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Life Support > Asthma and Lung Disease > Flashcards

Asthma and Lung Disease Flashcards

1
Q

What are the 4 properties of a receptor?

A

Tissue selectivity
Chemical selectivity
Extracellular/intracellular communication
Amplification

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2
Q

What is tissue selectivity?

A

Agonist only works in tissues where its receptor is found

Noradrenaline (NA) acts at adrenoceptors and not Ach receptors NA only works on tissues which express adrenoceptors –> But different receptor subtypes can bind the same drug
e.g. NA binds to
α-adrenoceptors – blood vessels
β-adrenoceptors – heart

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3
Q

What is chemical selectivity?

A

Molecular structure of a drug has a profound effect on its action,
e.g. (-)-adrenaline is 100 more potent that (+)-adrenaline
Drug binding sites within receptors have a high chemical selectivity

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4
Q

What is cellular communication?

A

Many drugs are hydrophilic – cannot cross plasma membrane
Drugs bind to receptors located in the plasma membrane to communicate information to the cell

e.g. adrenaline released into bloodstream from adrenal glands, acts at b1-adrenoceptors on sino-atrial node of heart to increase heart rate

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5
Q

What is amplification?

A

Receptors amplify signals – this means that drugs work at very low concentrations (<10-9M)
Type of receptor activated by a drug determines speed of amplified response (ms to days)

e.g. binding of Ach to Nic receptors at NMJ leads to immediate contraction of skeletal muscle (ms), but testosterone acts at steroid receptors to produce changes in gene expression over days-weeks

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6
Q

Name the 4 receptor families

A

Ligand-gated receptor/channel complexes
G-protein-coupled receptors
Tyrosine kinase receptors
Intracellular receptors

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7
Q

Describe the structure and action of ligand-gated receptors

A

Ligand-gated receptor/channel complexes

e.g. Nicotinic receptors (Ach at NMJ, Ach at autonomic ganglia)
Nicotinic receptors composed of five protein subunits
Subunits form a channel
Ligand-binding site on N-terminal region – extracellular site

Signal transduction mechanism:
Ligand binds to receptor -> conformation of protein subunits -> channel opening -> ion flux -> excitability

This is a very fast response: milliseconds (ms)

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8
Q

Describe the structure and action of G protein-coupled receptors

A

G-protein-coupled receptors

e.g. Muscarinic receptors (Ach at heart)
β1-adrenoceptors (NA at heart)
1000s of GPCRs, e.g. smell, taste

1 Single protein
7 transmembrane regions
N-terminal - ligand-binding site
C-terminal - G-protein binding region

Signal transduction mechanism:
Ligand binds to receptor -> Activation of G-proteins -> Production of intracellular messengers -> cellular function

Slower response than ligand-gated receptors: seconds to minutes

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9
Q

Which G protein subunits lead to changes in cAMP?

A

G-alpha s, G-alpha i

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10
Q

What is the target for G alpha s and G alpha i?

A

Adenylate cyclase

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11
Q

What is the target for G alpha q?

A

PLC (phospholipase C)

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12
Q

What is the G alpha q and PLC mediated reaction?

A

Phosphatidyl 4,5-bisphoshate (PIP2) phospholipid –> Diacylglycerol (DAG) (triglyceride) + Inositol 1,4,5-trisphoshate (IP3) (water soluble)

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13
Q

What is the pathway for G alpha S?

A

NA at B1-adrenoreceptors in heart to increase HR

NA to Gas -> stimulates adenylate cyclase (AC) -> ATP used -> increase cAMP levels -> stimulate protein kinase A (PKA) -> increased HR

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14
Q

What is the pathway for G alpha i?

A

Ach at M2-adrenoreceptors in heart to decrease HR

NA to Gai -> stimulates adenylate cyclase (AC) -> ATP used -> decrease cAMP levels -> inhibit protein kinase A (PKA) -> decreased HR

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15
Q

Describe the structure and action of Tyrosine kinase receptors

A

Tyrosine kinase receptors

e.g. Insulin receptor

Monomer – 1 single protein subunit
1 transmembrane domain
N-teminal extracellular- binds ligand
C-terminal intracellular- bind effector

Signal transduction mechanism:
Ligand binding to monomers induces dimerisation -> monomers phosphorylate tyrosine residue in each another -> phosphorylated intracellular domains bind enzymes/other cellular proteins -> cellular function

e.g. with insulin leads to glucose uptake by increased expression of GLUT transporters on cell surface

This is slow response: minutes, hours, days

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16
Q

Describe the structure and action of intracellular/nuclear receptors

A

Intracellular (or nuclear) receptorse.g. cortisol hormone receptorReceptor found within cytoplasm of cellMonomer – 1 single protein subunitDNA binding site N-teminal – binds heat shock protein (HSP) and also agonistC-terminal – control transcriptionSignal transduction mechanism:Drug crosses plasma membrane hormone displaces HSP and binds to N-terminal hormone/receptor complex enters nucleus and binds to hormone-responsive-element on a gene modulation of gene transcriptionThis is an even slower response: hours, days, months, beyond

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17
Q

What subunits are G proteins made of?

