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BS > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Conducting portion

A

Tubes to transport and condition air

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2
Q

Respiratory portion

A

Membranes for gas exchange

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3
Q

R lung (lobes and fissures)

A 
3 lobes
2 fissures (oblique and horizontal)
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4
Q

L lung (lobes and fissures)

A 
2 lobes
1 fissure (oblique)
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5
Q

Where does the trachea bifurcate?

A

Carina

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6
Q

Functions of thoracic cage (x 2)

A

Protection

Respiratory movements

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7
Q

Functions of fluid film (x 2)

A

Aid sliding

Create surface tension

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8
Q

What does increased surface tension help?

A

Inspiration

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9
Q

Pressures in inspiration

A

Pb > Pa

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10
Q

Pressures in expiration

A

Pb

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11
Q

Quiet inspiratory muscles (x 2)

A

Diaphragm

External intercostals

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12
Q

Increasing effort inspiratory muscles (x 4)

A

Diaphragm
External intercostals
Accessory
Neck/Shoulder girdles

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13
Q

Quiet expiratory muscles (x 1)

A

Elastic recoil of tissues

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14
Q

Increasing effort inspiratory muscles (x 2)

A

Internal intercostals

Abdominal wall

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15
Q

What type of pressure does expansion exert on the intrapleural space?

A

Negative

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16
Q

Tidal volume (TV)

A

Volume of air in and out in normal breathing (6-7 ml/kg)

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17
Q

Inspiratory reserve volume (IRV)

A

Deepest possible inspiration (3000 ml)

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18
Q

Expiratory reserve volume (ERV)

A

Deepest possible expiration (1500 ml)

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19
Q

Residual volume (RV)

A

Air remaining in the lungs after ERV (1000ml)

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20
Q

Why is there a residual volume?

A

Due to the rigidity of the thorax and pleural attachments

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21
Q

Total lung capacity (TLC)

A

TV + IRV + ERV + RV

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22
Q

Vital capacity (VC)

A

TV + IRV + ERV

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23
Q

Functional residual capacity (FRC)

A

ERV + RV

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24
Q

Restrictive lung disease

A

Lower RV, TLC, VC and FRC

FVC/FEV1 > 0.7

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25
Q

Obstructive lung disease

A

Higher RV, TLC (emphysema) and FRC
Lower TLC (COPD)
FVC/FEV1

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26
Q

When is compliance reduced?

A

Fibrosis and circumferential burns

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27
Q

When is compliance increased?

A

Emphysema

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28
Q

When will alveoli be poorly ventilated?

A

When closing capacity > FRC

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29
Q

Surface tension =

A

Energy needed to maintain gas-liquid interface

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30
Q

How is PE minimised?

A

By forming a sphere -> reduces SA : vol

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31
Q

Which cells make surfactant?

A

Type 2 alveolar cells

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32
Q

Functions of surfactant (x 5)

A 
Reduce surface tension
Increase compliance
Prevent atelectasis
Aid alveolar recruitment
Minimise fluid
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33
Q

Why is it important that surfactant becomes more dispersed as volume increases?

A

Helps to equalise pressure

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34
Q

How is energy used in inspiration?

A

To overcome elasticity stored as PE

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35
Q

In what form is energy dissipated in expiration?

A

Heat

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36
Q

Rate of oxygen uptake is proportional to…

A

Area x change in pressure

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37
Q

Rate of oxygen uptake is dependent on…

A

Physiochemical properties of the gas

Nature of the membrane

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38
Q

Pressure gradient

A

The difference in partial pressure of gas in alveolus and blood

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39
Q

Partial pressure

A

The pressure a gas would exert if it were the only gas in a mixture
= P x fractional constant

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40
Q

Why is pp inversely proportional to solubility?

A

As fewer molecules are available to exert a pressure

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41
Q

Why is CO2 transport more efficient than O2?

A

Because CO2 is 24 times more soluble

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42
Q

Alveolar fibrosis

A

Thickening of the alveolar wall

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43
Q

Pneumonia

A

Alveolar consolidation

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44
Q

Pulmonary oedema

A

Frothy secretions

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45
Q

Interstitial oedema

A

Fluid around alveoli

46
Q

Emphysema

A

Alveolar-capillary destruction

47
Q

Atelectasis

A

Alveolar collapse

48
Q

How are airways kept patent?

A

Through continuous muscle activity

49
Q

Pharyngeal dilator reflex

A

P receptor -> brainstem -> muscle

50
Q

Sleep disordered breathing

A

No pharyngeal contraction -> periods of airway destruction -> lack of deep sleep

51
Q

What is sleep disordered breathing associated with?

A

Obesity
Hypertension
Drugs
Alcohol

52
Q

Which cells produce airway lining fluid?

A

Ciliated epithelial cells

53
Q

What is airway lining fluid produced in response to?

A

Irritation
Smoke
Pollution

54
Q

Functions of airway lining fluid (x 2)

A

Humidifies alveoli

Forms part of the airway defence

55
Q

What are cilia inhibited by?

A

Smoke, anaesthetic, pollution and infection

56
Q

What determines where a particle is deposited?

A

Size

57
Q

Non-immune pulmonary defences

A

Physical barrier and removal
Chemical inactivation
Alveolar macrophages

58
Q

Immune pulmonary defences

A

Humoral (IgA, IgE and IgG)

Cell-mediated

59
Q

In what two forms is O2 carried?

A

Dissolved in the blood and combined with haemoglobin

60
Q

How many O2 molecules can each haemoglobin carry?

A

4 (4 chains)

61
Q

In which form of haemoglobin can O2 access the binding site?

