Lecture 2 Flashcards

1
Q

What are the 3 functions of surfactant

A
  1. reduces surface tension in the alveolar lining fluid, (reduces the tendency for the alveolus to collapse).
  2. increases lung compliance.
  3. prevents transudation of fluid into alveoli -> less negative pressure in the interstitial space, therefore lower hydrostatic pressure gradient between pulmonary capillary and interstitial space
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2
Q

Where can e observe a decrease in lung compliance

A
↓ Lung compliance:
Interstitial edema
Pulmonary edema
↓ ventilation of lung for an extended period
Diseases causing pulmonary fibrosis
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3
Q

Where can e observe a increase in lung compliance

A

↑ Lung compliance
Age
Emphysema

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4
Q

Why chronic bronchitis and emphysema have a hyperinflation?

A

Obstructive lund mx. -> emphysema -> incr lung compli, the tethering (elastic fibers in the lung) gets destroyed -> end up getting stretched more, more floppy -> FRC gett more larger -> hyperinflated

Chronic bronchitits (part of COPD)-> increased rsistance -> not bc of elasticity, but air trapping, to espirate you have to push harder -> increase FRC but the mecanism is diff between emphysema and chron bronc

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5
Q

What is resistance to airflow

A

Resistance to airflow (Raw) is equal to the pressure difference between alveolar and atmospheric pressure (AP) divided by airflow.
Raw= (Palv-Patm)/Flow

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6
Q

Name 4 Factors increasing airway resistance:

A
Reduced lung volumes
Increased bronchial motor tone
Reduced airway caliber
Increase in density and 
viscosity of inspired air

Resistance =8 η L/πr4

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7
Q

T/F

Major airway resistance is in the small airways

A

Major resistance NOT in the small airways - total cross-sectional area increases as descend the tracheo-bronchial tree - ↓↓ drop in flow.

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8
Q

Where is the EPP in healthy & emphysema

A

Heathly: at EPP there is cartilage
Emphys: at EPP no cartilage, happens deeper, further in the branching

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9
Q

Respiratory rhythm altered by inputs from the pons:

describe

A

Apneustic center  regulates the length and depth of inspiration.
Pontine respiratory group (PRG) regulates apneustic center & medullary rhythmicity area.

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10
Q

T/F
Cerebral cortex can override “automatic” control of breathing for voluntary activities i.e. deep breathing, breath holding, singing etc.

A

T

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11
Q

T/F

Inputs to brainstem from chemoreceptors, baroreceptors only regulate breathing

A

Inputs to brainstem from chemoreceptors, baroreceptors, and stretch receptors (lungs), irritant receptors (airways), proprioceptors (joints & muscles) and emotional input (limbic system) regulate breathing

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12
Q

where are the central chemoreceptor

A

Located just below the ventrolateral surface of the medulla

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13
Q

the central chemoreceptor respond to

A

Respond to H+ dissolved in the cerebrospinal fluid (CSF)

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14
Q

T/F

O2 and CO2 diffuses through the blood-brain barrier which separates the CSF & arterial blood

A

F

Only CO2 diffuses through the blood-brain barrier which separates the CSF & arterial blood

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15
Q

T/F

In CSF, CO2 cannot combines with H2O and forms H+ & HCO3-

A

F

Yes it can

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16
Q

Chemical control of breathin, how does it work

A

Increased H+ lowers the pH
As pH decreases, ventilatory rate increases which in turn lowers the CO2, eventually returning the body to a homeostatic balance.

17
Q

where are the peripheral chemoreceptor

A

Aortic bodies located on the aortic arch

Carotid bodies located at the bifurcation of the internal and external carotid arteries in the neck.

18
Q

what are the peripheral chemoreceptor sensing, to what do they react

A

Sense PO2, PCO2, and pH of arterial blood  the only chemoreceptors that respond to changes in PO2 . Response not clinically significant until PaO2falls below 60 mm Hg

19
Q

T/F

Because of the weight of the lung, the pleural pressure is less negative at the base than at the apex

A

T

20
Q

What is a shunt

What is dead space

A

Shunt:
perfusion but no ventilation

Dead space:
ventilation but no perfusion
no gas exchange
anatomical vs physiological