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ACEM Viva > Physiology - Respiratory > Flashcards

Physiology - Respiratory Flashcards

1
Q

What are the typical volumes of the lung?

A
  • tidal volume = 500ml
  • inspiratory reserve volume = 3L
  • vital capacity = 5L
  • residual volume = 1.2L
  • functional residual capacity = 3L
  • expiratory reserve volume = 1.2L
  • total lung capacity = 6L
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2
Q

What respiratory volumes can be measured in the ED and elsewhere

A

ED: spirometry measures FEV1 and FVC, ventilators measure TV

other: helium dilution can measure TLV, FRC and RV

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3
Q

Describe the components of total lung capacity

A

residual volume + expiratory reserve volume + tidal volume + inspiratory reserve volume

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4
Q

What is residual volume and describe methods of measuring it

A

the volume of gas remaining in the lung after maximum expiration

measured by helium dilution, body plethysmography or nitrogen washout method

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5
Q

What is anatomical dead space and physiological dead space (how do they differ) and how are they measured

A

dead space = portion of tidal volume that does not participate in gas exchange

anatomical dead space:

  • refers to the conducting zones of the lung, do not contain alveoli, normally contain a volume of 150ml
  • from trachea to terminal bronchiole and take no part in gas exchange
  • measured by Fowler method

physiological dead space:

  • parts of the lung with ventilation but no perfusion, does not eliminate CO2
  • usually the same as anatomical dead space, but increases in lung disease
  • measured by Bohr method
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6
Q

What will lead to increased physiological dead space?

A

ventilation perfusion mismatch = non-perfused alveoli and alveoli with wasted ventilation

e.g. PE, shock/hypovolaemia, RV failure, excessive PEEP, COPD

(dead space: physiological = anatomical + alveolar)

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7
Q

Explain Fick’s law of diffusion

A

amount of gas moving across tissue is:
proportional to area of the diffusion membrane
pressure gradient across the membrane
diffusion constant

inversely proportional to
thickness of membrane

-volume of gas transferred = (area of tissue/thickness of tissue) x diffusion constant x partial pressure difference

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8
Q

What is the difference between diffusion limited and perfusion limited

A

diffusion limited:

  • amount of substance transferred is limited by diffusion properties of the blood-gas barrier and not blood flow
  • partial pressure of gas does not reach equilibration in time the blood spends in capillaries
  • gas that is highly soluble and does not form a partial pressure in blood
  • examples = CO moves rapidly into RBC with minimal change in plasma

perfusion limited:

  • amount of gas taken up by blood depends on the amount of available blood flow and not diffusion properties
  • partial pressure on both sides of the membrane equilibrates rapidly so no further diffusion without increased flow
  • gas is highly insoluble and forms a rapid partial pressure in blood
  • examples = N2O does not combine with Hb and partial pressure rises rapidly, O2, CO2
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9
Q

which Law is involved

What factors influence the rate of oxygen transfer from the alveolus into the pulmonary capillary

A
  • ficks law: gas transferred = (area of tissue/thickness of tissue) x diffusion constant x partial pressure difference
  • mostly perfusion limited
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10
Q

How do you measure diffusion capacity

A

Diffusing capacity, aka. DLCO (Diffusing Capacity of the Lungs for Carbon Monoxide) measures how effectively gases can diffuse across the lung’s alveolar-capillary membrane.

CO is used for measurement because its uptake is solely diffusion limited (not limited by perfusion, as CO is so avidly taken up by Hb that it has a uniform distribution in the alveolar and pulmonary capillaries).

Fick’s law of diffusion: diffusion flux Vgas ∝ Area x Δ(Palveolar - Pcapillary) / Thickness

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11
Q

What conditions may affect the rate of transfer of oxygen from the alveolus into a pulmonary capillary

A

exercise
alveolar hypoxia
thickening of the blood gas barrier

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12
Q

What is the effect of heavy exercise on oxygen uptake in the pulmonary capillary

A
  • reduced time for combination with Hb with possible reduced Hb saturation
  • shifts saturation curve to the right
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13
Q

What factors influence the distribution of pulmonary arterial blood

A

alveolar hypoxia
gravity (Describewest zone)
vascular resistance
pulmonary disease
vasoactive substances
sympathetic stimulation

