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Pulmonary > Embryology > Flashcards

Embryology Flashcards

1
Q

Embryonic (4-7wks)

A

Trachea up to tertiary bronchioles

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2
Q

Pseudoglandular (5-16 wks)

A

Up to terminal bronchioles

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3
Q

Cannalicular (wks 16-26)

A

Alvelolar ducts and capillaries

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4
Q

Saccular (wks 26 - birth)

A

Alveolar ducts to terminal sacs

Pneumocytes develop

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5
Q

Alvelolar (wks 32 to 8 years)

A

Adult alveoli (secondary septation)

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6
Q

Pulmonary hypoplasia

A

Poorly developed bronchial tree

Associated with congenital diaphragmatic hernia and bilateral renal agenesis

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7
Q

Brochogenic cyst

A

Abnormal budding of the foregut and dilation/ cyst of terminal or large bronchi

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8
Q

Type I cells

A

Line the alveoli

Squamous, thin for optimal diffusion

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9
Q

Type II cells

A

Secrete pulmonary surfactant –> decrease alveolar tension

Increase compliance, decreases lung recoil

Precursors to Type I and II cells

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10
Q

Surfactant

A

Composed of dipalmitoylphosphatidylcholine

Synthesis begins at week 26, but mature levels not reached until week 35

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11
Q

Club cells

A

Contain secretory granules that degrade toxins

Act as reserve cells

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12
Q

NRDS

A

Caused by surfactant deficiency
Causes buildup of hyaline membrane
Screening test for fetal lung maturity: lecithin:sphingomyelin ratio (should be >2, if less than 1.5- NRDS is likely)

Can happen as a result of C-section delivery (decreased release of fetal glucocorticoids)

Tx: maternal steroids before birth; artificial surfactant for infant

Therapeutic supplemental oxygen –> dangerous; can result in retinopathy, intraventricular hemorrhage, and bronchopulmonary dysplasia

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13
Q

Conducting zone

A

Large airways up to terminal bronchioles –> warms and filters air, but does not participate in gas exchange (dead space- air, but no blood perfusion)

Cartilage and goblet cells up to bronchi

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14
Q

Respiratory zone

A

Respiratory bronchioles, alveolar ducts and alveoli

Gas exchange

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15
Q

Lung relations

A

Right- 3 lobes

Left- 2 lobes + Lingula

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16
Q

Aspiration

A

Most commonly affects right lobe
Upright: inferior segment of inferior right lobe
Supine: superior segment of inferior right lobe

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17
Q

Pulmonary artery to bronchus- RALS

A

Right Anterior

Left Superior

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18
Q

Intercostal n., a., and v.

A

Run inferior to the corresponding ribs

To avoid –> during thoracocentesis, needles are inserted superior to a rib

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19
Q

Diaphragm structures

A

T8: IVC (vena cava- eight letters)
T10: esophagus, vagus (CN 10 + esophagus)
T12: aorta, thoracic duct, azygos vein (red, white and blue)

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20
Q

Diaphragm innervation

A

C 3, 4, and 5- keep diaphragm alive

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21
Q

IRV

A

Amount you can inspire beyond a normal breath

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22
Q

Tidal volume

A

Normally 500mL

Amount that you can inspire (and expire) just with normal breathing

23
Q

Expiratory reserve volume

A

amount you can expire beyond normal expiration

24
Q

Residual volume

A

Amount that remains in lung (cannot be expired)

25
Q

Capacity

A

sum of 2 or more physiologic VOLUMES

26
Q

Inspiratory capacity

A

IRV + TV

27
Q

Functional residual capacity

A

ERV + RV

28
Q

Vital capacity

A

Everything but RV (IRV + TV + ERV)

Max inspiration + expiration

29
Q

Total lung capacity

A

Everything

IRV + TC + ERV + RV

30
Q

Physiologic dead space

A

V_dead = V_tidal * (PaCO2 - PeCO2)/ PaCO2

where PeCO2 is the expired air PCO2

V-dead = Taco Paco Peco Paco

31
Q

Minute ventilation

A

Volume of gas entering per minute

V_E = V_T * RR

32
Q

Alveolar ventilation

A

Volume of gas that reaches ALVEOLI (per unit time); discounts the dead space

V_A = (V_T - V_D) * RR

33
Q

Compliance

A

Change in volume / Change in pressure

The higher, the easier it is to fill

34
Q

Hemoglobin

A

Two forms: Taut in tissues, Relaxed in Respiratory areas

Tight- deoxygenated; low affinity for O2 –> good for releasing/ unloading O2 (e.g. tissues)

