1. 1

3. 3

4. Congenital anomalies
1- Agenesis or hypoplasia
2- 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
4

5. 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- Compression
3- Contraction
4- Patchy
5

6. • 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
Contraction
irreversible

7. Pulmonary edema
Normal
Hydrostatic pressure Oncotic pressure
Hydrostatic pressure Oncotic pressure
Causes:
- Heart failure
- Mitral stenosis
Hydrostatic pressure Oncotic pressure
Causes:
- Nephrotic
syndrome
- Liver diseases
Microvascular injury
Causes:
- Infections
- Aspiration
- Drugs
- Radiation
cardiogenic
Non-cardiogenic

8. Pulmonary Edema

9. 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
9

10. 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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11. 11

12. 12
Basic lesion is injury to alveolar type I pneumocytes
& capillary endothelial cells
By:-
* O2 free radicals.
* activated macrophages & neutrophils.
loss of surfactant.

13. Pathology
1st /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
13

14. 2nd /Proliferative or organizing stage
As 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
14