3. Risk Factors for COPD
Nutrition
Infections
Socio-economic
status
Aging Populations
4.
5. Percent Change in Age-Adjusted
Death Rates, U.S., 1965-1998
Proportion of 1965 Rate
3.0
Coronary Stroke Other CVD COPD All Other
2.5 Heart Causes
Disease
2.0
1.5
1.0
0.5
–59% –64% –35% +163% –7%
0
1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998
Source: NHLBI/NIH/DHHS
6. Prevalence of allergies and asthma in Pakistan
M.Y. Noori, S.M. Hasnain, and M.A. Waqar.
World Allergy Organization Journal & November 2007
• The frequency of wheezing was found to be 15.2%,
• while the diagnosed cases of asthma were 9.5%.
• The frequency of allergic rhinitis was found to be 34.3%.
• The frequency of those having allergic rhinitis as well as
wheezing episodes was 8%.
• There was no statistically significant difference between
asthmatics and non-asthmatics by sex (P-value:0.402).
• Socioeconomic status was found to affect significantly (p
value 0.001) as the prevalence of diagnosed asthma cases
was 6.17% in high socioeconomic class,13.11% in the
middle-class and 2.4% in the low socioeconomic class.
• Family history of atopy was also found to be significantly
higher in asthmatics.
7. NOCTURNAL ASTHMA IN SCHOOL CHILDREN OF SOUTH PUNJAB,PAKISTAN
Ghulam Mustafa, Pervez Akber Khan, Imran Iqbal
J Ayub Med Coll Abbottabad 2008;20(3)
• The parents reported nocturnal asthma in 177
(6%) of their children with an equal
prevalence in boys and girls,
9. Pathogenesis of
Cigarette smoke COPD
Biomass particles
Particulates
Host factors
Amplifying mechanisms
LUNG INFLAMMATION
Anti-oxidants
Anti-proteinases
Oxidative
stress Proteinases
Repair
mechanisms
COPD PATHOLOGY
Source : Peter J. Barnes,
10. Differences in Inflammation and its Consequences: Asthma and COPD
ASTHMA COPD
Allergens Cigarette smoke
Y Y
Y
Ep cells Mast cell Alv macrophage Ep cells
CD4+ cell Eosinophil CD8+ cell Neutrophil
(Th2) (Tc1)
Bronchoconstriction Small airway narrowing
AHR Alveolar destruction
Airflow Limitation
Reversible Irreversible
Source : Peter J. Barnes,
13. Changes in Large Airways of COPD Patients
Mucus hypersecretion Neutrophils in sputum
Squamous metaplasia of epithelium
No basement membrane thickening
Goblet cell
hyperplasia ↑ Macrophages
↑ CD8+ lymphocytes
Mucus gland hyperplasia
Little increase in
airway smooth muscle
Source : Peter J. Barnes,
MD
14. Air Trapping in COPD
Normal Mild/moderate Severe
Inspiration COPD COPD
small
airway
alveolar attachments loss of elasticity loss of alveolar attachments
Expiration
closure
↓ Health Dyspnea Air trapping
status ↓ Exercise capacity Hyperinflation
Source : Peter J. Barnes,
15. 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
Source : Peter J. Barnes,
MD
16. Changes in the Lung Parenchyma in COPD
Patients
Alveolar wall destruction
Loss of elasticity
Destruction of pulmonary
capillary bed
↑ Inflammatory cells
macrophages, CD8+ lymphocytes
Source : Peter J. Barnes,
MD
28. PFTs
ASTHMA COPD
FEV1 Decreased in active asthma Decreased-stage of disease
FVC Decreased Decreased
FEV1/FVC Decreased decreased
TLC Normal or increased Normal or increased
FRC Normal or increased Normal or increased
RV Normal or Increased Normal or increased
DLCO Normal or Increased Decreased in Emphysema
29. Therapy at Each Stage of COPD
I: Mild II: Moderate III: Severe IV: Very Severe
FEV 1 /FVC < 70%
FEV 1 /FVC < 70% FEV 1 < 30%
FEV 1 /FVC < 70% predicted
FEV 1 /FVC < 70% 30% < FEV 1 < or FEV 1 < 50%
50% < FEV 1 < 80% 50% predicted predicted plus
FEV 1 > 80% predicted chronic respiratory
Active reduction of risk factor(s); influenza vaccination
predicted failure
Add short-acting bronchodilator (when needed)
Add regular treatment with one or more long-acting
bronchodilators (when needed); Add rehabilitation
Add inhaled glucocorticosteroids if
repeated exacerbations
Add long term
oxygen if chronic
respiratory failure.
Consider surgical
treatments
Notas do Editor
Pathogenesis of COPD, illustrating the central role of inflammation
Changes in large airways of COPD patients. The epithelium often shows squamous metaplasia and there is goblet cell and submucosal gland hyperplasia, resulting in mucus hypersecretion. The airway wall is infiltrated with macrophages and CD8+ lymphocytes, whereas neutrophils predominate in the airway lumen and around submucosal glands. Airway smooth muscle and basement membrane are minimally increased compared to the findings in asthma.
Air trapping in COPD. During expiration small airways narrow but closure is prevented by the elasticity of alveolar attachments. In COPD patients there is a loss of elasticity with greater narrowing in small airways, which may close completely when there is loss of alveolar attachments as a result of emphysema. This results in air trapping and hyperinflation, leading to dyspnea and reduced exercise capacity.
Changes in small airways in COPD patients. The airway wall is thickened and infiltrated with inflammatory cells, predominately macrophages and CD8+ lymphocytes, with increased numbers of fibroblasts. In severe COPD there are also lymphoid follicles. The lumen is often filled with an inflammatory exudate and mucus. There is peribronchial fibrosis and airway smooth muscle may be increased, resulting in narrowing of the airway.
Changes in the lung parenchyma in COPD patients. There is loss of elasticity and alveolar wall destruction, and accumulation of inflammatory cells, predominantly macrophages and CD8+ lymphocytes. The destructive changes reduce the pulmonary capillary bed. The left panel shows a scanning electron micrograph of a patient with emphysema demonstrating the enlargement of alveoli and destruction of the alveolar walls.
Inflammatory cells involved in COPD. Cigarette smoke activates macrophages and epithelial cells to release chemotactic factors that recruit neutrophils, monocytes and CD8+ T-lymphocytes from the circulation. They also release factors that activate fibroblasts leading to small airway obstruction (obstructive bronchiolitis). Proteases released from neutrophils and macrophages may cause mucus hypersecretion and emphysema.
Oxidative stress in COPD has several detrimental consequences, including activation of the transcription factor nuclear factor-κB (NF-κB), reduction in antiproteases, plasma leakage and mucus hypersecretion. In addition it reduces histone deacetylase-2, resulting in amplified inflammation and reduced anti-inflammatory response to corticosteroids.
This provides a summary of the recommended treatment at each stage of COPD.