ASTHMA AND CHRONIC OBSTRUCTIVE PULMONARY DISORDER

INTRODUCTION
ASSESSMENT IN IMPROVING KNOWLEDGE , ATTITUDE AND PRACTICE
TOWARDS INHALERS USED IN ASTHMA AND COPD PATIENTS Page 1
1. INTRODUCTION
1.1 ASTHMA
Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular
elements play a role: in particular, mast cells, eosinophils, T-lymphocytes, macrophages,
neutrophils, and epithelial cells. In susceptible individuals, this inflammation causes recurrent
episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in
the early morning.[1]
CLASSFICATION OF ASTHMA
Asthma classification Signs and symptoms
Mild intermittent Mild symptoms up to two days a week and up to two
nights a month
Mild persistent Symptoms more than twice a week, but no more than
once in a single day
Moderate persistent Symptoms once a day and more than one night a
week
Severe persistent/ Symptoms throughout the day on most days and
frequently at night
Table 1: Classification of asthma. [2]
1.2 EPIDEMIOLOGY
Asthma affects 5-10% of the population or an estimated 23.4 million persons, including 7 million
children. The overall prevalence rate of exercise-induced bronchospasm is 3-10% of the general
population if persons who do not have asthma or allergy are excluded, but the rate increases to

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12-15% of the general population if patients with underlying asthma are included. Asthma
affects an estimated 300 million individuals worldwide. Annually, the World Health
Organization (WHO) has estimated that 15 million disability-adjusted life-years are lost and
250,000 asthma deaths are reported worldwide. [3]
1.3 TYPES OF ASTHMA
There are different types of asthma include:
 Exercise-induced asthma, which may be worse when the air is cold and dry
 Occupational asthma, triggered by workplace irritants such as chemical fumes, gases or
dust
 Allergy-induced asthma, triggered by airborne substances, such as pollen, mold spores,
cockroach waste or particles of skin and dried saliva shed by pets (pet dander).[1]
SIGNS AND SYMPTOMS:
Asthma signs and symptoms include:
 Shortness of breath
 Chest tightness or pain
 Trouble sleeping caused by shortness of breath, coughing or wheezing
 A whistling or wheezing sound when exhaling (wheezing is a common sign of asthma in
children)
 Coughing or wheezing attacks that are worsened by a respiratory virus, such as a cold or the
flu.
CAUSES
Factors that can contribute to asthma or airway hyperreactivity may include any of the following.
 Airborne substances, such as pollen, dust mites, mold spores, pet dander or particles of
cockroach waste.
 Respiratory infections, such as the common cold.

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 Physical activity (exercise-induced asthma)..
 Cold air.
 Air pollutants and irritants, such as smoke.
 Certain medications, including beta blockers, aspirin, ibuprofen (Advil, Motrin IB, others)
and naproxen (Aleve).
 Strong emotions and stress.
 Sulfites and preservatives added to some types of foods and beverages, including shrimp,
dried fruit, processed potatoes, beer and wine.
 Gastroesophageal reflux disease (GERD), a condition in which stomach acids back up into
your throat.
RISK FACTORS
A number of factors are thought to increase your chances of developing asthma. These include:
 Having a blood relative (such as a parent or sibling) with asthma.
 Having another allergic condition, such as atopic dermatitis or allergic rhinitis (hay fever).
 Being overweight.
 Being a smoker.
 Exposure to secondhand smoke
 Exposure to exhaust fumes or other types of pollution.
 Exposure to occupational triggers, such as chemicals used in farming, hairdressing and
manufacturing.[4]

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1.4 PATHOPHYSIOLOGY
Fig 1:Diagrammatic representation of Pathogenesis of Asthma.[5]
Asthma is associated with T helper cell type-2 (Th2) immune responses, which are typical of
other atopic conditions. Asthma triggers may include allergic (e.g., house dust mites, cockroach
residue, animal dander, mould, and pollens) and non-allergic (e.g., viral infections, exposure to
tobacco smoke, cold air, exercise) stimuli, which produce a cascade of events leading to chronic
airway inflammation. Elevated levels of Th2 cells in the airways release specific cytokines,
including interleukin (IL)-4, IL-5, IL-9 and IL-13, and promote eosinophilic inflammation and
immunoglobulin E (IgE) production. IgE production, in turn, triggers the release of inflammatory
mediators, such as histamine and cysteinyl leukotrienes, that cause bronchospasm (contraction of

INTRODUCTION
the smooth muscle in the airways), edema, and increased mucous secretion, which lead to the
characteristic symptoms of asthma .
The mediators and cytokines released during the early phase of an immune response to an
inciting trigger further propagate the inflammatory response (late-phase asthmatic response) that
leads to progressive airway inflammation and bronchial hyperreactivity. Over time, the airway
remodeling that occurs with frequent asthma exacerbations leads to greater lung function decline
and more severe airway obstruction. This highlights the importance of frequent assessment of
asthma control and the prevention of exacerbations.[6]
1.5 DIAGNOSIS
The diagnosis of asthma is based on history, physical exam, and diagnostic testing. There are
several diagnostic testing used to indicate the asthma includes:
1. Spirometry.
2. Peak expiratory flow.
3. Bronchial provocation test.
4. Chest X-ray .
 Spirometry: It measures obstruction and severity of asthma and confirms chronic airflow
limitation by assessing forced expiratory volume in 1 second (FEV1), forced vital capacity
(FVC), and FEV1/FVC, which represents the proportion of the vital capacity (maximum
amount of air expelled from the lungs) an individual expires in the first second of forced
expiration. Spirometry should be obtained to determine respiratory obstruction and
reversibility in patients age 5 years and older.
 Peak Expiratory flow: A peak flow meter is a simple device that measures how hard you
can breathe out. Lower than usual peak flow readings are a sign your lungs may not be
working as well and that your asthma may be getting worse. Your doctor will give you
instructions on how to track and deal with low peak flow readings.
 Bronchial provocation test: (also known as bronchial challenge test) is used to determine
airway hyper responsiveness. Bronchial provocation can be useful when asthma is a
differential diagnosis, but spirometry is near normal or normal. This test is considered

