The respiratory system

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The respiratory system

• The lung

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Normal lung structure

• Function gas exchange
• Embryological developmental from the ventral
  wall of the foregut .
• The right lung bud eventually divides into three
  branchesthe main bronchiand the left into two
  main bronchi .
• Three lobes on the right and two lobes on the
  left

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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.

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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.

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of normal structures within the acinus, the
fundamental unit of the lung. A terminal
bronchiole (not shown) is immediately proximal to
the respiratory bronchiole.
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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

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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.

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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

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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.

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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.

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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.
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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

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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

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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 )

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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.

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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

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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).

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Acute Lung Injury
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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)-ß. 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.

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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 .

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1-Hemodynamic Pulmonary Edema

• The most common hemodynamic mechanism of
  pulmonary edema is that attributable to increased
  hydrostatic pressure, as occurs in left-sided
  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).

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• 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.

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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.

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ACUTE RESPIRATORY DISTRESS SYNDROME (DIFFUSE
ALVEOLAR DAMAGE)
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• 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.

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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
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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.

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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).
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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
  anti-inflammatory 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.

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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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