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RC Test 3 > B4.058 Acute Lung Injury and Respiratory Distress Syndromes > Flashcards

B4.058 Acute Lung Injury and Respiratory Distress Syndromes Flashcards

1
Q

neonatal respiratory distress syndrome

A

most common cause of respiratory distress in premature infants
due to lack of surfactant
characterized histologically by the presence of hyaline membranes in peripheral airspaces

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2
Q

what cells produce surfactant

A

type 2 pneumocytes

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3
Q

what is surfactant

A

lecithin, phosphatidyl glycerol, and hydrophobic glycoproteins
reduce surface tension and make it so there is less pressure required to keep alveoli patent and aerated

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4
Q

what happens in lung parenchyma as gestation proceeeds

A

cuboidal epithelium surrounding alveoli is replaced for thinner type 1 pneumocytes
results in wider air spaces
capillaries migrate closer to air spaces

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5
Q

epidemiology of NRDS

A 
neonates = 0-4 weeks
observed in premature infants
60% infants born at < 28 weeks
30% born between 28-34 weeks
<5% 34 weeks or older
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6
Q

role of surfactant in initial respiration

A

first breath of life is high pressure to expand lungs
lungs retain up to 40% of the residual air volume after the first breath
subsequent breaths require much less pressure because surfactant reduce surface tension

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7
Q

what happens in initial respiration when there is a deficiency in surfactant

A

lungs collapse with each breath
successive breaths take as much effort as the first
stiff atelectatic lungs are further impeded by the soft thoracic wall that is pulled in as the diaphragm descends

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8
Q

what is the result of the atelectasis caused by lack of surfactant?

A 
uneven perfusion and hypoventilation
hypoxemia and CO2 retention
acidosis
pulm vasoconstriction
pulm hypoperfusion
endothelial/epithelial damage 
plasma leak into alveoli
fibrin and necrotic cells produce hyaline membrane
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9
Q

factors that lead to increased surfactant production

A

intrauterine stress
fetal growth retardation
glucocorticoids
labor

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10
Q

factors that lead to decreased surfactant production

A

infants of diabetic mothers
insulin
congenital deficiency

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11
Q

gross appearance of NRDS

A

congested, atelectatic lung

usually sink in water

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12
Q

what reparative changes occur after 48 hours of NRDS

A

alveolar epithelium grows under the hyaline membrane
may detach into the airspace
partial digestion or phagocytosis by macrophages

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13
Q

management of NRDS

A

assess lung maturity using amniotic fluid phospholipids
delay labor
induce lung maturity with steroids
surfactant replacement therapy
oxygenation/ventilation
survival for 3-4 days indicates an excellent chance of recovery

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14
Q

potential complications of NRDS

A

air leaks due to rupture of distended air spaces
complications of oxygen therapy
complications of prematurity

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15
Q

complications of oxygen therapy

A 
retrolental fibroplasia (retionopathy of prematurity)
bronchopulmonary dysplasia
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16
Q

pathogenesis of retinopathy of prematurity

A 
phase I: hyperoxic phase of therapy
-reduction in proangionic VEGF
-endothelial cell apoptosis
phase II: comparatively hypoxic room air
-VEGF levels recover
-retinal vessel proliferation and neovascularization
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17
Q

what is bronchopulmonary dysplasia

A

potentially reversible abnormality in alveolar septation > fewer, larger alveoli > reduction in surface area available for gas exchange
dysregulation of pulm vasculature development

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18
Q

cause and outcome of bronchopulmonary dysplasia

A

superimposed effects of hyperoxemia, hyperventilation, prematurity, inflammatory mediators and vascular maldevelopment play a role
most infants gradually improve in 2-4 months
severe disease required prolonged mechanical ventilation and may develop pulmonary hypertension and cor pulmonale

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19
Q

what is transient tachypnea of the newborn

A

pulm edema resulting from delayed resorption and clearance of fetal alveolar fluid
shortly after delivery in full or late preterm babies

20
Q

increased risk of transient tachypnea of the newborn

A

C-section

infants of diabetic mothers

21
Q

persistent fetal circulation

A

pulmonary vascular resistance fails to decrease after birth
pulm vascular resistance remains equal to or greater than systemic vascular resistance
blood continues to flow through the foramen ovale and ductus arteriosus