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moderately sensitive with low specificity for the diagnosis of asthma. Therefore, a positive
test can signify asthma, but it can also be indicative of other diagnoses (allergic rhinitis,
chronic obstructive pulmonary disease [COPD], or cystic fibrosis); conversely, a negative
test supports ruling out asthma as a diagnosis.
 Chest X-ray: Chest X-rays are not recommended to routinely assess or diagnose asthma.
Typically, a chest X-ray is normal or possibly displays hyperinflation. A chest X-ray is only
recommended when other conditions are suspected beyond asthma, such as cardiopulmonary
diagnoses in older adults.
Additional tests
Other tests to diagnose asthma include
 Methacholine challenge. Methacholine is a known asthma trigger that, when inhaled, will
cause mild constriction of your airways. If you react to the methacholine, you likely have
asthma. This test may be used even if your initial lung function test is normal.
 Nitric oxide test. This test, though not widely available, measures the amount of the gas,
nitric oxide, that you have in your breath. When your airways are inflamed a sign of asthma
you may have higher than normal nitric oxide levels.
 Allergy testing. This can be performed by a skin test or blood test. Allergy tests can identify
allergy to pets, dust, mold and pollen. If important allergy triggers are identified, this can
lead to a recommendation for allergen immunotherapy.
 Sputum eosinophils. This test looks for certain white blood cells (eosinophils) in the mixture
of saliva and mucus (sputum) you discharge during coughing. Eosinophils are present when
symptoms develop and become visible when stained with a rose-colored dye (eosin). [7]
1.6 TREATMENT
The pharmacologic agents commonly used for the treatment of asthma can be classified as
controllers (medications taken daily on a long-term basis that achieve control primarily through
anti-inflammatory effects) and relievers (medications used on an as-needed basis for quick relief
of bronchoconstriction and symptoms).
1) Controller medications include
 Inhaled corticosteroids (ICSs)

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 LABAs (Long acting beta agonists) in combination with an ICS (Inhaled corticosteroid)
 Leukotriene receptor antagonists (LTRAs)
 Long-acting muscarinic receptor antagonists (LAMAs), and
 Theophylline
2) Reliever medications include
 Short acting inhaled beta2-agonists
 Inhaled anticholinergics (Ex: Ipratropium)
 Systemic corticosteroids.
3) Allergen medication: It may help if your asthma is triggered or worsened by allergies. These
include:
 Anti-IL5 therapy
 Anti IgE monoclonal antibodies
1. Controller medications : These medications taken daily on a long-term basis that achieve
control primarily through anti-inflammatory effects
 Inhaled corticosteroids (ICSs)
Ex: Beclomethasone (Qvar, generics), Budesonide (Pulmicort), Ciclesonide (Alvesco),
Mometasone (Asmanex), Fluticasone propionate.
ICSs are the most effective anti-inflammatory medications available for the treatment of asthma
and represent the mainstay of therapy for most patients with the disease. Low-dose ICS
monotherapy is recommended as first-line maintenance therapy for most children and adults with
asthma. Regular ICS use has been shown to reduce symptoms and exacerbations, and improve
lung function and quality of life. ICSs do not, however, “cure” asthma, and symptoms tend to
recur within weeks to months of ICS discontinuation.
 Combination ICS/LABA inhalers (Inhaled corticosteroid/Long acting beta agonists)
Ex: Fluticasone propionate/Salmeterol, Budesonide/Formoterol, Mometasone/Formoterol and
Fluticasone furoate/Vilanterol.
LABA monotherapy is not recommended in patients with asthma as it does not impact airway
inflammation and is associated with an increased risk of morbidity and mortality. LABAs are
only recommended when used in combination with ICS therapy. The combination of a LABA

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and ICS has been shown to be highly effective in reducing asthma symptoms and exacerbations,
and is the preferred treatment option in adolescents or adults whose asthma is inadequately
controlled on low-dose ICS therapy, or in children over 6 years of age who are uncontrolled on
moderate ICS doses. Although there is no apparent difference in efficacy between ICSs and
LABAs given in the same or in separate inhalers, combination ICS/LABA inhalers are preferred
because they preclude use of the LABA without an ICS, are more convenient and may enhance
patient adherence.
 Leukotriene receptor antagonists (LTRSs)
Ex: Montelukast and Zafirlukast
The LTRAs are effective for the treatment of asthma and are generally considered to be safe and
well tolerated. Because these agents are less effective than ICS treatment when used as
monotherapy, they are usually reserved for patients who are unwilling or unable to use ICSs.
LTRAs can also be used as add-on therapy if asthma is uncontrolled despite the use of low-to-
moderate dose ICS therapy or combination ICS/LABA therapy. It is important to note, however,
that LTRAs are considered to be less effective than LABAs as add-on therapy in adults. In
children, if medium-dose ICS therapy is ineffective, LTRAs are considered the next-line
treatment option. If, however, the child has persistent airway obstruction, the addition of a
LABA may be preferred.
 Long-acting muscarinic receptor antagonists (LAMA)
Ex: Tiotropium
The LAMA are administered by mist inhaler can be used as add-on therapy for patients with a
history of exacerbations despite treatment with ICS/LABA combination therapy. It is only
indicated for patients 12 years of age and older.
 Theophylline
Theophylline is an oral bronchodilator with modest anti-inflammatory effects. Given its narrow
therapeutic window and frequent adverse events (e.g., gastrointestinal symptoms, loose stools,
seizures, cardiac arrhythmias, nausea and vomiting), its use is generally reserved for patients
over 12 years of age who are intolerant to or continue to be symptomatic despite other add-on
therapies.