A

Apha, beta and gamma

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18
Q

What is the alpha subunit bound to at rest?

A

GDP

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19
Q

When a drug binds to the end terminal of a G protein coupled receptor what happens to the structure?

A

CONFORMATIONAL CHANGE

Alpha subunit exposed to cytosol and now binds GTP (higher affinity for alpha subunit, replaces GDP)

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20
Q

Once alpha subunit binds to GTP it…

A

Dissociates from receptor and beta/gamma complex to produce change in cellular signalling

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21
Q

Describe the tissue distribution, mechanism of action, physiological effects and agonists of alpha 1 adrenoreceptors

A

TD: vascular smooth muscle
MoA: Gq protein coupled activates PhoC, IP3 and DAG
Effects: vasoconstriction
Agonist: phenylephrine, NE

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22
Q

Describe the tissue distribution, mechanism of action, physiological effects and agonists of beta 1 adrenoreceptors

A

TD: heart
MoA: Gs protein coupled activates adenyl cyclase
Effects: increase HR
Agonist: isoproterenol, NE

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23
Q

Describe the tissue distribution, mechanism of action, physiological effects and agonists and antagonist of beta 2 adrenoreceptors

A

TD: visceral smooth muscles, bronchioles, liver, skeletal muscles
MoA: Gs protein coupled activates adenyl cyclase and PKA, Ca- channels
Effects: bronchodilation
Agonist: salbutamol, salmeterol
Antagonist: propranolol

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24
Q

What occurs in alpha subunit instrinsic GTPase activity?

A

GTP phosphorylated into GDP allowing alpha and GDP to bind again and rejoin beta/gamma complex on receptor

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25
Q

What is the cellular mechanism of glucocorticoids?

A

Glucocorticoid passes through membrane
Binds to receptor and displaces protein its usually bound to
Translocation of glucocorticoid/receptor complex to nucleus
Expression of genes increased or decreased

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26
Q

Is there a big difference between kPa of oxygen in alveoli vs pulmonary circulation?

A

No, PaO2 is 14 kPa in alveoli and 13 kPa in pulmonary circulation normally, making it very efficient

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27
Q

What happens to O2 and CO2 if ventilation icnreases?

A

More ventilation = more O2 in lungs = more O2 diffusing into blood

More ventilation = less CO2 in lungs = less CO2 in blood

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28
Q

How does increased ventilation affect gas exchange?

A

More ventilation = increased partial pressure gradient (between alveoli and blood) = increased gas exchange

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29
Q

Why is pulmonary ventilation important?

A

Needed to maintain adequate O2 supply and Co2 removal from respiring tissues

Pulmonary ventilation (movement of air from the atmosphere to gas exchange surfaces within the lung) is required to maintain O2 and CO2 gradients between alveolar air and arterial blood.

This enables a sufficient level of gas exchange to take place, ensuring adequate O2 supply/CO2 removal to/from respiring tissues (via blood).

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30
Q

How does the respiratory system achieve movement of air?

A

Gases naturally move from (connected) areas of higher pressureto lower pressure, until an equilibriumis re-established.

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31
Q

What does Boyle’s law show?

A

Pressure is proportional to the number of gas molecules in a given space, divided by volume (positive relationship between number of gas molecules in a space and pressure, so more molecules = more pressure) and inverse relationship between pressure and volume so bigger volume = lower pressure

if n remains constant (P ~ n/V)

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32
Q

Using Boyle’s law, how would you move gases into the lungs?

A

Because gases move from areas of higher pressure to lower pressure, we would increase volume so that pressure in lungs is lower than the atmosphere and gas molecules move in. (P ~ n/V)

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33
Q

How do the lungs allow gases to move in and out?

A

Changes in lung volume induce changes in alveolar pressure, which generate pressure gradients between alveoli & atmosphere, causing air to flow.

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34
Q

Inspiration vs Expiration

A

INSPIRATION
Diaphragm contracts (arch state to flat state)
Thoracic cavity expands
Alveolar pressure decreases

EXPIRATION
Diaphragm relaxes (and lung recoils)
Thoracic cavity volume decreases
Alveolar pressure increases

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35
Q

What happens to pressure at the end of expiration?

A

Equal pressure, so P alveoli = P atmosphere and therefore no movement of air

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36
Q

How is air pushed out the lungs?

A

Elastic recoil of the lungs and relaxed diaphragm

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37
Q

Why is the pleural cavity resistant to changes in volume?

A

Fluid filled and sealed

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38
Q

What is the pleural cavity and why is it important in breathing?

A

Pleural cavity = fluid filled space between the membranes (pleura) that line the chest wall and each lung - helps to reduce friction between lungs and chest.

