Respiratory 2

Question 1

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

Answer 1

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

Question 2

what is pneumothorax?

Answer 2

collapsed lung

Question 3

how does pneumothorax arise?

Answer 3

interruption of the IP negative pressure

Question 4

types of pneumothorax?

Answer 4

traumatic and spontaneous

Question 5

what is traumatic PT?

Answer 5

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

Question 6

what is spontaneous PT?

Answer 6

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

Question 7

what is lung compliance?

Answer 7

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)

Question 8

what is pulmonary fibrosis, and what are the causes?

Answer 8

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

Question 9

what is emphysema?

Answer 9

increased stretching of lungs

Question 10

what causes emphysema?

Answer 10

cigarette smoke, mainly

Question 11

physiological causes for emphysema?

Answer 11

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

Question 12

describe surface tension

Answer 12

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)

Question 13

what produces the surfactant?

Answer 13

Type II alveolar cells

Question 14

what is surfactant?

Answer 14

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

Question 15

purposes of surfactant?

Answer 15

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

Question 16

what is infant respiratory distress syndrome?

Answer 16

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

Question 17

prevention and treatment of IRDS?

Answer 17

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

Question 18

how does a surfactant minimize fluid accumulation in alveoli?

Answer 18

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

Question 19

how does a surfactant regulate alveolar size?

Answer 19

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

Question 20

where does most airway resistance occur?

Answer 20

trachea and bronchi, is constant due to small CSA

Question 21

what regulates bronchoconstriction/dilation?

Answer 21

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

Question 22

how does an asmthatic inhaler work?

Answer 22

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

Question 23

how are frequent asthma attacks “resolved”?

Answer 23

More Frequent acacks:

• Weekly inhaled corticosteroid

Question 24

what is total pulmonary ventilation/minute entilation?

Answer 24

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

Question 25

why is alveolar ventilation advantageous to TPV?

Answer 25

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

Question 26

how are ventilation and alveolar blood flow matched?

Answer 26

via chemoreceptors and gravity

Question 27

what is eupnea?

Answer 27

normal, quiet breathing

Question 28

what is hyperventilation and an example?

Answer 28

increased resp rate and/or volume without increased metabolism; e.g. emotional hyperventilation, blowing up a balloon

Question 29

what is hypoventilation + e.g.?

Answer 29

decreased alveolar ventilation; e.g. shallow breathing–asthma, restrictive lung disease

Question 30

what is apnea?

Answer 30

cessation of breathing; e.g. voluntary breath-holding; depression of CNS control centres;

Question 31

how are ventilation and perfusion controlled?

Answer 31

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

Question 32

remember, an increase in O2 in alv will influence Po2 in blood–>and vv

Answer 32

ya