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2. Reliever medications: These medications used on an as-needed basis for quick relief of
bronchoconstriction and symptoms
 Short acting beta agonists
Ex: Albuterol (Proventil HFA, Ventolin HFA)
These inhaled , quick relief bronchodilators act within minutes to rapidly ease symptoms during
an asthma attacks. Short-acting beta agonists can be taken using a portable, hand-held inhaler or
a nebulizer, a machine that converts asthma medications to a fine mist ,so that they can be
inhaled through a face mask or a mouthpiece.
 Inhaled Anticholinergic
Ex: Ipratropium.
These prevent increase in intracellular calcium concentration that is caused by interaction of
acetylcholine with muscarinic receptors on bronchial smooth muscles.
Side effects : Shortness of breath, wheezing, chest tightness.
 Systemic corticosteroids
These medications — which include prednisone and methylprednisolone — relieve airway
inflammation caused by severe asthma. They can cause serious side effects when used long term,
so they're used only on a short-term basis to treat severe asthma symptoms.
Adverse events with short-term, high-dose oral prednisone are uncommon, but may include:
reversible abnormalities in glucose metabolism, increased appetite, edema, weight gain, rounding
of the face, mood alterations, hypertension, peptic ulcers and avascular necrosis of the hip .
3. Allergy medications : It may help if your asthma is triggered or worsened by allergies. These
include:
 Anti-IL5 therapy
Ex: Mepolizumab (Nucala), Reslizumab (Cinqair), Benralizumab (Fasenra)
These drugs reduces eosinophils and basophils through antibody-dependent cell mediated
cytotoxicity.
 Anti IgE monoclonal antibodies
Ex: Omalizumab (Xolair)

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It selectively binds to IgE and inhibits binding to IgE receptors on surface of mast cells and
basophils.
This medication, given as an injection every two to four weeks, is specifically for people who
have allergies and severe asthma. It acts by altering the immune system.[8]

INTRODUCTION
1.7 DOSAGE ADMINISTRATION FOR ASTHMA
Medications Usual adult dose Pediatric dose
information< 6 years
of age
6–18 years of age
ICSs
Beclomethasone
(Qvar, generics)
Budesonide
(Pulmicort)
Ciclesonide
(Alvesco)
PMDI: 100-800
µg/day,
divided bid
DPI: 400–2400 µg/day,
divided bid
Nebules: 1–2 mg bid
PMDI: 100–800 µg/day
DPI: 200–400 µg/day
PMDI
• Low 50 µg bid
• Med 100 µg bid
DPI not recommended
for children < 6 years
PMDI:
• Low 100 µg once
daily
• Med 200 µg daily
• High refer to
specialist
DPI not recommended
for children <6 years
PMDI
• Low 50–100 µg bid
• Med > 100 µg bid
• High > 200 µg bid
DPI
• Low 100 µg bid
• Med 200–400 µg bid
Nebules: 0.25–0.5 mg
bid (for children 3
months to 12 years)
PMDI:
• Low 100 µg once daily
• Med 200–400 µg daily
• High > 400 µg daily
DPI
• Low ≤ 200 µg daily
• Med > 100–200 µg bid

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Mometasone
(Asmanex)
Fluticasone
propionate
(Flovent HFA,
Flovent Diskus)
PMDI/DPI: 100–
500 µg bid
PMDI/DPI
• Low 50 µg bid
• Med 100–125 µg bid
• High refer to
specialist
PMDI/DPI
• Low ≤ 100 µg bid
• Med > 100–200 µg bid
• High ≥ 200 µg bid
Combination
ICS/LABA
inhalers
Budesonide/for
moterol
(Symbicort)
DPI (maintenance):
100/6 µg or 200/6 µg,
1–2 puffs od or bid;
max 4 puffs/day
DPI (maintenance and
reliever):
100/6 µg or 200/6 µg,
1–2 puffs bid or 2 puffs
od; plus 1 puff prn for
relief of symptoms (no
Refer to specialist DPI
• Low 100/6 µg 1 dose
bid
• Med 100/6 µg 2 doses
bid, 200/6 µg 1–2 doses
bid
• High > 200/6 µg 2
doses bid

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Fluticasone
furoate/salmeter
ol (Advair
PMDI, Advair
Diskus)
Mometasone/for
moterol
(Zenhale)
more than 6 puffs on
any single occasion);
max 8 puffs/day
PMDI: 125/25 µg or
250/25 µg, 2 puffs bid
Diskus: 100/50 µg,
250/50 µg or
500/50 µg: 1 puff bid
For patients previously
treated with
 Low-dose ICS:
50/5 µg, 2 puffs bid
 Medium-dose ICS:
100/5 µg, 2 puffs
bid
 High-dose ICS:
200/5 µg, 2 puffs
bid
Refer to specialist
Refer to specialist
DPI/PMDI
• Low 100/50 µg bid
• Med > 100–200 µg bid
• High ≥ 250/50 µg bid
PMDI
• Low 50/5–100/5 μg 1
dose bid
• Med 100/5 μg 2 doses
bid, 200/5 μg 1–2 doses
bid
• High > 200/5 μg
LTRAs
Montelukast
Zafirlukast
(Accolate)
10 mg tablet OD (taken
in the evenings)
20 mg tablet BID, at
least 1 h before or 2h
after meals
4 mg PO daily
Refer to specialist
5 mg PO daily (6–
14 years)
10 mg PO daily
(≥ 15 years)
20 mg tablet bid, at least
1 h before or 2 h after
meals

