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Pulmonary Flashcards

1
Q

what is respiratory tract derived from

A

endoderm
lung from the ventral bud of the esophagus that arises from the foregut

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2
Q

pulmonary vasculature forms from what branch of the aortic arch

A

6th

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3
Q

when are pre-acinar arteries development complete

A

16 weeks

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4
Q

when does intraacinar arteries complete development

A

8-10 years

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5
Q

vascular wall thickness:total vascular diameter in fetus

A

> than adults; remains constant in second half of gestation

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6
Q

what enhances alveolarization

A

vit A
thyroxine

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7
Q

what delays alveolarization

A

postnatal steroids
supplemental oxygen
nutritional deficiencies
mechanical ventilation
insulin
inflammation

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8
Q

stages and timing of pulmonary development

A

embryonic (0-5 weeks)
pseudoglandular (5-16 weeks)
canalicular (16-25 weeks)
saccular (25-36 weeks
alveolar (36 +)

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9
Q

what happens in embryonic stage of pulmonary development

A

lung from ventral bud of esophagus
evidence of 5 lobes
elongation of proximal airway
pulmonary vascular development (6th aortic arch)

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10
Q

what happens in pseudoglandular stage of pulmonary development

A
  • branching up to terminal bronchi
  • start making AF
  • pneumocyte precursors
  • vasculature of arteries and veins
  • separation of thoracic and peritoneal cavity (7)
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11
Q

what happens in canalicular stage of pulmonary development

A
  • canaliculi branching
  • preliminary gas exchange
  • type 2 into type 1 pneumocytes
  • lung becomes viable
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12
Q

what happens in saccular stage of pulmonary development

A

terminal sacs form - last generation of air spaces
gas exchange alveolar-capillary membrane

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13
Q

what happens in alveolar stage of pulmonary development

A

alveoli increase in diameter
microvascular growth and vessel maturation

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14
Q

disorders of embryonic stage

A

laryngeal cleft
tracheal stenosis
TEF
bronchogenic cyst

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15
Q

disorders of pseudoglandular stage

A

abnormal branching
CDH
congenital lobar emphysema
CPAM
pulmonary lymphangiectasia

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16
Q

disorders of canalicular stage

A

pulmonary hypoplasia
surfactant deficiency
ACD

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17
Q

disorders of saccular stage

A

pulmonary hypoplasia
surfactant deficiency

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18
Q

disorders of alveolar stage

A

surfactant deficiency
congenital lobar emphysema
pulmonary hypertension

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19
Q

which arteries have muscle?

A

pre-acinar not intra-acinar

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20
Q

type 1 vs type 2 pneumocytes

A

shape:
1. fried egg/tight junctions
2. cuboid

percentage of surface
1. 90%
2. 10%

more cells: 2

role in gas exchange: 1

surfactant: 2

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21
Q

what percent of FLF is cleared prenatally, during active labor, and postnatally

A

35 - 30 -35%

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22
Q

prenatal clearance

A
  1. decreased formation
  2. Cl secretion decreases & Na into cell increases - FLF follows
  3. increased lymphatic oncotic pressure promoting alveoli –> lymphatics
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23
Q

active labor clearance

A
  1. mechanical compression
  2. catecholamines –> increase Na transport into cells
  3. cortisol and thyroid –> increase Na transport into cells
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24
Q

postnatal clearance

A
  1. lung distension pressure –> fluid into interstitium
  2. lymphatic transition
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25
Q

components of surfactant

A

50% phosphatidylcholine disaturated
20% phosphatidylcholine monosaturated
8% SP A, B, C, D
8% neutral lipids
8% phosphatidyl glyerol
6% other

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26
Q

which surfactant proteins are excreted by type II and clara cells and which by type II alone?

A

both = A and B

only type II = C and D

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27
Q

what chromosomes express each surfactant protein

A

A = 10
B = 2
C = 8
D = 10

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28
Q

when in gestation is each surfactant protein expressed

A

A =early third
B= end of first
C = end of first
D = latest in third

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29
Q

which surfactant protein is most abundant

A

SP A

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30
Q

which surfactant proteins are hydrophillic and which are hydrophobic?

A

hydrophillic = A and D (both collectins)

hydrophobic = B and C

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31
Q

which surfactant proteins are induced by steroids

A

A, B, and C

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32
Q

what does SP A do?

