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

25
APNEA 1) define apnea 2) define periodic breathing
1) no airflow for >20 seconds 2) 3 respiratory pauses with more than 3 sec between for up to 20 seconds
26
Ventilation Ideal ventilation:perfusion
Va/Q should = 1 Anything else = VQ mismatch = hypoxemia
27
VENTILATION ventilation equation
Va= (tidal volume - dead space) x RR
28
MECHANICS 1) resistance equation 2) most respiratory resistance
R = change in pressure (cmH2O / change in flow(L/s) Chest wall (25%), airway (55%), lung tissue (20%)
29
What part of the respiratory system has the most resistance?
About 50% of airway resistance is due to nasal resistance
30
Poiseuille's Law
Flow = [change in pressure x constant x (radius)4] / [8 (length X viscosity)] Radius to the 4th power
31
What happens to the resistance if the diameter of an ETT increases from 2 to 4 mm
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
Compliance equation Elastance equation
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
How does compliance differ from neonates to adults?
Greater chest wall compliance because bones are more Cartlidge and soft and compliant compared to hard adult ribs.
34
1) How does compliance differ from premature to term infants? 2) How does RDS change compliance?
1) premature infants, have more compliant lungs 2) sentence with RDS have stiffer lungs. Flat volume pressure curve. Less compliant lungs
35
MECHANICS What happens to compliance at both high and low lung volumes?
Compliance decreases because very small volume changes require large pressure changes.
36
What are disease states that lead to low FRC, and high FRC
1) low: RDS-> atelectasis and collapse 2) high: MAS, chronic lung disease, using excessive vent pressures
37
MECHANICS Define "time constant" Time constant equation
How quickly the lungs can empty. Also, how long it takes for alveolar and proximal airway pressure to equilibrate. TC= resistance x compliance 
38
MECHANICS One time constant = ____% volume Two time constant Three time constants 3-5 time constants
63% 86% 95% 3-5: necessary to allow adequate time for inspiration and expiration
39
MECHANICS 1) Healthy, newborn time constant? 2) RDS 3) CLD
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
MECHANICS What is increase in neonates compared to adults?
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
MECHANICS What is decreases in neonates compared to adults?
Tidal volume Total lung capacity Inspiratory capacity Vital capacity Time Konstant Lung compliance (stiffer lungs) Muscle strength
42
MECHANICS What is the same in neonates and adults?
 Dead space Functional residual capacity
43
PATH Sequestration vs CPAM
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
OXYGEN 1) Define paO2 2)Each hemoglobin contains ___ sites that combine to oxygen 3) define O2 sat
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
OXYGEN 1) O2 content equation
1) O2 con= bound to hgb + dissolved = (1.34 x Hb x O2sat) + (0.003 x paO2)
46
CO2 1) how is majority transferred in blood
1) bicarb ions (70%) vs 10% dissolved
47
BPD classification
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
Factors associated with accelerated long maturation and surfactant production
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
Pulsus paradoxus occurs when the in blood pressure during is exaggerated and > ___mm Hg.
decrease in systolic blood pressure during inspiration is exaggerated and > 10 mm Hg.
50
Which surfactant protein is not associated with human disease.
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
La places law
P = 2T/r