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LAMAs
Tiotropium
(Spiriva
Respimat)
1.25 µg, 2 puffs OD Not indicated for
children < 18 years
Anti-IgE therapy
Omalizumab
(Xolair)
150–375 mg sc every
2–4 weeks (based on
patient’s weight and
pre-treatment serum
IgE level)
Not indicated for
children < 6 years
75–375 mg sc every 2–
4 weeks (based on
patient’s weight and pre-
treatment serum IgE
level)
Anti-IL5 therapy
Mepolizumab
(Nucala)
Reslizumab
(Cinqair)
Benralizumab
(Fasenra)
100 mg sc every
4 weeks
3 mg/kg IV every
4 weeks
30 mg sc every 4 weeks
for the first 3 doses,
then every 8 weeks
thereafter
Not indicated for
children < 18 years
Not indicated for
children < 18 years
Not indicated for
children < 18 years
Short acting
beta agonists
Albuterol
90 mcg(base) /
actuation (equivalent to
108 mcg albuterol
sulfate)
> 4 years: 90-180 mcg
(1-2puffs) inhaled PO
q4-6hr
180 mcg (2 puffs)
inhaled PO q4-6hr; not
exceed12 inhalations / 24
hrs
Inhaled
Anticholinergic
Ipratropium
17 mcg/actuation > 12years : 8
actuaions q20 min
PRN for upto 3hr
8 actuation (136 mcg)
q20min PRN for 3hr
ICS- inhaled corticosteroid,
PMDI pressurized metered-dose inhaler,
DPI dry powder inhaler,
LTRA leukotriene receptor antagonists,
IgE immunoglobulinE,
IL-5 interleukin 5,
bid twice daily,
SC - subcutaneously,
IV - intravenously,

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LABA - long acting beta agonist,
LAMA - long-acting muscarinic receptor antagonist,
PO - oral,
Prn - as needed
Table 2: Dosage administration for asthma.[9]
1.8 LIFESTYLE CHANGES
 Get regular exercise and yoga everyday.
 Maintain a healthy weight and diet.
 Reduces exposure to allergens or irritants that trigger asthma.
 Maintain optimal humidity and body temperature.
 Avoid smoking .[2]

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1.9 CHRONIC OBSTRUCTIVE PULMONARY DISEASES
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that
causes obstructed airflow from the lungs.
Emphysema and chronic bronchitis are the two most common conditions that contribute
to COPD.
Chronic bronchitis is inflammation of the lining of the bronchial tubes, which carry air to and
from the air sacs (alveoli) of the lungs. It's characterized by daily cough and mucus (sputum)
production.
Emphysema is a condition in which the alveoli at the end of the smallest air passages
(bronchioles) of the lungs are destroyed as a result of damaging exposure to cigarette smoke and
other irritating gases and particulate matter.[10]
1.10 PREVELANCE
According to the World Health Organization report, the prevalence of COPD ranges between 4%
and 20% in the Indian adults. According to a recent systematic review which includes estimates
from the INSEARCH and other major studies in India, the prevalence of CB seems to range
between 6.5% and 7.7% in rural and up to 9.9% in urban India. The review also mentions that
the included studies were mostly low quality, questionnaire-based and was conducted around
1990-2006. These figures may underestimate the true burden of COPD since questionnaire-based
prevalence estimates tend to be lower than the true spirometry-based estimates. This review
provides the best available estimate of COPD prevalence till date but is unlikely to reflect the
current disease burden across all Indian subpopulations. COPD led to 13% of all deaths in India
and 7.5 million were at risk of the disease in 2016. [11]
SIGN AND SYMPTOMS
Signs and symptoms of COPD may include:
 Shortness of breath, especially during physical activities
 Wheezing
 Chest tightness
 Having to clear your throat first thing in the morning, due to excess mucus in your lungs

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 A chronic cough that may produce mucus (sputum) that may be clear, white, yellow or
greenish
 Blueness of the lips or fingernail beds (cyanosis)
 Frequent respiratory infections
 Lack of energy
 Unintended weight loss (in later stages)
 Swelling in ankles, feet or legs [12]
CAUSES
The main cause of COPD in developed countries is tobacco smoking. In the developing
world, COPD often occurs in people exposed to fumes from burning fuel for cooking and heating
in poorly ventilated homes.
Only about 20 to 30 percent of chronic smokers may develop clinically apparent COPD,
although many smokers with long smoking histories may develop reduced lung function. Some
smokers develop less common lung conditions. They may be misdiagnosed as
having COPD until a more thorough evaluation is performed.[13]
a) Causes of airway obstruction
These causes of airway obstruction include:
 Emphysema: This lung disease causes destruction of the fragile walls and elastic fibers of
the alveoli. Small airways collapse when you exhale, impairing airflow out of your lungs.
 Chronic bronchitis: In this condition, your bronchial tubes become inflamed and narrowed
and your lungs produce more mucus, which can further block the narrowed tubes. You
develop a chronic cough trying to clear your airways.
b) Cigarette smoke and other irritants
In the vast majority of cases, the lung damage that leads to COPD is caused by long-term
cigarette smoking. But there are likely other factors at play in the development of COPD, such as
a genetic susceptibility to the disease, because only about 20 to 30 percent of smokers may
develop COPD.

