Definitions:

1) COPD :
Chronic Obstructive Pulmonary Disease is a preventable and
treatable disease with some significant extrapulmonary effects that may
contribute to the severity in individual patients. Its pulmonary component
is characterized by airflow limitation that is not fully reversible. The airflow
limitation is usually progressive and associated with an abnormal
inflammatory response of the lung to noxious particles or gases.

Chronic Bronchitis : It is define clinically by chronic cough and

sputum production for 3 consecutive months over 2 consecutive years
after excluding other causes of cough. Pathologically, hypertrophy and
hyperplasia of submucosal glands located predominately in proximal
airways is the characteristic feature.

Emphysema: It is defined pathologically

destruction of gas exchanging portions of the lung.
2)

by

distension

and

Bronchial Asthma :
Asthma is a chronic inflammatory disorder of the airways in which
many cells and cellular elements play a role. The chronic inflammation is
associated with airway hyper-responsive (AHR) that leads to recurrent
episodes of wheezing, breathlessness, chest tightness and coughing
particularly at night or in early morning. These episodes are usually
associated with widespread, but variable airflow obstruction within the
lung that is often reversible either spontaneously or with treatment.

3) Bronchiectasis :
Bronchiectasis is a chronic condition define as an abnormal and
irreversible dilatation of the bronchi and larger bronchioles.
4) Acute Exacerbation of COPD :
An exacerbation of COPD is an event in the natural course of COPD
characterized by an acute change in the patients baseline dyspnea or
breathing difficulty, cough and/or sputum production beyond day-to-day
variability sufficient to warrant a change in management.

Extrapulmonary Or Systemic Manifestation of

COPD
General :

Weight Loss and Muscle wasting

Nutritional Anomalies and Anemia

Musculoskeletal :

Skeletal Muscle Dysfunction

Osteoporosis
Reduction in Exercise Tolerance and Performance

Cardiovascular:

Cor Pulmonale
Supraventricular Arrhythmias
IHD
Cardiac failure
Stroke

Endocrinology :

DM
Metabolic syndrome
Dysfunction of pituitary, thyroid, gonads and adrenals

Neuropsychiatrics:

Depression
Anxiety
Sleep Disturbance
Decline cognitive function

1) Weight Loss and Wasting:

-

Exact mechanism is incompletely understood but likely due to

imbalance in an ongoing process of protein degradation and
replacement.It may include alteration in endocrine hormones
such as insulin, GH, Testosterone, Glucocorticosteroids.
Commonest seen in 20 to 40 %

Loss of FFM adversely affects muscle aerobic and exercise

capacity
Hypoxia and Increase work of breathing leads to increased Basal
metabolic rate which leads to weight loss
Acidosis (hypercapnia), infection, inadequate caloric intake
especially in acute exacerbation stage associated with increased
breakdown of muscle cell protein.
Quadricep muscle wasting is commonly seen .It is commonly
associated with low level of testosterone hormone in men.

2) Skeletal Muscle Dysfunction:

-

It is most likely to occur due to sedentary lifestyle, tissue hypoxia

and systemic inflammation.
Systemic inflammation raising level of TNF-alfa, IL-8, IL-6 And
oxidative and nitroactive stress which leads to muscle protein
inactivation and degradation which leads to dysfunction, atrophy
and apoptosis .
Increase in lung inflammation does not correlate with increased
level of systemic inflammatory markers.

3) Quality of Life:
-

Weight loss and skeletal muscle dysfunction limit the activities

and exercise tolerance
BMI, Degree of Airflow Obstruction, Dyspnea and Exercise
capacity (BODE Index) have been used as measures of disease
severity and mortality risk in COPD.

4) Osteoporosis & Osteopenia:

-

Osteopenia and osteoporosis were reported in 68% of patients

with COPD.
Osteoporosis may lead to generalized bony pains, compression
fracture of the spine and compromised lung function due to
kyphosis and thoracic vertebral compression.
Corticosteroid therapy, including inhaled steroids, is generally
considered responsible for osteoporosis; although in one study,
compression fractures were reported in 49% of patients who had
COPD and had never received steroids.

