lung-respiratory distress syndrome Flashcards
tell me about the pathogenesis of ARDS
leakage of protein rich fluid leads to edema that combines with necrotic epithelial cells to form hyaline membranes in alveoli
what are some clinical features of ARDS
hypoxemia and cyanosis with resp distress due to thickened diffusion barrier and collapse of air sacs
how does the xray look in ARDS
white out
tell me about the pathogenesis of ARDS when it is secondary to some other disease process
activation of neutrophils induce protease and free radical mediated damage of type I and II pneumocytes
how is recovery from ARDS complicated
complicated by interstitial fibrosis, damage and loss of type II pneumocytes leads to scarring and fibrosis
what is neonatal respiratory distress syndrome
resp distress due to inadequate surfactant levels
what cells make surfactant?
type II pneumocytes
what is the major component of surfactant
phosphatidylcholine (lecithin)
what does lack of surfactant lead to?
collapse of air sacs and formation of hyaline membranes
what gestational age does surfactant usually get produced
begins at 28 weeks and adequate levels are reached by 34 weeks
what is used to screen for surfactant maturity in amniotic fluid? what ratio value indicates adequate fluid production
lecithin to sphingomyelin ration (lecithin levels increase as surfactant is produced, sphingomyelin stays constant)
ratio >2 is adequate
what does C section put a baby at higher risk for neonatal RDS
due to lack of stress induced steroids
steroids increase the production of surfactant
what does maternal diabetes lead to higher risk of neonatal RDS
increased maternal glucose–>baby’s insulin levels increase–>insulin decreases surfactant production
what are some clinical features of neonatal RDS
increasing resp effort after birth, tachypnea with use of accessory muscles, grunting
hypoxemia with cyanosis
how does neonatal RDS appear on xray
diffuse granularity of lung (ground glass appearance)