The properties of the pleural cavity (sealed, fluid-filled) mean that it resists changes in volume. Thus, changes in the volume of the thoracic cavity only = changes in lung volume.

The opposing elastic recoil of the chest wall (outward) and lungs (inward) results in the pressure within the pleural cavity being sub-atmospheric.

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39
Q

What is the process of inspiration?

A

Respiratory muscles (e.g. diaphragm) contract
↓Volume of thoracic cavity increases
↓Lungs expand, increasing volume
↓PAlv (alveolar pressure) decreases below PAtm(atmospheric pressure)
↓Air moves down pressure gradient, through airways into alveoli, expanding the lungs

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40
Q

What is the process of expiration?

A

PASSIVE

Respiratory muscles (e.g. diaphragm) relax, lungs recoil due to elastic fibres (elastic recoil of lungs and relaxatio of resp muscles)
↓Lung volume & decreases (also causing thoracic cavity to decrease)
↓PAlv increases above Patm
↓Air moves down pressure gradient, into atmosphere, deflating lungs

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41
Q

How is movement of air in/out of lungs achieved?

A

Changing volume of thoracic cavity

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42
Q

What is the process of forced expiration?

A

Involves compression of thoracic cavity and lungs, as well as lung recoil

Inspiratory muscles (e.g. diaphragm) relax, expiratory muscles (e.g. int. intercostals) contract, lung tissue recoils
↓Volume of thoracic cavity decreases↓Lung volume decreases*
↓PAlv increases above PAtm
↓Air moves down pressure gradient, into atmosphere, deflating lungsExpiration (forced)

*Lung volume will also reduce due to lung recoil (as in passive expiration), however compression of the thoracic cavity will exert additional compressive force on the lungs, resulting in a greater level of expiration (in terms of volume change and rate of airflow)

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43
Q

What does the rate of airflow depend on?

A

Pressure gradient and level of airway resistance

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44
Q

What does Ohm’s law show?

A

An increase in change in pressure = increase in airflow
An increase in resistance = decrease in airflow

Airflow (V) = Pressure/Resistance

airflow is proportional to the pressure gradient and inversely proportional to resistance

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45
Q

What does the Hagen-Poiseulle equation show?

A

As airway radius decreases = resistance increases = airflow decreases dramatically

Resistance ~ 1/radius to the power 4

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46
Q

What is the impact of airway inflammation on resistance and airflow?

A

Obstructs airway so
Increased resistance
Decreased airflow

(less luminal area = more airway resistance = less airflow)

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47
Q

What are the features of airway inflammation in asthma?

A 
Obstructed
Smaller lumen
Smooth muscle contracted
Excess mucus secretion
Oedema/swelling

OVERALL EFFECT: decreased luminal area = increased airway resistance = decreased airflow (symptoms)

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48
Q

What is structural degradation in COPD?

A

Degradation of structural fibres (e.g. elastin) due to chronic inflammation
Less elastin fibres and radial traction so airwats collapse under compressive force = obstruction

Structural degradation can cause loss of patency and airway obstruction

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49
Q

How do airways resist collapse?

A

Elastin fibres connect airways to surrounding tissue producing radial traction

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50
Q

What forces act on airways and alveoli in insipiration vs forced expiration?

A

Expansive forces act during inspiration

Compressive forces act during forced expiration

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51
Q

What is transpulmonary pressure?

A

Overall level of force acting to expand/compress lungs

Transpulmonary pressure = alveolar presure - intrapleural pressure (difference between)

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52
Q

What is lung compliance?

A

Relationship between transpulmonary pressure and lung volume

Compliance (CL) = change in volume/change in pressure

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53
Q

What happens to lung stiffness when lung compliance is increased vs decreased?

A

↑ compliance = less force required to induce a specific change in volume (↓stiffness)

↓ compliance = more force required to induce a specific change in volume (↑stiffness)

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54
Q

What does a steeper curve for lung compliance indicate?

A

Increased lung compliance

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55
Q

What are the 3 factors involved in lung compliance?

A

Chest wall mechanics
Alveolar surface tension
Elastin fibres

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56
Q

How are chest wall mechanics negatively affected?

A

Scoliosis, muscular dystrophy and obesity DECREASE lung compliance

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57
Q

How is alveolar surface tension negatively affected?

A

NRDS (neonatal respiratory distress syndrome) decreases lung compliance

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58
Q

How are elastin fibres negatively affected?

A

Fibrosis (scarring of lung tissue making it stiff) decreases lung compliance and COPD increases it (degradation of fibres, lunsg expand too easily)

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59
Q

When ex vivo lungs are inflated with saline (rather than air) what happens to compliance?

A

Compliance increases

  • In classic experiments, physiologists compared compliance in ex vivo lungs inflated with air vs. lungs inflated with saline.
  • Saline-filled lungs required less pressure to inflate (↑ compliance).
  • Washing lungs with saline before inflating with air, produced lungs that required more pressure to inflate (↓ compliance).
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60
Q

Why do air-liquid interfaces ike alveoli resisr inflation?

