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Histology of the
Respiratory System
Clinical Slides
David L. McWhorter, Ph.D.


In persons afflicted with poliomyelitis, the muscles
of respiration may become so weakened that the
accessory muscles hypertrophy because they
become responsible for the elevation of the thoracic
cage
In other diseases, such as myasthenia gravis and
Guillain-Barré syndrome, the weakness of the
respiratory and accessory respiratory muscles may
lead to respiratory failure and consequent death
even though the lungs function normally
Immotile Cilia Syndrome causes
infertility in men and chronic respiratorytract infections in both sexes

Immobility of cilia and flagella

In some cases, due to deficiency of dynein

Protein involved in ciliary movement
With asthma, smooth
muscle undergoes prolonged
contraction during expiration


Difficulty in expelling air from lungs
Increased airway resistance is
believed to be due mainly to
contraction of bronchiolar smooth
muscle:
Thickness of bronchiolar muscle layers
is proportionately greater than bronchial
muscle layer
Epinephrine and other sympathomimetic
drugs frequently used to relax smooth
muscle during asthma attacks:



Increase in bronchiole diameter in response to
stimulation of the sympathetic nervous system
Cystic fibrosis is an autosomal
recessive disorder


Caused by defective transport of chloride ions in mucous cells of
seromucous glands in the respiratory tract as well as in cells producing
sweat, saliva, and pancreatic secretions elsewhere in the body
A defective gene alters a membrane-associated protein with an active
transport function, known as CF transmembrane conductance
regulator:


Defective chloride ion transport results in:



this protein is a channel that controls movement of chloride in and out of
cells
thick and sticky mucus that predisposes patients to chronic lung infections,
among other symptoms
Respiratory failure is the most dangerous consequence and can be
life-threatening
Patients with cystic fibrosis are good candidates for gene therapy
Respiratory
System:
Conducting
Portion
Laryngitis



Inflammation of the laryngeal tissues, including
the vocal folds
Prevents the vocal folds from vibrating freely
Persons suffering from laryngitis sound hoarse
or can only whisper
Cough Reflex




Caused by presence of chemical irritants or particulate
matter in the upper air passages, including the trachea or
bronchi
Produces an explosive rush of air in an effort to remove
the irritant
Begins with the inhalation of a large volume of air and the
closure of the epiglottis and glottis (abduction of the
vocal folds), followed by powerful contraction of the
muscles responsible for forced expiration (intercostal and
abdominal muscles)
Sudden opening of the glottis and epiglottis generates a
rush of air whose velocity can exceed 100 miles per hour,
removing the irritant with an enormous force
Acute bronchitis



Caused by viral or bacterial infection of the lining of
the tracheobronchial tree
Damages the ciliated epithelium and permits the
mucus to pass down (under the influence of gravity)
into the distal portions of the respiratory tract
If the mucus contains inhaled pathogenic bacteria
this may lead to bronchopneumonia:


bacterial infection passes into the lungs through many
small bronchioles
Because the direction of spread of infection is
under the influence of gravity:

basal portions of the lower lobes of the lungs are most
commonly affected
Interstitial (Pulmonary) Fibrosis

In some lung diseases, the fibroblasts in the
interalveolar septa increase in number and secrete
excess collagen and elastin:


This results in fibrocollagenous thickening of the septa
(interstitial fibrosis)
Interstitial fibrosis increases the rigidity of the lung
and limits expansion, but most importantly impairs
gaseous exchange because the presence of collagen
fibers between the capillary and alveolar walls ruins
their intimate contact
Emphysema

Characterized by
destruction of
interalveolar wall, resulting
in:
Enlargement of air space
distal to bronchioles
 Decreased gas-exchange
capability


Major cause is cigarette
smoking:

Irritation stimulates
destruction and/or impairs
synthesis of elastic fibers and
other components of
interalveolar septum
Chronic Obstructive Pulmonary
(Airways) Disease



The most common lung disease in the western world
Characterized by difficulty in getting air into and out of the distal
respiratory tree
There are three main disease processes that may be present alone or
in combination, causing chronic obstructive airways disease:
1.
2.
3.
Asthma is caused by a combination of bronchoconstriction and
excessive production of particularly viscid mucus, both of which obstruct
the airways
Chronic bronchitis, the bronchial walls are thickened by a combination
of muscle layer thickening and an increase in number and size of the
mucous glands
Emphysema is characterized by destruction of the walls of the alveolar
ducts, sacs and alveoli, with permanent dilatation of air spaces:

leading to loss of the elastic support for the bronchioles and their collapse,
particularly during exhalation:

trapping air (air is unable to pass the obstructed lumen)
Squamous Cell Carcinoma

Common form
of lung cancer



1/3 of all lung
cancers
Strongly
associated with
cigarette
smoking
Islands of
neoplastic
epithelial cells
(keratin pearls)
Respiratory Distress Syndrome (RDS) Of
Premature Newborns