5) Cardiovascular:
-

Structural changes in pulmonary arteries can occur early in COPD

before the onset of hypoxemia
Pulmonary hypertension and consequent right ventricular failure,
cor pulmonale, are usually the consequence of chronic alveolar
hypoxia, with secondary contributions from destruction of the
alveolar capillary bed, lung hyperinflation, and increased blood
viscosity.

Physical findings of venous engorgement, and right ventricular

hypertrophy and dilatation are late signs of Cor Pulmonale
Peripheral edema is poorly correlated with resting right atrial
pressure and may reflect fluid retention from activation of the
reninangiotensinaldosterone system.
Functional imaging studies including echocardiography or
radionuclide ventriculography are more probative for evaluation
of right ventricular function.
If the pulmonary artery pressure exceeds 25 mm Hg, the average 5year survival is diminished by 50%.
The primary treatment of cor pulmonale consists of continuous oxygen
to overcome hypoxemia and diuretic to optimize volume status.
Calcium channel blockers and other vasodilators can dilate the
pulmonary circulation, but they worsen hypoxemia and their benefit is
not established. Phlebotomy increases exercise capacity when the
hematocrit exceeds 55%, but persistent erythrocytosis suggests
inadequate oxygen supplementation or another cause. Anticoagulation,
which is considered beneficial in severe pulmonary vascular
hypertension of other causes, is of uncertain benefit in patients with
pulmonary hypertension caused by COPD.
Pulse inhalation of NO, a potent vasodilator, along with supplemental
O2 has shown promise as a treatment for Pulmonary Hypertension.It
reduce pulmonary vascular resistance by increasing cycline guanosine
monophosphate in vascular wall. Sildenafil has same action.

Systemic inflammation, atherosclerotic coronary heart disease

and cardiovascular deaths are known as important complications
of COPD. Atherosclerosis and coronary artery disease are associated
with decline in forced expiratory volume in one second
(FEV1).The risk for cardiovascular death was 75% greater for
patients who had lower FEV1
Supraventricular tachyarrhythmias are common in patients with
COPD, as a consequence of right atrial enlargement, increased
endogenous adrenergic tone, hypoxemia, and drug treatment
specifically theophylline and anticholinergic bronchodilators

6) Endocrinal Disorders:
-

Several mechanisms have been proposed to cause endocrine

dysfunctionhypoxemia, hypercapnia, systemic inflammation
and glucocorticoid administration for airway obstruction
The decreased protein anabolism and increased catabolism affect
the body mass and also accounts for muscle dysfunction
Altered renin-angiotensinaldosterone function affects the blood
flow, fluid balance and the renal function.
Other systemic effects of endocrinal disorders include the
disturbances of control in breathing, worsening of respiratory
mechanics and impairment of cardiac function

7) HYPERCAPNIA

Chronic hypercapnia secondary to alveolar hypoventilation can

be considered an adaptive response to obstructive lung disease
by decreasing the work of breathing, preventing respiratory
muscle fatigue, and allowing a diminished sensation of dyspnea.
The adverse effect of chronic hypercapnia is the development of
alveolar hypoxia and consequent pulmonary hypertension.
Accordingly, the approach to chronic hypercapnia is the use of
supplemental oxygen in controlled concentrations. In patients
who are very sensitive to oxygen, it is preferable to provide
oxygen in controlled concentrations with Venturi masks rather
than nasal cannula.
Nocturnal ventilation has been effective in reducing daytime
hypercapnia in patients with neuromuscular disease and
kyphoscoliosis And showing modest improvement in symptoms
and quality of life, and a trend toward reduced hospitalization.

