Midterm exam study Flashcards

(46 cards)

1
Q

what is the alveolar septum?

A

its the central site for gas exchange, elastic recoil, and disease pathogenesis

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2
Q

how could you describe the anatomy of the capillaries, alveoli, and alveoli septum?

A

the capillaries are sandwiched between the alveoli and alveoli septum

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3
Q

what are the cell types of the alveoli septum?

A
  • type 1 pneumocytes : gas exchange
  • type 2 pneumocytes : production of surfactant
  • macrophages
  • fibroblasts
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4
Q

what is the role of elastin and collagen found within the septum?

A
  • helps with stretching during inspiration and elastic recoil during expiration and restoring the lungs to its original shape at functional residual capacity
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5
Q

how is the diaphragm connected to the paricardium?

A

its is connected via the central tendons

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6
Q

what tendinous structure binds the diaphragm to the thoracic vertebrae?

A

the crura

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7
Q

which nerve/ spinal nerves keep the diaphragm alive?

A

the phrenic nerve and spinal nerves c3 - c5

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8
Q

what anatomy passes through the diaphragm

A

IVC, descending aorta, esophagus, lymphatics

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9
Q

during inspiration and expiration what happens to the diaphragm?

A

inspiration - contracts downward
expiration - relaxes upwards

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10
Q

what are pores of kohn?

A

alveoli - alveoli connection

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11
Q

why are pores of kohn important?

A

it helps with the redistribution of air during V/Q mismatch, it can also cause pathogens to move from one alveoli to another. it can help with the movement of surfactant

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12
Q

what are channels of martin?

A

bronchiole - bronchiole connection

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13
Q

why are channels of martin important?

A

it helps air to bypass obstructed areas or areas with reduced perfusion

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14
Q

what are channels of lambert?

A

bronchiole to alveoli connection

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15
Q

what is structural interdependence of alveoli?

A

alveoli share a septa, which means the expansion or collapse of one alveoli effects its neighbour

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16
Q

how does structural interdependence of alveoli work?

A

when the outer alveoli is exposed to interpleural pressure/ transpulmonary pressure and the alveoli expands, the septal traction pulls open the neighbouring alveoli in the inner region

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17
Q

how does structural interdependence effect expiration?

A

during expiration the alveoli pull on each other aiding in uniform emptying and prevents localized collapse and controlled deflation

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18
Q

what is elastic recoil caused by?

A
  • elastin and collagen
  • surface tension
  • structural interdependence
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19
Q

COMPRESSIVE atelectasis

A

caused by external pressure on the lungs such as blood, air, fluid, tumour

20
Q

Resorptive/ obstructive atelactasis

A

caused by an airway obstruction where no air enters. when this happens oxygen is diffused into the blood and co2 is not diffused out in the same rate which causes a drop in lung volume. this drop in lung volume causes a decrease in alveolar pressure leading to the collapse of the alveoli due to elastic recoil

21
Q

scarring atelactasis

A

lung tissues is destroyed and replaced with scar tissue. this can distort and compress adjacent lung tissue

22
Q

adhesive atelactasis

A

a deficiency in surfactant. surfactant decreases surface tension, without it the surface tension is too high and leads to a collapse of the alveoli as seen in IRDS

23
Q

talk about IRDS

A
  • a deficiency of surfactant usually in premature babies <37 weeks gestation
  • surfactant starts to be produced in babies at 4 months gestation and is fully matured by term
24
Q

what are the types of atelactasis?

A
  • COMPRESSIVE
  • obstructive
  • scarring
  • adhesive
25
what are the treatments for atelactasis
- breathing exercises - surgery - surfactant therapy
26
what are the imaging signs of atelactasis is the superior lobe appears to be collapsed?
minor fissures appear pulled upwards and hilum may be pulled upwards on the affected side. it can appear stretched or displaced on x-ray
27
resistance to airflow is caused by...
airway geometry and obstruction
28
in smaller airways there is ______ resistance per tube
higher
29
in larger airways there is ______ resistance per tube
lower resistance
30
what is laminar airflow
in the center of the airway, the airflow is more uniform and moves faster which allows it to reach the alveoli first and the outer airflow is slower due to friction against the airway wall
31
what is the cross sectional trend in early (proximal) airways.
because there is limited branching the airflow is less uniformed and it becomes turbulent which causes high resistance
32
cross sectional trend in distal airways
because there is more extensive branching the airflow slows and allows for the airflow to become more laminar. this drops airflow resistance alot
33
what is tissues resistance?
friction from tissues sliding against each other as the lungs and chest wall move during airflow
34
what is the purpose of the inspiratory hold maneuver?
to assess airway/tissue resistance in patients on ventilators
35
what are the steps/procedure of inspiratory hold maneuver?
1. ventilatory quickly inflates lungs to TLC 2. air is stopped by pressing the inspiratory hold button 3. there is a rapid decrease from PMAX to P1 = airway resistance 4. slow decrease from P1 to P2 = tissue resistance/ pendelluft
36
what is the driving force for passive eupinic expiration?
passive expiration is driven by the elastic recoil of the lungs which allows for alveolar pressure to be greater than atmospheric pressure pushing air out of the lungs
37
what is the driving force for airflow during dynamic compression?
internal intercostals muscle and abdominal muscles are used to increase intrapleural pressure which increases alveolar pressure above atmospheric pressure. this helps to push air out. however when intrapleural pressure rises above airway pressure it causes dynamic compression and collapse of the airways
38
what are fast alveoli?
fast alveoli have low resistance and low compliance because they are already large and stretched however they fill and empty quickly with a smaller change in volume per pressure
39
what are slow alveoli?
slow alveoli fill and empty slower. they have higher resistance and higher compliance but can accommodate more incomming air than fast alveoli
40
what is the pendelluft phenomenon?
the redistribution of air between alveoli with different time constants
41
what is a time constant?
time constant is the time required for an alveoli to inflate/deflate
42
what is relaxation volume?
when no muscles are active and the lung-chest wall system is fully relaxed
43
when does FRC does not equal relaxation volume?
- during increased breathing frequency when the next breath starts before the full exhalation ends - during increased airway resistance and expiration is prolonged and air cannot leave before next breath (air trapping) - both causes FRC to become greater than relaxation volume
44
what are three things that cause air trapping?
- dynamic compression - mucus plugging - loss of elastic recoil
45
what are the consequences of air trapping?
- increased RV and FRC - increased work of breathing - alveoli remained partially inflated after exhalation
46
how is transpulmonary pressure measured clinically?
1. an esophageal balloon measures esophageal pressure which equals intrapleural pressure 2. a mouth peice measures airway pressure which equals alveoli pressure under static conditions 3. transpulmonary pressure = Palv - Pip = Paw - Pes