Chapter 13 – The Lung
Atelectasis (Collapse)
Atelectasis, also known as collapse, is loss of lung volume caused by inadequate expansion of
air spaces. It results in shunting of inadequately oxygenated blood from pulmonary arteries
into veins, thus giving rise to a ventilation-perfusion imbalance and hypoxia. Atelectasis is
classified into three forms:
Resorption atelectasis
o Obstruction prevents air from reaching distal airways.
o Obstruction of bronchus
Compression atelectasis
o Accumulation of fluid, blood or air within the pleural cavity
Contraction atelectasis
o Local or diffuse fibrosis affecting the lung or the pleura hamper lung
expansion
Acute Respiratory Disease Syndrome
A respiratory failure within 1 week of known clinical insult with bilateral opacities on chest
imaging, not fully explained by effusions, atelectasis, cardiac failure, or fluid overload. Causes
are diverse; the shared feature is that all lead to extensive bilateral injury to alveoli. In ARDS,
the integrity of the alveolar-capillary membrane is comprised by endothelial and epithelial
injury. Neutrophils and their products have a crucial role in the pathogenesis of ARDS of
causing endothelial and epithelial injury. The characteristic histologic picture is that of
alveolar edema, epithelial necrosis, accumulation of neutrophils, and presence of hyaline
membranes lining the alveolar wall and ducts.
Obstructive versus Restrictive Pulmonary Diseases
Diffuse pulmonary diseases can be classified into two categories
1. Obstructive (airway) disease, characterized by an increase in resistance to air flow
caused by partial or complete obstruction at any level
2. Restrictive disease characterized by reduced expansion of lung parenchyma and
decreased total lung capacity.
Obstructive Lung (airway) Disease
It should be noted that emphysema is defined on the basis of morphologic and radiologic
features, whereas chronic bronchitis is defined on the basis of clinical features.
Emphysema
Emphysema is characterized by permanent enlargement of the air spaces distal to the
terminal bronchioles, accompanied by destruction of their walls without significant fibrosis.
There are four major types of emphysema:
Centriacinar (centrilobular) emphysema
o The central or proximal parts of the acini, formed by respiratory bronchioles
are affected, while distal alveoli are spared.
Panacinar (panlobular) emphysema
o The acini are uniformly enlarged.
, Distal acinar (paraseptal) emphysema
o The proximal portion of the acinus is normal, but the distal part is primarily
involved
Irregular emphysema
o The anicus is irregularly involved
o Almost invariable associated with scarring
Inhaled cigarette smoke and other noxious particles cause lung damage and inflammation
result in parenchymal destruction (emphysema) and airway disease. Factors that influence
the development:
Inflammatory cells and mediators
Protease-anti protease imbalance
Oxidative stress
Airway infection
The idea that proteases are important is based in part on the observation that patients with
genetic deficiency of the anti-protease alfa1-anti-trypsin have a predisposition to develop
pulmonary emphysema, which is compounded by smoking. Protease-mediated damage of
extracellular matrix has a central role in the airway obstruction seen in emphysema.
Dyspnea is usually the first symptom; weight loss is another common complaint. Dyspnea
and hyperventilation are common in patients with no bronchitic component.
Conditions related to Emphysema
Compensatory emphysema dilation of residual alveoli in response to loss of lung
substance elsewhere
Obstructive over inflation expansion of lung due to air trapping
Bullous emphysema produces large subpleural blebs or bullae
Mediastinal (interstitial) emphysema entry of air into the interstitium of the lung
Chronic Bronchitis
Chronic bronchitis is diagnosed on clinical grounds: it is defined by the presence of a
persistent productive cough for at least 3 consecutive months in at least 2 consecutive years.
The distinctive feature of chronic bronchitis is hypersecretion of mucus, beginning in the
large airways. The most important cause is cigarette smoke and other air pollutants. Chronic
airway obstruction largely results from small airway disease (chronic bronchiolitis) and
coexistent emphysema. Histological examination demonstrates enlargement of mucus
secreting glands, goblet cell metaplasia, and bronchiolar wall fibrosis. In some patients,
cough and sputum production persist indefinitely without ventilatory dysfunction, while
other develop COPD with significant outflow obstruction marked by hypercapnia, hypoxemia
and cyanosis.
