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

B4.058 - Acute Lung Injury and Respiratory Distress Syndrome Flashcards

1
Q
A

cardiogenic pulmonary edema

microhemorrhages –> hemosiderin-containing macrophages in thealveoli

“heart cells”

if prolonged, numerous hemosiderin laden macrphages nad fibrosis make brwon induration

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2
Q
A

B. Hemodynamic pulmonary edema

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3
Q
A

RDS gross appearance

congested, atelectatic lung (like liver)

usually sink in water

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4
Q
A

DAD fibrosis

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5
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. Chest radiographs show diffues aveolar infilatrates. May progress to extrapulmonary multisystem organ failure.

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6
Q
A

pulmonary hypoplasia

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7
Q

managemenf of RDS

A

assess lung maturity using amniotic fluid phospholipids

prevent labor

induce maturity with corticosteroids

surfactant replacement therapy

oxygenation/ventilation

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8
Q
A

immature lung

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9
Q

histo manifestation of ALI and ARDS

A

DAD

diffuse alveolar damage

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10
Q
A

lamellar bodies (precursor of surfactant) within a type 2 pneumocyte

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11
Q

pulmonary hypoplasia

A

another cause of acute respiratory distress in infants, due to poorly developed lungs

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12
Q

causes of ARDS

A

diffuse pulmonary infections (viral, mycoplasma, miliary TB, pneumocystis

gastric aspiration

sepsis

trauma (incl. head injury)

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13
Q

causes of pulmonary edema

A

hemodynaminc - cadiogenic

microvascular injury - direct increase in vasc permeability

undetermined origin - head injury, HAPE

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14
Q
A

cardiogenic pulmonary edema

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15
Q

resolution of ARDS/DAD

A

resorption of the exudate and dead cell removal by macrophages

macrophages also discharge fibrogenic cytokines (TGFbeta and PDGF) –> fibroblastic proliferation and collagen deposition –> alveolar wall fibrosis

Epithelial cell repopulation from proliferation fo bronchilar stem cells

endothelial repopulation from proliferation of undamaged capillaries

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16
Q

other causes of respiratory distress syndrome in neonate

A
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17
Q

pathogenesis of ARDS

A

endothelial activation

pneumocyte injury –> sensed by resident alveolar macrophages –> secrete mediators TNF –> endothelium

Circulating mediators activate pulmonary endothelium (severe tissue injury or sepsise)

endothlelial cells expresss increased adhesion molecules, procoagulant proteins and chemokines.

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18
Q

management of DAD

A

treat underlying cause and supportive care. average mortaility is 40%

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19
Q

potential complications of acute lung injury in adults

A

air leaks

unresolved fibrosis

superinfection

can be fatal

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20
Q
A

renal abnormalities seen with pulmonary hypoplasia due to oligohydramnios

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21
Q
A

pulmonar edema - cardiogenic

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22
Q

retinopathy of prematurity phases

A

1 - hyperoxic phase, marked reduction of VEGF, endothelial cell apoptosis

2 - comparatively hypoxic room air, retinal vessel proliferatiol (neovascularization)

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23
Q

pathophys of RDS

A

prematurity means reduced surfactant –> incfased ST –> atelectasis –> uneven perfusion and hypoventilation –> hypoxemia and CO2 retention –> acidosis, pulm vasoconstriction –> pulm hypoperfusion –> ednothelial and epithelial damage –> leaky plasma –> hyaline mebrane

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24
Q

commonest cause fo respiratory distress in infants

A

RDS lack of surfactant in immature lungs

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25
Q
A

organization phase of ARDS/DAD

26
Q

describe the adhesion and migration of neutrophils in ARDS

A

neutrophils degraulate –> inflammatory mediators, including proteases, reactive oxygen species, and cytokines. Macrophage migration inhibitory factor (MIF) helsp to sustain proinflammatory reponse –>increase recruitement of leukocytes –> more endothelial injury and local thrombosis

27
Q

what is acute lung injury

A

concardiogenic pulmonary edema

abrupt onset of significant hypoxemia nad diffuse pulmonary infiltrates in the absesce of cardiac failure

ARDS is severe ALI

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

28
Q

histo of RDS

A

presence of hyaline membranes in peripheral airspaces

29
Q

CXR for RDS

A

ground glass opacification

30
Q

what reparative changes happen after 48 hrs in RDS

A

alveolar epithelium growsn under hyaline membrane

may detach into airspace

partial digestion or phagocytosis by macrophages

31
Q

signs of cardiogenic pulmonary edema

A

perivascular and isterstitial fluid accumulation, particularly in theinterlobular septa, responsible for Kerleys B lines on x ray

progressive edematous widening of alveolar septa

accumulation of edema fluid in alveolar spaces –> wet, heavy lungs with frothy blood tinged fluid