8) Neuropsychiatric :
-

Depression
Anxiety
Disordered
sleep
is
commonly
ascribed
to
hypoxemia,hypercapnia and diminished ventilatory responses. It
is further aggravated by the concomitant presence of nocturnal
respiratory symptoms, anxiety and depression. Obstructive sleep
apnea is present in about 10 to 15% patients of COPD (overlap
syndrome)
The other sleep disturbances seen in more than half of the COPD
patients include the diminished arousal responses, longer latency
in falling asleep, more frequent awakenings or generalized
insomnia
Impairment of intellectual function
cognitive decline O2 improve it

9) Sexual Dysfunction :

Question : Etiology of Bronchiectasis. How to manage

Acute Exacerbation of Bronchiectasis.
Pathogenic mechanisms
Primary infective insult

Etiology

Primary impairment of mucous

clearance
Genetic, biochemical
Genetic, ultrastructural
Immunodeficiency syndrome,
congenital and acquired

Bronchitis/bronchiolitis
Pertussis
Measles
Adenovirus
Pneumonia
Tuberculosis

Cystic fibrosis
Primary ciliary dyskinesias

Common varied immune deficiency

Selective immunoglobulin deficiency
Functional immune deficiency
Secondary
hypogammaglobulinaemia
Human immunodeficiency virus
infection

Hyperimmune response

Allergic Bronchopulmonary mycoses

Infection secondary to bronchial

obstruction
Intraluminal

Slow-growing tumour, Aspirated foreign

body

Extraluminal

Lymphadenopathy

Autoimmune disease

Inflammatory bowel disease

Coeliac disease
Systemic lupus erythematosus

Inhalational/aspiration injury

Developmental defects
Structural

Biochemical

Rheumatoid disease
Cryptogenic fibrosing alveolitis
Primary biliary cirrhosis
Thyroiditis
Pernicious anaemia

Toxic fumes
Gastric contents

Pulmonary agenesis
Sequestrated segment
Tracheobronchomegaly
Bronchomalacia
1-Antitrypsin deficiency

Management of Acute Exacerbation of Bronchiectasis:

Most Common Cause : Fresh infection (Mostly Viral)

Bacterial Organisms: H.Influenza, P.Aerugenosa, Streptococcus
pneumoniae or Moraxella catarrhalis
An exacerbation causes the patient to have symptoms of one or more
symptoms such as increasing frequency of cough, sputum volume and
sputum purulence, Alteration in sputum colour, Shortness of breath, Fever
(not always).
On Examination, there is hypoxia, dyspnea , crackels with or without
wheeze.
Ensure oxygen saturations are adequate in air (>94%)
Chest x-ray - pleural effusion or a pneumothorax or Secondary infection
(Air fluid level)
Send sputum for microscopy, culture and sensitivity
Initially the treatment depends partly on the previous microbiology results
available
Even if you suspect a viral aetiology antibiotics are normally prescribed to
reduce the microbial load.
Oral, parenteral, and aerosolized antibiotics are used, depending on the
clinical situation.
If the patient is colonized with Pseudomonas aeruginosa, then treatment
can be done with an oral agent, such as ciprofloxacin 500 mg twice a day;
for more severe exacerbations, intravenous antibiotics may be more
effective
If the exacerbation is caused by MRSA, then often two antibiotics are
recommended either orally or intravenously.
Azithromycin has known anti-inflammatory properties and long-term use
has been studied in patients with both CF and non-CF bronchiectasis

Bacterial

First choice

Second line

infection
Haemophilus
influenza
Moraxella
catarrhalis
Streptococcus
pneumonia
MRSA

Pseudomonas
aeruginosa

MAC

treatment
Co-amoxiclav

Doxycycline
ciprofloxacin

Amoxicillin

Clarithromycin

Rifampicin and
trimethoprim
or IV vancomycin
or teicoplanin
Ciprofloxacin (Oral)

Rifampicin and doxycycline or

linezolid

Clarithromycin,
Rifampin, Ethambutol,
and possibly
Streptomycin that is
continued until the
patient's culture results
are negative for 1 year

Ceftazidime and tobramycin or

colistin
Aztreonam, Tazobactam,
Meropenem, gentamicin (IV)
----

Duration of Antibiotics : Due to difficulties with antibiotic penetration

into the damaged lung and airways, a prolonged course of antibiotics is
often required. however if there is a clinical improvement with a fall of
serum inflammatory markers, such as C-reactive protein, then this would
indicate improvement and often such a course of antibiotics would last for
10 to 14 days.
Aerosolized Antibiotics :
- it is capable of delivering relatively high concentrations of drugs locally
with relatively few systemic adverse effects.This is particularly
beneficial in treating patients with chronic infection from P aeruginosa.
Inhaled tobramycin is the most widely used nebulized treatment for
patients with bronchiectasis from either CF (More commonly) or non-CF
causes of bronchiectasis. Gentamicin and colistin have also been used.
- It may cause wheezing even after pre-dosing with inhaled -2 agonists

