Flashcards in Pulmonary Edema - Pathology Deck (17):
Distinction between "active" and "passive" congestion?
Active - associated with inflammation.
Passive - from increased pulmonary vein pressure.
Aside from distended capillaries, what's a histologic sign of of chronic passive congestion?
Hemosiderosis - iron deposition, and hemosiderin-laden macrophages.
(and mild alveolar wall thickening)
What are lungs with hemosiderosis like grossly?
Firm and rusty/brown.
Is permeability altered in hemodynamic edema?
No - the edema is possible due to the normal intrinsic permeability of the lung capillaries. (But, you can have both hemodynamic and permeability edema happening at the same time.
Example of a high molecular weight plasma protein that escapes from capillaries in permeability edema?
3 pathophysiological mechanisms of hemodynamic edema?
Increased capillary hydrostatic pressure.
Decreased capillary oncotic pressure (eg. hypoalbuminemia).
What region of the lungs does hemodynamic edema preferentially affect?
The lower lobes, due to gravity increasing the hydrostatic pressure more there.
What's the histologic pattern of pathology associated with ARDS?
Diffuse alveolar damage.
(if there isn't a clear etiology, can also be called Acute Interstitial Pneumonia -AIP)
3 consequences of diffuse alveolar damage directly affecting gas exchange?
Fibrin-rich exudates in interstitium and airspaces.
Loss of surfactant.
What follows the eptihelial and endothelial necrosis in diffuse alveolar damage?
Alveolar collapse and "reparative fibrosis".
When do you seen hyaline membranes in diffuse alveolar damage?
Early - the acute/exudative phase.
What happens to Type II pneumocytes in diffuse alveolar damage? Why?
Hyperplasia of Type II Pneumocytes - because these are stem cells that will differentiate into Type I pneumocytes to replace the damaged ones.
(during this phase, their nuclei enlarge, have nuclei / clumped chromatin - can be hard to distinguish from viral inclusions that could be causing the damage)
Gross pathology of early diffuse alveolar damage resembles that of chronic congest...
Yeah, the lungs are heavy and red.
But the slide notes that the cut surface "exudes blood or sanguineous fluid"...
Histology of late diffuse alveolar damage?
How does this relate to lung compliance?
Lots of fibroblasts. "proliferating / organizing phase"
This results in decreased lung compliance.
How do lungs appear grossly in the late phase of diffuse alveolar damage?
Heavy, firm white-grey lungs - lots of fibrosis.
Mortality rate of ARDS?