the Aimath reveiably lun preventable

CopD irrevelable / preventable

Normal ventilator function

Diaphragm contracts and descends, rib cage moves upwards and outward.

Pressure in the thorax is less than in the

mouth so air flow into the lungs occurs.

In expiration, diaphragm relaxes and

moves upwards, the rib cage moves
inward.

Expiration is passive so no muscular contraction is needed.

Lung tissue is intrinsically elastic and has a natural ability to recoil.
During exercise expiration is aided by the contraction of abdominal and
thoracic expiratory muscles.
Contractions generate positive pressure in the thorax pushing air out.
Definition
Chronic Obstructive Pulmonary
Disease (COPD) is a preventable and treatable disease
state characterized 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

Component of COPD
The definition Include chronic bronchitis, emphysema with airflow
limitation.

The definition excludes other causes of chronic airflow obstruction such as

Pulmonary cystic fibrosis

Diffuse panbronchiolitis
Bronchiectasis
 muso-pullent
or Not mat be "pullert"
-mua
Definition : recurrent mucoid or mucopurulent expectoration,
occurring on most days for a minimum of 2 months of the year for 2

and expectoration.
L
consecutive years in absence of other causes of cough
month 12 yew
2 dool and most be

and incoive year

much a Bronchictiv

The pathological basis of chronic bronchitis is mucus

hyper secretion secondary to hypertrophy of
the glandular elements of the bronchial mucosa

Types:
Simple chronic bronchitis chronic mucoid hyper-secretion
Mucopurulent bronchitis sputum persistently or intermittent mucopurulent
Obstructive bronchitis persistent widespread airway narrowing

~without Fibroi to be deflected

From I P P D
Pathological definition,
. . .

which is a condition where there is

permanent destructive enlargement
of the airspaces distal to the terminal
bronchioles without obvious fibrosis
(To exclude enlarged air spaces associated with gross fibrosis as in cryptogenic
fibrosing alveolitis).
A disease characterized by loss
Physiological definition of elastic recoil & thus
increasing lung compliance
Epidemiology
COPD is the fourth leading cause of
death in the USA and Europe, and COPD
mortality in females has more than doubled over
the last 20 years.

Risk factors of COPD

Host factors:
Genes (Alpha-1 antitrypsin deficiency) Hyperresponsiveness
Lung growth Sex
Exposure:
Tobacco smoking Recurrent bronchopulmonary Infections
Occupational dust and chemicals Diet
Environmental Pollution Perinatal events and Childhood illness
 X
&

and
masophage - Lymphocyte

Pathogenesis of COPD
The inflammation in the respiratory tract of COPD
patients appears to be an amplification of the normal
inflammatory response of the respiratory tract to chronic
irritants such as cigarette smoke.
Inflammatory Cells
Involve neutrophils, macrophages, and lymphocytes.

These cells release inflammatory mediators and interact with

structural cells in the airways and lung parenchyma.
Inflammatory Mediators
The inflammatory mediators attract inflammatory cells from the circulation
(chemotactic factors), amplify the inflammatory process (proinflammatory
cytokines), and induce structural changes (growth factors).
Oxidative Stress
Oxidative stress may be an important amplifying mechanism in COPD.

Oxidants are generated by cigarette smoke and other inhaled particulates,

and released from activated inflammatory cells such as macrophages and
neutrophils.
Protease-Antiprotease Imbalance
Protease-mediated destruction of elastin, a major connective tissue
component in lung parenchyma, is an important
feature of emphysema and is likely to be
irreversible.

