CHRONIC

OBSTRUCTIVE
PULMONARY DISEASE

JOSHI MARMIK
What Is COPD?

Chronic obstructive pulmonary disease (COPD) is

defined as a disease state characterized by
persistent respiratory symptoms and airflow
limitation that is not fully reversible.
• Emphysema- an • CHRIONIC
anatomically defined BRONCHITIS- a
condition clinically defined
characterized by condition with chronic
destruction of the lung cough and phlegm
alveoli with air space
enlargement

SMALL AIRWAY DISEASE- a

condition in which small
bronchioles are narrowed and
reduced in number.
• copd is third leading cause of death and affects
>10 million people in US.
• Airflow limitation is a major physiolgic change in
copd, it can result from small airway disease
and/or emphysema.
• Small airways may become narrowed by
cells(hyperplasia and accumulation),mucus and
fibrosis, and extensive small airway destruction is
a Hallmark of copd.
• (1) Chronic exposure to cigarette smoke in genetically
susceptible individuals triggers inflammatory and immune cell
recruitment within large and small airways and in the terminal air
spaces of the lung.
(2) Inflammatory cells release proteinases that damage the
extracellular matrix supporting airways, vasculature, and gas
exchange surfaces of the lung.
(3) Structural cell death occurs through oxidant-induced damage,
cellular senescence, and proteolytic loss of cellular-matrix
attachments leading to extensive loss of smaller airways, vascular
pruning, and alveolar destruction.
(4) Disordered repair of elastin and other extracellular matrix
components contributes to air space enlargement and emphysema.
• Cigarette smoke • Airway inflammation,
exposure affect the destruction and the
large and small development of
airways and alveoli. emphysema are
present in most with
COPD.
Gold 1,2- little or no Emphysema
Gold 3,4- Extensive Emphysema
At Greatest Risk Of Progression In
COPD= THOSE WITH AGGRESSIVE
AIRWAY DISEASE AND EMPHYSEMA
• LARGE AIRWAYS • SMALL AIRWAYS
• cigarette smoking • Major site of
often results in mucus increased resistance
gland enlargement in airway <or= 2mm
and goblet cell
hyperplasia, leading
to COUGH and
MUCUS production
that define as
CHRONIC
BRONCHITIS
• Emphysema is characterized by destruction
of gas-exchanging air spaces(respiratory
bronchioles, alveolar ducts,alveoli)
• Types of emphysema
• Centrilobular-mostly with cigarette smoking,most
prominent in upper lobes and superior segment of
lower lobes.
• Panlobular- commonly in patient with Alpha1AT
deficiency, mostly in lower lobes.
• Paraseptal- In 10-15% cases and is distributed
along the pleural margins with relative sparing of
lung central region
• Most typical finding- persistent reduction in
forced expiratory flow rates.

Airflow obstruction determined by spirometry

key parameters include the volume of air
exhaled within the first second of Forcd
expiratory maneuver (FEV1) and total volume of
air exhaled during the entire spirometric
maneuver(FVC)
• Hyperinflation
• in copd there is often air-trapping(increase
residual volume and increased ratio of
residual volume to TLC)
• Hyperinflation can push the diaphragm into a
flattened position
• cigarette smoking
• respiratory infections
• occupational exposure
• ambient air pollution
• passive or second hand, smoking exposure
• alpha 1 antitrypsin deficiency
 CLINICAL PRESENTATION
• HISTORY • PHYSICAL FINDING
• Three most common • Early stages can have
symptoms- entirely normal PE
cough,sputum • in patient with more sever
disease the pe of lung is
production, exertional
notable for a prolonged
dyspnea expiratory phase and may
include expiratory
wheezing
• hyperinflation-barrel chest
and enlarged lung
volumes, triopd position
to facilitate action of
scm,scalene, intercostal
muscles
• some patient with advanced disease have
paradoxical inward movement of the rib cage
with inspiration= HOOVER'S SIGN
• Two main goals
• 1) provide symptomatic relief (reduce
respiratory symptom, improve exercise
tolerance, improve health status)
• 2) reduce future risk (prevent disease
progression,prevent and treat exacerbation,
reduce mortality
• mMRC Dyspnea Scale CAT-COPD ASSESSMENT TEST
• 1—hurrying on level
ground or walking up a
slight hill
• 2— walk slower than
peers or stop walking
at their own pace 3—
walking about 100 yards
or after a few minutes on
level ground 4—too
breathless to leave the
house or when dressing
• Smoking Cessation- • Bronchodilator-
nicotine replacement primary treatment for
therapy available as all patient with copd
gum, patch,nasal and used for
spray, buporpion and symptomatic benefits
varenicline and to reduce
exacerbation.
• Anticholinergic • Beta Agonist- short
Muscarine acting ease symptoms
with acute improvement
Antagonists- short
in lunf function. LABA-
acting ipratropium symptomatic benefits and
bromide. LAMA- reduce exacerbation
aclidinium,glycopyrrol (arformoterol,formoterol,i
ate,tiotropium. ndacaterol,salmeterol)
Improve symptoms and • Side effect- Tremors and
Tachycardia
reduce exacerbations.
 NONPHARMACOLOGIC THERAPIES
• Pulmonarynary • Lung Transplant-
Rahabilitation
COPD is 2nd leading
• Lung volume reduction
surgery- patient with indication for lung
upper lobe predominant transplant. Candidate
emphysema and low post should have very
rehabilitation exercise severe airflow
capacity are likely to limitation,severe
benefit from LVRS
disability despite
• patient with FEV1<20% maximal medical
and diffusely distributed
emphysema on ct scan
therapy and no
have increased mortality comorbid condition
after the procedure and
thus are not candidate for
LVRS
• Episode of acute • Patient with
worsening of severe(FEV1 <50%)
respiratory symptom, very severe
increased (FEV1<30%) have
dyspnea,cough,whee and average 1-3
zing, change in episode per year
amount or character
of sputum.
• Strongest predictor of
exacerbation is
history of previous
exacerbation
• Bronchodilator • Mechanical ventilatory
support- initiation of
• Antibiotics- bacteria NIPPV in patient with
frequently implicated respiratory failure which
in COPD is defined as PaCO2
exacerbation include >45mmHg .
S.pneumoniae, Contraindication include
H.influenza, cardiovascular instability,
impaired mental status,
Morexella catarrhalis inability to
• Oxygen- maintain cooperate,copious
>or=90% secretions or inability to
clear secretion, significant
burns
• Following a hospitalization for COPD- 20%
re-hospitalized in 30days,
• 45% in next year

• Mortality following hospital discharge is 20%

in following year.
THANK YOU!!