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الجمعة، 12 أكتوبر، 2012

صور باثولوجى - Pathology Slides : Pulmonary Pathology


Patholgy Slides : Pulmonary pathology

 
اضغط على الصورة للتكبير -ـ Click on image to enlarge size
 

Edema

Edema represents the accumulation of excess liquid in the interstitial (extracellular) spaces of a tissue or in pre-existing cavities. It may affect any organ, but most often it appears in : subcutaneous tissues, lung and brain.
According to the etiology, edema may be localized (in inflammation or in impaired venous drainage) or systemic (in right heart failure or in nephrotic syndrome). A generalized and severe edema is called anasarca.
Accumulation of transudate or non-inflammatory fluid (effusions) in body cavities :
  • Peritoneal cavity - ascites
  • Pleural cavity - hydrothorax
  • Pericardial cavity - hydropericardium
Pulmonary edema
Etiology of pulmonary edema : acute left heart (ventricular) failure, pulmonary failure in syndrome of adult respiratory distress, pulmonary infections and hypersensitivity reactions
Pulmonary edema. Alveolar walls are thickened due to acute distention of capillaries and interstitial edema. Alveolar lumen is filled with transudate (pale-eosinophilic, finely granular), a liquid which replaces the air. (H&E, ob. x20)

Pulmonary edema (detail)

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Passive congestion (Passive hyperemia) (lung)

Hyperemia (congestion) represents the increase of blood in a territory, due to dilatation of small vessels. According to the mechanism, it may be active or passive.
Active hyperemia (congestion) is a result of arteriolar distension (e.g., skeletal muscle activity, inflammation, local neuro-vegetative reaction).
Passive hyperemia (congestion), also termed stasis, is a consequence of an impaired venous drainage (heart failure, compression or obstruction of veins), followed by dilatation of venules and capillaries.

Etiology of passive congestion of the lung : chronic left heart (ventricular) failure.
Alveolar walls are thickened due to dilated capillaries. Alveolar lumens are filled with transudate (amorphous, eosinophilic and homogenous) which replaced the air, red blood cells (microhemorrhages) and hemosiderin-laden macrophages (also called "heart failure cells"). (H&E, ob. x20)
With progression, interstitial fibrosis may appear and, together with hemosiderin pigmentation, generates the aspect of "brown induration". Extensive fibrosis leads to intrapulmonary hypertension.


Passive congestion (Passive hyperemia) (lung) (detail)

Passive congestion of the lung. Hemosiderin-laden macrophages contain in cytoplasm hemosiderin pigment (brown, granular), resulted from destruction of red blood cells in alveolar lumen. (H&E, ob. x40)
Perls reaction is useful in distinguishing hemosiderin pigment from anthracotic (carbon) pigment : trivalent iron from hemosiderin stains in green-blue, while anthracotic pigment remains dark-brown and is mainly located perivascular.

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Hemorrhagic infarct lung

Pulmonary infarct (hemorrhagic infarct of the lung) is an area of ischemic necrosis produced by venous thrombosis on a background of passive congestion of lung. In infarct area, alveolar walls, vascular walls and bronchioles are necrotic. They appear eosinophilic (pink), homogenous, lacking the nuclei, but keep their shapes - "structured necrosis". Alveolar lumens from infarcted area are invaded by red blood cells - hemorrhagic infarct (red). (H&E, ob. x10)

Hemorrhagic infarct lung (detail)
Pulmonary infarct in an area of passive congestion. The hemosiderin-laden macrophages present inside the alveolar lumen are witnesses of pre-existent passive congestion. (H&E, ob. x20)

Hemorrhagic infarct lung venous thrombosis


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Lobar pneumonia (leukocytic alveolitis)

