Pharmacotherapy for COPD
Prepared by:-Mr. Ujjval P. Vaghela
1
2 Content
DEFINITION
EPIDEMIOLOGY
CAUSES
SIGNS & SYMPTOMS
TYPES
PATHOGENESIS
PATHOPHYSIOLOGY
CELLULAR MECHANISM
DIAGNOSIS
REFERENCES
3 Introduction
The term COPD means
Chronic i.e. continual, permanent, incurable
Obstructive i.e. blocks
Pulmonary i.e. pertaining to the lungs
Disease i.e. condition with signs and symptoms
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)
4 Definition
Chronic obstructive pulmonary disease
(COPD) is a preventable and treatable disease
state characterised by airflow limitation that is
not fully reversible.
The airflow limitation is usually progressive
and is associated with an abnormal
inflammatory response of the lungs to noxious
particles or gases, primarily caused by
cigarette smoking.
Although COPD affects the lungs, it also
produces significant systemic consequences.
5 Epidemiology
COPD is the fifth leading cause of death in
the UK and the fourth in the world.
It is expected to rise to third position by
2020.
30% of smokers develop COPD
20% of adult males have COPD
15% of COPD patients are severely
symptomatic
Tuberculosis in smokers predisposes to
COPD.
6
7 Risk factor
Smoking
Age
Gender
Occupation
Genetic factor
Air pollution
Socio economic status
Airway hyper-responsiveness and allergy
Inflammation
Proteinase and antiproteinase imbalance
Oxidative stress
8 Sign & symptoms
Large barrel shaped
chest
(hyperinflation)
Use of accessory
muscle in respiration
Shortness of breath,
especially during
physical activity
Low, flat diaphragm
Chronic cough
Sputum production
9 Cont…
Wheezing
Chest tightness
Dyspnoea
Weight loss
Respiratory insufficiency
Respiratory infections
10
COPD
CHRONIC
EMPHYSEMA
BRONCHITIS
11 Emphysema
Emphysema is the permanent
destructive enlargement of the
airspaces distal to the terminal
bronchioles without obvious fibrosis.
Destruction of the alveolar walls,
which contain the protein elastin,
reduces the elasticity of the lungs,
causing collapse of bronchioles, thus
obstructing airflow out of the
lung.The alveolar wall destruction
also decreases the number of
capillaries available for gas exchange.
Emphysema makes breathing
inefficient.
12
13 Chronic bronchitis
Chronic bronchitis is defined
clinically by the presence of
chronic bronchial secretions,
enough to cause expectoration,
occurring on most days for a
minimum of 3 months of the year
for 2 consecutive years.
The pathological basis of chronic
bronchitis is increased secretion of
mucus due to inflammation, which
can lead to further obstruction of
the airways and an increased
likelihood of bacterial infection.
14
15 Pathogenesis of COPD
16
17
Inflammation
Small Airway Disease, Parenchymal Distruction,
Airway inflammation Decrease elastic recoil,
Air flow
limitation
18 The overlap of asthma & COPD
Emphysema Chronic
bronchitis
Asthma
Airflow
limitation
19
Asthma COPD
COPD Airway
Asthmatic Airway
Inflammation ,
Inflammation ,
CD8-T lymphocytes,
CD4-T lymphocytes,
Macrophages,
Eosinophils ,
Neutrophils
Fully Not Fully
Airflow limitation
Reversible Reversible
20 Pathophysiology
Abnormal inflammatory response of the
lungs due to toxic gases.
Response occurs in the airways
,parenchyma & pulmonary vasculature.
Narrowing of the airway takes place
Destruction of parenchyma leads to
emphysema.
