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BOONE/WALTERS NEO BOARDS > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Lung development
1) respiratory tract is derived from ___
2) what first branches from esophagus to form the lungs?
3) does this arise from forgot, Midgut, or hindgut

A

1) Endoderm
2) Ventral Bud
3) Foregut

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2
Q

Vascular Supply
1) which aortic arch does the pulmonary vasculature form from?
2) where do the bronchial arteries come from? What did they supply?
3) how do pre-Acenar arteries develop? When are they complete?
4) how do intra-Acenar arteries develop? When are they complete?

A

1) sixth aortic arch
2) aorta to the conducting airways, visceral, pleura, connective tissue
3) angiogenesis (16 weeks)
4) vasculogenesis (alveolar development to 8-10 years)

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3
Q

Alveolarization
1) what phase does this occur? (Timeline)
2) how many alveoli at term? Adult?
3) what enhances alveolarization?
4) what delays alveolarization?

A

1) alveolar phase (36 weeks to 8 years)
2) 50 – 150million -> 200–600 million
3) vitamin a and thyroxine
4) postnasal steroids, oxygen, malnutrition, ventilation, insulin, inflammation

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4
Q

Lung development
List the stages of lung development and gestational age

A

Embryonic (0–5)
pseudoglanular (5–15)
canalicular (15–25)
Sacular (25–35)
Alveolar (36+)

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5
Q

Embryonic
1.) structures?
2.) developmental abnormalities?

A

-Ventral bud, bronchi, five branches/lobes (“5 branches by 5 weeks”)
-Pulmonary vasculature from 6th aortic arch
-laryngeal cleft, tracheostenosis, tracheoesophageal fistula, bronchogenic cyst

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6
Q

Pseudoglandular
1) structures?
2) developmental abnormalities

A

Branching up to terminal bronchi
Bronchopulmonary epithelium -> amniotic fluid
Pneumocyte precursors
Vasculature (artery/veins)
Separation of thorax/peritoneal (7wk)

Branching abnormalities, CDH, CLE, CPAM, pulmonary lymphangiectasia

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7
Q

Cannulicular
1) structures?
2) developmental abnormalities?

A

-Terminal bronchioles/respiratory bronchioles
-Type two-> type one pneumocytes
-Viable lung at 25 weeks

Pulmonary hypoplasia, surfactant deficiency, alveolar capillary dysplasia

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8
Q

SACCULAR
1) structures?
2) developmental abnormalities?

A

-alveolar ducts
-Complete bronchial division
-Gas exchange = alveolar/capillary membrane

2) pulmonary hyperplasia, surfactant deficiency

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9
Q

ALVEOLAR
1) structures?
2) developmental abnormalities?

A

1) alveoli
-Microvasculature

2) surfactant deficiency, CLE, PHTN

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10
Q

PNEUMOCYTES
1) percent surface area of alveoli?
2) which secrete surfactant?
3) which is progenitor cell?

A

1) I = 90% II = 10%
2) type 2
3) type 2

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11
Q

FETAL LUNG FLUID
1) how much volume? Equal to what on PFT?
2) production rate near term?
3) how is Cl- transported and pulmonary epithelia?
4) what inhibits fetal lung fluid production?

A

1) 20–30 ML/KG; FRC
2) 4–5, ML/KG/HR
3) actively on basal side
4) Epi (delivery stress), B-adrenergic agonists

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12
Q

ABSORPTION OF FLF
1) prior to birth, function of respiratory epithelium changes from _____ secreting to _____ absorbing.
2) FLS decreases by ___, prenatally, ___ during active labor and ___ postnatal.
3) why is it helpful to have fluid in lungs at birth?

A

1) chloride, sodium

2) 1/3

3) P~T/r ⬆️ radius of airways allows for a lower pressure to overcome surface tension

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13
Q

SURFACTANT
1) what is the largest composition?