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c) Alpha-1-antitrypsin deficiency
In about 1 percent of people with COPD, the disease results from a genetic disorder that causes
low levels of a protein called alpha-1-antitrypsin. Alpha-1-antitrypsin (AAt) is made in the liver
and secreted into the bloodstream to help protect the lungs. Alpha-1-antitrypsin deficiency can
affect the liver as well as the lungs. Damage to the lung can occur in infants and children, not
only adults with long smoking histories.[14]
RISK FACTORS
Risk factors for COPD include:
 Exposure to tobacco smoke. The most significant risk factor for COPD is long-term
cigarette smoking. The more years you smoke and the more packs you smoke, the greater
your risk. Pipe smokers, cigar smokers and marijuana smokers also may be at risk, as well as
people exposed to large amounts of secondhand smoke.
 People with asthma who smoke. The combination of asthma, a chronic inflammatory
airway disease, and smoking increases the risk of COPD even more.
 Occupational exposure to dusts and chemicals. Long-term exposure to chemical fumes,
vapors and dusts in the workplace can irritate and inflame your lungs.
 Exposure to fumes from burning fuel. In the developing world, people exposed to fumes
from burning fuel for cooking and heating in poorly ventilated homes are at higher risk of
developing COPD.
 Age. COPD develops slowly over years, so most people are at least 40 years old when
symptoms begin.
 Genetics. The uncommon genetic disorder alpha-1-antitrypsin deficiency is the cause of
some cases of COPD. Other genetic factors likely make certain smokers more susceptible to
the disease.
COMPLICATIONS
COPD can cause many complications, including:
 Respiratory infections. People with COPD are more likely to catch colds, the flu and
pneumonia. Any respiratory infection can make it much more difficult to breathe and could

INTRODUCTION
cause further damage to lung tissue. An annual flu vaccination and regular vaccination
against pneumococcal pneumonia can prevent some infections.
 Heart problems. For reasons that aren't fully understood, COPD can increase your risk of
heart disease, including heart attack. Quitting smoking may reduce this risk.
 Lung cancer. People with COPD have a higher risk of developing lung cancer. Quitting
smoking may reduce this risk.
 High blood pressure in lung arteries. COPD may cause high blood pressure in the arteries
that bring blood to your lungs (pulmonary hypertension).
 Depression. Difficulty breathing can keep you from doing activities that you enjoy. And
dealing with serious illness can contribute to development of depression. Talk to your doctor
if you feel sad or helpless or think that you may be experiencing depression.[15]
1.11 PATHOPHYSIOLOGY
Cigarette smoking or exposure to noxious agents induces an inflammatory process in the lungs
and airways of the bronchial tree that leads to small airway disease and parenchymal destruction.
Loss of elasticity of the alveolar attachments, or their destruction, is a hallmark of emphysema.
The inability of the lungs to empty results in air trapping and hyperinflation, manifested as
dyspnea on exertion. Over time, this can cause the diaphragm to flatten and the rib cage to
enlarge. In the late stages of COPD, hypoxemia develops. Pulmonary hypertension is a
consequence of thickening of the intima and vascular smooth muscle and indicates a poor
prognosis.
The net result of the pathophysiologic processes of COPD is increased resistance to airflow and
decreased expiratory flow rate. Removing the inflammatory stimulus (eg, stopping smoking)
does not diminish the inflammatory process.

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Fig 2: Pathophysiology of chronic obstructive pulmonary diseases.[16]
DIAGNOSIS
COPD is commonly misdiagnosed. Many people who have COPD may not be diagnosed until
the disease is advanced.
To diagnose your condition, your doctor will review your signs and symptoms, discuss your
family and medical history, and discuss any exposure you've had to lung irritants — especially
cigarette smoke. Your doctor may order several tests to diagnose your condition.
Tests may include:
 Lung (pulmonary) function tests. Pulmonary function tests measure the amount of air you
can inhale and exhale, and if your lungs are delivering enough oxygen to your blood.
 Spirometry: It is the most common lung function test. During this test, you'll be asked to
blow into a large tube connected to a small machine called a spirometer. This machine
measures how much air your lungs can hold and how fast you can blow the air out of your
lungs. Spirometry can detect COPD even before you have symptoms of the disease. It can

INTRODUCTION
also be used to track the progression of disease and to monitor how well treatment is
working. Spirometry often includes measurement of the effect of bronchodilator
administration. Other lung function tests include measurement of lung volumes, diffusing
capacity and pulse oximetry.[17]
Staging of COPD
• Stage I (mild) - FEV1 80% or greater of predicted
• Stage II (moderate) - FEV1 50-79% of predicted
• Stage III (severe) - FEV1 30-49% of predicted
• Stage IV (very severe) - FEV1 less than 30% of predicted or FEV1.[18]
 Chest X-ray. A chest X-ray can show emphysema, one of the main causes of COPD. An X-
ray can also rule out other lung problems or heart failure.
 CT scan. A CT scan of your lungs can help detect emphysema and help determine if you
might benefit from surgery for COPD. CT scans can also be used to screen for lung cancer.
 Arterial blood gas analysis. This blood test measures how well your lungs are bringing
oxygen into your blood and removing carbon dioxide.
 Laboratory tests. Laboratory tests aren't used to diagnose COPD, but they may be used to
determine the cause of your symptoms or rule out other conditions. For example, laboratory
tests may be used to determine if you have the genetic disorder alpha-1-antitrypsin (AAt)
deficiency, which may be the cause of some cases of COPD. This test may be done if you
have a family history of COPD and develop COPD at a young age, such as under age 45.[17]
1.12 TREATMENT
Medications
Several kinds of medications are used to treat the symptoms and complications of COPD. You
may take some medications on a regular basis and others as needed.
Bronchodilators
Bronchodilators are medications that usually come in inhalers — they relax the muscles around
your airways. This can help relieve coughing and shortness of breath and make breathing easier.
Depending on the severity of your disease, you may need a short-acting bronchodilator before
activities, a long-acting bronchodilator that you use every day or both.
a) Examples of short-acting bronchodilators include:

INTRODUCTION
 Albuterol (ProAir HFA, Ventolin HFA, others)
 Ipratropium (Atrovent HFA)
 Levalbuterol (Xopenex)
b) Examples of long-acting bronchodilators include:
 Aclidinium (Tudorza Pressair)
 Arformoterol (Brovana)
 Formoterol (Perforomist)
 Indacaterol (Arcapta Neoinhaler)
 Tiotropium (Spiriva)
 Salmeterol (Serevent)
 Umeclidinium (Incruse Ellipta)
Inhaled steroids
Inhaled corticosteroid medications can reduce airway inflammation and help prevent
exacerbations. Side effects may include bruising, oral infections and hoarseness. These
medications are useful for people with frequent exacerbations of COPD.
Examples of inhaled steroids include:
 Fluticasone (Flovent HFA)
 Budesonide (Pulmicort Flexhaler)
Combination inhalers
Some medications combine bronchodilators and inhaled steroids.
Examples of these combination inhalers include:
 Fluticasone and vilanterol (Breo Ellipta)
 Fluticasone, umeclidinium and vilanterol (Trelegy Ellipta)
 Formoterol and budesonide (Symbicort)
 Salmeterol and fluticasone (Advair HFA, AirDuo Digihaler, others)
Combination inhalers that include more than one type of bronchodilator also are available.
Examples of these include:

INTRODUCTION
 Aclidinium and formoterol (Duaklir Pressair)
 Albuterol and ipratropium (Combivent Respimat)
 Formoterol and glycopyrrolate (Bevespi Aerosphere)
 Glycopyrrolate and indacaterol (Utibron)
 Olodaterol and tiotropium (Stiolto Respimat)
 Umeclidinium and vilanterol (Anoro Ellipta)
Oral steroids
For people who experience periods when their COPD becomes more severe, called moderate or
severe acute exacerbation, short courses (for example, five days) of oral corticosteroids may
prevent further worsening of COPD. However, long-term use of these medications can have
serious side effects, such as weight gain, diabetes, osteoporosis, cataracts and an increased risk of
infection.
Phosphodiesterase-4 inhibitors
A medication approved for people with severe COPD and symptoms of chronic bronchitis is
roflumilast (Daliresp), a phosphodiesterase-4 inhibitor. This drug decreases airway inflammation
and relaxes the airways. Common side effects include diarrhea and weight loss.
Theophylline
When other treatment has been ineffective or if cost is a factor, theophylline (Elixophyllin, Theo-
24, Theochron), a less expensive medication, may help improve breathing and prevent episodes
of worsening COPD. Side effects are dose related and may include nausea, headache, fast
heartbeat and tremor, so tests are used to monitor blood levels of the medication.
Antibiotics
Respiratory infections, such as acute bronchitis, pneumonia and influenza, can aggravate COPD
symptoms. Antibiotics help treat episodes of worsening COPD, but they aren't generally
recommended for prevention. Some studies show that certain antibiotics, such as azithromycin

INTRODUCTION
(Zithromax), prevent episodes of worsening COPD, but side effects and antibiotic resistance may
limit their use.[18]

INTRODUCTION
1.13 Medications Available for the Treatment of COPD
Drugs Inhaler
(mcg/use)
Maintainance Dose Side effects
Beta2 agonists
a) Short acting
 Albuterol
b) Long acting
 Formoterol
 Salmeterol
 Arformeterol
90 MDI
20 DPI
50 DPI
15 DPI
180 mcg (2 puffs )
inhaled PO every 4-
6hr
20 mcg every 12 hr
50 mcg every 12 hr
15 mcg every 12 hr
Tremor
Palpitation, Bronchitis
Chest pain, Back pain,
Sinusitis
Anticholinergics
a) Short acting
Ipratropium
b) Long acting
Tiotropium
17 MDI
18 DPI
2 inhalation every 6 hr
18 mcg per day
Palpitation, Bronchitis
Xerostomia, Sinusitis
Combination
short acting beta2
agonists +
Anticholinergic
Albuterol +
Ipratropium
100/20 MDI 2 inhalation every 6hr Albuterol: Tremor, Sinus
tachycardia, Anxiety
Ipratropium: Bronchitis,
Upper respiratory tract
infection
Combination long
acting beta2
agonist + Inhaled
corticosteroid
 Salmeterol +
Fluticasone
50+250
50+500 DPI
250/50 mcg PO every
12 hr
Headache, Palpitation,
Bronchitis

INTRODUCTION
 Formoterol +
Budesonide
4.5+80
4.5+160 DPI
2 inhalations every
12hr
Headache, Pharyngitis
Methylxanthines
Theophylline Tablets/Capsule
12 h: 100, 125,
200, 300, 450 mg
Initial >45 kg: 10
mg/kg/d titrate to max
800 mg/d in divided
doses every 6–8 hrs
Tachycardia, nausea.
vomiting, nervousness,
restlessness
Systemic
corticosteroids
 Prednisone
 Methyl-
prednisolone
1, 2.5, 5, 10, 20,
50 mg tablets
4, 8, 16, 32 mg
tablets
5–60 mg/d single or
divided dose
4–48 mg/d in 4
divided doses
Short-term: Insomnia,
indigestion, increased
appetite, nervousness
Long-term: Cataracts,
hypertension, thinning bones,
easier bruising, slower wound
healing, muscle weakness
MDI – Metered Dose inhalers, DPI – Dry Powder Inhalers, PO – Orally , hr – Hours
Table 3: Medication available for treatment for chronic obstructive pulmonary diseases [19]
Stepwise approach to the management of COPD
4 Stages of COPD Pharmacologic Intervention
Mild
FEV1/FVC <70% Add a short-acting bronchodilator when needed
(anticholinergic or beta2-agonist)
Moderate
 FEV1 ≥80%
 FEV1/FVC <70%
 50% FEV1 <80%
Prescribe an annual influenza vaccination
Add 1 or more long-acting bronchodilators on a scheduled
basis
Consider pulmonary rehabilitation
Severe
FEV1/FVC
<70% 30% FEV1 <50%
Add inhaled glucocorticosteroids if repeated exacerbations
occur
Very severe