Regular Monthly Antibiotics : Some patients with chronic bronchial

infections may need regular antibiotic treatment of 7 to 10 days per
month to control the infectious process

Bronchial Hygiene & Physiotherapy :

- Its very Important to clear the airway and relieve spasm.
- Maintaining adequate general hydration, which may improve the
viscidity of secretions, is important.
- Postural drainage with percussion and vibration is used to loosen and
mobilize secretions.

Bronchodilators, including beta-agonists and anticholinergics, may help

some patients with bronchiectasis, presumably reversing
bronchospasm associated with airway hyperreactivity and improving
mucociliary clearance.
Devices available to assist with mucus clearance include flutter
devices, intrapulmonic percussive ventilation devices, and incentive
spirometry Proper Technique Required
Nebulization with concentrated (7%) sodium chloride solutions appears
to be beneficial, particularly in patients with CF-related bronchiectasis.
Aerosolized recombinant DNase has been shown to benefit patients
with CF. This enzyme breaks down DNA released by neutrophils, which
accumulates in the airways in response to chronic bacterial infection.
However, improvement has not been definitively shown in patients with
bronchiectasis from other causes.
Inhaled mannitol as agents to help aid sputum production .

Anti-inflammatory Drugs:
- Inhaled corticosteroids,[oral corticosteroids,leukotriene inhibitors used
to modify the inflammatory response caused by the microorganisms
associated with bronchiectasis and subsequently reduce the amount of
tissue damage.

NIV : Noninvasive ventilation may be useful for those patients who slip
into type 2 respiratory failure

Question : How to Differentiate COPD from Bronchial

Asthma?
COPD

BRONCHIAL ASTHMA

Definition
It is a preventable and treatable
disease with some significant
extrapulmonary effects that
may contribute to the severity
in
individual
patients.
Its
pulmonary
component
is
characterized
by
airflow
limitation that is not fully
reversible. The airflow limitation
is usually progressive and
associated with an abnormal
inflammatory response of the

Asthma
is
a
chronic
inflammatory disorder of the
airways in which many cells
and cellular elements play a
role.
The
chronic
inflammation is associated
with
airway
hyperresponsive (AHR) that leads
to recurrent episodes of
wheezing,
breathlessness,
chest
tightness
and
coughing
particularly
at

lung to
gases.

noxious

particles

or

night or in early morning.

These episodes are usually
associated with widespread,
but
variable
airflow
obstruction within the lung
that is often reversible either
spontaneously
or
with
treatment.

It is a preventable and treatable

disease.
It has abnormal inflammatory
response of the lung to noxious
particles or gases.

It is a not preventable but

treatable disease.
It is chronic inflammatory
disorder of the airways with
AHR in which many cells and
cellular elements play a role
It has airflow obstruction
within the lung that is often
reversible either
spontaneously or with
treatment.

It has airflow limitation is

usually progressive and is not
fully reversible.

Classification
The severity of airways
obstruction in COPD is best
classified with spirometry
FEV1 cutoffs of <80%, 50% and
30% of predicted values are
used to further stage disease
severity to Mild, Moderate,
Severe and Very severe COPD

Asthma severity is determined on the

basis of both impairment* and risk*

FEV1 cutoffs of >80%, 60%80% and <60% of predicted

values are used to further
stage disease severity Into
Intermittent and Persistent
(Mild, Moderate & Severe).