A

They generate surface tension

Alveoli are lined with fluid to enable gas exchange (the gas molecules dissolve into water before diffusing.

Within the bubble formed by the air-liquid interface, surface tension arises due to H-bondsbetween the water molecules, exerting a collapsing force toward the centre of the alveoli, resisting expansion during inspiration.

61
Q

What reduces alveolar surface tesnion and what impact does this have on lung compliance?

A

Alveolar surface tension is reduced by pulmonary surfactant secreted by type 2 pneumocytes

The presence of pulmonary surfactant therefore increases lung compliance, as less expansionary force (ΔPtranspulmonary) is required to overcome the collapsing force generated by surface tension and inflate the lung.

62
Q

What impact does pulmonary surfactant have on alveolar oedema?

A

Pulmonary surfactant helps to prevent alveolar oedema

Surface tension produced at the air-liquid interface also reduces hydrostatic pressure in the alveolar fluid. If a pressure gradient is formed between the alveolar lining fluid and a nearby capillary, fluid will be pulled into the alveoli.

By reducing surface tension, pulmonary surfactant helps to prevent alveolar oedema, as observed in patients with insufficient surfactant.

63
Q

How does pulmonary surfactant prevent fluid from alveoli going into lungs?

A

Pulmonary surfactant removes surface tension which would normally go through the below steps to cause pulmonary oedema:

Collapsing force produced by surface tension
Hydrostatic pressure decreases in alveolar lining fluid
Fluid pulled from capillary into alveolus

64
Q

What causes neonatal respiratory distress syndrome and what is the process through which this occurs?

A

Caused by insufficient production of pulmonary surfactant

Process:
Premature birth, maternal diabetes, congenital developmental issues
Insufficient surfactant production
Stiff (low compliance) lungs, alveolar collapse, oedema
Respiratory failure
Hypoxia
Pulmonary vasoconstriction, endothelial damage, acidosis, pulmonary + cerebral haemorrhage.

65
Q

How can you treat neonatal respiratory distress syndrome?

A

Artificial surfactant supplementation of infant

Maternal glucocorticoid supplementation

66
Q

What happens if pleura are ruptured?

A

Rupture of parietal pleura means air to move from atmosphere to pleural space, no longer sealed
Now a pressure gradient between pleural space and atmosphere, so because air moves from area of low pressure to high pressure it will move into pleural space, fills with air at expense of lungs
If losing this seal then chest wall and lungs recoil in oppsoite directions causing collapse of lung like in pneumothorax (damage to one doesnt mean damage to other lung)

67
Q

Define asthma

A

Chronic inflammatory and obstructive disease of airways (sllergic asthma induces inflammatory response in airways which impairs airway function leading to wheeze, cough and dyspnoea)

68
Q

What genetic, immunological development and lifestyle factors make developing asthma more or less likely?

A

Genetics:
Parental asthma
ADAM33, GSTP1- genes
(none of these and protective genes make it less likely)

Immunological development:
infant resp virus infection
modern hygeine
c-section birth
(vaginal birth, healthy microbiota, older siblings and helminth exposure make it less likely)
Lifestyle:
Urban dwelling
Pollution exposure
Poor diet
Obesity
(rural dwelling, lower pollution environment, healthy diet make it less likely)
69
Q

What happens to ventilation due to impaired airway function?

A

Insufficient ventilation leads to decreased blood gas homeostasis and decreased acid base balance

70
Q

What is the relationship between resistance and airflow when resistance INCREASES?

A

More resistance = less airflow

UNLESS pressure gradient is increased to compensate

71
Q

Describe what is meant by airflow being proportional to the size of the airway lumen

A

Increased lumen diameter = increased luminal area = decreased resistance and increased airflow

Decreased lumen diameter = decreased luminal area = increased resistance and decreased airflow

72
Q

What is the normal patern of airflow?

A

Laminar (low resistance manner)

73
Q

What is the pattern of airflow in asthma?

A

Turbulent (produces noise = wheezing)

Multidirectional, more airway resistance because more molecules making contact with airway wall and vibrations (noise)

74
Q

What 2 things to allergic responses require?

A

Prior exposure and sensitisation

75
Q

What is allergen sensitisation vs allergic response?

A

Allergen Sensitisation:
Allergen exposure -> Allergen ecnountered and processed by adaptive immune system -> Antibodies generated and immune system ‘primed’

AND THEN

Allergic Response:
Subsequent (same) allergen exposure
Allergen binds antibodies -> immune cell activation -> inflammatory response
Symptoms

76
Q

What is the sensitisation process/

A

Allergen inhaled, enters airway tissue
Antigen presenting cell eg dendritic cell (APC) engulfs and processes allergen, presents allergen to naïve T helper cell. (himbo cell)

Naïve CD4+ T helper cell becomes mature Th2 cell (an now recognise allergen fragments and release cytokines IL5, IL4 and IL13)
IL5 binds to eosinophils and these cells proliferate
T cell also releases IL4 which interacts with B cell displaying antigen
B cell proliferates and produces IgE antibodies
Antibodies bind FceRI (IgE) receptor on mast cells (granulocyte)
Mast cell will release inflammatory granules into tissue of airway

77
Q

What triggers the asthmatic response?

