Lungs Flashcards
describe atelectasis and name the 3 types
- loss of lung volume secondary to alveolar collapse → decreased oxygenation → ventilation perfusion imbalance
- types:
- resorption
- compression
- contraction
describe resorption atelectasis
- consequence of complete airway obstruction
- obstruction in bronchi, subsegmental bronchi or bronchioles
- prevents air from reaching alveoli
- resorption of air trapped in distal airspaces through the pores of Kohn
- lack of air in distal airspaces
- collapse
name causes of resorption atelectasis
- cause of obstruction:
- mucus/mucopurulent plug following surgery
- aspiration of foreign material
- bronchial asthma, bronchitis, bronchiectasis
- bronchial neoplasms (caveat–needs to be TOTAL obstruction)
describe clinical findings in resorption atelectasis
- fever and dyspnea within 24-36 hours of collapse (commonest cause of fever 24-36 hrs following surgery)
- ipsilateral deviation of trachea
- ipsilateral diaphragmatic elevation
- absent breath sounds and absent vocal vibratory sensation (tactile fremitus)
- collapsed lung does not expand on inspiration
describe compression atelectasis
- air or fluid accumulation in pleural cavity → increased pressure → collapses underlying lung
- examples:
- tension pneumothorax
- pleural effusion
- trachea and mediastinum shift away from the atelectatic lung
name examples of compression atelectasis
- examples:
- tension pneumothorax
- pleural effusion
describe contraction atelectasis
- fibrotic changes in lung or pleura prevent full expansion → NOT reversible
describe the loss of surfactant (neonatal atelactasis)
- surfactant
- lipoprotein
- phosphatidylcholine (lecithin)
- phosphatidylglycerol
- proteins
- surfactant proteins (SP) A and D → innate immunity
- surfactant proteins (SP) B and C → reduction of surface tension at air-liquid barrier in alveoli
- synthesized by type 2 pneumocytes
- synthesis begins by 28th week of gestation
- stored in lamellar bodies
- lipoprotein
what is the role of surfactant proteins (SP) A and D?
innate immunity
what is the role of surfactant proteins (SP) B and C?
reduction of surface tension at air-liquid barrier in alveoli
describe the role of surfactant
reduces surface tension in small airways and prevents collapse on expiration
describe how the synthesis of surfactant is modulated by hormones
- cortisol and thyroxine INCREASE surfactant production
- insulin DECREASES surfactant production
describe respiratory distress syndrome (RDS) in newborns and name 3 conditions where this can occur
- decreased surfactant in fetal lungs
- prematurity
-
maternal diabetes
- fetal hyperglycemia stimulates insulin release → decreased surfactant production
-
Cesarean section
- labor and vaginal delivery increases stress-related cortisol secretion → increases surfactant production
describe what is seen in the image
describe the clinical findings of neonatal atelectasis
- clinical findings:
- respiratory distress within a few hours of birth
- hypoxemia and respiratory acidosis
- “ground glass appearance” on CXR
describe the complications of neonatal atelectasis
- complications:
- intraventricular hemorrhage
- PDA (persistent hypoxemia)
- necrotizing enterocolitis (intestinal ischemia)
- bloody diarrhea
- hypoglycemia (excessive insulin release)
- O2 therapy: damage to lungs (bronchopulmonary dysplasia) and cataracts (blindness because of ROS → free radical injury)
describe the sequence of events seen in reduced surfactant production in neonates
describe clinical symptoms of acute respiratory distress syndrome (ARDS)
- clinical syndrome:
- rapid onset
- severe hypoxemia
- bilateral pulmonary infiltrates
- often refractory (unresponsive) to O2 therapy
- secondary to both direct and indirect lung injury
- alveolar-capillary membrane compromise
- alveolar epithelium/capillary endothelium
- increased vascular permeability, loss of diffusion and surfactant deficiency (type II cell damage)
- alveolar-capillary membrane compromise
describe the etiology of ARDS
list the mediators of acute lung injury
- cytokines, oxidants, growth factors
- TNF, IL-1, IL-6, IL-10, TGF-B
describe the histology of ARDS
- diffuse alveolar damage
- acute (exudative) phase = 0-4 days
- heavy and firm lungs
- interstitial and intra-alveolar edema/hemorrhage
- necrosis and sloughing of alveolar epithelial cells
- HYALINE MEMBRANES
- organizing (proliferative) phase = 4 days - 3 weeks
- proliferation of type II cells
- organization of fibrin exudates→ fibrosis
- alveolar septal thickening
- acute (exudative) phase = 0-4 days
list poor prognostic indicators of ARDS
- advanced age
- bacteremia/sepsis
- progression to multisystem organ failure