poorly defined lung pathologies Flashcards
what are some examples of direct pulmonary insults leading to adults RDS (5)
- pneumonia
- aspiration
- emboli
- drowning
- oxygen toxicity
which types of atelectasis are reversible which are irreversible?
reversible: resorption and compression
irreversible: contraction
what are some important findings in the exudative/acute phase of ARDS?
- HYALINE MEMBRANES
- interstitial and intralveolar edema/hemorrhage
- necrosis and sloughing of epithelial cells
what are some indirect pulmonary causes of ARDS?
- sepsis
- trauma with shock
- acute pancreatitis
- severe burns
- transfusion of blood products
- uremia
- drugs
what phase does alveolar septal thickening occur in ARDS?
proliferative phase/ organizing phase
in neonatal RDS, what is a classic histopathological finding?
hyaline membranes with minimal inflammation
surfactant is produced by _______, around the ______ week of gestation and is stored in ______
type 2 pneumocytes; 28 weeks;
stored in lamellar bodies
ventilation or perfusion is the cause of the V/Q mismatch in atelectasis
ventilation
normal perfusion
compression atelectasis is caused by ________
air or fluid accumulation in the pleural cavity which then compresses and collapses underlying lung
proliferation of type ___ cells occurs in the proliferative phase of ARDS
type II cells
_____ atelectasis is due to fibrotic changes in the lung for pleura
contraction
severe burns is an ____ injury to the lungs that can cause _____
indirect; ARDS
surfactant reduces surface tension in small airways and prevents collapse on _____
EXPIRATION; the alveoli have ↑ tendency to collapse on expiration as radius ↓
“ground glass appearance” on X ray is seen in _____
neonatal atelectasis / neonatal RDS
bronchopulmonary dysplasia is a complication of ______ q
oxygen therapy in treating neonatal RDS
what are the phases and time frames of each in the progression of acute respiratory distress syndrome in adults
- acute (exudative phase): 0-4 days
- organizing (proliferative phase): 4 days - 3 weeks
hyaline membranes are composed of ____ and ____
fibrin (endothelial cell damage) + necrotic cells (alveolar epithelial cell damage)
insulin ___ levels of surfactant in the fetus
↓
____ and _____ are examples that can lead to compression atelectasis
pneumothorax (air in the pleural cavity) or hydrothorax / pleural effusion (fluid in pleural cavity)
neonatal atelectasis occurs as a result of the loss of ______
surfactant
what are the complications of oxygen therapy in treating neonatal atelectasis?
- retinopathy of prematurity (cataracts/blindness)
- intraventricular hemorrhage
- bronchopulmonary dysplasia
(RIB)
atelectasis causes a V/Q mismatch because ______
loss of lung volume → ↓ oxygenation
however, the lung is still getting perfused thus leads to a V/Q mismatch
respiratory acidosis/alkalosis is seen in neonatal atelectasis
respiratory acidosis and hypoxemia
the collapsed alveoli in neonatal RDS is lined by ______
hyaline membranes
hyaline membranes in the collapsed alveoli will _______ the diffusion gradient
↑
_______ atelectasis is associated with COMPLETE airway instruction
resorption; resorption of air trapped in the distal airspaces back into the blood
what are some manifestations of acute lung injury?
- pulmonary edema (must make sure no cardiac dysfunction)
- diffuse alveolar damage (RDS)
- inflammatory infiltrate in alveoli
- hyaline membrane formation
drowning is a ______ cause of ARDS
direct
what are some risk factors for neonatal respiratory distress syndrome?
- maternal diabetes (↑ insulin will ↓ surfactant)
- C section birth (↓ in cortisol will ↓ surfactant)
- premature birth (surfactant production starts at 28 weeks but does reach max levels till week 35)
_______ atelectasis can occur following surgery
resorption atelectasis due to the mucus plugs that can form post surgery (still unable to cough them out) and they cause COMPLETE obstruction
which RDS is refractory to oxygen therapy: adult or neonatal
ADULT
in resorption atelectasis, you will see ______ deviation of the trachea and _____ elevation of the diaphragm
IPSILATERAL deviation of the trachea and IPSILATERAL elevation of the diaphragm
cortisol ____ levels or surfactant in the fetus
↑
what are some findings in the organizing phase of ARDS?
- proliferation of type II cells
- fibrosis
- alveolar septal thickening
MAINLY: interstitial inflammation and fibrosis
what are some other names for adult respiratory distress syndrome
- shock lung syndrome
- acute lung injury
- diffuse alveolar damage
- non cardiogenic pulmonary edema
in adults, the RDS is due to _______
underlying inflammation; rapid onset, severe hypoxemia with bilateral pulmonary infiltrates in the absence of cardiac failure
hypoxia in the lungs lead to pulmonary vasoCONSTRICTION → pulmonary _________ →endothelial and alveolar epithelial damage → plasma leak into alveoli → fibrin + necrotic cells (hyaline membrane)
HYPOperfusion because of the vasoconstriction in the pulmonary vasculature
(all other parts of the body will respond to hypoxia with vasodilation)
what is the difference between direct and indirect lung injury causes of adult RDS?
direct: direct pulmonary insult the alveoli resulting in inflammation while indirect: systemic causes of inflammation that goes to the lungs via capillaries
trachea and mediastinum shift ______ to the site of the affected side in compression atelectasis
SHIFT AWAY from lesion (CONTRALATERAL SHIFT)
what are some complications of neonatal RDS?
- PDA (due to persistent hypoxemia because it closes due to oxygen in the lungs)
- necrotizing enterocolitis (due to intestinal ischemia) = bloody diarrhea
- HYPOglycemia (excessive insulin release in the case RDS is caused by maternal diabetes)
acute lung injury is precipitated by ________ injury
endothelial and epithelial injury
