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Congenital anomalies1- Agenesis or hypoplasia2- Tracheal & bronchial anomalies (atresia, stenosis, tracheoesophageal fistula)3- vascular anomalies.

4- foregut cysts (abnormal detachment of primitive foregut) ,depending on wall structure ,it classified into bronchogenic (most common), esophageal or enteric cyst Bronchogenic cyst, 1-4cm in diameter, rarely connected to the tracheobronchial tree microscopically lined by respiratory epithelium with sq.metaplasia.

5- pulmonary sequestration. presence of a discrete mass of lung tissue without any normal connection to the airway system & with separate blood supply (not from pulmonary arteries but from aorta or its branches). - extralobar---- external to the lung anywhere in the thorax or mediastiunum. - intralobar---- within lung substance & usually associated with recurrent localized infection

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Atelectasis (collapse) Incomplete expansion of the lungs(neonatal) or to the collapse of previously inflated lung (acquired or adult), producing relatively airless pulmonary parenchyma

Types: 1- Obstructive (resorption) 2- Compression3- Contraction4- Patchy

• Resorption (reversible) – Secretions (mucus plug)– Aspiration of foreign bodies– Tumors– Mediastinum: toward

• Compression (reversible)– Hydrothorax (pl.effusion)– Pneumothorax– Hemothorax– Exudate in pleural cavity– Tumor– Mediastinum : away

Contractionirreversible

Pulmonary edema

Normal

Hydrostatic pressure Oncotic pressure

Hydrostatic pressure Oncotic pressure

Causes: - Heart failure - Mitral stenosis

Hydrostatic pressure Oncotic pressureCauses: - Nephrotic syndrome - Liver diseases

Microvascular injury

Causes: - Infections - Aspiration - Drugs - Radiation

cardiogenic

Non-cardiogenic

Pulmonary Edema

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Acute respiratory distress syndrome (ARDS)

Diffuse alveolar damage, shock lung Is a clinical syndrome caused by diffuse alveolar capillary damage

Clinically rapid onset of severe life-threatening respiratory insufficiency& severe arterial hypoxemia that is refractory to oxygen therapy & may progress to extrapulmonary multisystem organ failure

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Etiology:- 1)pulmonary ARDS" (caused by direct lung injury) 2)"extra-pulmonary ARDS" (a remote effect of injury elsewhere).

By:- * Infection (viral), sepsis * gas inhalation or liquid(gastric)aspiration. * drugs, chemicals, radiation. * trauma (head injury), sepsis.

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Basic lesion is injury to alveolar type I pneumocytes & capillary endothelial cellsBy:- * O2 free radicals. * activated macrophages & neutrophils. loss of surfactant.

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Pathology1st /acute (exudative) stage When the alveolar+/or endothelial cells are injured fluid leaks into the interstitial spaces and alveolar air spaces -- this is Non-Cardiogenic PULMONARY EDEMA.

Later, with cell necrosis, FIBRIN is released into the alveoli, producing HYALINE MEMBRANES. Of course there is LOSS OF SURFACTANT, so many alveoli COLLAPSE. During this early stage, the patient is very tachypneic and dyspneic

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2nd /Proliferative or organizing stageAs type I pneumocytes are destroyed, TYPE II PNEUMOCYTES DIVIDE to replace them (regenerative epithelial hyperplasia" ).FIBROSIS ensues as the intra-alveolar hyaline membranes and the interstitial exudate organize