A

tubular myelin formation
phospholipid uptake and inhibits its secretion
host defense: opsonization, inflammation modulation
helps regulate the expression and uptake of surfactant

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33
Q

what does SP B do?

A

SURFACTANT FUNCTION
tubular myelin formation
surface absorption of phospholipids

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34
Q

what does SP C do?

A

SURFACTANT FUNCTION
surface absorption of phospholipids

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35
Q

what does SP D do?

A
  • host defense:
    – opsonization
    – inflammation modulation
    – antioxidant
  • surfactant lipid homeostasis
  • regulates reuptake and recycling
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36
Q

ABCA3 pathophys

A

AR
transport of lipids –> lack of DPPC and PG –> decreased lamellar bodies

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37
Q

Surfactant metabolism

A
  1. transport
  2. lamellar storage
  3. secretion
  4. adsorption
  5. turnover
  6. recycling
  7. clearance
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38
Q

which pregnancy related factors delay lung development?

A

diabetes
rh immunization
2nd born twin
male
c-sec
prematurity
insulin
tgf beta
androgen

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39
Q

phosphatidylinositol change over time

A

peaks around 35 then drops
present before phosphotidylglycerol

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40
Q

sphingomyelin change over time

A

does NOT reflect lung maturity
decreases after 32 weeks

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41
Q

what is ratio that is used to reflect lung maturity?

A

lecithin/sphingomyelin

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42
Q

lecithin change over time

A

increases with GA
reflects lung maturity
> 2 = mature; 2 at 35 weeks

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43
Q

phosphatidylglycerol change over time

A

increases last; after 34-35 weeks
not necessary for surfactant function
reflects lung maturity

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44
Q

what is foam stability or shake test

A

if AF mixed with ethanol forms foam then phosphatidyl glycerol is present suggesting mature lung

high false negative

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45
Q

what is lamellar body solubilization test

A

detects unraveling or solubilization of lamellar bodies in amniotic fluid if mature lung tissue

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46
Q

laplace law

A

P = 2T/r
P = pressure to resist alveolar collapse
T = surface tension
r - alverolar radius

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47
Q

boyles law

A

P1V1 = P2V2

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48
Q

what is the hering breuer inflation reflex

A

lung overinflation –> inspiration stops as pulmonary stretch receptors in smooth muscle send signals to afferent neural input in medulla causing vagal nerve to inhibit inspiration

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49
Q

what zone does neonatal lung mimic?

A

zone 3
Pa > Pv > PA

50
Q

what zone does air trapping or alveolar distension cause neonatal lung to mimic?

A

zone 1 or 2 leading to decreased pulmonary venous compression and decreased pulmonary blood flow

51
Q

what zone does extravascular fluid cause neonatal lung to mimic?

A

zone 4 with increase PVR and decreased pulmonary ventilation and alveolar collapse

52
Q

physiologic dead space =

A

(arterial CO2 - Expired CO2)/arterial CO2 X TV

53
Q

resistance =

A

change P/change flow

54
Q

% shunt =

A

(O2 content pulm capillary - O2 content systemic artery)/
(O2 content pulm capillary - O2 content mixed venous)

55
Q

total respiratory system resistance components

A

25% chest wall
55% airway
20% lung tissue

usually: 40-55 cm H20/L/s

56
Q

airway system resistance components

A
  • 50% nasal
  • rest first few generation of bronchi
  • distal contribute very little
57
Q

poiseulles law for laminar flow
flow =

A

(change P x pi x r^4)/(8 x length x viscosity)

58
Q

compliance =

A

change V/change P

59
Q

elastance =

A

change P / change V

60
Q

work of breathing =

A

P x V

61
Q

Power =

A

work x force

62
Q

time constant =

A

resistance x compliance

63
Q

one time constants =

A

time for alveoli to discharge 63%

64
Q

two time constants =

A

alveoli discharges 86%

65
Q

three time constants

A

alveoli discharges 95%

66
Q

which respiratory mechanics increase in neonates

A

RR
residual volume
MV
alveolar ventilation = TV - deadspace x RR
chest wall compliance
lung tissue resistance
oxygen consumption

67
Q

which respiratory mechanics decrease in neonates

A

TV
TLC
IC
VC
time constant
lung compliance - neonates stiffer lungs
muscle strength and endurance