INTRODUCTION
FEV1/FVC <70%
FEV1 <30%
Evaluate for adding oxygen
Consider surgical options
COPD indicates chronic obstructive pulmonary disease; FEV1, forced expiratory volume in 1 second; FVC, forced
vital capacity.
Table 4: Treatment approach for management of chronic obstructive pulmonary diseases [20]
1.14 LIFESTYLE CHANGES
 Avoid alcohol consumption.
 Do yogas and Exercise regularly.
 Eat healthy foods.
 Avoid smoke and air pollution.
 Avoid close contact with people who have respiratory infections .
 Avoid exposure to environmental irritants. [21]

INTRODUCTION
COMPARISION BETWEENASTHMAAND CHRONIC OBSTRUCTIVE
PULMONARY DISEASES
ASTHMA CHRONIC OBSTRUCTIVE
PULMONARY DISEASES
Age Any age, Common in childhood Generally above 40 years
Causes Genetics and environmental factors Usually smoking related but also
related to genetics and environmental
factors
Co-
morbidities
Others allergic conditions,
Including hay fever
Smoking related co-morbidities, such
as coronary heart diseases and
systemic problems such as
osteoporosis
Triggers Poor control due variety of reasons,
including under treatment, infection
or exposure to allergens
Poor treatment because treatment is
suboptimal or condition is
deteriorating
Diagnosis Careful history taking, trial of
therapy, lung function and others
tests
Spirometry and others test
Prognosis Symptoms can be well controlled
and patients can maintain activities
of daily life in old age.
Symptoms deteriorate over time –
patients become increasingly reliant
on intensive health sciences
Predictability Diseases is not progressive but can
be unpredictable
Progression is relatively predictable
– functions declines with time
Management Largely in primary care, specialist
services in severe asthma
Required many different types of
input to co-ordinate care
Treatment Inhaled steroids are the cornerstone
of treatment, with add-on long acting
bronchodilators or others agents if
necessary. Others anti-inflammatory
or anti-allergics medication
sometimes needed .
Oxygen only used during severe
Regular bronchodilations with high
dose steroids or inhaled
corticosteroids long acting
bronchodilators combination
reserved for many severe cases.
Long term oxygen therapy improves

INTRODUCTION
exaberations prognosis in other diseases
Table 5: Comparision between Asthma and COPD. [22]

INTRODUCTION
1.15 INHALERS
Inhaler devices are an important part of the armamentarium of clinicians who treat asthma and
COPD.
Figure 3 : Inhalers [24]
There are a broad range of options available for the management of asthma and COPD. [23]
Inhalation therapy is the most effective treatment for almost all people with asthma and COPD.
The major advantage of the inhaled route is that drug is delivered directly to the airways, where
it has rapid onset of action with minimal dose, thus limiting systemic side effects. Inhalers are
also portable and compact which makes them suitable for ambulatory therapy. [24]
Today, commonly used inhaled therapies include; short acting beta agonists( SABA’s ) Eg
salbutamol, short acting muscarinic antagonist (SAMA’s) Eg: ipratropium, long acting beta
agonists (LABA’s) Eg salmeterol , long acting muscarinic antagonist (LAMA’s) Eg tiotropium
and inhaled corticosteroids (ICS ) Eg Beclomethasone .[24]

INTRODUCTION
These medications can be used as required to relieve acute symptoms of asthma (SABA’s,
SAMA’s) or for daily maintenance to prevent worsening of symptoms (ICS with LABA’s ,
LAMA’s) . Sustained use of ICS reduces airway inflammation, improves symptoms and reduce
asthma related morbidity and mortality. [24]
Asthma and COPD Medicines are commonly administered using either pressurized metered dose
inhaler (PMDI ) or a dry powder inhaler (DPI).[23]
Pressurized metered dose inhaler (MDI) is the most commonly used and cheapest device,
which may also be used in conjunction with a spacer device [25]. A MDI is a small, aluminium
canister that contains a mixture of both medication and pressurized propellant . The pressure
from the growing propellant forces the medication from inside the canister through the device
each time the canister is pushed down into the plastic container or boot/actuator [26] . MDI
require patient to co-ordinate pressing down on inhaler canister whilst initiating a slow and deep
inhalation. [27] But their correct use require simultaneous device activation and inspiration, a
challenge for many patients. In addition to coordination problems, elderly patient, patient with
osteoarthritis or weak hands may not have the grip, strength or dexterity needed to fire inhaler.
[26]

INTRODUCTION
Figure 4 : Pressurized metered dose inhalers[25].
METERED DOSE INHALER
For those who find coordination required to use MDI difficult , a modified breath actuated
pressurized metered dose inhaler can be prescribed or an add on device can be used with the
inhaler such as spacer or a holding chamber. Spacers provide added advantage of improving
delivering of the drug to the appropriate portion of the airway while preventing oropharyngeal
deposition which is particularly important for ICS.[27] Breath Actuated MDI’s enable the patient
to prime the inhaler which is then only actuated when patient takes a breath, avoiding need to
coordinate actuation with breathing. [25]
Figure 5: Breathe actuated metered dose inhalers [25].

