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Emphysema
• Pulmonary emphysema is
described in clinical,
radiological and
physiologic terms, but the
condition is best defined
morphologically
• Definition:Abnormal
enlargement of airspaces
distal to the terminal
bronchioles with
destruction of their wall
• It is characterized by
destruction and
enlargement of alveoli
Cont.
• Although the normal lung has about
35,000 terminal bronchioles and their
total internal cross-sectional area is at
least 40 times as great as that of the
lobar bronchi but the bronchioles are
more delicate and vulnerable.
Cont
• Bronchioles may be obstructed partially
or completely, temporarily or
permanently, by thickening of their
walls, by collapse due to loss of
elasticity of the surrounding
parenchyma, or by influx of exudates.
Cont
• In advanced emphysema, the lungs are
large, pale, and relatively bloodless.
• They do not readily collapse.
• They many contain many superficial
blebs or bullae, which occasionally are
huge.
• The right ventricle of the heart is often
enlarged (cor pulmonale), reflecting
pulmonary arterial hypertension.
Emphysema: Pathophysiology
• Structural changes
– Hyperinflation of
alveoli
– Destruction of alveolar
& alveolar-capillary
walls
– Small airways narrow
– Lung elasticity
decreases
Emphysema
• Early stages
– Dyspnea
– Non productive cough
– Diaphragm flattens
– A-P diameter increases
• “Barrel chest”
– Hypoxemia may occur
• Increased respiratory rate
• Respiratory alkalosis
– Prolonged expiratory phase
• Tripod position
Emphysema:
Clinical Manifestations
• Later stages
– Hypercapnea
– Purse-lip breathing
– Muscle retraction
– Use of accessory muscles to
breathe
– Underweight
• No appetite & increase
breathing workload
• Loss of subcutaneous fat
– Lung sounds diminished
Clinical Manifestations
• Pulmonary function
• residual volume, lung
capacity, DECREASED
FEV1, vital capacity
maybe normal
• Arterial blood gases
– Normal in moderate disease
– May develop respiratory
alkalosis
– Later: hypercapnia and
respiratory acidosis
• Chest x-ray
– Flattened diaphragm
– hyperinflation
Classification
• Anatomical Distribution
– Cetriacinar
– Panacinar
– Paraseptal
– Irregular
Pathogenesis
• Protease anti Protease Theory
– Hereditary deficiency of the major protease inhibitors
– Laurell and Eriksson –1963 – deficiency of α1-antitrypsin
and emphysema
• Pollutants in environment
– smoking of cigarettes
– exhalations from cars, dust from grain
• Recruitment of neutrophils
• stimulation of macrophages and epithelial cells to produce TNF-
α, IL-8 and LTB4
• Elastase release from leukocytes and tissue macrophages
• Inactivation of α1-antitrypsin by oxidants in tobacco smoke or
free radicals released from the neutrophils
Diseases in which misfolding of a given
protein results in improper trafficking
Diseases in which misfolding of a
given protein results in improper
trafficking
Emphysema – Total
Lung Capacity (TLC) &
Residual Volume (RV) are elevated. P = 2t/r.
Bullous Emphysema
Other types of Emphysema
1 Bullous Emphysema (also known as
Bullous Lung Disease):