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Physiology and Pharmacology > Lecture 10 > Flashcards

Lecture 10 Flashcards

1
Q

What is compliance?

A

Distensibility: The ease with which the lungs and thorax expand during pressure changes

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2
Q

What is the equation for compliance?

A

C= change in Volume / change in Pressure

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3
Q

What does low compliance entail?

A

More work required to inspire in the muscle and diaphram; need to overcome elastic nature

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4
Q

What is a disease in which low compliance can be seen?

A

Pulmonary fibrosis - lung paranchyma is more rigid

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5
Q

What does high compliance entail?

A

Little work to expand lungs and inspire but involved more difficulty expiring (loss of elastic recoil)

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6
Q

What is a disease in which high compliance can be seen?

A

Emphysema

  • breakdown of walls, loss of elastic recoil
  • when expiring, tend to collapse the airway because of high compliance
  • have to overcome force to open airway
  • can cause problems
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7
Q

Why do emphysema patients tend to have a higher starting volume?

A

It prevents the airways from collapsing

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8
Q

What happens when lungs recoil and collapse down?

A

Collapse down to residual volume

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9
Q

What are the two major components of elastic recoil?

A

“Anatomical” component
- elastic nature of cells and extracellular matrix
- tissues binding together: elastin etc
Surface tension generated at air-fluid interface
- helps cause lungs to contract
- has to overcome surface tension to expand lungs

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10
Q

Why is there surface tension at the air-fluid interface?

A

Due to differences in the forces on water molecules at the air-water interface
- in a gas bubble, there is a balance between the pressure exerted by the gas and the surface tension at the gas-water border

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11
Q

What happens in a gas bubble when it comes to surface tension?

A

Net downward force on molecules at surface

Droplet contracts to take lowest energy state - sphere

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12
Q

How is the relationship between pressure and surface tension described?

A

By Laplace’s equation

P = 2T / r

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13
Q

According to Laplace’s equation what would happen to the smaller sacs?

A

Air will flow down from smaller alveoli to larger alveoli leading to their collapse

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14
Q

What prevents smaller alveoli from collapsing?

A

Surfactant

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15
Q

Which cells produce surfactant?

A

Type II pneumocytes

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16
Q

What are surfactants composed of?

A

Lipids and proteins

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17
Q

What do Surfactant (lipoprotein) Type II cells do?

A

Prevents alveolar collapse by decreasin the surface tension
Alveolar size regulation - spread of surfactant shows rate of inflation
Increases compliance - allows lungs to inflate much more easily
Prevents edema - reduces fluid entering alveoli

18
Q

What disease shows a decrease in surfactant production?

A

Pneumonia - lungs are harder to inflate

19
Q

When do the surfactants begin to be produced?

A

Fully forms after 37 weeks of gestation

20
Q

What happens by partitioning phospholipids?

A

Disrupts the effect of surface tension

Reduces surface tension

21
Q

Which has a larger density of surfactant, larger or smaller alveoli? Why?

A

Smaller alveoli

  • reduces effect of surface tension
  • helps prevent over-inflation of the alveoli to maintain millions of alveoli of different volumes
22
Q

What is the type of lung volume that cannot be measured using a spirometer?

A

Residual lung volume

23
Q

What are the two types of dead space?

A

Anatomical dead space

Physiological dead space

24
Q

What is anatomical dead space?

A

Volume of conducting airways

- at rest approximately 30% of inspired air volume (150ml)

25
Q

What is physiological dead space?

A

Volume of lungs not participating in gas exchange

  • conducting zone + non-functional areas of respiratory zone
  • normally the two values are almost identical
26
Q

What are the different lung volumes and their values?

A

Inspiratory reserve volume (IRV) = 1.9 - 2.5 L
Tidal volume (TV) = 0.4 - 0.5 L
Expiratory reserve volume (ERV) = 1.1 - 1.5 L
Residual Volume (RV) = 1.5 - 1.9 L
Total lung capacity (TLC) = 4.9 - 6.4 L
Inspiratory capacity (IC) = 2.3 - 3L
Functional residual capacity (FRC) = 2.6 - 3.4 L
Vital capacity (VC) = 3.4 - 4.5 L

27
Q

What changes can be seen in the lung volumes during exercise?

A

IRV, ERV: decrease
TV: increase
VC and RV: same

28
Q

What is an equation that shows the relationship between airflow and pressure and resistance?

A

Airflow = Change in Pressure / Resistance

Change in pressure = Alveolar pressure - Atmospheric pressure

29
Q

What is Poiseuille’s law?

A

It shows that airway resistance is proportional to gas viscosity and the length of the tube but is inversely proportional to the fourth power of the radius

30
Q

What is the equation for Poiseuille’s law?

A

R = 8 ( viscosity x length) / (pi x r4)

31
Q

What has the most impact on resistance and flow rate?

A

Airway diameter (radius)

32
Q

What is the total airway resistance in a normal individual?

A

1.5 cm H2O x s / liters

33
Q

Which anatomical structures contribute to total airway resistance and by how much?

A

Pharynx-Larynx: 40%
Airways > 2mm diameter: 40%
Airways<2mm diameter: 20%

34
Q

How is the total resistance in the upper airways determined and why?

A

Sum of resistance

- resistances are in series

35
Q

How is the total resistance in the lower airways determined and why?

A

Inverse resistance is the sum of inverse resistances

- resistances are in parallel

36
Q

When would the lower airways increase resistance?

A

inflammation

37
Q

What are factors that have an impact on airway resistance?

A

Airway diameter:
Increased mucus secretion will effectively reduce airway diameter - increased resistance
Oedema - increased fluid retention in the lung tissue will cause swelling and narrowing of the airways - increases resistance
Airway collapse - e.g. during forced expiration, narrows airways, increases resistance

38
Q

What are the two pathways involved in the control of bronchial smooth muscle?

A

ANS

Humoral factors

39
Q

How is the ANS involved in the control of bronchial smooth muscle?

A

Parasympathetic:
ACh is released from the vagus, acts on muscarinic (type 3) receptors = (GPCR)
- leads to constriction

Sympathetic:
Release of adrenaline from nerves
- weak agonist binds to beta-2 adrenergic receptors
- leads to relaxation of smooth muscle then dilation of the airways

40
Q

How are humoral factors involved in the control of bronchial smooth muscle?

A

Adrenaline circulating in the blood - better agonist binds to dilation

  • acts on beta-2 adrenergic receptor
  • stronger agonist than noradrenaline
  • leads to dilation

Histamine - released during inflammatory process

  • binds to H1 receptor (GPCR)
  • leads to constriction

Physiology and Pharmacology (27 decks)

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