2) what percentage is surfactant proteins

A

1) 50% disaturated Phosphatidylcholine

2) 8%

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14
Q

SURFACTANT
1) chromosome for SP-A
2) chromosome for SP-B
3) chromosome for SP-C
4) chromosome for SP-D

A

1) 10
2) 2
3) 8
4) 10

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15
Q

SURFACTANT
1) which is the most abundant?
2) hydrophobic?
3) express last (early third trimester)
4) assist w/ tubular myelin formation?
5) promotes surface absorption of phospholipid?
6) aids in host defense?

A

1) SP-A
2) SP-B, C
3) SP-D
4) SP-A, B
5) SP-B, C
6) SP-A, D

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16
Q

SURFACTANT
1) which SP has no known mutations?
2) which homozygotes deficiency is autosomal recessive? Timeline of symptoms?
3) which is autosomal dominant? Timeline?

A

1) SP-A, D
2) SP-B @birth
3) SP-C months ➡️ interstitial lung disease

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17
Q

SURFACTANT
1) what is the most common known genetic cause of surfactant deficiency? Inheritance?
2) mechanism of action of this protein?
3) timeline?

A

1) ATP-binding Cassatt member A3 deficiency (ABCA3 deficiency); autosomal recessive

2) assist with transport of lipids; deficiency lacks DPPG, and PG. Decreased lamellar bodies.

3) soon after birth to childhood

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18
Q

SURFACTANT
1) ___ % of secreted surfactant is recycled

2) what is the turnover time?

A

1) 95%

2) 10 hours

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19
Q

SURFACTANT
what is Survanta made from and what does it contain?

A

Minced bovine long
SP-B and C (small amounts.)
No SP -A

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20
Q

SURFACTANT
What is infasurf and what does it contain?

A

Bovine lung lavage

SP-B, C
No SP -A

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21
Q

SURFACTANT
What is Curosurf made from and what does it contain?

A

Minced porcine lungs

SP-B, C
No SP-A

22
Q

SURFACTANT
What is Alveofact made from and what does it contain?

A

Bovine lung lavage

SP-B, C
No SP-A

23
Q

SURFACTANT
Laplace’s Law

A

P=2T/r

“LaPressure’s Law”
Pressure is directly proportional to ST and indirectly to radius.

24
Q

CONTROL OF BREATHING
Boyles Law

A

P1V1=P2V2

25
Q

APNEA
1) define apnea
2) define periodic breathing

A

1) no airflow for >20 seconds
2) 3 respiratory pauses with more than 3 sec between for up to 20 seconds

26
Q

Ventilation
Ideal ventilation:perfusion

A

Va/Q should = 1
Anything else = VQ mismatch = hypoxemia

27
Q

VENTILATION
ventilation equation

A

Va= (tidal volume - dead space) x RR

28
Q

MECHANICS
1) resistance equation
2) most respiratory resistance

A

R = change in pressure (cmH2O / change in flow(L/s)

Chest wall (25%), airway (55%), lung tissue (20%)

29
Q

What part of the respiratory system has the most resistance?

A

About 50% of airway resistance is due to nasal resistance

30
Q

Poiseuille’s Law

A

Flow = [change in pressure x constant x (radius)4] / [8 (length X viscosity)]

Radius to the 4th power

31
Q

What happens to the resistance if the diameter of an ETT increases from 2 to 4 mm

A

If the diameter goes from 2 to 4 than the radius will increase from 1 to 2. And the resistance will be 16 times less because resistance is indirectly proportional to r ^ 4.

32
Q

Compliance equation

Elastance equation

A

C=changing vol / changing pressure
-Compliance is the slope of the volume pressure curve

E= changing pressure / changing vol
-elastance is inverse of compliance

33
Q

How does compliance differ from neonates to adults?

A

Greater chest wall compliance because bones are more Cartlidge and soft and compliant compared to hard adult ribs.

34
Q

1) How does compliance differ from premature to term infants?
2) How does RDS change compliance?