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14
Q

What extra-pulmonary factors influence pulmonary blood flow

A

Patient factors:

blood volume
cardiac output
pathology
exercise
posture

Environmental factors:

atmospheric pressure
temperature

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15
Q

Describe the normal distribution of pulmonary blood flow in an upright lung

A

-decreases linearly from base to apex
-influenced by gravity and divided into 3 zones:
Zone 1 = V/Q >1 PA>Pa>Pv, capillaries are squashed, no flow, does not normally occur
Zone 2 = V.Q=1 Pa>PA>Pv, capillaries are partly squashed, flow occurs
Zone 3 = V/Q <1 Pa>Pv>PA, capillaries are distended, flow is based on normal arterial-venous pressure difference

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16
Q

How does the distribution of blood change in lungs when the subject becomes supine

A
  • blood flow from base to apex becomes almost uniform
  • flow in posterior segments exceeds that in anterior segments
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17
Q

How is the distribution of pulmonary blood flow actively controlled

A

pulmonary vasoconstrictors =
local hypoxia
serotonin
histamine
thromboxane A2
endothelin
acidosis

pulmonary vasodilators =
NO
PGI2
phosphodiesterase inhibitors
calcium channel blockers

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18
Q

Explain how cardiogenic pulmonary edema occurs

A
  • via starling’s law: differences in capillary and interstitial hydrostatic pressure and colloid osmotic pressures
  • increased hydrostatic pressure caused by heart failure pushes fluid out of capillary, leading to interstitial edema
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19
Q

How do you calculate pulmonary vascular resistance

A
  • vascular resistance = (input pressure - output pressure) / blood flow
  • pulmonary vascular resistance is normally very low
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20
Q

What are the determinants of pulmonary vascular resistance

A

-increased pressure causes a reduction in resistance by recruitment and distension

  • large lung volumes causes increased resistance by narrowing pulmonary capillaries
  • small lung volumes cause increased resistance if critical opening pressure is not reached
  • hypoxic pulmonary vasoconstriction directs blood away from hypoxic lung
  • drugs = increased by serotonin, histamine, NA and decreased by acetylcholine
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21
Q

Describe hypoxic pulmonary vasoconstriction

A
  • alveolar hypoxia constricts pulmonary blood vessels via direct effect of alveolar pO2 on smooth muscle
  • important at birth and directs blood away from hypoxic areas
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22
Q

What 2 mechanisms allow pulmonary vascular resistance to fall

A
  • recruitment: opening of previously closed vessels as pressure in pulmonary artery increases
  • distension: increase in caliber of vessel at higher vascular pressure
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23
Q

Describe the relationship between pulmonary vascular resistance and pulmonary vascular pressure

A
  • resistance decreases with increased pressure
  • mechanisms: vascular recruitment and distension
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24
Q

How does lung volume influence pulmonary vascular resistance

A
  • vascular resistance initially decreases as lung volumes increase, then rises
  • very low lung volumes: lungs collapse and must reach a critical opening pressure to enable any flow
  • very high lung volumes: alveolar pressure exceeds pulmonary capillary pressure, squashes pulmonary capillaries
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25
Q

What are the metabolic functions of the lung

A

synthesis of: surfactant, phospholipids, proteins, prostaglandins, histamine, kallikrein, IgA

activation of: angiotensin I converted to angiotensin II by ACE

inactivation/removal of: bradykinin, adenine, serotonin, NA, acetylcholine

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26
Q

What is the alveolar gas equation

A

-describes the relationship between fall in PO2 and rise in PCO2
PAO2 = PIO2 - (PACO2 / 0.8) [PIO2 = FiO2 x (Patm - PH2O) = 0.21 x (760 - 47) = 149] [PACO2 = 40]
-if ventilation is halved, PACO2 is doubled to 80

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27
Q

How do you calculate the Aa gradient and why is it important

A
  • Aa gradient = alveolar PO2 - arterial PO2 = (149-PACO2/0.8) - PaO2 [PaCO2 is used to estimate PACO2]
  • normal Aa gradient is 5-10mmHg
  • high gradient indicates ventilation-perfusion inequality such as in a pulmonary embolism
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28
Q

Explain the reason for the normal Aa gradient

A
  • there is normally a ventilation perfusion inequality and most blood flow comes from the base
  • the addition of shunted blood with low O2 reduces arterial O2 concentration
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29
Q