Pathological changes characteristic of COPD are

found in
the proximal airways peripheral airways pulmonary vasculature
lung parenchyma
These changes include chronic inflammation, and structural
changes.
Proximal airways (trachea, bronchi > 2 mm internal
diameter) epithel metaple
-
Goblet cells, enlarged submucosal glands (both leading to mucus
hypersecretion), squamous metaplasia of epithelium
Peripheral airways (bronchioles < 2mm i.d.)
Airway wall Thickening, peribronchial Fibrosis, luminal inflammatory
Exudate, airway Narrowing (obstructive bronchiolitis)
Increased inflammatory response and
exudate correlated with disease severity

Lung parenchyma (respiratory bronchioles and alveoli)

Alveolar wall destruction, apoptosis of epithelial and endothelial cells.

Centrilobular emphysema dilatation and destruction of respiratory

bronchioles
Most commonly seen in smokers
Panacinar emphysema destruction of alveolar sacs as well as
respiratory bronchioles
Most commonly seen in alpha-1 antitrypsin
deficiency
Pulmonary vasculature
Thickening of intima, endothelial cell dysfunction, smooth muscle
Pulmonary hypertension
bothr a
categ
a
 Changes in Small Airways in COPD Patients

Inflammatory exudate in lumen

Disrupted alveolar attachments

Thickened wall with inflammatory cells

+
Macrophages, CD8 cells, fibroblasts

Peribronchial fibrosis
Lymphoid follicle
· both mpe-inflated chest but

empisema mot

Changes in Lung Parenchyma in COPD

Alveolar wall destruction

Loss of elasticity
Destruction of
pulmonary
Capillary bed

↑ Inflammatory cells
+
macrophages, CD8 lymphocytes
Pathophysiology
1-Airflow Limitation and Air Trapping
The inflammation, fibrosis, and luminal exudates
in small airways are correlated with the reduction in
FEV1and FEV1/FVC ratio.

The peripheral airway obstruction traps air during expiration, resulting in

hyperinflation.
Emphysema is more associated with gas exchange abnormalities
than with reduced FEV1

2-Gas Exchange Abnormalities

VA/Q imbalance
Reduced pulmonary vascular bed

3-Mucus Hypersecretion
Pulmonary Hypertension
Hypoxicvasoconstriction of small pulmonary arteries eventually results
instructural changes that include intimal hyperplasia and later smooth
muscle hypertrophy/hyperplasia.

The loss of the pulmonary capillary bed in emphysema may also

contribute to increased pressure in the pulmonary circulation.

Progressive pulmonary hypertension may lead to right ventricular

hypertrophy and eventually to right-side cardiac failure (cor
pulmonale).
 Are
Chronic hypoxia -
treger u

Of pulet, hapeten

Pulmonary vasoconstriction

Muscularization
Pulmonary hypertension Intimal hyperplasia
Fibrosis
Obliteration
Cor pulmonale

Death Edema

Systemic features
They have a major impact on survival and comorbid diseases.

Cachexia
A loss of skeletal muscle Mass and Weakness
Increased concentrations of inflammatory mediators,
including TNF, IL-6, and oxygen-derived free radicals
increased likeliness of having osteoporosis, depression
and chronic anemia
There is an increase in the risk of cardiovascular
diseases multi-fuel
·
tach, and

More Rise of C.
Arefy die

otcopoxir "chronic striod"

.

· depposition
·
obeity
Diagnosis and assessment of COPD
History:
History of exposure to risk factors, Tobacco smoke,
Occupational dusts and chemicals and Smoke from
home cooking and heating fuels.

Age of onset: After middle age

Season: winter
Symptoms:
Gradually progressive dyspnea is the most common presenting character.
~> shorth of broth
 Dyspnea that is Progressive (worsens over time),
usually worse with exercise, Persistent (present every day),
Described by the patient as an “increased effort to breathe,
“Heaviness,” “air hunger,” or “gasping.”

 Chronic Cough

May be intermittent and may be

unproductive.

