3. 3
COPD(CHRONIC OBSTRUCTIVE PULMONARY DISEASES)
A Hypercapnia disease characterized by progressive airflow limitation
,usually both progressive and associated with an abnormal inflammatory
response of the lungs to noxious particles or gases
4. PATHOPHYSIOLOGY OF COPD
4
ACTIVATION OF WBC’S ACTIVATION OF OXIDATIVE STRESS
Etiologic factors like tobacco smoke, noxious
gases,etc
Activates neutrophils, macrophages and CD8+
lymphocytes
Causes release of chemical mediators like tnfα, IL-8,
LTB4
Leads to destructive changes in the airways,
pulmonary vasculature and lung parenchyma
Imbalance between aggressive and protective
defense system in lungs
Increased oxidants generated by cigarette smoke
reacts and damages various proteins and lipids
Leading to cell and tissue damage
Oxidants also promote inflammation directly and
inhibits anti-protease activity
Leads to protease-antiprotease imbalance
5. “An anatomic alteration of the lung characterized by an abnormal airspace
enlargement distal to the terminal bronchioles accompanied by destructive
changes of the alveolar walls”
EMPHYSEMA
6. TYPES OF EMPHYSEMA
6
CENTRIACINAR
(CENTRILOBULAR)
PANACINAR
(PANLOBULAR)
DISTAL ACINAR
(PARASEPTAL)
An abnormal enlargement of
airspaces centered on the respiratory
bronchiole with coalescence of
destroyed lobules
An abnormal dilation distributed
throughout the pulmonary
lobule
Emphysematous change adjacent to a
pleural surface
Central or proximal parts of the acini Uniform injury Effect peripheral parts (dilate) alveolar
duct & alveoli
Smoking Alpha1-antitrypsin deficiency Unknown (spontaneous pneumothorax
is thought to result from rupture of a
paraseptal bleb/bulla.)
7. ETIOLOGY OF EMPHYSEMA
• Age and gender
• Smoking
• Alpha 1 antitrypsin
Deficiency
• Exposure to second
hand smoke.
7
• Exposure to indoor
or outdoor pollution
• IV Drug users
• Occupational
exposure to fumes
and dust
8. EPIDEMIOLOGY
8
• In US emphysema is estimated to be third leading cause of death.
• The prevalence of emphysema in the United States is approximately 14
million which includes 14% white male smokers and 3% white male non-
smokers.
• Around 90% of COPD deaths occur in low and middle-income countries.
• In the most socioeconomically deprived parts of the country, one in 32
people were diagnosed with COPD, compared with one in 98 in the
most affluent areas.
• 25 million people may have COPD if currently undiagnosed cases are
included.
9. • Doctor will start diagnosis by medical
examination , asking about history and
symptoms and observing signs as well.
CLINICAL MANIFESTATION:
• Two key symptoms are chronic cough and
SOB.
• These symptoms appear in early stages.
As disease progress following symptoms also
observed:
• Wheezing, having hard time getting air out of
lungs
• Dyspenoea , difficulty in catching breaths
• Morning headaches 9
DIAGNOSIS
10. • Tachypnoea with prolonged expiration,
inadequate O2 due to lung infection
• Use of accessory muscles for ventilation ,
malfunctioning of lungs)
• Barrel chest (rounding of chest),
Overinflated lungs with air
• Pursed lips to prevent expiratory airway
collapse
• Cardiac enlargement due inadequate
oxygen supply
• Clubbing of nails in which end of the
fingers appear as upside down spoon
• Sleep disturbance 10
DIAGNOSIS Cont….
11. DIAGNOSIS (LAB TEST)
11
X-RAY & CT-SCAN
Chest X-rays & CT-scan can help confirm a diagnosis of emphysema and rule out
other lung conditions.
Lungs are large and hyper inflated.
Signs of hyperinflation are:
•Low set diaphragm
•Hyper lucent lung fields
Signs of hyperinflation can be seen in emphysema
12. 12
COMPLETE BLOOD COUNT
In emphysema , your body produces more RBCs
to makeup for decreased oxygen. These cells
carry oxygen.
WBCs higher than normal.
ARTERIAL BLOOD GAS
The test measures the oxygen level in your blood
and carbon dioxide (CO2) is removed properly. It
can also determine the acidity (pH) of your blood.
Imbalances in the amount of oxygen, carbon
dioxide, or pH can serve as a way to evaluate
emphysema.
• In emphysema, the blood is more acidic, as the
pH levels are low and the PaCO2 levels are above
than normal.
