Lungs

Question 1

describe atelectasis and name the 3 types

Answer 1

• loss of lung volume secondary to alveolar collapse → decreased oxygenation → ventilation perfusion imbalance
• types:
  
  • resorption
  • compression
  • contraction

Question 2

describe resorption atelectasis

Answer 2

• 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

Question 3

name causes of resorption atelectasis

Answer 3

• cause of obstruction:
  
  • mucus/mucopurulent plug following surgery
  • aspiration of foreign material
  • bronchial asthma, bronchitis, bronchiectasis
  • bronchial neoplasms (caveat–needs to be TOTAL obstruction)

Question 4

describe clinical findings in resorption atelectasis

Answer 4

• 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

Question 5

describe compression atelectasis

Answer 5

• 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

Question 6

name examples of compression atelectasis

Answer 6

• examples:
  
  • tension pneumothorax
  • pleural effusion

Question 7

describe contraction atelectasis

Answer 7

• fibrotic changes in lung or pleura prevent full expansion → NOT reversible

Question 8

describe the loss of surfactant (neonatal atelactasis)

Answer 8

• 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

Question 9

what is the role of surfactant proteins (SP) A and D?

Answer 9

innate immunity

Question 10

what is the role of surfactant proteins (SP) B and C?

Answer 10

reduction of surface tension at air-liquid barrier in alveoli

Question 11

describe the role of surfactant

Answer 11

reduces surface tension in small airways and prevents collapse on expiration

Question 12

describe how the synthesis of surfactant is modulated by hormones

Answer 12

• cortisol and thyroxine INCREASE surfactant production
• insulin DECREASES surfactant production

Question 13

describe respiratory distress syndrome (RDS) in newborns and name 3 conditions where this can occur

Answer 13

• 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

Question 14

describe what is seen in the image

Answer 14

Question 15

describe the clinical findings of neonatal atelectasis

Answer 15

• clinical findings:
  
  • respiratory distress within a few hours of birth
  • hypoxemia and respiratory acidosis
  • “ground glass appearance” on CXR

Question 16

describe the complications of neonatal atelectasis

Answer 16

• 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)

Question 17

describe the sequence of events seen in reduced surfactant production in neonates

Answer 17

Question 18

describe clinical symptoms of acute respiratory distress syndrome (ARDS)

Answer 18

• 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)

Question 19

describe the etiology of ARDS

Answer 19

Question 20

list the mediators of acute lung injury

Answer 20

• cytokines, oxidants, growth factors
  
  • TNF, IL-1, IL-6, IL-10, TGF-B

Question 21

describe the histology of ARDS

Answer 21

• 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

Question 22

list poor prognostic indicators of ARDS

Answer 22

• advanced age
• bacteremia/sepsis
• progression to multisystem organ failure