 Chronic sputum production

 Recurrent respiratory infection

Recurrent attacks leading to cor pulmonal

 Heart disease
 Unexpected weigh loss
 Decreased food appetite
Physical Signs:
Earlier period:
None or prolonged expiratory phase wheeze with forced exhalation
Advanced Stage:
Inspection:

Barrel-shaped chest
accessory respiratory muscle participate
prolonged expiration during quiet breathing
Palpation:

Diminished TVF palpable rhonchi

Percussion:

Hyperresonant depressed diaphragm (tidal percussion)

Resonant Bare area of the heart.
Auscultation:

Prolonged expiration
Reduced breath sounds
The presence of wheezing during quiet breathing
Crackle can be heard if infection exist
The heart sounds are best heard over the xiphoid area
Pulmonary function Test crapatation at Loben
cover preia
-

fine aspartate e presea Bent

Late-> will besog

co
andDur
-ware
Determination of a forced vital capacity and FEV1 is necessary for the
diagnosis and assessment of the severity of the disease and helpful in following
its progress.

FEV1 /FVC is the best index of airflow obstruction

 A post-bronchodilator (FEV1)/forced vital capacity
(FVC) ≤70%
Confirm the presence of airflow limitation that is not fully
reversible
·
Pt with Frank plany all over char you can near Admatch
· and ent, vented Frilar
 FEV1 % pred is used for evaluation of the severity of pulmonary function
status.
 The FEV1 and the FEV1/FVC ratio fall progressively as the severity of
COPD increases

 Elevations of Total Lung Capacity (TLC)

 Functional Reserve Capacity (FRC)
 Residual Volume (RV)
 RV/TLC > 40% for emphysema
 Vital Capacity (VC)
 Peak Expiratory Flow(PEF)

FEV1/FVC FEV1%pred
Mild <70% ≥80%
Moderate <70% 50~80%
Severe <70% 30~50%
Very severe <70% ≤ 30% or <50% following with
respiratory failure & right heart failure
Radiology
Chest Radiograph (X-Ray)
1-Chronic bronchitis
Non apparent abnormality or thickened and increased of the
lung markings are noted.
2-Chest X-Ray --emphysema
At Choic bronchite - - No chaf
Chest findings are also variable.

Marked over inflation is noted with flattened and low

diaphragm

Intercostal space becomes widen

A horizontal pattern of ribs
A long thin heart shadow
Decreased markings of lung peripheral vessels
CT (Computed tomography)
Greater sensitivity and specificity for
emphysema than CXR, especially for the
diagnosis of bronchiectasis and evaluation of
bullous disease spainten buli
-

Laboratory Examination
In exacerbation or acute infection in
Blood examination
airway, leucocytosis may be detected
Sputum examination
Streptococcus pneumonia Haemophilus influenzae
Moraxella catarrhalis klebsiella pneumonia

Blood gas analysis

Arterial blood gas analysis may reveal hypoxemia, particularly advanced
disease.
In patients with severe hypoxemia, CO2 retention, it
shows low arterial PO2 and high arterial PCO2
 Differential Diagnosis of COPD

E
COPD
Suggestive features

Mid-life onset Dyspnea during exercise

Slowly progressing symptoms
Long history of smoking largely irreversible airflow limitation

Asthma
Early onset Airflow limitation that is largely reversible
Symptoms vary from day to day Allergy, Rhinitis, Eczema
Symptoms at the night/early morning
A family history

Pulmonary carcinoma
Suggestive features

Commonly occurs in patients over 40 years old cigarette smoking

Obvious radiological abnormality

Pulmonary carcinoma
Onset at all ages
Tuberculosis toxic syndrome
Lung infiltrate on chest radiography
Microbiological confirmation
Sputum examination of positive TB bacterium can confirms the diagnosis
 Congestive Heart Failure
Suggestive features

Fine basilar crackles on auscultation

Chest X-ray shows dilated heart, pulmonary edema
Pulmonary function tests indicate volume restriction, not airflow
limitation
Bronchiactesis
Large volumes of purulent sputum
Commonly associated with bacterial infection
Coarse crackles/clubbing on auscultation
Chest X-ray/CT shows bronchial dilation, bronchial wall thickening

TREATMENT
Aim
prevention of further progress of disease
preservation and enhancement of pulmonary functional capacity
avoidance of exacerbations in order to improve the quality of life
1-Avoid risk factors
 Education and smoking cessation
Smoking cessation has the greatest
capacity to influence the natural history of
COPD.