Asthma
Asthma is a chronic inflammatory disorder of the airways that causes recurrent episodes of
wheezing, breathlessness, chest tightness, and cough. The hallmarks are intermittent,
reversible airway obstruction; chronic bronchial inflammation with eosinophils; bronchial
smooth muscle cell hypertrophy and hyperreactivity; and increased mucus secretion. Major
factors contributing to the development of asthma include genetic predisposition to type I
hypersensitivity (atopy), acute and chronic airway inflammation, and bronchial
hyperresponsiveness to a variety of stimuli. Two waves of reactions:
Atelectasis (Collapse)
Atelectasis, also known as collapse, is loss of lung volume caused by inadequate expansion of
air spaces. It results in shunting of inadequately oxygenated blood from pulmonary arteries
into veins, thus giving rise to a ventilation-perfusion imbalance and hypoxia. Atelectasis is
classified into three forms:
Resorption atelectasis
o Obstruction prevents air from reaching distal airways.
o Obstruction of bronchus
Compression atelectasis
o Accumulation of fluid, blood or air within the pleural cavity
Contraction atelectasis
o Local or diffuse fibrosis affecting the lung or the pleura hamper lung
expansion
Acute Respiratory Disease Syndrome
A respiratory failure within 1 week of known clinical insult with bilateral opacities on chest
imaging, not fully explained by effusions, atelectasis, cardiac failure, or fluid overload. Causes
are diverse; the shared feature is that all lead to extensive bilateral injury to alveoli. In ARDS,
the integrity of the alveolar-capillary membrane is comprised by endothelial and epithelial
injury. Neutrophils and their products have a crucial role in the pathogenesis of ARDS of
causing endothelial and epithelial injury. The characteristic histologic picture is that of
alveolar edema, epithelial necrosis, accumulation of neutrophils, and presence of hyaline
membranes lining the alveolar wall and ducts.
Obstructive versus Restrictive Pulmonary Diseases
Diffuse pulmonary diseases can be classified into two categories
1. Obstructive (airway) disease, characterized by an increase in resistance to air flow
caused by partial or complete obstruction at any level
2. Restrictive disease characterized by reduced expansion of lung parenchyma and
decreased total lung capacity.
Obstructive Lung (airway) Disease
It should be noted that emphysema is defined on the basis of morphologic and radiologic
features, whereas chronic bronchitis is defined on the basis of clinical features.
Emphysema
Emphysema is characterized by permanent enlargement of the air spaces distal to the
terminal bronchioles, accompanied by destruction of their walls without significant fibrosis.
There are four major types of emphysema:
Centriacinar (centrilobular) emphysema
o The central or proximal parts of the acini, formed by respiratory bronchioles
are affected, while distal alveoli are spared.
Panacinar (panlobular) emphysema
o The acini are uniformly enlarged.
, Distal acinar (paraseptal) emphysema
o The proximal portion of the acinus is normal, but the distal part is primarily
involved
Irregular emphysema
o The anicus is irregularly involved
o Almost invariable associated with scarring
Inhaled cigarette smoke and other noxious particles cause lung damage and inflammation
result in parenchymal destruction (emphysema) and airway disease. Factors that influence
the development:
Inflammatory cells and mediators
Protease-anti protease imbalance
Oxidative stress
Airway infection
The idea that proteases are important is based in part on the observation that patients with
genetic deficiency of the anti-protease alfa1-anti-trypsin have a predisposition to develop
pulmonary emphysema, which is compounded by smoking. Protease-mediated damage of
extracellular matrix has a central role in the airway obstruction seen in emphysema.
Dyspnea is usually the first symptom; weight loss is another common complaint. Dyspnea
and hyperventilation are common in patients with no bronchitic component.
Conditions related to Emphysema
Compensatory emphysema dilation of residual alveoli in response to loss of lung
substance elsewhere
Obstructive over inflation expansion of lung due to air trapping
Bullous emphysema produces large subpleural blebs or bullae
Mediastinal (interstitial) emphysema entry of air into the interstitium of the lung
Chronic Bronchitis
Chronic bronchitis is diagnosed on clinical grounds: it is defined by the presence of a
persistent productive cough for at least 3 consecutive months in at least 2 consecutive years.
The distinctive feature of chronic bronchitis is hypersecretion of mucus, beginning in the
large airways. The most important cause is cigarette smoke and other air pollutants. Chronic
airway obstruction largely results from small airway disease (chronic bronchiolitis) and
coexistent emphysema. Histological examination demonstrates enlargement of mucus
secreting glands, goblet cell metaplasia, and bronchiolar wall fibrosis. In some patients,
cough and sputum production persist indefinitely without ventilatory dysfunction, while
other develop COPD with significant outflow obstruction marked by hypercapnia, hypoxemia
and cyanosis.
Asthma
Asthma is a chronic inflammatory disorder of the airways that causes recurrent episodes of
wheezing, breathlessness, chest tightness, and cough. The hallmarks are intermittent,
reversible airway obstruction; chronic bronchial inflammation with eosinophils; bronchial
smooth muscle cell hypertrophy and hyperreactivity; and increased mucus secretion. Major
factors contributing to the development of asthma include genetic predisposition to type I
hypersensitivity (atopy), acute and chronic airway inflammation, and bronchial
hyperresponsiveness to a variety of stimuli. Two waves of reactions:
