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L2 physiology of cells and systems > Respiration > Flashcards

Respiration Flashcards

1
Q

What is the flow of air into/out of the lungs proportional to?

A

Pressure gradient

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2
Q

What is the flow of air into/out of the lungs inversely proportional to?

A

Resistance

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3
Q

What is the main relationship demonstrated by Poiseuille’s law?

A

Airway resistance is inversely proportional to the fourth power of the radius

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4
Q

What do small changes in airway diameter impact?

A

The resistance of airflow (small change in diameter = big change in resistance)

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5
Q

What percentage of the total airway resistance is made up by the pharynx-larynx?

A

40%

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6
Q

What percentage of the total airway resistance is made up by the large airways (>2mm diameter)?

A

40%

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7
Q

What percentage of the total airway resistance is made up by the small airways (<2mm diameter)?

A

20%

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8
Q

What factors impact airway diameter and therefore resistance? (3)

A
  • Increased mucus secretion
  • Oedema
  • Airway collapse/expansion during normal breathing
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9
Q

What are the 2 categories of lung disease?

A
  • Obstructive
  • Restrictive
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10
Q

What is obstructive lung disease?

A

Narrowing of the airways causes a reduction in flow

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11
Q

What is restrictive lung disease?

A

Causes a reduction in lung expansion

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12
Q

What is the effect of both obstructive and restrictive lung disease?

A

Both reduce ventilation

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13
Q

What is FEV1?

A

Forced expiratory volume in 1 second

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14
Q

What is VC?

A
  • Vital Capacity
  • Maximum volume of air that can be expelled from the lungs after biggest possible deep breath
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15
Q

What is the ratio of FEV1:VC in healthy lungs?

A

Greater than 80%

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16
Q

Which graphs are used to diagnose lung diseases? (2)

A
  • Volume/time
  • Flow/volume
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17
Q

What causes narrowing of the airways in obstructive lung disease? (3)

A
  • Excess secretions
  • Bronchoconstriction (airway smooth muscle contraction - asthma)
  • Inflammation
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18
Q

What is FVC?

A
  • Forced Vital Capacity
  • Volume of air exhaled with maximal effort after maximum inspiration
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19
Q

Which measurement is affected in obstructive lung disease?

A
  • FEV1 decreased
  • FVC usually unaltered
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20
Q

What is a sign of obstructive lung disease on a flow/volume graph?

A

Concave shaped decline in flow rate

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21
Q

What are examples of obstructive lung disease? (4)

A
  • Asthma
  • COPD
  • Chronic bronchitis
  • Emphysema
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22
Q

What does COPD stand for?

A

Chronic Obstructive Pulmonary Disease

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23
Q

What happens in emphysema?

A

Loss of elastin

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24
Q

Which diseases are classed as subtypes of COPD? (2)

A
  • Chronic bronchitis
  • Emphysema
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25
Q

What forces are interacting to keep the pressure of the intrapleural space less than atmospheric pressure?

A
  • Elastic recoil of the lungs tends to make them collapse inwards
  • Elastic recoil of the chest wall tends to make it expand
  • Inward and outward forces balance
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26
Q

What are the 4 types of airflow?

A
  • Laminar
  • Unstable (switching between)
  • Turbulent
  • Transitional
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27
Q

What factors influence the Reynolds number? (4)

A
  • Viscosity
  • Density
  • Radius of vessel
  • Velocity
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28
Q

What state of airflow is the fluid in if the Reynolds number is <2000?

A

Laminar

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29
Q

What state of airflow is the fluid in if the Reynolds number is between 2000 and 3000?

A

Unstable

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30
Q

What state of airflow is the fluid in if the Reynolds number is >2000?

A

Turbulent

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31
Q

What is the pressure gradient in the lungs?

A

Difference in pressure between the alveoli and the atmospheric pressure

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32
Q

How do you calculate airflow in a laminar state?

A
  • Airflow is proportional to the pressure gradient and inversely proportional to the resistance
  • Airflow = difference in pressure over resistance
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33
Q

Where in the airway is the flow rate the fastest?

A
  • Centre
  • Slows as you move towards the edges
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34
Q

What kind of airflow occurs in most of the areas of the lungs?