 Control the occupational and environmental

pollution
2-Drug therapy
 Prevent and control symptoms.
 Increase exercise capacity.
 Reduce the frequency and
severity of exacerbations
 Improve health status

1. Bronchodilators
Bronchodilators are central to the symptomatic management of COPD.

Improve emptying of the reduce dynamic improve exercise

lungs hyperinflation performance
Three major classes of bronchodilators:
β2 - agonists
Short acting: salbutamol & terbutaline
Long acting :Salmeterol & formoterol

Anticholinergic agents
Ipratropium,tiotropium

Theophylline
agents
A weak bronchodilator, which may have some anti-inflammatory properties

2. Glucocorticoids
Regular treatment with inhaled glucocorticoids is appropriate for
symptomatic patients with an FEV1<50%pred and repeated
exacerbations. Chronic treatment with systemic glucocorticoids should be
avoided??? because of an unfavorable benefit-to-risk ratio.
3. Others
Immunoregulators Alpha-1 antitrypsin augmentation
Vaccine Mucolytic (mucokinetic,mucoregulator) agents Antitussives
Oxygen >15 h /d
Long-Term Oxygen Therapy (LTOT) improves survival, exercise, sleep and
cognitive performance in patients with respiratory failure.
The therapeutic goal is to maintain
SaO2 ≥ 90% and PaO2 ≥ 60
mmHg at sea level and rest
For patients with a PaO2 ≤ 55 mmHg
or SaO2≤88%, with or without
hypercapnia
For patients with a PaO2 of
55~70（60）mmHg or
-
> No Need for AISG
SaO2≤89% as well as pulmonary hypertension / heart failure / polycythemia
(hematocrit >55%) palpite in Load 52 toknow it cimely

Pulmonary rehabilitation
Nutrition
Surgery
 Bullectomy
 Lung volume reduction surgery
 Lung transplantation >
-
cardioplut
translat
 Acute exacerbation of COPD
Definition
An exacerbation is a
sustained worsening of
the patient’s symptoms
from his or her usual stable state that is and is acute in
onset.

Commonly reported worsening

symptoms are
breathlessness, cough, and increased sputum
production and change in sputum color
Etiology
The most common causes of an exacerbation are
infection of the tracheobronchial tree and air
pollution, but the cause of about one-third of severe
exacerbations cannot be identified.

Secondary Causes
-- -j
Pneumonia Spontaneous pneumothorax Poor nutritional stage
Left or Right heart failure Inappropriate oxygen therapy acute disease
(GI Bleeding)
Arrhythmias Drugs (hypnotics, diuretics)
Pulmonary embolism Metabolic diseases End-Stage disease
(fatigue resp. muscles)
Clinical features
Symptoms:
Worsening of dyspnea, sometimes at rest, increase cough, increased
sputum production, often with change in character from mucoid to
purulent, development or increase in wheezing.

Signs:
Fever>38.5 °C
Increased respiratory rate
Tachycardia

Development or increased cyanosis

Use of accessory muscles of respiration

Peripheral edema

Loss of alertness
Criteria for severe acute exacerbation:
Loss of alertness or two or more of the following:
Dyspnea at rest
Respiratory rate > 25 cycle/min
Pulse > 110 beats/min
increase Cyanosis
use of accessory Muscles of respiration

Home management:
Initiate or increase bronchodilator therapy combined with
antibiotics, then reassess within hours.
If no improvement, add oral corticosteroids, after hours, if no improvement
refers to hospital. If there is improvement refers for long term management

Hospital management
Controlled Oxygen therapy
Bronchodilator therapy
Glucocorticosteroids
Antibiotics
Ventilatory support