Respiratory 2 Flashcards

(32 cards)

1
Q

How does the pleura play a role in lung expansion (inspiration)?

A

inspiratory muscles pull the parietal layer of pleura away from visceral layer, increasing the volume of the intrapleural cavity and thus decreasing the intrapleural pressure; creates negative pressure n the intrapleural space, pulls visceral layers (attached the lung walls) towards the parietal layer–>lungs expand

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2
Q

what is pneumothorax?

A

collapsed lung

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3
Q

how does pneumothorax arise?

A

interruption of the IP negative pressure

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4
Q

types of pneumothorax?

A

traumatic and spontaneous

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5
Q

what is traumatic PT?

A

puncture of the lungs (and thus, the pleura) causes air to go from a high pressure (atm) to low pressure (IP space)–>IP pressure because more positive, lung collapses

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6
Q

what is spontaneous PT?

A

visceral layer thins and eventually ruptures (via creation of blebs); air from inspiration enters the IP space and creates a more positive pressure, leading to lung collapse

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7
Q

what is lung compliance?

A

The degree of lung expansion at any 6me is propor6onal to the change in pressure; the stretchability; compliance = change in lung volume/ change in pressure (Palv-Pip)

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8
Q

what is pulmonary fibrosis, and what are the causes?

A
Formation or development of excess fibrous connective tissue in the lungs; decreased compliance; 
•  Inhalation of pollutants 
      •  Metals, asbestos,
       certain gases.
•  Infections
•  Idiopathic
      •  Age related 
      •  Genetic
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9
Q

what is emphysema?

A

increased stretching of lungs

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10
Q

what causes emphysema?

A

cigarette smoke, mainly

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11
Q

physiological causes for emphysema?

A

Proteolytic enzymes
secreted by leukocytes (neutrophils) attack alveolar tissue; weakens alveoli tissue–> becomes more compliant, has less elastic recoil (elastance); initially easier to breath in, difficult to breathe out; severe emph: tough to breathe in (so stretchy, it collapses on itself), tough to breathe out

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12
Q

describe surface tension

A

a major determinant of both compliance and elastic recoil, at the air-water interface of the airways; surface tension creates a force that opposes the pressure in the alveoli to hold them open (more surface tension = more pressure needed to hold alveoli open)

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13
Q

what produces the surfactant?

A

Type II alveolar cells

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14
Q

what is surfactant?

A

~90% phospholipids (dipalmitoylphospha6dylcholine), 10% protein (amphipathic)

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15
Q

purposes of surfactant?

A
  1. Increases compliance.
  2. Minimizes fluid accumula6on in alveoli.
  3. Regulates alveolar size by dynamically adjusting their rates of inflation and deflation.
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16
Q

what is infant respiratory distress syndrome?

A

surfactant production in premature infants is low; large amount of ST, less compliance, need lots of pressure to inflate lungs;

17
Q

prevention and treatment of IRDS?

A

-Preven3on: glucocorticoid
injection (happens in the mother; believed to jumpstart surfactant production in fetus)
Treatment:
-Artificial surfactant
-Continuous Positive Airway Pressure (CPAP)
-Intubate

18
Q

how does a surfactant minimize fluid accumulation in alveoli?

A

not super important; pure air-water interface (not surfactant)= alveolar collapse, fill up with fluid and draw fluid from interstitial space

19
Q

how does a surfactant regulate alveolar size?

A

for big alveoli: surfactant ‘cules move further apart, water ‘cules allow to reform bonds—>increase in surface tension, stops inflation

for small: allows them to inflate more, as well

20
Q

where does most airway resistance occur?

A

trachea and bronchi, is constant due to small CSA

21
Q

what regulates bronchoconstriction/dilation?

A

CO2, histamine from mast cells, and parasym nrves which innervate bronchioles–> activates PLC-IP3 pathway via M3 muscarinic receptor (causes constriction)

22
Q

how does an asmthatic inhaler work?

A

β2-adrenergic agonist; opposes bronchoconstriction, competes for Epi?

23
Q

how are frequent asthma attacks “resolved”?

A

More Frequent acacks:

• Weekly inhaled corticosteroid

24
Q

what is total pulmonary ventilation/minute entilation?

A

the volume of air moved into and out of the resp system each minute

25
why is alveolar ventilation advantageous to TPV?
amount of air in resp system =/= the amount that reaches alveoli; Alv vent = vent rate x (tidal volume- dead space); Alv ventilation rate indicates efficiency of resp system
26
how are ventilation and alveolar blood flow matched?
via chemoreceptors and gravity
27
what is eupnea?
normal, quiet breathing
28
what is hyperventilation and an example?
increased resp rate and/or volume without increased metabolism; e.g. emotional hyperventilation, blowing up a balloon
29
what is hypoventilation + e.g.?
decreased alveolar ventilation; e.g. shallow breathing--asthma, restrictive lung disease
30
what is apnea?
cessation of breathing; e.g. voluntary breath-holding; depression of CNS control centres;
31
how are ventilation and perfusion controlled?
via altering bronchioles and arterioles; pulmonary arterioles are primarily influenced by O2-->constricts in low levels of O2; bronchioles primarily influenced influenced by CO2 levels-->dilates during an increase of CO2 gravity
32
remember, an increase in O2 in alv will influence Po2 in blood-->and vv
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