What are the causes of hypoxia

A

1) hypoventilation = due to drugs, chest damage, respiratory muscle paralysis, resistance
2) diffusion limitation = impaired diffusion due to exercise or thickened blood gas barrier state
3) shunt = blood that enters arterial circulation without going through ventilated areas of the lung
4) ventilation-perfusion inequality = hypoxaemia due to V/Q mismatch cannot be corrected with hyperventilation

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30
Q

How does hypoxia affect oxygenation

A
  • alveolar to pulmonary capillary oxygen gradient is decreased, oxygen diffusion is decreased
  • rate of rise of pO2 for a given O2 concentration in blood is less
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31
Q

What does the ventilation perfusion ratio mean

A
  • the concentration of oxygen in any respiratory unit is determined by the ratio of alveolar ventilation to blood flow
  • normal V/Q ratio is 0.8
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32
Q

Describe the relationship between ventilation and perfusion in the upright lung, draw a graph

A
  • blood flow and ventilation both increase from top to bottom of the lung with blood flow increasing more rapidly
  • ventilation perfusion ratio decreases from top to bottom of lung
  • apex: ventilation is greater than perfusion, high V/Q (but both ventilation and perfusion are lower than in the base)
  • base: perfusion is greater than ventilation, low V/Q
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33
Q

What is the effect of ventilation perfusion inequality on gas exchange

A
  • impedes exchange of oxygen and carbon dioxide
  • hypoxia cannot be corrected by increased ventilation
  • hypercapnia can be corrected by increased ventilation
34
Q

Explain why V/Q inequality causes a reduction in arterial PO2 while arterial PCO2 remains relatively normal

A
  • due to the differences in their dissociation curves
  • V/Q inequality causes decreased O2 and increased CO2 which stimulates chemoreceptors to increase ventilation
  • CO2 dissociation curve is linear and increased ventilation is able to blow off CO2
  • O2 dissociation curve is s shaped so increasing ventilation to units with high V/Q cannot compensate for shunt
35
Q

What effect does increasing ventilation have on arterial PO2 and PCO2

A

PCO2 reduces much more than PO2 increases

36
Q

In the alveolus, what factors affect oxygenation

A

ventilation, perfusion, diffusion across the blood gas barrier and the alveolar-pulmonary capillary pressure gradient

37
Q

Describe the oxygen uptake along a pulmonary capillary

A
  • alveolar pulmonary capillary gradient: alveolar pO2 = 100mmHg, pulmonary capillary pO2 = 40mmHg
  • blood gas barrier thickness: 0.3 microns
  • RBC transit time: 0.75 seconds
  • oxygen uptake normally perfusion limited and complete in 0.25 seconds
  • alveolar end capillary oxygen difference if minimal
38
Q

What conditions cause V/Q mismatch and what tests can be done in clinical medicine to identify this

A
  • pulmonary embolism, pulmonary edema, pneumonia, emphysema
  • tests: Aa gradient
39
Q

How is oxygen transported in the blood

A

1) dissolved O2 = minimal
2) haemoglobin = most important, made up of 2 beta and 2 alpha chains, each with one heme unit containing iron

one oxygen molecule binds to one Fe+2

40
Q

Describe and draw the oxygen dissociation curve and what causes it to shift left and right

A
  • shows the change in Hb saturation at different partial pressures of oxygen
  • 50% oxygen saturation is associated with oxygen partial pressure of 27mmHg
  • 75% oxygen saturation is associated with oxygen partial pressure of 40mmHg
  • left shift (increased Hb affinity): high pH, low CO2, low DPG, low temperature, CO
  • right shift (reduced Hb affinity): low pH, high CO2, high DPG, high temperature
41
Q

Draw the oxygen concentration and pressure curve

A
  • anaemia causes a decrease in oxygen concentration
  • carbon monoxide causes the curve to shift to the left
42
Q

Draw and explain the carbon dioxide dissociation curve

A
  • shows the relationship between pCO2 and the total CO2 in the blood
  • more linear than the oxygen dissociation curve
  • shows that oxygenated blood carries less CO2 for the same PCO2
  • curve moves up in venous blood due to the haldane effect
43
Q

Draw the pressure volume curve of a normal lung

A
  • as transpulmonary pressure becomes more negative, volume is increased
  • hyteresis = fact that inflation and deflation curves are different
  • non-linear because lung is stiffer at higher pressure
44
Q

What are the implications of the shape of the oxygen dissociation curve?

