atelectasis and acute lung injury

Question 1

Atelectasis

Answer 1

Definition- atelectasis is defined as a state in which the lung, in whole or in par is collapsed or without air, loss of lung volume due to inadequate expansion of airspaces

Types: resorption, compression, loss of surfactant, contraction

Question 2

Resorption atelectasis

Answer 2

censequence of complete airway obstruction, obstruction in bronchi subsegmental bronchi or bronchioles, prevents air from reaching the alveoli, resorption of air trapped in distal airspace thru the pores of Kohn, lack of air in distal airspace, collapse

Cause of obstruction, mucus, mucopurulent plug following surgery, aspiration of foreign material, bronchial asthma, bronchitis, bronchitis, bronchiectasis, bronchial neoplasms (caveat- total obstruction)

Clinical findings: fever and dyspnea- within 24-36 hours of collapse (commonest cause of fever follwoing surgery)
Ipsilateral deviation of trachea, ipsilateral diaphragmatic elevation,, absent breath sounds, collapsed lung doesnt expand on inspiration

Question 3

compression atelectasis

Answer 3

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 lng

Question 4

neonatal atelactasis loss of surfactant

Answer 4

Lipoprotein, phosphatidylcholine (lecithin), phosphatidylglycerol, proteins (surfactant proteins SP A and D innate immunity), 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

Synthesis modulated by different hormones: increased by cortisol and thyroxine, decreased by insulin

Respiratory distress syndrome in newborns: decreased surfactant in fetal lungs, premature, maternal diabetes fetal hyperglycemia stimulates insulin release, cesarean section labor and vag delivery increase stress cortisol to increase surfactant production

Question 5

acute lung injury

Answer 5

endothelial or epithelial injury, initiated by numerous factors, non heritable and heritable, response and survival depends on multiple loci on different chromosomes

Mediators- cytokines, oxidants, growth factors TNF IL1, 6 and 10 TGF B

Manifestation: pulmonary edema, diffuse alveolar damage

Question 6

Pulmonary edema

Answer 6

edema due to alterations in starling pressure, increased hydrostatic pressure in pulmonary capillaries, left sided hear failure, volume overload, mitral stenosis, hemodynamic disturbances, cardiogenic pulmonary edema

Decreased oncotic pressure, nephrotic syndrome, liver cirrhosis, transudate, edema fluid accumulation in alveoli with HF cells and brown induration

Microvascular or alveolar injury- increase in capillary permeability

Question 7

Acute respiratory distress syndrome

Answer 7

noncardiogenic pulmonary edema resulting from diffuse alveolar capillary damage, direct lung injury, indirect lung injury (gram neg sepsis, aspirations, severe trauma, pulmonary infection heroin smoke inhalation)

Pathogenesis: acute injury to alveolar epithelial or endothelial cells , Alveolar macrophages and other cells release cytokines (OMN chemotaxis, transmigration, hyaline membrane, damage to pneumocytes–> low surfactant), repair by type 2 pneumocytes, progressive intersititial fibrosis

PAthology: diffuse alveolar damage with hyaline