21 Destruction of lung parenchyma leads to an
imbalance of proteinases/antiproteinases. (this
proteinases inhibitors prevents the destructive
process)
Pulmonary vascular changes : Thickening of vessels,
Collagen deposit , Destruction of capillary
beds. , Mucus hypersecretion(cilia
dysfunction,airflow limitation,cor pulmonale(RVF))
Chronic cough and sputum production
22 Cellular mechanism of COPD
Cigarette smoke
Alveolar macrophage
CD8+ MCP-1
lymphocyte
Neutrophil chemotactic factors
Cytokines (IL-8)
Mediators (LTB4)
Neutrophil
PROTEASE
PROTEASES
INHIBITORS
-
Alveolar wall destruction Mucus hypersecretion
23 TNF- and IL-8 in COPD
Cigarette
smoke
TNF-
Alveolar macrophage
NF-B
TNF- Epithelial
cells
IL-8
IL-8 gene
IL-8 Neutrophils IL-8
24 Diagnosis
1. History
2. Assessment of symptoms:
Cough
Dyspnea
Sputum production
3. PFT (pulmonary function testing)
PFT is complete evaluation of the
respiratory system including patient history,
physical examinations, chest x-ray examinations,
arterial blood gas analysis, and tests of
pulmonary function. The primary purpose of
pulmonary function testing is to identify the
severity of pulmonary impairment.
25 4. Spirometry (to find out airflow
obstruction) :
The diagnosis of COPD is confirmed by
spirometry, a test that measures breathing.
Spirometry measures the forced expiratory
volume in one second (FEV1) which is the
large volume of air that can be breathed
out in the first second of a single breath.
Spirometry also measures the forced vital
capacity (FVC) which is the volume of air
inhaled & exhaled during forced maximum
expiration after full inhalation. Normally
at least 70% of the FVC comes out in the
first second (i.e. the FEV1/FVC ratio is
>70%).
26 In COPD, this ratio is less than normal, (i.e.
FEV1/FVC ratio is <70%) even after a
bronchodilator medication has been given.
Spirometry can help to determine the severity
of COPD .
Severity of COPD FEV1 % predicted
Mild ≥80
Moderate 50–79
Severe 30–49
<30 or Chronic respiratory
Very severe
failure symptoms
27 5. An x-ray of the chest may show an over-
expanded lung(hyperinflation) and can be
useful to help exclude other lung diseases.
28 6. ABG analysis (arterial blood gas test)
These blood tests measure how the lungs transfer
oxygen to bloodstream and how effectively they
remove carbon dioxide.
7. Screening of alpha antitrypsin deficiency
8. A high-resolution computed tomography scan
of the chest may show the distribution of
emphysema throughout the lungs
(Axial CT image of the lung of a person with end-stage bullous emphysema)
29 9. Peak Flow Rate Measurement
Start with meter indicator at lowest level
Take in deep inspiration while standing
Exhale forcefully and rapidly with lips sealed
around mouthpiece.
These steps are repeated 2 more times. If the
patient coughs or does not perform the
technique correctly, the turn is ignored and
repeated. The highest number from the 3
attempts is recorded by the patient.
30 Treatment
AIM :
Prevent disease progression
Relieve symptoms
Improve exercise tolerance
Improve health status
Prevent and treat complications such as
hypoxaemia and infections
Prevent and treat exacerbations
Reduce mortality
31 Cont...
The most essential step in any treatment plan for
smokers with emphysema is stopping smoking;
it's the only way to stop the damage to lungs from
becoming worse.
But quitting is never easy, and people often need the
help of a comprehensive smoking cessation plan,
which may include:
A target date to quit
Relapse prevention
Advice for healthy lifestyle changes
Social support systems
Nicotine patch
ASTHMA vs COPD
32
Inflammation ASTHMA COPD
CELLS Mast cells
Eosinophils Neutrophils
CD4 T cells CD8 T cells
predominate
MEDIATORS LTD4 , LTB4,
histamine,IL-4 , IL-8 , TNFα,
IL-5, ROS + ROS+++
EFFECTS All airways Peripheral
Little fibrosis airways
Lung
destruction
Fibrosis
Response +++ ±
steroids
33
34 References
1. Clinical pharmacy and therapeutics, Edited by
Roger Walker ,fifth edition. Page no. :431-445.
2. Rang H.P., Dale M. M. Pharmacology , 6th
edition,1996. page no. 365-366.
3. Essential of medical pharmacology , seventh
edition, K. D. TRIPATHI page no. 222-230
4. Alfred Goodman Gilman, The
Pharmacological basis of Therapeutics,
Eleventh edition , page no. 470-474
Thank you