Lobar pneumonia is an acute exudative inflammation of an entire pulmonary lobe, produced in 95 % of cases by Streptococcus pneumoniae (pneumococci).
If not treated, lobar pneumonia evolves in four stages :
  • Congestion (first 2 days)
  • Red hepatisation (fibrinous alveolitis) (2nd to 4th day)
  • Grey hepatisation (leukocytic alveolitis) (4th to 8th day)
  • Resolution (after 8th day)
    Leukocytic alveolitis is the 3rd phase of the lobar pneumonia. Alveolar lumens are filled with leukocytic (suppurative) exudate (neutrophils and macrophages, in order to remove the fibrin). Alveolar walls are thickened due to capillary congestion and edema. (H&E, ob. x20)

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    Bronchopneumonia (Lobular pneumonia)

    Bronchopneumonia (Lobular pneumonia) is an acute exudative inflammation of the lungs characterised by foci of consolidation surrounded by normal parenchyma. Usually, bronchopneumonia affects one or more lobes and is bilateral.

    Bronchopneumonia : focus of inflammatory condensation centred by a bronchiole with acute bronchiolitis (suppurative exudate in the lumen and parietal inflammation). Alveolar lumens surrounding the bronchia are filled with neutrophils ("leukocytic alveolitis"). Inflammatory foci are separated by normal, aerated parenchyma. (H&E, ob. x10)



    Bronchopneumonia (detail) : central area of a focus of inflammatory condensation - bronchiola with acute bronchiolitis. (H&E, ob. X20)

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    Aspiration bronchopneumonia


    Aspiration bronchopneumonia appears when early respiratory movements during labor, facilitate filling of alveolar ducts and alveolar lumens with elements of amniotic fluid : amniotic cells, squames and squamous cells from fetal skin, lanugo, meconium. Reduced inflammatory infiltrate (neutrophils) and capillary congestion is present. (H&E, ob. x20)

    Aspiration bronchopneumonia with amniotic fluid. (H&E, ob. x20)

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    Pulmonary tuberculosis

    Tuberculosis is a chronic inflammation caused by Mycobacterium tuberculosis (tubercle bacillus, Koch bacillus) - human type or bovine type. The most affected organ by tuberculosis is the lung. Microscopically, the characteristic lesion in tuberculosis is the tuberculous granuloma

    Pulmonary tuberculosis. Tuberculous granuloma is localized in the pulmonary interstitium, compressing the surrounding alveoli and destroing the parenchyma. (Hematoxylin-eosin, ob. x4) (For detailed histological description of granuloma

    Pulmonary tuberculosis (detail 1)

    Tuberculous granuloma in the pulmonary interstitium. (Hematoxylin-eosin, ob. X20)

    Pulmonary tuberculosis (detail 2)

    Tuberculous granuloma in the pulmonary interstitium. (Hematoxylin-eosin, ob. x20)

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    Pneumoconiosis - Silicosis

    Silicosis is a pneumoconiosis produced by chronic exposure to silica dust (workers in glass industry, sand blasters, miners, grinders and polishers, cement workers). After inhalation, silica particles are phagocytated by macrophages which shortly after die and so, the released silica particles will be phagocytated by other macrophages. These macrophages seems to secrete a fibroblast grown factor which stimulates the fibrosis.
    Pulmonary silicosis. Continuous accumulation of collagen around inhaled silica crystals produces pulmonary fibrotic hyalinized (silicotic) nodules. They present concentric laminated collagen fibers (blue) and tend to become confluent, compressing adjacent alveoli. Silica crystals appear as empty cleft-like spaces. With progression, perivascular and peribronchiolar collagen deposits will produce pulmonary hypertension. (Simionescu trichromic staining, ob. x4)

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    Neonatal respiratory distress syndrome - NRDS (Hyaline membrane disease)

    Neonatal Respiratory Distress Syndrome - NRDS (Hyaline membrane disease) is characterized by collapsed alveoli alternating with hyperaerated alveoli, vascular congestion and hyaline membranes (resulted from fibrin, cellular debris, red blood cells). Hyaline membranes appear like an eosinophilic, amorphous material, lining or filling the alveolar spaces and blocking the gases exchange. (H&E, ob. x10)

    Hyaline membrane disease (detail 1)

    Hyaline membrane disease. (H&E, ob. x40)

    Hyaline membrane disease (detail 2)
    Hyaline membrane disease. (H&E, ob. x40)

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