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Title:

COPD

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Chronic bronchitis: inflammation of small and medium sized airways ... Chronic Bronchitis ... Chronic Bronchitis Emphysema. Cough excessive sputum production ... – PowerPoint PPT presentation

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Title: COPD


1
COPD
  • Review

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  • Progressive
  • Syndrome
  • Expiratory airflow obstruction
  • Chronic airway and lung parenchyma inflammation

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  • Preventable, treatable
  • 24 million adults in US
  • 4th leading cause of death in US
  • Heart disease
  • Cancer
  • Stroke
  • COPD
  • Accidents
  • Diabetes

6
  • GOLD global initiative for chronic obstructive
    lung diseasae
  • Expiratory airflow not fully reversible
  • Progressive, association with an abnormal lung
    response to noxious gases and particles

7
  • Two major clinical types
  • Chronic bronchitis inflammation of small and
    medium sized airways
  • Leads to expiratory defect, chronic cough, sputum
    production and dyspnea

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  • Emphysema
  • Inflammation of lung parenchyma
  • Loss of elastic recoil of lungs
  • Airflow limitation
  • Hypoxemia
  • dyspnea

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COPD
  • Irreversible airflow (as measured by FEV1 or
    FEV1/FVC) caused by
  • Increased airway resistance in the conducting
    airways, or,
  • Increased lung compliance due to destruction of
    lung parenchyma/elasticity
  • Or a combination of both the above

14
Chronic Bronchitis
  • Inflammation of the central airways (airways gt4mm
    diameter and peripheral airways lt 2 mm)
  • Extends to gland ducts and into the mucus
    producing glands
  • This produces increase mucus
  • Defective mucociliary clearance
  • Disruption (destruction) of epithelial barrier

15
  • Airflow obstruction occurs primarily in the small
    airways which are lt2mm diameter

16
Emphysema
  • Decrease in elastic recoil force needed to drive
    air out of lung (paper sack)
  • Centrilobular or centriacinar form is associated
    with cigarette smoking
  • Major destruction of the acinus at the
    respiratory bronchiole level

17
  • Panlobular or panacinar form is associated with
    alpha-1 antitrypsin disease
  • Destruction of the entire acinus
  • Occurs as a result of an imbalance of proteolytic
    enzymes in lung tissue

18
  • In both forms of the disease, the cause of COPD
    is inflammation, both in the airways and in lung
    tissue

19
Inflammation
  • Smoking, in
  • Chronic Bronchitis
  • Neutrophils and macrophages, lymphocytes
  • Emphysema
  • Cellular changes in terminal bronchioles
  • Destruction (protease enzymes) extracellular
    matrix of aleveoli
  • Ineffective repair mechanism

20
COPD vs Asthma
  • Asthma
  • Anatomical location of inflammation
  • With bronchodilators and steroids, lung function
    returns to normal or near-normal with occasional
    transient inflammation
  • COPD
  • Anatomical (airways and lung parenchyma)
  • Some degree of irreversible deterioration

21
  • Cellular differences
  • Asthma
  • Eosinophils
  • Mast cells
  • Lymphocytes
  • CD4 T cells

22
Same cells CB Emphysema
  • COPD
  • Neturophils
  • Macrophages
  • No mast cells
  • CD8 T cells

23
COPD Asthma
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  • A 20 pack year smoking history indicates that
    the subjects lungs have received 20 of these
    short cyclic exposures per day for a cumulative
    total of 7300 exposures per year and 146,000
    exposures over the lifetime of their smoking
    habit.

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GOLD Stages
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In Sum
  • Toxic gases and particles generated in tobacco
    smoke come into contact with lung tissues each
    time a puff of smoke is inhaled
  • Tissue injury recurs in a cyclic fashion as each
    cigarette is smoked

28
Chronic Bronchitis
  • Inflammation
  • mucociliary clearance disrupted
  • epithelial barrier/defense lost
  • increased sputum production (goblet cells)
  • irreversible airway remodeling
  • airflow obstruction

29
Emphysema
  • In lung tissue, the chronic inhalation also
    causes inflammation, destroys elastic recoil,
    disrupts balance of protective, anti-protease
    enzymes
  • proteinase-antiproteniase theory
  • elastase-antielastase
  • extracellular matrix

30
Toxins/free radicals Cigarette
smoke Toxins/free radicals Stimulation of
alveolar macrophages other inflammatory
cells chemotactic factors
Airway inflammation Lung (pulmonary)
inflammation Injury to parenchymal
cells Airflow obstruction Proteinase
inhibitors (alpha1-antitrypsin) Injury to
extracellular matrix Repair of
extracellular matrix Chronic Bronchitis
Emphysema Cough excessive sputum
production dyspnea at rest
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Alpha1-antitrypsin
  • Neutrophil elastase linked to alpha-1 antitrypsin
    deficiency
  • Other cells producing proteinase enzymes
    macrophages, lymphocytesstill not determined

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  • Decreased airflow resistance (airways) and
    decreased elastic recoil lead to
  • Hyperinflation
  • V/Q mismatching, which further leads to decreases
    in Pa02, increases in PaC02 with decreased
    ventilation

45
  • In end-stage COPD
  • Cor pulmonale
  • Pulmonary vasoconstriction (in presence of
    chronic low Pa02)
  • Increased pulmonary vascular resistance
  • Increased pressure, leading eventually to right
    heart enlargement

46
CXR
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COR Pulmonale
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Emphysema
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