The respiratory system
The lung
Normal lung structure
• Function – gas exchange
• Embryological developmental – from the
ventral wall of the foregut .
• The right lung bud eventually divides into
three branches—the main bronchi—and
the left into two main bronchi .
• Three lobes on the right and two lobes on
the left
Normal lung structure
• so the left lung is smaller than the right.
The right main stem bronchus is more
vertical and more directly in line with the
trachea than is the left
• So aspirated foreign material, such as
vomitus, blood, and foreign bodies, tends
to enter the right lung rather than the left.
Normal lung structure
• The main right and left bronchi branch , giving
rise to progressively smaller airways
• The lung have double arterial supply , the
pulmonary and bronchial arteries.
• Progressive branching of the bronchi forms
bronchioles, which are distinguished from
bronchi by the lack of cartilage and submucosal
glands within their walls. Further branching of
bronchioles leads to the terminal bronchioles, .
The part of the lung distal to the terminal
bronchiole is called the acinus.
of normal structures within the acinus, the fundamental unit of the lung. A
terminal bronchiole (not shown) is immediately proximal to the respiratory
bronchiole.
Normal lung structure
• an acinus is composed of respiratory
bronchioles (emanating from the terminal
bronchiole), which give off several alveoli from
their sides. These bronchioles then proceed into
the alveolar ducts, which immediately branch
into alveolar sacs, the blind ends of the
respiratory passages,
• A cluster of three to five terminal bronchioles,
each with its appended acinus, is usually
referred to as the pulmonary lobule
Normal lung structure
• From the microscopic standpoint, except
for the vocal cords, which are covered by
stratified squamous epithelium, the entire
respiratory tree, including the larynx,
trachea, and bronchioles, is lined by
pseudostratified, tall, columnar, ciliated
epithelial cells, heavily admixed in the
cartilaginous airways with mucus-secreting
goblet cells.
Normal lung structure
• The microscopic structure of the alveolar
walls (or alveolar septa) consists, from
blood to air, of the following .
• The capillary endothelium lining the
intertwining network of anastomosing
capillaries.
• • A basement membrane and surrounding
interstitial tissue separating the endothelial
cells from the alveolar lining
Normal lung structure
• Alveolar epithelium, which contains a continuous
layer of two principal cell types: flattened,
platelike type I pneumocytes (or membranous
pneumocytes) covering 95% of the alveolar
surface and rounded type II pneumocytes. Type
II cells are important for at least two reasons: (1)
They are the source of pulmonary surfactant,
and (2) they are the main cell type involved in
the repair of alveolar epithelium after destruction
of type I cells.
Normal lung structure
• Alveolar macrophages, loosely attached to
the epithelial cells or lying free within the
alveolar spaces, derived from blood
monocytes and belonging to the
mononuclear phagocyte system. Often,
they are filled with carbon particles and
other phagocytosed materials.
Microscopic structure of the alveolar wall. Note that the basement membrane (yellow) is
thin on one side and widened where it is continuous with the interstitial space. Portions
of interstitial cells are shown.
Pathology
• Primary respiratory infections, such as bronchitis and
pneumonia, are common place in clinical and pathologic
practice .
• In these days of cigarette smoking, air pollution, and
other environmental inhalants, chronic bronchitis and
emphysema have become imporatnt and common
disease .
• malignancy of the lungs had been rising now a day .
• Moreover, the lungs are secondarily involved in almost
all forms of terminal disease, so some degree of
pulmonary edema, atelectasis, or bronchopneumonia is
present in virtually every dying patient
Congenital Anomalies
• Developmental defects of the lung include
the following
– • Agenesis or hypoplasia of both lungs, one lung, or
single lobes
– • Tracheal and bronchial anomalies (atresia, stenosis,
tracheoesophageal fistula)
– • Vascular anomalies
– • Congenital lobar overinflation (emphysema)
– • Foregut cysts
– • Congenital pulmonary airway malformation
– • Pulmonary sequestrations
Atelectasis (Collapse)
• Definition :_ Atelectasis refers either to
incomplete expansion of the lungs
(neonatal atelectasis) or to the collapse of
previously inflated lung, producing areas
of relatively airless pulmonary
parenchyma. Acquired atelectasis,
• it divided into resorption (or obstruction),
compression, and contraction atelectasis )
1-Resorption atelectasis
• Definition :-is the consequence of complete obstruction
of an airway, which in time leads to resorption of the
oxygen trapped in the dependent alveoli, without
impairment of blood flow through the affected alveolar
walls. Since lung volume is diminished, the mediastinum
shifts toward the atelectatic lung.
• cause :- principally by excessive secretions (e.g.,
mucous plugs) or exudates within smaller bronchi and is
therefore most often found in bronchial asthma, chronic
bronchitis, bronchiectasis, and postoperative states and
with aspiration of foreign bodies.
2-Compression atelectasis
• atelectasis results whenever the pleural cavity is partially
or completely filled by fluid exudate, tumor, blood, or air
(the last-mentioned constituting pneumothorax) or, with
tension pneumothorax, when air pressure impinges on
and threatens the function of the lung and mediastinum,
especially the major vessels. Compression atelectasis is
most commonly encountered in patients with cardiac
failure who develop pleural fluid and in patients with
neoplastic effusions within the pleural cavities. Similarly,
abnormal elevation of the diaphragm, such as that which
follows peritonitis or subdiaphragmatic abscesses or
occurs in seriously ill postoperative patients, induces
basal atelectasis. With compressive atelectasis, the
mediastinum shifts away from the affected lung
3-Contraction atelectasis
• occurs when local or generalized
fibrotic changes in the lung or pleura
prevent full expansion .