INTRODUCTION
Figure 6: Metered dose inhalers with spacer. [25]
Dry powder inhaler (DPI) is a different type of inhaler that delivers medication as a fine, dry
powder. Instead of a force propellant, this require rapid and forcible inhalation activated by
inspiration by the patient through mouthpiece. This deep breath also helps to carry the powdered
medication further into the lungs.
There are many different types of DPI’s available today. [26]

INTRODUCTION
Figure 7: Types of Dry powder inhalers [26].
Actuating the DPI device is problematic for children, elderly and extremely breathless patients
who may not be able to achieve a fast and forceful inhalation enough to activate the device.
Breathless patient may also not be able to maintain 10 second breathe hold that is recommended
immediately after inhalation. [26]
Both inhaler types require a full exhalation before use and breath holding is recommended after
use. [27]

INTRODUCTION
Figure 8: Steps involved in Dry Powder inhalation technique
IMPORTANCE OF ASSESSING INHALATION TECHNIQUE:
As many as 70% to 80% of people with asthma and COPD are unable to use their inhaler device
correctly . This means that drug is not delivered properly to the lungs. Poor inhalation technique
has been associated with age, sex, educational level, emotional problems. Mistakes in inhaler
have been associated with poor clinical outcomes, including more frequent emergency

INTRODUCTION
department ED visits, hospitalizations, prescription of oral steroids and antimicrobials. Hence,
assessment of inhaler technique is an essential component of asthma and COPD care. [27]
Poor inhalation technique may be also due to confusion if patients are using more than one type
of inhaler.[26]
It has been estimated that the degree of compliance with inhaled drug therapy in patient with
asthma and COPD does not surpass 50%. Factors related to adherence with inhaled therapy:
 Complexity of inhalation regimen
 Peculiarities of inhaled devices
 Types of inhaled agent
 A variety of patient beliefs and sociocultural and psychological factors. [27]
The efficacy of inhaled medicines depends on proper inhaler technique and treatment adherence
by patients. Deep rooted beliefs and society imparted stigma in the patients mind affects the
patient’s attitude towards inhalers.
Changing the patients concepts by imparting education in this regard will improve treatment
outcomes of patients facilitating optimum utilization of available resources. [27]

INTRODUCTION
Development of questionnaire
A questionnaire is a technique for collecting data in which a respondent provides answers to a
series of questions. [28] To develop a questionnaire that will collect the data you want takes effort
and time. However, by taking a step-by-step approach to questionnaire development, you can
come up with an effective means to collect data that will answer your unique research question.
Perhaps the most important part of the survey process is the creation of questions that accurately
measure the opinions, experiences and behaviors of the public. Accurate random sampling and
high response rates will be wasted if the information gathered is built on a shaky foundation of
ambiguous or biased questions. Creating good measures involves both writing good questions
and organizing them to form the questionnaire.
Item generation
The content of the questionnaire was developed by the members on this project. An extensive
literature review was carried out by the team to retrieve already published instruments and to
identify the common domains. After the review of literature, the team decided to include three
domains namely knowledge, attitude and practice domain and each domain consisted of five
questions to assess the patient’s knowledge, attitude about their disease and practice on disease
management.
Item review
The rationale of KAP questionnaire was reviewed by a panel of experts namely pulmonologists,
clinical pharmacologists, language and public health experts. A content validity ratio was then
calculated for each item and the value higher than 0.78 was considered satisfactory. [29] Questions
about knowledge were corresponding to patient’s awareness of disease, part of the body affected,
causative factors, symptoms and physiological changes during asthma.

INTRODUCTION
Figure. 9: Flowchart of Development of questionnaire[29]
Second part of this questionnaire was about patient’s attitude on the curability of the disease,
convenient dosage form, continuation of medications, opinion on self-adjustment of doses and
contagiousness of disease. Patient’s practice of disease management was assessed by questions
regarded their habit of carrying medications, inhalation techniques followed, dosage timings,
avoiding food items and involving in activities which might exacerbate asthma.

INTRODUCTION
Many of the question in few research surveys have been asked in prior polls. However, asking
the same questions at different points allows us to report on changes in the overall view of the
general public . when measuring change overtime , it is important to use the same question
wording and to be sensitive to where the question is asked in the questionnaire to maintain a
similar context as when the question was asked previously
Figure 10 : Steps involved in validate the questionnaire [29]

INTRODUCTION
Validation of questionnaire
Questionnaire validation is a process in which the creators review the questionnaire to determine
whether the questionnaire measures what it was designed to measure. If a questionnaire's
validation succeeds, the creators label the questionnaire as a valid questionnaire. This validity
comes in different forms, all relying on the method used for the validation procedure.
Figure 11: Types of validation of questionnaire
Cross-cultural validation was adopted as shown in the below Figure 3. Internal consistency and
test-retest reliability were performed.

INTRODUCTION
Figure 12: schematic steps in cross - cultural validation
Measurement of KAP
For the purpose of statistical analysis, scoring was given to each domain. Each correct answer
yielded 1 point and wrong statement yielded 0 point. Each domain scores were calculated by
summing up correct answers and the score ranged from 0 to 5 for each domain and totally 0 to 15 for
KAP.
Patient education
In the usual practice, patients receive a general counseling from the physicians or their assistants.
Apart from these, a patient education material recommended by the GINA, which is available as
‘patient guide was used in educating the study patients in all their clinic visits [30]. The impact of
education on study patients was compared between the baseline and end visit KAP report. All the
patients were educated on day 0 (visit 1), 30, 60, 90, 120, 150 and 180 (end visit).

INTRODUCTION
Medication compliance assessment
Patient’s compliance with the study medication was assessed with the help of Medication
Compliance Cards (MCCs) which were provided to the patients at all the clinic visits except the
end visit. All the patients were instructed to mark on the respective date and time
(morning/evening) after taking the study medication. The patients were also instructed to bring
back the MCCs at their follow-up visits.
 Consumed medication = Medication issued – Returned medication of previous visit
 Score (% compliance) = (consumed medication / medication issued) x 100
 ≥80% of study medication consumed according to the prescribed regimes were
considered as complaint and ≤80% of study medication consumed according to the
prescribed regimes were considered as non-compliant.
Patient adherence assessment
An adherence form, which was maintained at the study site, was used to document the
observations from investigator side. The visit date was entered in the data sheet with the weight
of the inhaler at the time of medication issue. The compliance as per the MCCs was cross
checked with the canister weights.[30]

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