A

Turbulent

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35
Q

How do you calculate airflow in a turbulent state?

A

Airflow is proportional to the square root of the pressure difference

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36
Q

Which type of airflow needs a greater pressure gradient to achieve the same flow rate?

A

Turbulent (proportional to square root of pressure gradient)

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37
Q

What is transitional flow?

A
  • Jumping between laminar and turbulent type flow at the branching points of the airways
  • Bifurcations disrupt flow
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38
Q

What is COPD characterised by? (2)

A
  • Increase in airway resistance
  • Decrease in airflow
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39
Q

What is Chronic Bronchitis?

A

Long term inflammation of the bronchi and bronchioles

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40
Q

What is Emphysema?

A

Destruction of alveoli walls

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41
Q

How is COPD treated? (2)

A
  • Bronchodilators (anticholinergics or beta-2 adrenoreceptor agonists)
  • Glucocorticosteroids
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42
Q

What is the total airway resistance in a healthy individual?

A

1.5cm H2O .s.litres^-1

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43
Q

What is the total airway resistance in an individual with COPD?

A

5.0cm H2O .s.litres^-1

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44
Q

Why does the total ariway resistance increase in COPD patients?

A

Massive increase in resistance in the small airways (<2mm)

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45
Q

What percentage of the total airway resistance is made up by the small airways (<2mm diameter) in COPD patients?

A

70%

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46
Q

What happens to the diameter of the airways during inspiration?

A

Increases - dilation

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47
Q

What happens to the diameter of the airways during expiration?

A

Decreases - collapse

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48
Q

What happens to the resistance of the airways during inspiration?

A

Decreases

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49
Q

What happens to the resistance of the airways during expiration?

A

Increases

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50
Q

What is the pressure in the intrapleural space?

A

Sub-atmospheric

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51
Q

What keeps the lungs from collapsing?

A

The sub-atmospheric pressure in the intrapleural space

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52
Q

What happens in Emphysema?

A
  • Loss of elastic tissue and breakdown of alveolar walls
  • Collapse of airways during expiration is exaggerated
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53
Q

What is the resting lung volume like in an Emphysema patient compared to a healthy individual?

A

Higher than a healthy person

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54
Q

What is tidal volume?

A

Volume of air you breathe in with one breath

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55
Q

What effect does COPD have on the rate of inflation?

A

Decreases due to increased resistance in the airways

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56
Q

What are the 2 zones of the lungs?

A
  • Conducting zone
  • Respiratory zone
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57
Q

What is the respiratory zone?

A
  • Alveoli
  • Where gas exchange occurs
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58
Q

What is the conducting zone?

A
  • All the airways which get the air to the alveoli (respiratory zone)
  • Trachea to bronchioles
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59
Q

What are the 2 types of dead space?

A
  • Anatomical dead space
  • Physiological dead space
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60
Q

What is anatomical dead space? (2)

A
  • Volume of the conducting conducting airways
  • 30% of inspired air
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61
Q

What is physiological dead space? (2)

A
  • Volume of lungs not participating in gas exchange
  • Made up of the conducting zone and the non-functional areas of the respiratory zone
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62
Q

How do physiological and anatomical dead space differ in healthy individuals?

A

Values should be the same

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63
Q

What is compliance? (2)

A
  • Measure of elasticity/distensibility
  • The ease with which the lungs/thorax expand during pressure changes
64
Q

How is compliance effected by emphysema?

A
  • High compliance
  • Airways collapse more easily during expiration
65
Q

How is compliance effected by fibrosis?

A
  • Low compliance
  • More rigid
66
Q

What is total ventilation?

A

Volume of air moved out of the lungs per unit time

67
Q

What is the normal tidal volume at rest?

A

0.5 litres

68
Q

What is normal breathing frequency?

A

12 breaths a minute

69
Q

What is alveolar ventilation?

A

Volume of ‘fresh’ air reaching the respiratory zone

70
Q

How do you calculate alveolar ventilation?

A

Total ventilation - dead space ventilation

71
Q

What volume of air is in the dead space?

A

0.15 litres

72
Q

What happens to alveolar and arterial gas composition during hyperventilation?