A

Allergen induced degranulation and airway inflammation

78
Q

What is the impact of mast cells on airways in asthma?

A

Mast cell undergoes degranulation and releases inflammatory mediators (PGs, LTs, chemokines) AND eosinophils release inflammatory mediators ROS, enzymes and leukotrienes resulting in airway changes:

contraction of smooth muscle
excess mucus secretion
oedema/swelling
less luminal area = more resistance and less airflow

79
Q

What two cells are degranulated in asthmatic response?

A

Mast cells and recruited Eosinophils from further T cell activation

80
Q

Why does asthma have an early and late response?

A

Inhale allergen gets an early response of initial wave of degranulation and bronchospasm

After several hours the mucus secretion, microvascular leak, trafficking of leukocytes to airways and airway hyperresponsiveness culminates into the late response, so while early response is resolved the inflammation is still there

81
Q

Why is someone more likely to have another asthma attack after having a first one?

A

Threshold of allergen exposure to have further asthma atacks is significantly lowered

82
Q

What negative long term changes can occur in airway structure due to chronic uncontrolled asthma?

A

Allergen exposure and inflammatory mediator release lead to activation of airway eosinophils and Th2 cells = TISSUE DAMAGE

Inflammatory mediator release = bronchoconstriction, mucus hypersecretion and airway oedema -> all this can increase in chronic cases due to airway remodelling

83
Q

What is peak expiratory flow?

A

Measures fastest flow rate achieved during forced expiration
Units - litres per minute
Mostly used as chart of repeat measurements to diagnose or monitor variable airways obstruction
Most useful in ASTHMA

84
Q

What is the clinical use of PEF?

A

Diagnosis of reversible airways obstruction:
–Peak flow chart shows DIURNAL variation in peak flow measurements

Monitoring of treatment success:
–Acute asthma: planning discharge from hospital
–Chronic asthma: step up/step down inhaler treatment, then give written self management plan

85
Q

In a peak flow chart for asthma what would you typically see?

A

Bronchoconstriction is worst at night and in morning

86
Q

What is spirometry?

A

Spirometry is used to measure the volume and flow during maximal expiratory effort after maximal inhalation

It can be useful in differentiating between obstructive and restrictive lung disorders

‘Normal’ spirometry is determined by predicted values

87
Q

What are the spirometry values?

A

FEV1–Absolute value (in litres)–Percent predicted

FVC–Absolute value (in litres)–Percent predicted

FEV1 and FVC – normal range is 80-120% of predicted value

FEV1/FVC ratio (%, calculated from absolute values) – normal is 70-75%

88
Q

What is the difference between asthma and COPD spirometry?

A

In asthma, spirometry may be normal or show reversible changes during an attack
In COPD, altered spirometry is invariable and NOT fully reversible

89
Q

What happens to FEV1 and FVC in a restrictive lung disease?

A

In restrictive diseases, the lung volumes are small, FEV1 and FVC are both reduced by the same amount so the FEV1/FVC ratio is either normal or slightly elevated

Causes include lung fibrosis (scarring), obesity or respiratory muscle weakness

90
Q

What is transfer factor?

A

Lung function test in which haemoglobin is measured
Patient inhales a low, known concentration of carbon monoxide
CO taken up by circulating Hb
Amount left in breath is measured (reflects amount absorbed)

91
Q

What affects gas transfer in lungs?

A

Haemoglobin binding (anaemia), ventilation and perfusion deficit, alveolar capillary membrane (pneumonia, heart failure filling alveolus with fluid)

92
Q

What changes are seen in transfer factor?

A

REDUCTION
Thickening of alveolar-capillary membrane:
interstitial lung disease eg pulmonary fibrosis

SEVERE REDUCTION in ventilation or perfusion:
severe emphysema (holes in lung tissue)
heart failure
pneumonia
pulmonary emboli

INCREASE
Pulmonary haemorrhage

93
Q

If a patient has an FEV1 of half the normal percentage and FVC on the lower end of normal, what is their condition most likely to be?

A

FEV1 to FVC ratio is low so OBSTRUCTIVE deficit
So is it asthma or COPD?
In asthma airways normal so gas transfer should be normal, whereas COPD has emphysema so gas transfer is abnormal

So look at CO2 collected, if CO2 absorption is less than what it should be then it is COPD (if normal, asthma)

94
Q

What would you expect to happen to FEV1 and FVC in someone with a restrictive deficit?

A

For both numbers to drop by the same amount

Also see gas transfer to see if lung tissue is affected (if it is very low, could be fibrosis)

95
Q

What muscles are used in inspiration vs expiration?

