you use oral
corticosteroids.
 Problems with weight. If chronic bronchitis is
the main part of your COPD.
 Heart failure affecting the right side of the
heart (cor pulmonale).
 A collapsed lung (pneumothorax).
 Sleep problems.