Clinical Profile
Age
History of
Allergy
History of
Atopy

Mostly in Old Peoples over 40

years
Absent

Mostly in Children and Adults

Absent

Commonly present. History

of allergic rhinitis (hay fever)
or atopic dermatitis
(eczema)
Present

Seasonal
Variation
Family History

Absent

Symptoms

They are Persistent and

Progressive.
Most patients with COPD usually

Not always present

Present

Mostly Family member have

asthma
They are Variable and
Episodic.
The typical symptoms of

Exacerbation

History of
Smoking
Systemic
Effects
Environmental
Causes

first develop a chronic

productive cough followed by
dyspnea.
COPD aggravations are largely
caused by respiratory tract
infections such as pneumonia
and the flu, Exposure to
environmental pollutants.
Chronic Smoking
In more than 50% of COPD
patients
inhalation exposures to
cigarette smoke, occupational
dusts and chemicals and indoor
and outdoor pollution

asthma are wheeze,

dyspnoea, cough and a
sensation of chest tightness
Asthma is usually made
worse by exposure to
allergens, cold air, and
exercise.
Smoking make asthma
worse
Uncommon
sensitization to indoor and
outdoor aeroallergens and a
history of viral respiratory
infections, in particular,
rhinovirus infections
Chest is Normally Elliptical

Inspection

Chest is Barrel Shapped

Chest X Ray
Flattening of
Diaphragm
Widening of
ICS
Straightening
of Rib

Hyperinflatted Lung fields

Present

Usually normal Chest X Ray

Absent

Present

Absent

Present

Absent

Radiological

Laboratory Investigation
Sputum
Microscopy &
Peripheral
Blood smear

T lymphocytes, with
macrophages and Neutrophils,
are the predominant
inflammatory cell types

Post
Bronchodilator
Reversibility

Absent

Eosinophils and lymphocytes

are the major inflammatory
cells in asthma

Spirometry
Good - more than 12% or >
200 ml increase in FEV1
after giving short acting
inhaled bronchodilator

Treatment

Pharmacologic
al

COPD is treated to reduce

symptoms and Prevent systemic
co-morbidities
AS PER GOLD GUIDELINES
Inhaled Bronchodilators :
glucocorticoids, 2-agonists,
anticholinergics (Either single or

Asthma is treated to
suppress chronic
inflammation
AS PER GINA GUIDELINE
Inhaled Bronchodilators :
glucocorticoids, 2agonists(Either single or in

in combination)
Oral/Paranteral :
methylxanthines ,
glucocortecoids

Non
Pharmacologic
al

Long term O2 Therapy is

required in severe case to
prevent development of
systemic co-morbidities
1) Health education on
managing chronic illnesses,
2) Pulmonary rehabilitation with
focus on physical and dietary
measures
3) Smoking cessation
intervention programs.

combination)

Oral/Paranteral :
methylxanthines ,
glucocortecoids
Severe and Resistant cases :
Anti IgE Therapy
1)Patient-physician
partnership (e.g., asthma
action plan)
2) Identification and
reduction of exposure to risk
factors
3) Individualized care during
pregnancy and for
rhinosinusitis and nasal
polyps, gastroesophageal
reflux, aspirin-exacerbated
respiratory disease, and
anaphylaxis.

Prevention
Primary
prevention

Tobacco cessation strategies

Secondary
prevention

Early diagnosis, risk factor

modification and treatment

Prevention of allergic
sensitization (e.g Excessive
BF) & Prevent exposure to
smoke during perinatal
period
Prevention of exposure to
known Indoor Triggers* and
Outdoor triggers*
Antihistamines and allergenspecific immunotherapy may
play a role in preventing the
development of asthma in
atopic children
Prevention of exposure to
NSAIDS
specially Aspirin to
asthmatics who are allergic
to it.
Asthmatics with a history of
nasal polyps should go for

surgical intervention to
prevent repeated
exacerbation.

Vaccination

All patients, regardless of

disease severity, should be
offered the yearly influenza
vaccine. Pneumococcal vaccines
should be offered to patients
with COPD who are 65 years
and older and to patients with
COPD younger than 65 who
have an FEV1 of <40%

Treat GERD if present.

inactivated influenza vaccine
for patients (aged 6 months
to adult) who have asthma
to prevent exacerbation

* Impairment : is a function of the frequency of daytime and nocturnal

symptoms, short-acting 2-agonist (SABA) use, the degree to which normal
activity is affected and lung function.
* Risk : It is defined by the frequency of exacerbations requiring oral corticosteroid (OCS) use.
* Indoor Triggers : Tobacco smoke, Dust mites, Furry animals, Cockroaches and
Fungi
* Outdoor triggers : Aeroallergens and Air pollutants