A

1) premature infants, have more compliant lungs

2) sentence with RDS have stiffer lungs. Flat volume pressure curve. Less compliant lungs

35
Q

MECHANICS
What happens to compliance at both high and low lung volumes?

A

Compliance decreases because very small volume changes require large pressure changes.

36
Q

What are disease states that lead to low FRC, and high FRC

A

1) low: RDS-> atelectasis and collapse

2) high: MAS, chronic lung disease, using excessive vent pressures

37
Q

MECHANICS
Define “time constant”

Time constant equation

A

How quickly the lungs can empty.
Also, how long it takes for alveolar and proximal airway pressure to equilibrate.

TC= resistance x compliance 

38
Q

MECHANICS
One time constant = ____% volume
Two time constant
Three time constants
3-5 time constants

A

63%
86%
95%
3-5: necessary to allow adequate time for inspiration and expiration

39
Q

MECHANICS
1) Healthy, newborn time constant?
2) RDS
3) CLD

A

1) 0.09-0.15
2) lower 0.05 (decreased lung compliance, and mildly increased airway resistance)
3) higher >0.15 (decreased lung compliance, and markedly, increased airway resistance

40
Q

MECHANICS
What is increase in neonates compared to adults?

A

Respiratory rate
Residual volume
Minute ventilation (TV x RR)
Alveolar ventilation
Chest wall compliance (soft compliant ribs)
Lung tissue resistance (more dense)
Oxygen consumption

41
Q

MECHANICS
What is decreases in neonates compared to adults?

A

Tidal volume
Total lung capacity
Inspiratory capacity
Vital capacity
Time Konstant
Lung compliance (stiffer lungs)
Muscle strength

42
Q

MECHANICS
What is the same in neonates and adults?

A

 Dead space
Functional residual capacity

43
Q

PATH
Sequestration vs CPAM

A

Sequestration: “sequestered in time out” not functioned, not connected to bronchial tree, systemic circulation, most likely to cause respiratory distress

CPAM: fed by Pulm circulation,

Both unilateral, both regress in utero.

44
Q

OXYGEN
1) Define paO2

2)Each hemoglobin contains ___ sites that combine to oxygen

3) define O2 sat

A

1) Partial pressure of oxygen dissolved in the plasma of arterial blood. (Not bound to Hgb)

2) 4 Fe++ Heme

3) % hgb O2 binding sites that are saturated with O2.

45
Q

OXYGEN
1) O2 content equation

A

1) O2 con= bound to hgb + dissolved

= (1.34 x Hb x O2sat) + (0.003 x paO2)

46
Q

CO2
1) how is majority transferred in blood

A

1) bicarb ions (70%) vs 10% dissolved

47
Q

BPD
classification

A

mild: 02 at 28d + room air at 36 wks
Moderate: 02 at 28D + < 30% at 36WKS
Severe: 02 at 28D + >= 30% at 36WKS or CPAP

48
Q

Factors associated with accelerated long maturation and surfactant production

A

1) chorioamnionitis
2) chronic maternal hypertension
3) hemoglobinopathy
4) incompetent cervix
5) IUGR
6) maternal cardiovascular disease
7) placenta, infarction
8) pregnancy, induced, hypertension
9) prolong rupture of membranes 

49
Q

Pulsus paradoxus occurs when the <increase/decrease> in <systolic/diastolic> blood pressure during <inspiration/expiration> is exaggerated and > ___mm Hg.

A

decrease in systolic blood pressure during inspiration is exaggerated and > 10 mm Hg.

50
Q

Which surfactant protein is not associated with human disease.

A

A, B, C are associated with human disease. D Does not

Most critical: b chromosome 2 (b is the second letter), c on chromosome 8 causes disease later.

A tubular myelin formation.

8% of surfactaht.

51
Q

La places law

A

P = 2T/r

BOONE/WALTERS NEO BOARDS (21 decks)

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