A
  • flat upper part of curve: a fall in alveolar pO2 has little effect on loading of O2
  • steep low part of curve: large O2 liberated to tissues for small reduction in pO2
45
Q

What effect does carbon monoxide have on haemoglobin oxygen transport and why

A
  • CO has 240 times higher affinity for Hb than O2 and displaces most of the oxygen (coordinate covalent bond)
  • presence of CO causes marked reduction in oxygen carrying capacity
  • unoccupied heme groups have an increased affinity for oxygen, shifting the oxygen dissociation curve to the left
46
Q

How is CO2 transported in the blood

A

1) dissolved CO2 = 5%, CO2 is 24 times more soluble in blood than O2
2) bicarbonate = 90%, H2O + CO2 ⥧ H2CO3 (carbonic acid) ⥧ H+ + HCO3-
3) carbamino compounds = 5%, formed by combination of CO2 with blood proteins (Hb most important)

47
Q

What is the role of red blood cells in CO2 transport

A
  • carbonic anhydrase only found in significant numbers in RBC, contributing to the bicarbonate buffering system
  • some CO2 binds directly to Hb forming carbaminohaemoglobbin
48
Q

How is bicarbonate formed in the blood

A
  • H2O + CO2 ⥧ H2CO3 (carbonic acid) ⥧ H+ + HCO3-
  • first reaction is very slow in plasma, faster in Hb due to presence of carbonic anhydrase
  • second reaction is fast without an enzyme
49
Q

What is the chloride shift

A
  • HCO3- diffuses easily out of the cell but H+ does not
  • to maintain cell neutrality, Cl- diffuses into the cell from the plasma
50
Q

What is the haldane effect

A
  • H+ cannot cross the RBC membrane, so it combines to Hb (preferentially to deoxygenated Hb)
  • haldane effect = deoxygenation of blood increases its ability to carry CO2: H+Hb + O2 ⥧ H+ + HbO2
  • enhances the removal of CO2 from O2 consuming tissues
  • promotes the dissociation of CO2 from Hb in the presence of O2
51
Q

Describe how respiration compensates for acid base changes and the causes of metabolic acidosis and alkalosis

A
  • central chemoreceptors: CO2 diffuses into the CSF, liberates H+ that stimulates receptors increasing respiration
  • peripheral chemoreceptors: respond to hypoxia (mostly) but also increased PCO2, causing increased respiration
metabolic acidosis: caused by DKA, lactic acidosis, diarrhoea

increased ventilation causes decreased CO2 and thus decreased H+ and HCO3- (base deficit)

metabolic alkalosis: vomiting, diuretics, hypokalaemia

decreased ventilation causes increased CO2 and thus increased H+ and HCO3- (base excess)
52
Q

What is pulmonary compliance, what are the main determinants and what factors increase or decrease compliance

A

definition:

  • a measure of the elastic recoil of the lungs, normally 200ml/mmHg
  • compliance = change in volume / change in pressure

determinants:

  • surface tension of alveoli (determined by pressure/radius/surfactant), elastin/collagen fibers (elastic recoil)
  • greatest when measure in deflation, smaller at higher expanding pressures

factors that increase or decrease compliance:

  • increased compliance = pulmonary emphysema, asthma, age
  • decreased compliance = pulmonary fibrosis, alveolar edema, atelectasis, consolidation, loss of surfactant
53
Q

How does compliance vary throughout the upright lung

A

higher at the base than at the apex because the apex is already more distended

54
Q

What is the relationship between intrapleural pressure and lung volume

A
  • more negative intrapleural pressure causes higher lung volume
  • at any given intrapleural pressure, lung volume is higher in deflation than inflation
  • compliance decreases at higher lung volumes (reaches limits of elasticity)
55
Q

Describe how regional differences in intrapleural pressure affect ventilation

A
  • intrapleural pressure is higher at the apex than the base of the lung to keep lung expanded against its own weight
  • there is increased compliance at the base, hence better ability to ventilate at the base than at the apex
56
Q

What is surfactant and how does it work

A
  • molecule secreted by type II alveolar cells formed relatively early in foetal life
  • phospholipid with DPPC, also contains proteins and carbohydrates
  • DPPC is bipolar, when aligned, repulsive forces oppose normal attractive forces between liquid surface molecules
  • lowers alveolar surface tension, increases compliance, reduces work, improves alveolar stability, keeps alveoli dry
57
Q