A
  • Same amount of CO2 is being expelled in a larger volume of air so the partial pressure of CO2 in the alveolar gas decreases
  • The partial pressure of CO2 in the arterial blood also decreases to reach equilibrium
  • Results in respiratory alkalosis
73
Q

What happens to alveolar and arterial gas composition during hypoventilation?

A
  • Same amount of CO2 is being expelled in a smaller volume of air so the partial pressure of CO2 in the alveolar gas increases
  • The partial pressure of CO2 in the arterial blood also increases to reach equilibrium
  • Results in respiratory acidosis
74
Q

What causes respiratory acidosis?

A

Hypoventilation

75
Q

What causes respiratory alkalosis?

A

Hyperventilation

76
Q

Where in the lungs has the lowest ventilation?

77
Q

Where in the lungs has the highest ventilation?

78
Q

Why is ventilation low at the apex of the lungs?

A
  • Lung weight pulling down causes a more negative intrapleural pressure so alveoli have a greater starting volume
  • This means they have a lower compliance because they can’t expand that much
79
Q

Why is ventilation high at the base of the lungs?

A
  • Less negative intrapleural pressure so the alveoli have a smaller starting volume
  • Alveoli have a greater capacity to expand so have a higher compliance
80
Q

What are the 2 circulation systems?

A
  • Pulmonary
  • Systemic
81
Q

Is systemic circulation high or low pressure?

A

High pressure, high resistance

82
Q

Is pulmonary circulation high or low pressure?

A

Low pressure, low resistance

83
Q

When is pulmonary resistance at its lowest?

A

When the lungs are at functional residual capacity

84
Q

What is functional residual capacity?

A

Volume of air left in the lungs after a normal exhalation

85
Q

What are the 2 types of blood vessels in the lungs?

A
  • Alveolar vessels
  • Extra-alveolar vessels
86
Q

What are alveolar vessels?

A

Capillaries/small blood vessels which are surrounded by alveoli

87
Q

What are extra-alveolar vessels?

A

Blood vessels not surrounded by alveoli

88
Q

How does an increase in intrapleural pressure affect the extra-alveolar vessels?

A
  • More negative intrapleural pressure (bigger vacuum) causes extra-alveolar vessels to expand
  • Resistance goes down
89
Q

How does a decrease in intrapleural pressure affect the extra-alveolar vessels?

A
  • Less negative intrapleural pressure (smaller vacuum) causes the diameter of extra-alveolar vessels to decrease
  • Resistance increases
90
Q

How do you calculate the total pulmonary resistance?

A

Sum of alveolar and extra-alveolar vessel resistances

91
Q

What is residual volume?

A

Volume of air remaining in the lungs after a maximum forceful expiration

92
Q

When is intrapleural pressure most negative?

A

During inspiration

93
Q

What happens to alveolar vessel resistance during inspiration?

A
  • Alveoli expand which puts pressure on the alveolar vessels so they can’t expand as much
  • Resistance increases
94
Q

What happens to extra-alveolar vessel resistance during inspiration?

A
  • Intrapleural pressure becomes more negative which causes extra-alveolar vessels to expand
  • Resistance decreases
95
Q

What is capillary recruitment?

A
  • At rest some capillaries are conducting blood, some are open and NOT conducting blood and some are collapsed
  • As perfusion pressure increases (e.g. during exercise), previously non-conducting vessels start conducting blood and the collapsed vessels open
  • Further pressure increase causes all vessels to conduct blood which lowers system resistance
96
Q

Where in the lungs has the lowest perfusion?

97
Q

Where in the lungs has the highest perfusion?

98
Q

Why is perfusion lower at the top of the lungs?

A

Blood is being pumped against gravity

99
Q

What are the zones of the lungs?

A
  • Zone 1 to 4
  • Only zone 2-4 in healthy lungs
100
Q

What effect does a decrease in oxygen have on perfusion?

A

Causes vasoconstriction because the lungs sense a problem and direct the blood elsewhere

101
Q

What effect does an increase in oxygen have on perfusion?

A

Causes vasodilation

102
Q

What effect does a decrease in carbon dioxide have on perfusion?

A

Causes vasodilation

103
Q

What effect does an increase in carbon dioxide have on perfusion?

A

Causes vasoconstriction

104
Q

What is the ventilation-perfusion ratio?

