Pathology - Lecture 1 Flashcards
FEV1
Volume of air exhaled with force during the 1st second
FVC
Volume of air exhaled with force following maximal inhalation
DLCO
used to assess whether there is a problem with diffusion barrier
DLCO is reduced if:
increased thickness of diffusion barrier (fibrosis, fluids)
- loss of surface area (emphysema)
Cardiogenic Pulmonary Edema
-increased hydrostatic pressure
-CHF/mitral stenosis
-Transudate/heart failure cells
-Bilateral bibasilar infiltrates (dependent edema)
Pulmonary Edema - non cardiogenic - ARDS
-Abrupt onset of dyspnea (within 1 week of insult)
• Hypoxemia (on ABG)
• Bilateral pulmonary edema
-injury to pneomocytes (direct) or pulmonary endothelium (indirect for e.g sepsis )
-increased vascular permeability
-
ARDS Pathogenesis
-endothelial cells are activated after injury
-Neutrophils adhere to the activated endothelium and migrate into the Inflammatio interstitium and alveoli
-Alveolar inflammation : loss of diffusion and surfactant deficiency + debris organizes into hyaline membrane
Resolution of injury for ARDS
-fibrosis of alveolar walls
-type 2 pneomocytes proliferate to replace the type 1
-endothelial restoration due to proliferation of uninjured capillary endothelium
Morphology of ARDS - day 1-7 (acute and educative phase )
-edema
-hyaline membranes
Morphology of ARDS - day 7-21(organizing phase )
-proliferation of type 2 cells
-interstitial inflammation
-fibrosis