DIAGNOSIS (LAB TEST) Cont....
13. 13
DIAGNOSIS (LAB TEST) Cont....
SPUTUM EXAMINATION SPIROMETRY
Analysis of cells in your sputum can help
determine the cause of some lung
problems
It is a simple test that is often done to
monitor emphysema. It measures the
amount and how fast you can breathe in
and breathe out.
14. 14
DIAGNOSIS (LAB TEST) Cont....
PULMONARY FUNCTIONING TEST HIGH RESOLUTION COMPUTED
TOMOGRAPHY (HRCT)
This test involves a series of breathing maneuvers
that measure the airflow and volume of air in our
lungs.
It is used in the diagnosis of various health
problems, though most commonly for lung
disease, by assessing the lung parenchyma.
18. MEDICATIONS
• Bronchodilators. These drugs can
help relieve coughing, shortness
of breath and breathing problems
by relaxing constricted airways.
• Steroids. Corticosteroid drugs
inhaled as aerosol sprays reduce
inflammation and may help
relieve shortness of breath.
• Antibiotics. If you have a bacterial
infection, like acute bronchitis or
pneumonia, antibiotics are
appropriate.
19. BRONCHODILATORS
19
Short-acting beta-agonist
bronchodilators – called
“SABAs”
SABAs are the most common
type of rescue inhaler. SABAs
can start providing relief for
symptoms in 3 to 5 minutes,
but are only effective for
about 4 to 6 hours.
Short-acting anti
muscarinic
bronchodilators – called
“SAMAs”
SAMAs start working a little
more slowly than SABAs do.
They take about 15 minutes to
start working, so they cannot
be used as a rescue inhaler
but are used as a
maintenance therapy for
COPD
Long-acting beta-agonist
bronchodilators – called
“LABAs”
Long-acting
bronchodilators are often
used as maintenance
therapy for COPD patients
in later stages.
Long-acting muscarinic
agonists bronchodilators –
called “LAMAs”
Patients need to take long-
acting bronchodilators every
day in order for them to work
well. Having a regular amount
of the drug in the patient’s
body all the time helps to
provide more constant relief
for COPD symptoms.
1 2 3 4
22. 22
CORTICOSTERIODS
Several types of corticosteroids
are available. Some are
inhalable and should be used
every day as directed. They’re
usually prescribed in
combination with a long-acting
COPD drug.
Other corticosteroids are
injected or taken by mouth.
These forms are used on a
short-term basis when your
COPD suddenly gets worse.
• Fluticasone (Flovent), which comes as an
inhaler that you use twice daily. Side effects
can include headache, sore throat, voice
changes, nausea, cold-like symptoms.
• Budesonide (Pulmicort), which comes as a
handheld inhaler or for use in a nebulizer.
Side effects can include colds.
• Prednisolone, which comes as a pill, liquid.
It’s usually given for emergency rescue
treatment. Side effects can include
headache, muscle weakness, upset stomach,
and weight gain.
23. OTHER THERAPY
• Pulmonary rehabilitation:
Include breathing exercises and
techniques that may help reduce
your breathlessness.
• Nutrition therapy: Give advice
about proper nutrition.
• Oxygen supplements: Using
oxygen regularly at home and
when you exercise may provide
some relief.
24. SURGERY
• Lung volume reduction surgery:
Surgeons remove small wedges
of damaged lung tissue.
Removing the diseased tissue
helps the remaining lung tissue
expand and work more
efficiently and helps improve
breathing.
• Lung transplant: Lung
transplantation is an option if
you have severe lung damage.
25. HOME REMEDIES
• Stop smoking.
• Avoid other respiratory
irritants.
• Exercise regularly.
• Protect yourself from cold
air.
• Get recommended
vaccinations.
• Prevent respiratory
infections.
26. MONITORING
26
Mild stable COPD patients
may be followed up at 6-
month intervals, while
patients with severe and
recently hospitalized
patients need follow-up at 2-
week to 1-month intervals.
PFTs should be
monitored at least
every 3 years, to
evaluate response to
therapy and possible
need for change in
medications.
2
1
27. 27
Oxygen saturation should be monitored and patients
evaluated periodically for the need of supplemental
oxygen.
3
MONITORING
28. PROGNOSIS
28
MILD EMPHYSEMA
80% of patients are alive after 4 years.
MODERATE EMPHYSEMA
60-70% of patients are alive after 4 years.
SEVERE EMPHYSEMA
50% are alive after 4 years.
VERY SEVERE EMPHYSEMA
short life expectancy.