• Significant atelectasis reduces
oxygenation and predisposes to infection.
Because the collapsed lung parenchyma
can be re-expanded, atelectasis is a
reversible disorder (except that caused by
contraction).
Acute Lung Injury
Acute Lung Injury
•
•
•
The term "acute lung injury" encompasses a spectrum of
pulmonary lesions (endothelial and epithelial), which can be
initiated by numerous factors. Susceptibility to lung injury
appears to be heritable, and response and survival depend on
the interaction of multiple loci on different chromosomes.
Mediators include cytokines, oxidants, and growth factors, such
as tumor necrosis factor (TNF), interleukin (IL)-1, IL-6, IL-10,
and transforming growth factor (TGF)-β. Lung injury may
manifest as congestion, edema, surfactant disruption, and
atelectasis, and these may progress to acute respiratory
distress syndrome or acute interstitial pneumonia.
Each of these forms of pulmonary injury is described below.
PULMONARY EDEMA
• Pulmonary edema can result from
hemodynamic disturbances
(hemodynamic or cardiogenic pulmonary
edema) or from direct increases in
capillary permeability, owing to
microvascular injury .
1-Hemodynamic Pulmonary
Edema
• The most common hemodynamic mechanism of
pulmonary edema is that attributable to
increased hydrostatic pressure, as occurs in leftsided congestive heart failure.
• Grossly ;-congestion and edema are
characterized by heavy, wet lungs. Fluid
accumulates initially in the basal regions of the
lower lobes because hydrostatic pressure is
greater in these sites (dependent edema).
• Histologically :- the alveolar capillaries are
engorged, and an intra-alveolar granular pink
precipitate is seen. Alveolar microhemorrhages
and hemosiderin-laden macrophages ("heart
failure" cells) may be present. In long-standing
cases of pulmonary congestion, such as those
seen in mitral stenosis, hemosiderin-laden
macrophages are abundant, and fibrosis and
thickening of the alveolar walls These changes
not only impair normal respiratory function, but
also predispose to infection.
2-Edema Caused by
Microvascular Injury
• The second mechanism leading to pulmonary edema is
injury to the capillaries of the alveolar septa. Here the
pulmonary capillary hydrostatic pressure is usually not
elevated, and hemodynamic factors play a secondary
role. The edema results from primary injury to the
vascular endothelium or damage to alveolar epithelial
cells (with secondary microvascular injury). This results
in leakage of fluids and proteins first into the interstitial
space and, in more severe cases, into the alveoli
• When the edema remains localized, as it does in most
forms of pneumonia, it is overshadowed by the
manifestations of infection. When diffuse, however,
alveolar edema is an important contributor to a serious
and often fatal condition, acute respiratory distress
syndrome, discussed in the following section.
ACUTE RESPIRATORY
DISTRESS SYNDROME
(DIFFUSE ALVEOLAR DAMAGE)
• Acute respiratory distress syndrome (ARDS)
(synonyms include "shock lung," "diffuse
alveolar damage," "acute alveolar injury," and
"acute lung injury") is a clinical syndrome caused
by diffuse alveolar capillary damage. It is
characterized clinically by the rapid onset of
severe life-threatening respiratory insufficiency,
cyanosis, and severe arterial hypoxemia that is
refractory to oxygen therapy and that may
progress to extra-pulmonary multisystem organ
failure. Chest radiographs show diffuse alveolar
infiltration.
Conditions Associated with Development of Acute Respiratory Distress Syndrome
Infection
Sepsis *
Diffuse pulmonary infections *
Viral,
Mycoplasma, and Pneumocystis pneumonia; miliary tuberculosis
Gastric aspiration *
Physical/Injury
Mechanical trauma, including head injuries *
Pulmonary contusions
Near-drowning
Fractures with fat embolism
Burns
Ionizing radiation
Inhaled Irritants
Oxygen toxicity
Smoke
Irritant gases and chemicals
Chemical Injury
Heroin or methadone overdose
Acetylsalicylic acid
Barbiturate overdose
Paraquat
Hematologic Conditions
Multiple transfusions
Disseminated intravascular coagulation
Pancreatitis
Uremia
Cardiopulmonary Bypass
Hypersensitivity Reactions
Organic solvents
Drugs
Morphology
• In the acute stage, the lungs are heavy, firm,
red, and boggy. They exhibit congestion,
interstitial and intra-alveolar edema,
inflammation, and fibrin deposition. The alveolar
walls become lined with waxy hyaline
membranes that are morphologically similar to
those seen in hyaline membrane disease of
neonates . Alveolar hyaline membranes consist
of fibrin-rich edema fluid mixed with the
cytoplasmic and lipid remnants of necrotic
epithelial cells.
Diffuse alveolar damage (acute respiratory distress syndrome) shown in a
photomicrograph. Some of the alveoli are collapsed; others are distended. Many contain
dense proteinaceous debris, desquamated cells, and hyaline membranes (arrows).
Pathogenesis.
• Acute lung injury occurs as a result of a cascade
of cellular events initiated by either infectious or
noninfectious inflammatory stimuli. An elevated
level of pro-inflammatory mediators combined
with a decreased expression of antiinflammatory molecules is a critical component
of lung inflammation .
• there is increased synthesis of IL-8, a potent
neutrophil chemotactic and activating agent, by
pulmonary macrophages. Release of this and
other cytokines, like IL-1 and TNF, leads to
pulmonary microvascular sequestration and
activation of neutrophils. Neutrophils are thought
to play an important role in the pathogenesis of
acute lung injury and ARDS.
Histological
• examination of lungs early in the disease
process has shown increased numbers of
neutrophils within the vascular space, the
interstitium, and the alveoli
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