A

Inspiration – active process, descent of diaphragm and movement of ribs upwards and outwardsforced
inspiration – accessory muscles

Expiration – passive process due to elastic recoil
forced expiration – abdominal muscles

96
Q

What controls respiration?

A

Respiratory centre – ill-defined group of neurones in reticular substance of brainstem

Motor discharges travel down via the phrenic nerve (C3,4,5 to diaphragm) and intercostal nerves to respiratory musculature

97
Q

What neurogenic factors are involved in breathing?

A

Impulses – limb receptors during exercise•Pulmonary receptors sensitive to stretch
Juxtapulmonary receptors stimulated by pulmonary congestion
Impulses from receptors in muscles and joints of chest wall
Consciously induced changes

98
Q

What abnormal stimuli lead to problems in respiration?

A

Lesions in pons and midbrain – hyper or hypoventilation

Medullary compression – respiratory depression

99
Q

What is the strongest signal to start breathing faster and deeper? What else stimulates this?

A

Rise in CO2 is the strongest respiratory stimulant (central chemoreceptors)

Rise in hydrogen ions – increases ventilation

Reduced pO2 increases breathing (peripheral chemoreceptors)

100
Q

Type 1 vs Type 2 respiratory failure

A

Exists when pO2 < 8kPa

Type I (hypoxic) - pCO2 < 6.5kPa

  • VQ mismatch
  • increased rep rate leads to fall in pCO2

Type II (hypercapnic) – pCO2 > 6.5kPa

  • ventilatory failure
  • insufficieny to excrete CO2 being produced by tissues
101
Q

What physiological mechanism accounts for hypoxia?

A

Ventilation-perfusion mismatch

102
Q

What is ventilation-perfusion mismatch?

A

If there is a mismatch between the alveolar ventilation and the alveolar blood flow, this will be seen in the V/Q ratio. If the V/Q ratio reduces due to inadequate ventilation, gas exchange within the affected alveoli will be impaired. As a result, the capillary partial pressure of oxygen (pO2) falls and the partial pressure of carbon dioxide (pCO2) rises.

A mismatch in ventilation and perfusion can arise due to either reduced ventilation of part of the lung or reduced perfusion.

103
Q

What happens to haemoglobin in ventilation-perfusion mismatch?

A

No ventilation from one lung but there is from another. So all blood from lung with blocked airway is not ventilated and Hb unsaturated- no O2.

Blood from unventilated alveoli (one lung) and blood from ventilated alveoli (other lung) (where Hb is 100% saturated) would mix together so oxygen in blood from ventilated alveoli is all bound to Hb, but none spare to bind to deoxyHb from unventilated alveoli.

104
Q

How does ventilation increase/decrease pCO2?

A

Increased ventilation decreases pCO2 (bigger breaths, reducing alevolar CO2 = reduce blood Co2)
Decreased ventilation increases pCO2 (cannot breathe as well, underbreathing, increased alveolar CO2 = increase blood CO2)

105
Q

What is the difference between metabolic and respiratory acidosis?

A

Metabolic acidosis – increased production of acids – H+
less HCO3- -> lower pH -> less pCO2

Respiratory acidosis – reduced ventilation leading to raised pCO2
more pCO2 -> lower pH -> more HCO3-

106
Q

What is the difference between metabolic and respiratory alkalosis?

A

Metabolic alkalosis –loss of acids – H+
more HCO3- -> higher pH -> more pCO2

Respiratory alkalosis – increased ventilation leading to low pCO2
less pCO2 -> higher pH -> less HCO3-

107
Q

What thoracic levels are the:
Vena cava
Oesophagus
Aortic hiatus ?

A

T8: Vena cava (phrenic nerve)
T10: Oesophagus (vagus nerve)
T12: Aortic hiatus (azygous vein and thoracic duct)

108
Q

What innervates the parietal pleura?

A

Phrenic and intercostal nerves

109
Q

What innervates the visceral pleura?

A

Autonomic innervation by pulmonary plexus

110
Q

Which pleura produces sensation?

A

Parietal: pain, temp, pressure and produces well localised pain -> referred pain to shoulder

111
Q

What type of hypersensitivity reaction is asthma?

A

Asthma is a Type I hypersensitivity reaction characterised by classical symptoms (more than one of wheeze, chest tightness, breathlessness, or cough) and variable, but reversible, airflow obstruction.

Airway hyper-responsiveness and airway inflammation are also components of the disease.

112
Q

What are the classical symptoms of asthma?

A

variable
worse at night/early hours of the morning
associated with triggers (e.g., exercise, allergen exposure, cold air, smoking)

113
Q

What are clinical features of asthma?

A

cough, wheeze, chest tightness, sputum production, dyspnoea, low exercise tolerance

114
Q

What immunoglobin mediated response is a Type 1 hypersensitivity reaction?