A

R State (not in T state)

62
Q

Thalassemia

A

Absent globin chain

63
Q

HbS (Sickle Cell)

A

Defective globin chain

64
Q

Methaemoglobin

A

Defective Fe atom

65
Q

CO Hb

A

Wrong ligand (CO)

66
Q

In which 3 forms is CO2 carried?

A

Dissolved in plasma
In carbamino compounds
As bicarbonate

67
Q

Respiratory alkalosis

A

Low PCO2
Normal HCO3-
Due to hyperventilation

68
Q

Respiratory acidosis

A

High PCO2
High HC03-
Due to ventilatory failure

69
Q

Metabolic alkalosis

A

Normal PCO2
High HCO3-
Due to loss of H+

70
Q

Metabolic acidosis

A

Low PCO2
Low HCO3-
Due to renal failure/shock/diabetic ketoacidosis

71
Q

When do lung buds form?

A

Week 1

72
Q

When do main and secondary bronchi form?

A

Week 5

73
Q

When do tertiary bronchi form?

A

Week 6

74
Q

When do terminal bronchioles form?

A

Week 16

75
Q

When do respiratory bronchioles form

A

Week 26

76
Q

When do alveoli form?

A

Week 36

77
Q

What are tracheoesophageal fistulas (TOF)?

A

Incomplete division of foregut into oesophageal and tracheal portions
- most common with oesophageal atresia

78
Q

What is oesophageal atresia?

A

When the upper oesophagus end abruptly, and the lower forms a fistula with the trachea -> milk regurgitated and acid into trachea

79
Q

Pseudoglandular lung maturation

A

5-17 weeks

Resp tree -> terminal bronchioles

80
Q

Canicular lung maturation

A

16-25 weeks

Terminal bronchioles -> resp bronchioles -> alveolar duct

81
Q

Terminal sac lung maturation

A

26 weeks - birth
Formation of primitive alveoli, blood-air barrier and surfactant film
Foetus can survive

82
Q

Alveolar lung maturation

A

36 weeks - 8 years

83
Q

What is pulmonary agenesis?

A

When the lung bud fails to split-

  • bi (incompatible with life)
  • uni (prompts respiratory stress)
84
Q

What is pulmonary hyperplasia?

A

All components are present, but are underdeveloped

85
Q

What is respiratory distress?

A

Damage to alveolar lining -> laboured/fast breathing and chronic lung injury

86
Q

Treatment of RDS

A

Glucocorticoid and surfactant therapy

87
Q

Differences between apical and basal alveoli

A

Apical are

  • 4 x larger
  • better ventilated
  • less expanded
88
Q

Hydrostatic pressure

A

Force exerted by the weight of fluid due to gravity (greatest at bottom)

89
Q

What are the 3 lung zones?

A

Dead space, recruitment and distension

90
Q

Ventilation-perfusion mismatch

A

Ideally 1, but 3.3 at apex and 0.6 at base

91
Q

Anatomical dead space

A

Conducting airways- no gas exchange

92
Q

Alveolar dead space

A

Unperfused alveoli

93
Q

Physiological dead space

A

Anatomical + alveolar

94
Q

Shunt

A

Where deoxygenated blood reaches the L side by bypassing the lungs or failing to be oxygenated eg pneumothorax

95
Q

How does the medulla oblongata function as a respiratory centre?

A

Dorsal respiratory group (DRG) fires on inspiration

Ventral RG fires on inspiration and expiration

96
Q

How does the pons function as a secondary respiratory centre?

A

It regulates the medulla- apneustic centre stimulates DRG and pneumotaxic centre inhibits insp neurones in VRG

97
Q

Oxygen cascade

A

Humidification -> alveolar gas -> alveolar-capillary diffusion -> ventilation-perfusion mismatch/shunt -> tissue diffusion -> diffusion in cell

98
Q

Oxygen delivery

A

Amount of O2 leaving the heart in a minute

= O2 content x CO

99
Q

Oxygen consumption (VO2)

A

Amount of O2 used in a minute

100
Q

Respiratory exchange ration/quotient

A

CO2 production : O2 consumption (should be 1)

101
Q

How does oxygen generate energy?

A

Glyolysis
Tricarboxylic acid cycle
Oxidative phosphorylation

102
Q

When does cellular hypoxia occur?

A

When there is insufficient O2 to mitochondria

103
Q

What are the 3 causes of cellular hypoxia?

A

Anoxic (lack of O2)
Stagnant (poor blood supply)
Anaemia (lack of haemoglobin)

104
Q

What is VO2 max?

A

The plateaued VO2. An indicator of fitness and anaerobic threshold

105
Q

How are changes to normal respiration controlled?

A

Neural input
Proprioreceptors
Changes in arterial blood gases
Temperature regulation

106
Q

Responses to altitude (x5)

A 
Hyperventilation
Better unbinding of O2
Polycythaemia
HCO3- excretion
Duiresis/hyponatraemia
107
Q

What are the symptoms of acute mountain sickness?

A

Headache, nausea, vomiting, loss of appetite, difficulty sleeping/exercising, amnesia and dizziness

108
Q

Effects of diving

A

Compression of lungs, chest and abdomen
Increased pressure in pleural cavity
Reduced volume of O2 and blood
Increased pp of O2

109
Q

Treatments of dry cough

A

Cough suppressants
Stop smoking
Opioids/non-opioids
Sedatives

110
Q

Treatments of productive cough

A

Expectorants and mucolytics

111
Q

Selective B2 antagonists

A

Inhalers or nebulisation
Short (salbutamol) or long-lastin (salmeterol)
SE= palpitation, tachycardia, tremor and restlessness

BS (5 decks)

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