32
Q

pathogenensis of intraalveolar fluid and hyaline membranes in ARDS

A

endothelial damage –> pulmonary capillaries leaky –> interstitial and itraaveolar edema

necrosis of type 2 alveolar pneumocytes leads to surfactant abnormailities –> comprominsing alveolar gas exchange

protein rich edema fluid and debris from dead alveolar epthelial cells organize int hyaline membranes

33
Q

what is wide spread pulmonary edema from microvascular injury

A

significant contributor to ARDS

34
Q

causes of hemodynaic pulonary edema

A

increased hydrostatic pressure - left sided heart failure, volume overload, pulm vein obsturction

decreased oncotic pressure - low protein states, hypoalbuminemia, renal disease

lymphatic obstruction

35
Q

bronchopulmonary dysplasia

A

potentially reversible abnormality in avleolar septation –> fewer, larger alveoli –> reduction in surface area available for gas exchange

dysregulation of pulmonary vasculature

superimposed effects of hyperoxia, hyperventilation, prematurity, inflammation, vascular maldevelopment

36
Q

causes of pulmonary edema from microvascular injury

A

infections

inhaled gases

liquid aspiration

drugs and chemicals

shock

trauma

radiation

transfusion related

37
Q
A

normal mature alveoli

38
Q

what are hyaline membranes

A

debris consisting of damaged cells, exudative necrosis, leaked protein lining the alveolar sacs

39
Q
A

hyaline membrane disease

hyaline membrane is composed of fibrin and necrotic cells within peripheral airspaces

40
Q
A

DAD - fibrosis

41
Q

role of surfactant in initial respiration

A

first brewth of life needs high inspiratory pressures to expand lungs, in subsequent breaths it requries much less

in surfactant deficiency each breath takes as much effort as the first because the lungs collapse with additional breath

42
Q

pulmonary edema

anatomic compartment

pathogenesis

pathphys

histo

A

anatomic compartment - alveolar-capillary interface

pathogenesis - hemodynamic disturbances or injury to the the alveolar septa leading to extravasation of fluid

pathophys - decreased diffusing capacity and compliance

histo - congestion of alveolar capillaries and fluid filled aveoli

43
Q

what is persistent fetal circulation

A

PDA

foramen ovale

44
Q

pulmonary edema

A

increase in insterstitial fluid which then accumulates within the alveolar sacs

45
Q

what kinds of inhalants can cause ARDS

A

oxygen in high concentrations

46
Q

pathogenesis of pulmonary edema form microvascular injury

A

alveolar septa affected

damage to vascular endo/epithelium with secondary vascular injury

inflammatory exudate –> interstitial space –> alveoli (severe)

47
Q

increased risk of transient tachypnea of the newborn

A

C section

diabetic mother

48
Q

what produces surfactant

A

T2 pneumocytes

lecithin, phosphatidyl, glycerol are components of surfactant

49
Q

summarize ARDS effects of epithelial and endothelial injury

A
50
Q

neonatal respiratory distress syndrome

A

observed worldwide in premature infants of all racial and ethnic groups

lack of surfactant and lung immaturity

51
Q

complications of bronchopulmonary dysplasia

A

severe disease requires prolonged mechanical ventilation, may develop pulmonary hypertension and cor pulmonale

52
Q

pathogenic factors of RDS

A

insulin (moms diabetic) and congenital surfacatnt deficiency lead to decreaseds surfactant - baby senses high blood sugar and increases insulin production which negatively affects surfactant production

glucocorticoids lead to increased surfactant - this is why labor instead of C section is protective, it puts stress on the body which increases endogenous steroid release which helps produce surfactant. C sections do not cause endogenous steroid release

53
Q
A

full term lung

54
Q
A

diaphragmantic hernia seen with pulmonary hypoplasia due to chest wall abnormalities

55
Q

typical clinical scenario of RDS

A

preterm, male infant, maternal diabetes, delivered by C section

labored breathing and cyanosis

fine rales, flaring nostrils, increased RR

56
Q

potential complications of neonatal RDS

A

air leaks

complications of oxygen therapy - bronchopulmonary dysplasia, retrolental fibroplasia

PDA

intraventricular hemorrhage

necrotizing enterocolitis

57
Q

what is acute interstitial pneumonia

A

ALI/DAD of unknown etiology

rare, usually older

usually follows upper respiratory tract like illness

58
Q

a male infant born at 28 weeks to a diabetic mother develops severe respiratory difficulty 30 minutes after birth. Most likely Dx>

A

RDS of the neonate

59
Q

what is transient tachypnea of the newborn

A

pulmonary edema resulting from delayed resoption and clearance of fetal aveolar fluid

shortly after deliveryin full term or late preterm babies

60
Q
A

DAD hyaline membranes

RC Test 3 (15 decks)

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