A

Ratio = V/Q

105
Q

What happens to the ventilation-perfusion ratio when there is no ventilation?

A

Ratio is 0

106
Q

What happens to the ventilation-perfusion ratio when there is no perfusion?

A

Ratio is infinity

107
Q

Where in the lungs is the ventilation-perfusion ratio the highest?

108
Q

Where in the lungs is the ventilation-perfusion ratio the lowest?

109
Q

What happens to the ventilation-perfusion ratio during pulmonary embolism? (4)

A
  • Perfusion reduced
  • Alveolar gas composition becomes the same as inspired air due to no gas exchange
  • Ratio becomes infinity
  • Blood directed elsewhere
110
Q

What happens to the ventilation-perfusion ratio when something blocks airflow in the lungs? (4)

A
  • Ventilation reduced
  • Alveolar gas composition becomes the same as venous blood
  • Ratio becomes 0
  • Air and blood directed elsewhere
111
Q

What is the effect of stimulating a Gq protein coupled receptor? (4)

A
  • Alpha subunit dissociates and activates phospholipase C (PLC)
  • PLC cleaves PIP2 into diacylglycerol (DAG) and IP3
  • DAG stimulates protein kinase C (PKC)
  • IP3 causes release of Ca2+ from stores
112
Q

Which molecule is Gq linked to?

A

Phospholipase C (PLC)

113
Q

Which molecule is Gs linked to?

A

Adenylyl cyclase

114
Q

Which molecule is Gi linked to?

A

Adenylyl cyclase

115
Q

Which molecule is Gi linked to?

A

Adenylyl cyclase

116
Q

What is the effect of stimulating a Gs protein coupled receptor?

A
  • Alpha subunit dissociates and activates adenylyl cyclase
  • Causes increase of cAMP and activation of protein kinase A
117
Q

What is the effect of stimulating a Gi protein coupled receptor?

A
  • Alpha subunit dissociates and inhibits adenylyl cyclase
  • Causes a reduction in cAMP and reduction of protein kinase A activity
118
Q

What are the divisions of the autonomic nervous system? (3)

A
  • Sympathetic
  • Parasympathetic
  • Enteric
119
Q

What effect does the parasympathetic nervous system have on bronchial smooth muscle?

A

Vagus nerve releases acetylcholine which acts on muscarinic receptors, causing constriction

120
Q

What effect does the sympathetic nervous system have on bronchial smooth muscle?

A

Nerves release noradrenaline which acts on adrenergic receptors, causing dilation

121
Q

What humoral factors can affect bronchial smooth muscle?

A
  • Adrenaline
  • Histamine
122
Q

What effect does adrenaline have on bronchial smooth muscle?

123
Q

What effect does histamine have on bronchial smooth muscle?

A

Constriction

124
Q

What is a short acting asthma treatment?

A

Salbutamol

125
Q

How does salbutamol work?

A
  • Short-acting beta-2 adrenoreceptor agonist
  • Causes airway dilation
126
Q

What is a long-term asthma treatment? (2)

A
  • Glucocorticoids e.g. beclomethasone
  • Long acting beta adrenoreceptor agonists
127
Q

How does beclomethasone work?

A
  • Inhaled steroids
  • Reduce inflammation
128
Q

What is the mechanism of smooth muscle contraction? (6)

A
  • Increase in intracellular Ca2+
  • Ca2+ binds to calmodulin creating active Ca2+-calmodulin complex
  • Complex activates Myosin Light Chain Kinase (MLCK)
  • MLCK phosphorylates myosin light chain
  • Causes contraction
  • Contraction is maintained while the myosin light chain remains phosphorylated
129
Q

What is the mechanism of smooth muscle relaxation? (2)

A
  • Myosin Light Chain Phosphatase (MLCP) dephosphorylates the myosin light chain
  • Causes relaxation
130
Q

Which receptors present on smooth muscle are Gq coupled? (3)

A
  • M3 muscarinic receptors
  • H1 histamine receptors
  • BK bradykinin receptors
131
Q

What is the effect of stimulating Gq receptors on smooth muscle? (2)

A
  • IP3 causes Ca2+ release and therefore muscle CONTRACTION
  • DAG activates PKC which causes growth in the long term
132
Q