68
Q

which respiratory mechanics are same in neonates and adults

A

dead space
FRC

69
Q

normal PaO2 and normal O2 sat
decreased O2 content

A

severe anemia

70
Q

decreased PaO2, decreased O2 saturation, decreased O2 content

A

severe V/Q mismatch
high altitude

71
Q

normal paO2, decreased O2 saturation and content

A

CO poisoning

72
Q

O2 content =

A

O2 bound to Hb + dissolved O2
{1.34 x Hb X O2 sat} + {0.003 x paO2}

73
Q

what does O2 saturation represent

A

percentage of heme binding sites that are saturated with O2

74
Q

A-a gradient =

A

pAO2 - paO2 =
[FiO2 x (Pb - pH20)] - {paCO2 / R} - paO2

Pb = 760
pH20 = 47
R = 0.8

75
Q

oxygen delivery =

A

CO x O2 content =
CO x (O2 bound to Hb + dissolved O2)

76
Q

fick principle for O2 consumption

A

O2 delivered to tissue - O2 returning to heart

= blood flow x O2 arterial - blood flow x O2 venous
= blood flow (O2 artery - O2 venous)
= CO x [Hb] x 1.34 (O2 artery - O2 venous)

77
Q

increased oxygen consumption in:

A
  1. increased caloric intake
  2. decreased temp
  3. neonate > adult
  4. term > preterm
  5. AGA > SGA
78
Q

shift right oxy Hb curve

A

acidosis
higher paCO2
increased adult Hb
increased temp
increased 2,3 DPG

79
Q

bohr vs haldane

A

bohr = changes in O2 bound to Hb based on pCO2

haldane= change in CO2 bound to Hb based on amount O2

80
Q

oxygenation index =

A

(MAP x FiO2)/postductal paO2 x 100

81
Q

increase in flow does what to PIP?

A

get to PIP faster

82
Q

theories on how gas transport works in HFOV

A
  • bulk convection - bulk axial gas flow
  • pendelluft - gas moving between neighboring alveoli due to different time constants
  • asymmetric velocity
  • taylor dispersion - parabolic movement - increased area for diffusion
  • molecular diffusion- transport of gases across alveoli
83
Q

differences in HFOV and HJV

A
  1. expiration type :
    HFOV - active expiration (less gas trapping)
    HJV = passive
  2. inspiration time : HFOV
  3. expiration time : HJV
  4. frequency
    HJV 4-11; HFOV 3-15
  5. fixed inspiratory time HFOV adjustable with HJV
  6. sigh breaths with HJV not HFOV
  7. TV independent of frequency with HJV not HFOV
84
Q

early pneumonia causes

A

GBS
E coli
klebsiella
listeria

85
Q

late pneumonia causes

A

s.aureus
pseudomonas
fungal
chlamydia

86
Q

how do supraglottic, laryngeal and intrathoracic obstructions change with inspiration/expiration?

A

supraglottic - worsens with inspiration
laryngeal - fixed so no change
intrathoracic - worsens with expiration

87
Q

types of complete vascular rings

A
  1. double aortic arch (40%) from right and left 4th branchial arch
  2. right AoA with ligamentous arteriosum/PDA (30%) - persistence of right 4th branchial arch
88
Q

types of incomplete vascular ring

A
  1. aberrant right subclavian artery (20%); rSCA from descending aorta
  2. anomalous origin of the innominate artery (10%)
  3. aberrant LPA (rare)
89
Q

MC locations of chylothorax

A

R > L > bilateral

90
Q

why MCT for chylothorax?

A

bypasses lymphatic system

91
Q

how does octreotide work for chylothorax?

A

mild vasoconstriction of splanchnics???

92
Q

location of congenital lobar emphysema

A

LUL 45%
RML 30%
RUL 20%

93
Q

CPAM vs BPS
tracheobronchial communication

A

CPAM = yes
BPS = no

94
Q

CPAM vs BPS
blood supply

A

CPAM = pulmonary circulation
BPS = anomolous systemic vessels - ie aorta

95
Q

epi of types of CPAM

A

0 rare
1 MCC 50-70%
2 20-40%
3 10%
4 rare

96
Q

which CPAM has most associated anomalies

A

type 2

97
Q

timing of defects by type of CPAM

A

0 early
1 7-10wk
2 3rd wk
3 26-28d
4 ??