Relaxed- oxygenated; high affinity for O2 –> exhibits cooperatively (in lungs)

Acts as a buffer for H+ (which is released- along with CO2- when more O2 is binding; Haldane effect)

35
Q

Methemoglobinemia

A

Oxidized form of Hb (Fe 3+); doesn’t bind O2 as readily, but binds cyanide

S&S: cyanosis with chocolate colored blood

Can be induced using nitrates (+ thiosulfate)

Can be corrected with methylene blue

36
Q

Carboxyhemoglobin

A

Carbon monoxide

Causes left shit and decreased O2 binding

Tx: 100% oxygen

37
Q

Cyanide vs. CO poisoning

A

Both present very similarly, but cyanide poisoning will be associated with an acrid (bitter almond) smell on breath

Both will present with brightly colored venous blood, due to decreased oxygen extraction

38
Q

Things that shift curve right

A 
Altitude
CO2
Exercise
2,3 BPG
Acid
Temperature
39
Q

Fetal hemoglobin

A

curve shifted left

40
Q

Oxygen content of blood

A

O2 content = (1.34 * Hb * SaO2) + .003*PaCO2

Where PaCO2- is determined by plasma O2 concentration (generally unchanged)

SaO2: affected by poisoning (e.g. CO)

Hb: affected by anemia/ polycythemia

41
Q

Perfusion limited

A

Normal- O2, CO2, N2O

The amount of O2 exchange with blood is dependent on the blood flow (the O2 immediately diffuses through capillaries)

42
Q

Diffusion limited

A

Pathologic- seen in emphysema, fibrosis

Diffusion is slow, so it is the limiting factor in gas exchange (blood leaves lungs without being oxygenated)

43
Q

Diffusion

A

Proportional to the area (cross-sectional area- more area, more oxygen can diffuse), and partial pressure gradiant

Inversely proportional to the thickness of the alveolar wall (increased in pulmonary fibrosis)

44
Q

Pulmonary vascular resistance

A

Gradient in pressure between pulmonary artery and left atrium divided by the cardiac output

Resistance is inversely proportional to the r^4 (radius of the vessel)
Resistance is directly proportional to the length of the vessel

45
Q

Alveolar gas equation

A

PA_O2 = 150 - Pa_CO2/ 0.8

46
Q

Things that cause decreased O2 delivery to tissue (hypoxia)

A

Decreased cardiac output
Hypoxemia
Anemia
CO poisoning

47
Q

Thing that cause hypoxemia (decreased PaO2)

A

Normal A-a gradient (10-15)
High altitude
Hypoventilation

Abnormal A-a gradient
V/Q mismatch
Diffusion limitation
Right to left shunt

48
Q

Things that cause ischemia (decreased blood flow)

A

Impeded arterial flow (emboli)

Decreased venous drainage (HF)

49
Q

V/Q mismatch

A

V/Q= infinity: ventilation present, but perfusion is not: “dead space”; normal in upper portion of lung, but pathologic with emboli –> 100% O2 helps because there is not blockage of ventilation

V/Q = 0; ventilation is not present, but perfusion is: “shunt”; 100% does not help because there is a ventilation block (e.g. aspiration)

50
Q

V/Q through body

A

Gas floats, liquid sinks

so V/Q is high at the apex (more V) and low at the base (more Q)

With exercise –> more vasodilation of capillaries so V/Q approaches 1

51
Q

CO2 transport

A

Carried as HCO3- in the plasma

Haldane effect: in lungs, O2 binding to Hb causes release of H+ and HCO3- (converted to CO2)

Bohr effect: in peripheral tissue, high CO2 content causes, release of O2 and uptake of HCO3- + H+ into blood

52
Q

High altitude

A

Hyperventilation due to decreased PO2
Increased 2,3 BPG (to favor unloading to tissue)
Increase in mitochondria
Increase in renal excretion of HCO3- (to compensate for respiratory alkalosis –> this is what acetazolamide treats

Can lead to pulm HTN and RVH –> due to pulmonary vasoconstriction

53
Q

Response to exercise

A

Increased CO2 production
Increased O2 consumption
Increased ventilation rate and increased perfusion (due to opening of capillaries at the apex)

NO CHANGE to PaO2 or PaCO2 (this is a function of the PLASMA)

increased venous CO2 content and venous O2 content (because more is being extracted/ released from the peripheral tissue)

Pulmonary (2 decks)

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