A

IgE mediated, histamine release, onset within an hour eg anaphylaxis

115
Q

What are the 4 types of hypersensitivity reactions?

A

ACID

Allergy (IgE)
Cell mediated (IgG or IgM cytotoxic)
Immune complex (Immune complex mediated)
Delayed (T cell mediated)

116
Q

What happens in the immediate and late phase of a Type 1 reaction?

A 
Immediate phase:
vasodilation
increased vascular permeability
increased adhesion molecules
bronchoconstriction

Late-phase:
cellular infiltration
t cell activation

117
Q 
What is the difference between:
Moderate acute asthma
Acute severe asthma
Life-threatening asthma
Near-fatal asthma ?
A

Moderate acute asthma:
increasing symptoms
PEF >50-75% best or predicted
no features of acute severe

Acute severe asthma: any one of 
PEF 33-50% best or predicted
RR ≤ 25/min
HR ≤ 110/min
inability to complete sentences in 1 breath
Life-threatening asthma: patient with acute severe PLUS any of the following
PEF <33% best or predicated
SpO2 <92%
PaO2 <8 kPa
‘normal’ PaCO2 (4.6-6.0 kPa)
altered conscious level
exhaustion
arrhythmia
silent chest
hypotension
cyanosis
poor respiratory effort

Near fatal asthma:
Raised PaCO2 and/or requiring mechanical ventilation and raised inflation pressures

118
Q

What is the management for acute asthma?

A

MI POO SHIT

Magnesium sulphate (IV)
Inform consultant#

Prednisolone (tablet)
Oxygen
Oxygen (mechanical ventilation)

Salbutamol
Hydrocortisone (IV)
Ipratropium bromide
Theophylline

119
Q

What is the management for life-threatening asthma?

A

Call senior team
IV magnesium sulphate over 20 mins
more salbutamol – every 15-30 mins or 10mg over 1 hour

120
Q

If pO2 less than 8kPa and there are NO signs of hypoxia what has happened?

A

TYPE 1 RESPIRATORY FAILURE
caused by a ventilation perfusion disruption (V/Q mismatch)
air flowing in and out is not matching blood flow to the lungs
there is inadequate oxygenation of the blood. however, the lung is still able to excrete CO2 so there is low O2 but a normal or low CO2
examples: shunts, altitude, asthma, COPD, MI, PE, pneumothorax

121
Q

If pO2 less than 8kPa and there ARE signs of hypoxia what has happened?

A

TYPE 2 RESPIRATORY FAILURE
caused by ventilation failure
inadequate alveoli ventilation affecting CO2 and O2 levels
this affects the excretion of CO2 and therefore, these levels start to rise
examples: COPD, life-threatening alveoli, chest-wall deformities, CNS depression, iatrogenic (sedatives/strong opioids)

122
Q

Asthma

A

Asthma is characterised by classical
symptoms (more then one of wheeze, chest
tightness, breathlessness or cough) and
variable airflow obstruction

Airways hyper-responsiveness and airway
inflammation are components of the disease

123
Q

Asthma pathophysiology

A

Condition of intermittent airway obstruction caused by:

  • Chronic airway inflammation (eosinophils, lymphocytes, mast cells)
  • Airway hyper-responsiveness →smooth muscle contraction
  • ↑ mucus production
124
Q

If asthma is not controlled what can occur?

A

Airway remodelling and fixed airway changes

125
Q

Asthma aetiology

A

Genetics:

  • Multiple genes may be involved
  • 2-3x risk if parent is asthmatic, 5-6x if both parents

Immunology:
- Allergy (IgE mediated inflammation)

Environment:

  • Increased exposure to allergen
  • Pollution
126
Q

Asthma clinical features

A 
Cough + nocturnal cough
Wheeze
Dyspnoea
Chest tightness
Sputum production - white/yellow
Reduction in exercise tolerance
127
Q

Asthma symptoms are (behaviour wise):

A

Variable
Worse at night/early hours of morning (diurnal)
Associated w triggers ie exercise, allergen exposure, (tree/grass pollen), cold air

128
Q

Asthma on examination

A

May be completely normal
Expiratory wheeze
Silent chest (severe life threatening asthma)

129
Q

What tests are done to check for asthma?

A

Spirometry

Peak flow

130
Q

Spirometry for asthma diagnosis

A

FEV1/FVC (forced expiratory volume / forced vital capacity)
-May be normal if not symptomatic
BUT if ratio less than 70% then supports diagnosis of asthma
- <0.70 ie obstructive

Reversibility:
i.e. if they have obstructive airway disease, does lung function get better with inhaler/nebuliser?
-Measurement of FEV1 pre and post bronchodilator (eg nebulised or inhaled
salbutamol) to see if they improve
- ∆ if > 12% improvement + 200ml increase supports asthma diagnosis
if increase > 400ml without % also supports

131
Q

What are the steps to asthma diagnosis?