22
Q

causes of pulmonary hypoplasia

A

diaphragmatic hernia

renal abnormalities

23
Q

what is pulmonary edema

A

increase in interstitial fluid which then accumulated within alveolar spaces

24
Q

causes of pulmonary edema

A
  1. hemodynamic disturbances (cardiogenic)
  2. microvascular injury leading to direct increases in cap permeability
  3. undetermined origin (head injury, high altitude)
25
Q

hydrostatic pressure

A

pushes blood out of caps

26
Q

osmotic pressure

A

protein content that pulls plasma into caps

27
Q

3 causes for hemodynamic pulmonary edema

A
  1. increased hydrostatic pressure- increased pulm venous pressure (L sided heart failure, volume overload, pulm vein obstruction)
  2. decreased oncotic pressure (low protein states)
  3. lymphatic obstruction
28
Q

pathogenesis of cardiogenic edema

A

perivascular and interstitial fluid accumulation, particularly in the interlobular septa
progressive edematous widening of alveolar septa
accumulation of edema fluid in the alveolar spaces

29
Q

imaging findings in pulm edema

A

wet, heavy lungs with frothy blood tinged fluid
microhemorrhages (hemosiderin containing macrophages in the alveoli)
brown induration
congestion of capillaries

30
Q

pathogenesis of pulm edema from microvascular injury

A

alveolar septa affected
damage to vascular endothelium
damage to alveolar epithelium with secondary vascular injury
inflammatory exudate > interstitial space > alveoli

31
Q

causes of pulm edema from microvascular injury

A 
infections
inhaled gases
liquid aspiration
drugs and chemicals
shock, trauma
radiation
transfusion
32
Q

what happens with pulm edema from microvascular injury becomes widespread

A

significant contributors to ARDS

33
Q

what is acute lung injury

A

noncardiogenic pulmonary edema
abrupt onset of significant hypoxemia and diffuse pulmonary infiltrates in the absence of cardiac failure
severe ALI = ARDS

34
Q

what leads to ALI?

A

inflammation associated increase in pulm vascular permeability
epithelial and endothelial cell death

35
Q

histo manifestation of ALI

A

diffuse alveolar damage (DAD)

36
Q

what is ARDS

A

clinical syndrome characterized by the rapid onset of severe, life threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia that is refractory to oxygen therapy
CXR shows diffuse infiltrates
may progress to multisystem organ failure

37
Q

4 primary causes of ARDS

A 
diffuse pulm infections
gastric aspiration
sepsis
trauma
account for >50% of cases
38
Q

pathogenesis of ARDS

A

endothelial activation
adhesion and migration of neutrophils
intraalveolar fluid and hyaline membranes
loss of diffusion capacity

39
Q

discuss the process of endothelial activation in ARDS

A

pneumocyte injury > sensed by resident alveolar macrophages > secrete mediators > circulating mediators activate pulmonary endothelium
endothelial cells express increased adhesion molecules, procoag proteins, and chemokines

40
Q

discuss the process of adhesion and migration of neutrophils in ARDS

A

neutrophils degranulate and release inflamm mediators including proteases, ROS, and cytokines
macrophage migratory inhibition factor (MIF) helps sustain proinflamm response > increased recruitment of leukocytes

41
Q

discuss the intraalveolar fluid and hyaline membrane formation in ARDS

A

endothelial damage > leaky caps > interstitial and intraalveolar edema
necrosis of type 2 pneumocytes leads to surfactant abnormalities > compromising gas exchange
protein rich fluid and debris from deal alveolar epithelial cells organize into hyaline membranes

42
Q

resolution of ARDS/DAD

A

resolution is by resorption of the exudate and dead cell removal by macrophages
macrophages also discharge fibrogeneic cytokines > fibroblastic proliferation and collagen deposition > alveolar wall fibrosis
epithelial cell repopulation is from proliferation of bronchiolar stem cells
endothelial cell repopulation transpires by proliferation of undamaged capillaries

43
Q

management of ARDS/DAD

A

treatment of underlying precipitating and secondary conditions (sepsis) as well as supportive care (intubation and mechanical ventilation)
avg mortality is 40% depending on cause and severity

44
Q

potential complications of ALI in adults

A 
air leaks
unresolved fibrosis (V/Q mismatch)
superinfections
can be fatal
minority have chronic pulm disease with interstitial fibrosis
45
Q

pathophysiology of DAD

A

reduction in lung compliance and functional residual capacity
ventilation perfusion mismatch
impaired gas exchange

46
Q

what is acute interstitial pneumonia

A

ALI/DAD of unknown etiology
rare
acute resp failure follows an upper rest tract infection like illness
radiographically and pathologically identical to organizing ALI

47
Q

acute interstitial pneumonia mortality

A

33-75%
most deaths within 1 to 2 months
recurrences and chronic disease may develop

RC Test 3 (22 decks)

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