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The respiratory system

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Since lung volume is ... lung 3-Contraction atelectasis occurs when local or generalized fibrotic changes in the lung or pleura prevent full expansion . – PowerPoint PPT presentation

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Title: The respiratory system


1
The respiratory system
  • The lung

2
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

3
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.

4
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.

5
of normal structures within the acinus, the
fundamental unit of the lung. A terminal
bronchiole (not shown) is immediately proximal to
the respiratory bronchiole.
6
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

7
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.

8
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

9
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.

10
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.

11
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.
12
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

13
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

14
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 )

15
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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.

17
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

18
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).

19
Acute Lung Injury
20
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.

21
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 .

22
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).

23
  • 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.

24
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.

25
ACUTE RESPIRATORY DISTRESS SYNDROME (DIFFUSE
ALVEOLAR DAMAGE)
26
  • 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.

27
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
28
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.

29
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).
30
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.

31
Histological
  • examination of lungs early in the disease process
    has shown increased numbers of neutrophils within
    the vascular space, the interstitium, and the
    alveoli

32
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