Deficiency of surfactant in immature
infants born before 7 months
gestation
Respiratory bronchiole and alveolar
duct are dilated and contain fibrin-rich
eosinophilic material called hyaline
membrane



Deposits of pink staining proteinaceous
material in collapsed alveoli
RDS initially called hyaline membrane
disease
Treated with combination of:


synthetic surfactant to immediately
reduce surface tension
glucocorticoid therapy to induce
surfactant synthesis
Chronic Obstructive Pulmonary
(Airways) Disease



The most common lung disease in the western world
Characterized by difficulty in getting air into and out of the distal
respiratory tree
There are three main disease processes that may be present alone or
in combination, causing chronic obstructive airways disease:
1.
2.
3.
Asthma is caused by a combination of bronchoconstriction and
excessive production of particularly viscid mucus, both of which obstruct
the airways
Chronic bronchitis, the bronchial walls are thickened by a combination
of muscle layer thickening and an increase in number and size of the
mucous glands
Emphysema is characterized by destruction of the walls of the alveolar
ducts, sacs and alveoli, with permanent dilatation of air spaces:

leading to loss of the elastic support for the bronchioles and their collapse,
particularly during exhalation:

trapping air (air is unable to pass the obstructed lumen)
Acute Respiratory Distress Syndrome
(ARDS)

Results from a disruption of the normal barrier that
prevents leakage of fluid from the alveolar capillaries
into the interstitium and alveolar spaces
Two mechanisms can alter the
alveolar barrier

In the first mechanism, an increase in hydrostatic pressure in the
alveolar capillaries-caused, for example, by failure of the left
ventricle or stenosis of the mitral valve-results in increased fluid
and proteins in the alveolar spaces:


The resulting edema is called cardiogenic or hydrostatic pulmonary
edema
In the second mechanism, the hydrostatic pressure is normal,
but the endothelial lining of the alveolar capillaries or the
epithelial lining of the alveoli is damaged:



Inhalation of agents such as smoke, water (near drowning), or
bacterial endotoxins (resulting from sepsis); or trauma can cause a
defect in permeability
A cardiac component may or may not be involved
Although the resulting edema is called noncardiogenic, it can coexist
with a cardiogenic condition
A common pathologic pattern of diffuse
alveolar damage can be observed in
cardiogenic and noncardiogenic ARDS

The first phase of ARDS is an acute exudative
process defined by:
interstitial and alveolar edema, neutrophil infiltration,
hemorrhage, and deposits of fibrin
 Cellular debris, resulting from dead type I alveolar cells,
and fibrin deposited in the alveolar space form hyaline
membranes

The second phase of ARDS is a
proliferative process


Alveolar cells proliferate and differentiate to restore
the epithelial alveolar lining, returning gas exchange to
normal in most cases
In other cases, the interstitium displays inflammatory
cells and fibroblasts:
Fibroblasts proliferate and invade the alveolar spaces
through gaps of the basal lamina
 The hyaline membranes either are removed by
phagocytosis by macrophages or are invaded by fibroblasts

The third phase of ARDS is chronic
fibrosis and occlusion of blood vessels




Because ARDS is part of a systemic inflammatory
response, the outcome of the lung process depends on
improvement of the systemic condition
Prognosis for return to normal lung function is good
Diagnosis of ARDS is based on clinical (dyspnea,
cyanosis, and tachypnea) and radiologic examination
Treatment is focused on neutralizing the disorder
causing ARDS and providing support of gas exchange
until the condition improves
Pleurisy

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


When the normally smooth and slippery surfaces of the visceral
and parietal pleura become abnormally roughened they scrape
against each other roughly, instead of sliding smoothly and
effortlessly
This scraping can be heard through a stethoscope (pleural
friction rub) as a scratching noise in time with inspiration and
expiration
The pleura are equipped with sensory nerves, so the condition is
painful, the pain being most obvious when big inspiratory or
expiratory movements are made, particularly coughing
This condition is called pleurisy and occurs when the pleura is
damaged by inflammation, particularly with bacterial infection of
the lungs where the infection spreads out to the pleural surface
Because of the pain on breathing, patients with pleurisy have
shallow breathing and are loth to cough
Mesothelioma is a tumor that originates in
the mesothelial cell lining of the pleura, the
peritoneum, and the pericardium




Mesothelioma is associated with previous long exposure
(15 to 40 years) to asbestos
Pleural mesothelioma spreads within the thoracic cavity
(pericardium or diaphragm) and metastasis can involve
any organ, including the brain
Symptoms include pleural effusion, chest pain, or dyspnea
Organ imaging studies of the thorax can detect thickening
of the pleura (asbestos plaques) and fluid containing
tumoral cells