What factors keep fluid out of the alveoli

A
  • hydrostatic pressure = pressure exerted by a fluid due to gravity
  • colloid osmotic pressure = due to proteins in blood
  • surfactant
58
Q

What is the relationship of pressure and wall tension in connected bubbles

A
  • laplace law describes wall tension as the force in an alveoli that resists the force trying to expand it
  • wall tension is proportional to the pressure of the contents and the radius
  • if the pressure inside is greater than the wall tension, the alveoli will expand
  • small radius means more pressure is required for a container to expand
  • 2 connected bubbles with the same surface tension, smaller bubble has a high pressure
  • smaller bubble will blow up the larger bubble, small bubble will collapse
59
Q

Describe the factors affecting airway resistance

A
  • poiseuille law: Resistance = 8 x viscosity x length / pie x radius^4
  • main site of resistance is medium-sized bronchi
  • resistance is low in small airways due to large number
  • resistance decreases as lung volumes rise because airways are pulled open by radial traction

increased resistance: parasympathetic stimulation causing bronchoconstriction, histamine, reduced lung volume

decreased resistance: stimulation of beta-receptors causing bronchodilation, increased lung volume

60
Q

Describe dynamic compression of airways and its effect on flow

A
  • occurs when the pressure surrounding the airway exceeds the pressure within the airway lumen
  • causes compression of the airway and limits airflow
61
Q

What factors cause turbulent flow in airways

A
  • turbulent flow occurs when flow rate increases and there is separation of stream lines causing eddies
  • occurs when there is a high reynolds number: Re = (diameter x velocity x density) / viscosity
  • normally seen in the trachea
  • most areas in lung have transitional flow and laminar flow is only seen in small airways
62
Q

What factors affect the radius of the airway

A
  • bronchial smooth muscle tone, influenced by sympathetic and parasympathetic activity
  • high lung volume pulls airways open and increases radius by radial traction
63
Q

What factors determine the work of breathing?

A

1) elastic workload of the lungs and chest wall
- larger tidal volumes increases elastic workload
- reduced compliance (pulmonary congestion, fibrosis, loss of surfactant) increases the elastic workload
2) resistance of the airways and tissues
- decreased airway radius
- increased air viscosity (high temperature increases both dynamic and kinematic viscosities)

64
Q

What part of the brain controls respiration

A

1) Voluntary control
- located in the cerebral cortex and can override the brainstem and provide voluntary control of respiration
2) Autonomic control
- medulla = medullary respiratory center, main control center
- pons = pneumotaxic and apneustic center, modifies medulla activity

65
Q

What are the basic elements of the respiratory control system

A

sensors (chemoreceptors)

central controller (medulla, pons)

effectors (respiratory muscles)

66
Q

What is the role of central and peripheral chemoreceptors in the control of ventilation

A

central:

  • located on the ventral surface of the medulla responsible for breathing during sleep
  • directly monitors H+ and indirectly monitors CO2
  • with high blood CO2, CO2 diffuses into CSF, liberates H+ which stimulates chemoreceptors
  • efferents stimulate medullary respiratory center to increase ventilation and return CO2 to normal

peripheral:

  • located in carotid bodies (afferents via glossopharyngeal nerve) and aortic bodies (afferents via vagus nerve)
  • respond mostly to low O2 (<100mmHg) but also to low pH (carotid) and high CO2
  • impulses transmitted to the medullary respiratory center to increase ventilation
  • the only receptors that respond to hypoxia
67
Q

What other sensors (other than chemoreceptors) are involved in the control of ventilation?

A

Lung receptors:

  • Pulmonary stretch receptors = in airway SMC, respond to distension of lung to cause reduction in RR
  • Irritant receptors = stimulated by noxious gas causing bronchoconstriction
  • J-receptors = in alveolar cells, activated by engorgement of pulmonary capillaries

Others:

  • Muscle and joint proprioceptors = stimulated by movement and cause increase in RR
  • Arterial baroreceptors = stimulation may cause reflex hypoventilation
  • Pain and temperature receptors = may initially cause apnoea and then hyperventilation
68
Q

How does hypoventilation affect respiration

A
  • increase in CO2 diffuses into CSF and releases H+ that stimulate central chemoreceptors and increases RR
  • low O2 causes stimulation of peripheral chemoreceptors and increases RR
69
Q

Describe the ventilatory response to metabolic acidosis

A
  • low arterial pH stimulates peripheral chemoreceptors to increase ventilation
  • peripheral chemoreceptors dominate the response
70
Q

What are the physiological responses to high altitude

A

initial:

  • hyperventilation = occurs by hypoxic stimulation of peripheral chemoreceptors
  • results in low arteriolar PCO2 and alkalosis, which initially inhibits further increase in RR
  • after 24 hours, CSF pH returns back to normal by movement of HCO3- out
  • after 48 hours, blood pH returns back to normal by renal excretion of HCO3-
  • further increase in RR at day 4
  • initial left shift in oxygen dissociation curve due to hyperventilation causing increased pH

longer-term:

  • increased 2,3 DPG in 2-3 days causes a right shift in the oxygen dissociation curve
  • higher altitude then causes left shift in oxygen dissociation curve due to alkalosis
  • polycythemia = hypoxia induces EPO from kidneys in 2-3 days, causes increased RBC from bone marrow
  • pulmonary vasoconstriction causing pulmonary hypertension resulting in RVH
  • increased blood viscosity, mitochondria, capillaries in peripheral tissues, oxygen carriage and oxidative enzymes
71
Q

Describe the symptoms of acute mountain sickness

A

headache

irritability

insomnia

breathlessness

nausea, vomiting

72
Q

What are the effects of exercise on the respiratory system

A

1) increased ventilation due to muscle and joint proprioceptors and reduction in pH from increased lactate
- increased respiration rate, tidal volume and minute ventilation, decreased functional residual capacity

2) increased cardiac output

3) reduced V/Q inequality due to more uniform distribution of blood flow and increased pulmonary blood flow

4) increased diffusing capacity (5x increase in DLCO, partly due to increased diffusing capacity of the membrane)

5) oxygen dissociation curve shifts to the right due to increased pCO2, H+ and temperature, helping to offload O2

6) peripheral capillary dilation leading to reduced peripheral vascular resistance

(in broad categories, first pumping more air and blood, then better gas exchange, lastly better offloading the cargos, just like a truck driver, load more and faster, then unload faster)

73
Q

What happens to the pulmonary circulation during exercise

A

flow increases

distension and recruitment of vessels

increased cross sectional area

74
Q

What changes occur in arterial blood gases during exercise

A
  • arterial blood gases are little affected by moderate exercise
  • at high workloads, pH falls due to lactic acidosis, PaCO2 falls to compensate and PaO2 rises
75
Q

What changes occur in venous blood gases during exercise

A

total CO2 carried rises

decreased O2 because of increased extraction

lactic acidosis

76
Q

What are the different types of tissue hypoxia

A

1) hypoxic hypoxia = decreased arterial PO2
2) anaemic hypoxia = normal arterial PO2 but reduced overall O2 carrying capacity due to reduced Hb
3) stagnant (ischaemic) hypoxia = blood flow to tissue is reduced
4) histotoxic hypoxia = amount of O2 delivered to a tissue is normal but it cannot be used due to a toxic agent

77
Q

Describe the respiratory mechanisms leading to hypoxaemia and given examples

A
  • hypoventilation = drugs, chest damage, respiratory muscle paralysis
  • diffusion limitation = acute pulmonary edema, pulmonary fibrosis
  • shunt = coronary venous blood draining directly into LV via thesbian veins, pulmonary arteriovenous malformation
  • V/Q mismatch = pulmonary embolism
78
Q

Describe the clinical features of acute hypoxia

A

disorientation

confusion

headache

loss of consciousness

tachycardia

hypertension

hypotension

AMI

arrest

79
Q

What are the common causes of respiratory acidosis

A
  • central respiratory depression –> hypoventilation: opioids, sedatives, CVA, raised ICP, seizure, neuromuscular disorders, OSA
  • lung or chest wall abnormality: infection, trauma, pulmonary oedema, obesity, scoliosis
  • airway obstruction: COPD, asthma
80
Q

Describe the lung defense mechanisms

A
  • upper airways = humidification, nasal hairs, lymphoid tissue from tonsils and adenoids
  • conductive airways = cough reflex, bronchoconstriction, mucus secreting goblet cells, mucociliary escalator
  • cellular defence = pulmonary alveolar macrophages, IgA in bronchi

ACEM Viva (39 decks)

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