P2s1 medicine COPD SYnurhTS

TREATMENT OF COPD
Lifestyle
Smoking cessation
Bronchodilators
Beta agonist
Anticholinergic agents
Inhaled corticosteroids
Oral corticosteroid
Combined bronchodilators
Steroid
Theophylline
Oxygen
Others:
N- acetylcysteine :
Mucolytic
Antioxidant
IV alpha antitrypsin

Clinical features

Cough with sputum for more than three

months per year for more than two
successive years before seeking
medical attention.

Sputum , mucous , worse in the

morning ( yellowish or purulent when it
is acute infective exacerbation)

Exertional dyspnea and then

progressive ( severe in acute
exacerbation) later restricted daily and
social activities , house bound and bed
bound

Surgery
i.
ii.
iii.
iv.
v.
vi.

Lung volume reduction

surgery
Lung transplantation
Others
Prophylactic vaccination
against influenza virus
Chest physiotherapy
(pulmonary rehabilitation)
Good nutrition
Exercise

PHYSICAL SIGN

Use of accessory muscles

( supraclavicular and
suprasternal hollow, less
distance between cricoid
cartilage and sternal ) tracheal
tug

Purse lip breathing with out

without cyanosis , plethoric
face

Signs of type 2 respi failure

such as tachycardia ( AF) with
bounding pulse, flapping

During exacerbation
Admission
Assess severity and obtain
previous data
Antibiotic :
Strep pneumonia
Haemophilus influenza
Moraxella catarrhalis
Penicillin grp
Amoxicillin, ampicillin,
augmentin, Cephalosporin grp
Mycoplasma pneumonia,Chlamydia
pneumonia
Macrolides:
Erythromycin
Azithromycin

Acute exacerbation
1. Oral prednisolone 30mg, 10
days to 2 weeks
(reduce duration of stay), decrease
chance of subsequent exacerbation and
relapse
2.

Supplement Oxygen- keep

arterial saturation above 90%
3. Mechanical ventilator support
(NIPPV)
Non invasive positive pressure
ventilation
PCO2 > 45mmHg
(reduce mortality, need
intubation, complication
therapy, duration of stay in
hospital)
Containdicated NIPPV
1. CVS instability
2. Impaired mental status
3. Lack of cooperation
4. Copious secretion inability to
clear secretions
5. Craniofacial abnormalities
6. Extreme obesity- severe
degree of burns

INVESTIGATION

Spirometry for FEV1 and FEV1/FVC ratio

symptoms
Spirometry

0
at risk chronic cough and
Normal

sputum production

1
Mild
FEV1/FVC <0.7
&FVC>80% predicted

11
moderate
<0.7,
FEV1 < 50% and < 80% predicted

111
severe
<0.7,
FEV1<30% and < 50% predicted

Chest X-ray
Bullae, paucity of lungs
marking, increased lung
volume, hyper
translucency, low flat
diaphragm, tubular heart
/ cardiomegaly,
Signs of infection such
as pneumonia,
pneumothorax
Serum 1anti-trypsin if
patient is < age of 50,

P2s1 medicine COPD SYnurhTS

Confusion, irritability, fits and

convulsions, coma ( respi failure)
chest tightness /pain, swelling of the
legs ( cor-pulmonale)
CAD, stroke, PE , pneumonia,
pneumothorax, ( complications)

Etiology

Definition by GOLD ( Global

Initiative for Chronic Obstructive
Lung Disease)

Airflow limitation which not fully

reversible such as

1. emphysema (anatomically
defined condition characterized by
destruction and enlargement of the
lung alveoli

2. Chronic bronchitis ( clinically

defined as chronic cough with
productive sputum)

3.small air way disease (a

condition in which small bronchioles
are narrowed)

tremors, drowsiness
Hyperinflation of lungs with
loss o cardiac and liver
dullness
Parasternal heave, palpable P2
and loud P2 ( corpulmonale)
Raised JVP and edema of legs
( right heart failure)

Epidemiology

Infections

Childhood:
difficult o assess

Adult :
important cause of acute
exacerbations

Occupational exposure

Coal, Gold and Mining and

Cadmium

Cadmium only is associated

with low FEV1 , FEV1/FVC and
Dlco

Ambient Air Pollution

( much less important risk
factor for COPD than
smoking)

Urban and rural ( cooking )

1V
very severe
FEV1 <30% or >50% with

<0.7,

signs of

predominant basilar
disease and no
history of smoking

respi failure or right heart failure

Positive or Second-and ,
Smoking Exposure
Exposure of children to
maternal smoking
Although passive smoke
exposure has been associated
with reduction in pulmonary
function , the importance of
this risk factor in the
development of severe
pulmonary function is
uncertain.
Genetic
Many variants of the protease
inhibitor (PI) locus which
encodes 1 anti-Tripsin ( AT)
M ( normal allele), S ( slightly
reduced) Z ( markedly reduced
allele )
ZZ or PiZ ( most common form
of severe aAT deficiency

Pathology and pathogenesis

Cigarette smoking affect large and

small airways ( <2mm in diameter)
and alveolar space

Changes in large airways cause

cough with mucous sputum

Changes in slam airways cause

physiologic alteration

( small airways obstruction and

emphysema changes contribution
vary in individuals. The former is
changes in early part of the disease
and the latter is later part of the
disease)

Large airways: mucous gland

enlargement and goblet cell
hyperplasia. These changes are not
related to airflow limitation. Bronchi
may undergo squamous cell
metaplasia which not only
predispose to bronchogenic
carcinoma but also disruption of
mucociliary clearance. Neutrophil
influx , its peoteolytic activity and
neutrophil elastase , the most
secretagogues. Cytokine and
chemokine release , accumulation
of macrophages and TCD8 > TCD4
cells