Which receptors present on smooth muscle are Gs coupled? (2)

A
  • Beta-2 adrenergic receptors
  • VIP (Vasoactive Intestinal Peptide) receptors
133
Q

What is the effect of stimulating Gs receptors on smooth muscle? (6)

A
  • RELAXATION
  • Protein Kinase A activated
  • Causes stimulation of BK K+ channels so K+ leaves and hyperpolarises the membrane
  • Inhibits MLCK and activates MLCP
  • Gene regulation
  • Inhibits growth
134
Q

What is the effect of stimulating Gi receptors on smooth muscle? (3)

A
  • Counteracts the action of Gs
  • Opposes the relaxation of smooth muscle
  • Inhibits the BK K+ channel
135
Q

Which receptors present on smooth muscle are Gi coupled?

A

M2 muscarinic receptors

136
Q

Which receptors cause smooth muscle contraction?

A

M3 receptors

137
Q

What is the negative feedback mechanism which prevents over-contraction of airway smooth muscle?

A
  • ACh released from postganglionic nerve fibre and activates M3 receptors on smooth muscle causing contraction
  • Some of the ACh activates M2 receptors on the postganglionic nerve fibre which inhibits further ACh release
138
Q

What kind of receptors are adrenergic receptors?

A

G protein coupled

139
Q

Which G protein are beta-2 adrenergic receptors coupled to?

140
Q

What is NANC signalling?

A

Nonadrenergic/noncholinergic signalling

141
Q

What are the 2 pathways of NANC signalling?

A
  • eNANC (excitatory)
  • iNANC (inhibitory)
142
Q

What happens in eNANC?

A

Causes bronchoconstriction

143
Q

Which transmitters are involved in eNANC? (2)

A
  • Substance P
  • Neurokinin A
144
Q

Which transmitters are involved in iNANC? (3)

A
  • Vasoactive Intestinal Peptide (VIP)
  • Nitric Oxide
  • Neuropeptide Y
145
Q

What happens in iNANC?

A

Causes bronchodilation

146
Q

What are the 2 classes of asthma?

A
  • Atopic (extrinsic)
  • Non-atopic (intrinsic)
147
Q

What is the effect of histamine on airway smooth muscle?

A

Bronchoconstriction

148
Q

What are the characteristics of atopic asthma? (4)

A
  • Associated with allergies
  • Linked to elevated serum IgE and positive skin-prick test
  • Allergen causes activation of mast cells which release histamine (bronchoconstriction)
  • Other inflammatory cells activated e.g. eosinophils
149
Q

What are the characteristics of non-atopic asthma? (3)

A
  • Normal serum IgE and no positive skin-prick test
  • Induced by exercise, cold air, inhaled irritants, stress, drugs
  • May have a localised increase in IgE
150
Q

Which division of the nervous system is overactive in asthma?

A

Parasympathetic

151
Q

What is the effect of increased parasympathetic activity in asthma? (5)

A
  • Increased basal tone
  • Increased muscle constriction in response to irritants
  • ACh activates M3 receptors on goblet cells causing increased mucus secretion
  • ACh activates M3 receptors on smooth muscle causing bronchoconstriction and long term growth of cells (thicker layer of muscle)
  • Inflammatory cells activated
152
Q

How are M2 receptors linked to asthma?

A
  • Reduced neuronal M2 receptor activity leads to increased parasympathetic activity
  • M2 receptors are involved in negative feedback which prevents over-activation of smooth muscle
153
Q

How are eosinophils involved in asthma? (3)

A
  • Eosinophils cluster around the nerve fibres
  • Activated eosinophils release Major Basic Protein (MBP)
  • MBP inhibit M2 receptors which inhibits negative feedback
154
Q

How can anticholinergics be used to treat asthma? (2)

A
  • Competitive inhibitors of M1, M2 and M3 receptors
  • Block the effects of endogenous ACh
155
Q

What is Ipratropium?

A

Short-lasting anticholinergic drug used in combination with short-acting beta-2 adrenoreceptor agonists e.g. salbutamol

156
Q

What is Tiotropium?

A

Long-lasting anticholinergic drug used in combination with long-acting beta-2 adrenoreceptor agonists and inhaled corticosteroids

L2 physiology of cells and systems (6 decks)

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