98
Q

size and location of cysts by CPAM type

A

0 very small, all lobes (upper tracheobronchial tree)
1 large, usually just 1
2 multiple small
3 very large microcystic entire lobe or multiple lobes
4 large

99
Q

which types of CPAM have mass effect

A

type 1 3 and 4

100
Q

cell types in CPAM?
Which have mucus cells?

A

0 and 1 ciliated pseudostratified
2 ciliated cuboid
3 nonciliated cuboid
4 nonciliated flattened

mucus cells in type 0 and 1 only

101
Q

prognosis by type of CPAM

A

excellent 1 and 4 - excision is curative
poor 0 and 2 for associated anomalies
poor 3 because of pulmonary hypoplasia

102
Q

bronchogenic cyst pathophys

A

anomalous budding of foregut leading to cystic mass that communicates with airway
central or peripheral
may be posterior to trachea

103
Q

congenital pulmonary lymphangiectasia types

A

primary (tri 21, noonan, turner)
secondary (HLHS, thoracic duct agenesis, intrauterine infection)

failure of lymphatic vessel regression at 20 weeks or lymphatic obstruction

poor prognosis

104
Q

bronchopulmonary sequestration pathophys

A

nonfunctioning lung tissue without communication with tracheobronchial tree

105
Q

types of BPS

A

intralobar 75% (lower > upper, L > R); 10-20% risk anomalies

extralobar 25% (L>R often between LLL and diaphragm); 40-60% risk of anomalies

106
Q

alveolar capillary dysplasia pathophys

A

inadequate vascularization of alveoli with decreased number of capillaries adjacent to alveoli
malaligned pulmonary veins

107
Q

MoA acetazolamide

A

carbonic anhydrase inhibitor
inhibits NaHCO3 reabsorption
acts on proximal tubule

108
Q

MoA furosemide/bumetanide

A

blocks active Cl transport
ascending loop of henle

109
Q

MoA chlorothiazide

A

inhibits NaCl reabsorption
acts on distal tubule
inhibits pancreatic release of insulin; risk of hyperglycemia

110
Q

MoA spironolactone

A

antagonist of aldosterone
acts on collecting duct
K sparing

111
Q

Surfactant Metabolism

A
  1. transport SP B and SPC into multivesicular bodies
  2. lamellar storage
  3. secretion into alveolar sub space and interact with SP-A to form tubular myelin reservoir
  4. adsorption + film creation to reduce tension
  5. turnover by endocytosis by alveolar type II cells
  6. recycling into multivesicular and lamellar bodies
  7. alveolar macrophages clear and catabolize surfactant remnants
112
Q

what percent of secreted surfactant is recycled?

A

95%

113
Q

how long does surfactant turnover take?

A

10 hours

114
Q

teratogenic agents associated with CDH

A

mycophenolate mofetil, allopurinol, and lithium

115
Q

syndromes associated with CDH

A

Fryns
Denys Drash
Cornelia de Lange
Marfan
spondylocostal dysostosis
craniofrontonasal syndrome

116
Q

ventilation equations for conventional and HFV

A

Conventional ventilation: Q ∝ f × VT

HFV (jet and oscillatory): Q ∝ f × (VT)2

117
Q

Episodic interruption of fetal breathing mediator

A

Prostaglandin

118
Q

hallmark of “new” BPD

A

disruption of normal alveolar and vascular development with subsequent diffuse alveolar and capillary hypoplasia

119
Q

SP B deficiency associated with what genetic mutation

A

121ins2 SFTB gene chr 2
N. Euro

120
Q

MoA caffeine

A
  • stimulation medullary respiratory center
  • increased sensitivity to CO2
  • diaphragmatic contractility
  • antagonism adenonsine 1+2 R in brain > inhibit phosphodiesterase > increase cAMP and intracellular Ca release
  • upregulates GABA-R
121
Q

antiinflammatory effect of glucocorticoids mediator

A

annexin A1
- decreased phospholipid A2–> decreased PG, thromboxane, PC, leukotrienes

  • suppression COX1/2
  • regulation of surfactant production
  • antioxidant production
  • enhanced adrenergic activity

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