asthma copd

COPD-Asthma

Risk Factors for COPD

NutritionNutrition

InfectionsInfections

Socio-economic Socio-economic statusstatus

Aging PopulationsAging Populations

Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998

Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998

00

0.50.5

1.01.0

1.51.5

2.02.0

2.52.5

3.03.0Proportion of 1965 Rate Proportion of 1965 Rate

1965 - 19981965 - 1998 1965 - 19981965 - 1998 1965 - 19981965 - 1998 1965 - 19981965 - 1998 1965 - 19981965 - 1998

–59%–59% –64%–64% –35%–35% +163%+163% –7%–7%

CoronaryHeart

Disease

CoronaryHeart

Disease

StrokeStroke Other CVDOther CVD COPDCOPD All OtherCauses

All OtherCauses

Source: NHLBI/NIH/DHHSSource: NHLBI/NIH/DHHS

Prevalence of allergies and asthma in PakistanM.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.

NOCTURNAL ASTHMA IN SCHOOL CHILDREN OF SOUTH PUNJAB,PAKISTANGhulam 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,

Anatomy

LUNG INFLAMMATIONLUNG INFLAMMATION

COPD PATHOLOGYCOPD PATHOLOGY

OxidativeOxidativestressstress ProteinasesProteinases

Repair Repair mechanismsmechanisms

Anti-proteinasesAnti-proteinasesAnti-oxidantsAnti-oxidants

Host factorsAmplifying mechanisms

Cigarette smokeCigarette smokeBiomass particlesBiomass particles

ParticulatesParticulates

Pathogenesis of COPD

Source: Peter J. Barnes, MD

Differences in Inflammation and its Consequences: Asthma and COPD

YYYY YY

Mast cellMast cell

CD4+ cellCD4+ cell(Th2)(Th2)

EosinophilEosinophil

AllergensAllergens

Ep cellsEp cells

ASTHMAASTHMA

BronchoconstrictiBronchoconstrictionon

AHRAHR

Alv macrophageAlv macrophage Ep cellsEp cells

CD8+ cellCD8+ cell(Tc1)(Tc1)

NeutrophilNeutrophil

Cigarette smokeCigarette smoke

Small airway narrowingSmall airway narrowingAlveolar destructionAlveolar destruction

COPDCOPD

Reversible IrreversibleAirflow LimitationAirflow Limitation

Source: Peter J. Barnes, MD

COPD airway

Asthma airway

Mucus gland hyperplasia

Goblet cellhyperplasia

Mucus hypersecretion Neutrophils in sputum

Squamous metaplasia of epithelium

↑ Macrophages

No basement membrane thickening

Little increase in airway smooth muscle

↑ CD8+ lymphocytes

Changes in Large Airways of COPD Patients

Changes in Large Airways of COPD Patients

Source: Peter J. Barnes, MD

NormalNormalInspiration

Expiration

alveolar attachments

Mild/moderateMild/moderateCOPD COPD

loss of elasticity

Severe Severe COPD COPD

loss of alveolar attachments

closure

small small airwayairway

Dyspnea↓ Exercise capacity

Air trappingAir trappingHyperinflationHyperinflation

↓ ↓ HealthHealthstatusstatus

Air Trapping in COPD

Source: Peter J. Barnes, MD

Disrupted alveolar attachments

Inflammatory exudate in lumen

Peribronchial fibrosisLymphoid follicle

Thickened wall with inflammatory cells- macrophages, CD8+ cells, fibroblasts

Changes in Small Airways in COPD Patients

Source: Peter J. Barnes, MD

Alveolar wall destruction

Loss of elasticity

Destruction of pulmonarycapillary bed

↑ Inflammatory cells macrophages, CD8+ lymphocytes

Changes in the Lung Parenchyma in COPD Patients

Source: Peter J. Barnes, MD

Cigarette smoke Cigarette smoke (and other irritants)(and other irritants)

PROTEASES PROTEASES Neutrophil elastaseNeutrophil elastaseCathepsinsCathepsinsMMPsMMPs

Alveolar wall destructionAlveolar wall destruction(Emphysema)(Emphysema)

Mucus hypersecretionMucus hypersecretion

CD8CD8+ +

lymphocytelymphocyte

Alveolar Alveolar macrophagemacrophage

EpithelialEpithelialcellscells

FibrosisFibrosis(Obstructive(Obstructivebronchiolitis)bronchiolitis)

FibroblastFibroblast

MonocyteMonocyteNeutrophilNeutrophil

Chemotactic factorsChemotactic factors

Inflammatory Cells Involved in COPD

Source: Peter J. Barnes, MD

Anti-proteases

SLPI 1-AT

Proteolysis

OO22--, H, H220022

OHOH.., ONOO, ONOO--

Mucus secretion

Plasma leak Bronchoconstriction

NF-NF-BB

IL-8IL-8

NeutrophilNeutrophilrecruitmentrecruitment

TNF-TNF-

IsoprostanesIsoprostanes

↓ ↓ HDAC2HDAC2

↑↑InflammationInflammationSteroidSteroid

resistanceresistance

Macrophage NeutrophilOxidative Stress in COPD

Source: Peter J. Barnes, MD

Chronic hypoxiaChronic hypoxia

Pulmonary vasoconstrictionPulmonary vasoconstriction

MuscularizationMuscularization

Intimal Intimal hyperplasiahyperplasia

FibrosisFibrosis

ObliterationObliteration

Pulmonary hypertensionPulmonary hypertension

Cor pulmonaleCor pulmonale

DeathEdemaEdema

Pulmonary Hypertension in COPD

Source: Peter J. Barnes, MD

Asthma

Emphysema- CT scan

Emphysema

Chronic bronchitis

PEF meters

Spirometry: Normal and Patients with COPD

Lung Volumes and Capacities

PFTsASTHMA 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

IV: Very Severe III: Severe II: Moderate I: Mild

Therapy at Each Stage of COPD

FEV1/FVC < 70%

FEV1 > 80% predicted

FEV1/FVC < 70%

50% < FEV1 < 80%

predicted

FEV1/FVC < 70%

30% < FEV1 < 50% predicted

FEV1/FVC < 70%

FEV1 < 30% predicted

or FEV1 < 50% predicted plus chronic respiratory failure

Add regular treatment with one or more long-acting bronchodilators (when needed); Add rehabilitation

Add inhaled glucocorticosteroids if repeated exacerbations

Active reduction of risk factor(s); influenza vaccinationAdd short-acting bronchodilator (when needed)

Add long term oxygen if chronic respiratory failure. Consider surgical treatments