A

Classic symptoms/signs (cough, nocturnal cough, wheezing, SOB, chest tightness, sputum production, reduction in exercise tolerance- variable)

Tests for variability:
Reversibility (FEV1/FVC)
Peak flow charting
Challenge tests

Tests for eosinophilic inflammation or atopy

  • FeNO (fractional exhaled nitric oxide) above 40 suggests inflammation -> asthma
  • Blood eosinophils - if increased
  • Skin prick tests, IgE - allergy marker
132
Q

Peak flow charting for asthma diagnosis

A

Peak flow recording

  • may be normal between attacks
  • rather than single recording do it 2x a day for time period, recording in peak flow diary

Peak flow diaries
- more sensitive and accurate
- ∆ confident if mean variability > 20% or
>15% diurnal variability on > 3 days/week
supports asthma diagnosis

133
Q

Assessment of PEFR variability

A

PEFR (max) - PEFR (min) / PEFR (max) (x 100)

eg, 450 - 290 / 450 = 0.35 (x 100)
= 35% variability

= significant variability (over 20%)
supports asthma diagnosis

134
Q

When do we use challenge tests (for bronchial hyper-responsiveness)?

A

If spirometry and peak flow charts normal

  • Methacholine/histamine/acetylcholine - varying doses of these drugs given to inhale and then FEV1 measured
  • > looking for concentration of drug that will provoke 20% fall in FEV1
  • PC20 = dose of agent provoking 20% fall in FEV1
  • asthma if PC20 equal to or less than 8mg/ml
135
Q

Skin prick testing

A

Intradermal inoculation of tiny quantity of allergen

Allergen -> bridging of IgE molecule on mast cell -> mast cell degranulation -> histamine release -> wheal and flare

136
Q

How to investigate an allergy?

A

CLINICAL HISTORY
specifically hay fever/eczema/nasal polyps and recognised triggers

BLOODS
total IgE
specific IgE (prev called RAST)

137
Q

Aims for chronic asthma management?

A
  • no daytime symptoms
  • no night-time awakening due to asthma
  • no need for rescue medication
  • no asthma attacks
  • no limitations on activity including exercise
  • normal lung function (in practical terms FEV1 and/or PEF>80% predicted or best)
  • minimal side effects from medication
138
Q

Non-pharmacological chronic asthma management

A

Allergen avoidance

Smoking cessation

Weight loss

Breathing technique training

139
Q

Asthma treatment according to BTS guidelines

A

Asthma suspected- consider monitored inhalation of low dose corticosteroids

Diagnosed adult asthma- escalation to improve control as needed:

  • > regular preventer and low dose ICS
  • > initial add-on therapy, inhaled LABA added to low dose ICS
  • > additional controller therapies, consider increasing ICS to medium dose or adding LTRA (if no response to LABA, consider stopping it)
  • > specialist therapies - refer patient for specialist care

Alongside all- short acting beta agonists as required unless using MART

140
Q

What is an asthma ‘action’ plan and what does it involve?

A

Personalised action plan written by doc/asthma nurse
Self management education -> improved health outcomes for people with asthma

  • Details about asthma ie peak flow, medication
  • How to tell when asthma control is poor
  • What you should do if control is poor
  • What to do in an emergency
  • Allows self adjustment of medication in the event to deterioration
  • Details frequently of medical/asthma nurse review
  • Adults should have at least annual review
141
Q

Asthma review

A

Ensures patient on correct level of treatment for severity and level of control

142
Q

What is involved in assessment of control for asthma?

A

Review of peak flow diaries, inhaler technique and checking spirometry

143
Q

What to do regarding asthma therapy if control is poor?

A

Increase therapy in stepwise approach if
markers of poor control

If stable, aim to reduce inhaled steroid dose
to the minimum dose which maintains control
(↓ no faster than at 3/12 intervals)

144
Q

Asthma severity scale

A

MODERATE ACUTE ASTHMA
increasing symptoms
PEF > 50-75% best or predicted
no features of acute sever asthma

ACUTE SEVERE ASTHMA
any ONE of:
- PEF 33-50% best or predicted
- resp rate equal or > 25/min
- HR equal or > 110/min
- can't complete sentences in one breath
LIFE THREATENING ASTHMA
any ONE in patient w severe asthma:
Clinical Signs:
altered conscious level
exhaustion
arrhythmia
hypotension
cyanosis
silent chest
poor resp effort
Measurements:
PEF <33% best or predicted
SpO2 <92%
PaO2 <8 kPa
'normal' PaCO2 (4.6-6.0 kPa)

NEAR FATAL ASTHMA
raised PaCO2 and/or require mechanical ventilation with raised inflation pressures

145
Q

IMMEDIATE TREATMENT for acute asthma

A
146
Q

SUBSEQUENT MANAGEMENT for acute asthma

A
147
Q

Monitoring after treating acute asthma

A
148
Q

When to discharge asthma patient

A

Life Support (5 decks)

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