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year 1 flash cards > BS respiratory strand > Flashcards

BS respiratory strand Flashcards

1
Q

what is the main function of the respiratory system?

A

gas exchange

O2 from air to blood and CO2 from blood to air

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2
Q

what are the other functions of the respiratory system?

A

speech - exhalation and vibration of vocal chords

smell - inspiration through nasal cavity - in roof specialised epithelium detect small particles in the air

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3
Q

what are the two functional divisions of the respiratory system?

A

conducting and respiratory portion

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4
Q

what is the role of the conducting portion?

A
  • transports air from external environment to exchange surfaces
  • conditions the air (warms, moistens and filters as exchange structures are v delicate
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5
Q

what is the role of the respiratory portion?

A

where the actual gas exchange occurs

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6
Q

what makes up the conducting portion?

A

nasal cavity to the terminal bronchi

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7
Q

what are conchae?

A

3 inundations in the nasal cavity that increase the surface area for conditioning of air

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8
Q

what are meatuses?

A

the 4 pathways for air to flow created by the conchae, flow is disrupted creating a turbulent flow and conditioning it

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9
Q

why do we need turbulent flow?

A

viruses and bacteria in the air can be passed into the sinuses and immune response can be mounted –> prevents infection

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10
Q

what is the hard pallate?

A

roof of mouth

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11
Q

what is the soft palate?

A

the uvula is part of it

pushes food to back of throat and can almost seal of nasal cavity to prevent food going up nose

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12
Q

what barrier is there between nasal cavity and brain?

A

ethmoid bone

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13
Q

what is the role of the epiglottis?

A
  • stop food going into respiratory system by sealing it

- swallowing pushes food posterior

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14
Q

what is the nasopharynx?

A

upper part of the pharynx posterior to nasal cavity - only air

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15
Q

what is the oropharynx?

A

middle part of the pharynx posterior to mouth, uvula can be line of demarcation - air and food

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16
Q

what is the langopharynx?

A

most inferior portion of the pharynx

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17
Q

What is the upper airway composed of?

A

The nasopharynx, oropharynx, laryngopharynx and associated structures

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18
Q

What muscle is important in nasal breathing?

A

The genioglossus

  • the muscle that makes up most of the tongue
  • it prevents posterior tongue displacement and upper airway closure
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19
Q

What muscle is important in mouth breathing?

A

The tensor palati

  • it acts to tense and elevate the soft in order to prevent entry of food into the nasopharynx during swallowing
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20
Q

Describe the pharyngeal dilator reflex

A

Pressure receptors > brain stem > pharyngeal muscle contraction

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21
Q

What is the afferent nerve of the pharyngeal dilator reflex?

A

The trigeminal nerve

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22
Q

What is the efferent nerve of the pharyngeal dilator reflex?

A

The vagus nerve

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23
Q

What percentage of people are affected by sleep disorder breathing and sleep apnoea?

A

Sleep disordered breathing - 25%

Sleep apnoea - 10%

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24
Q

What are clinical features of sleep disordered breathing?

A

Snoring and daytime somnolence

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25
Q

What features is sleep disordered breathing associated with?

A

Obesity and hypertension

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26
Q

How is sleep disordered breathing treated?

A

Weight loss and CPAP (continuous positive airway pressure)

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27
Q

Airway lining fluid is produced by…

A

Ciliated epithelial cells

Goblet cells

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28
Q

In the nose and pharynx the ciliated epithelial cells are classified as…

A

Pseudostratified

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29
Q

In the trachea and bronchi the ciliated epithelial cells are classified as…

A

Columnar

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30
Q

In the bronchioles the ciliated epithelial cells are classified as…

A

Cuboidal

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31
Q

Goblet cells produce…

A

Mucin granules

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32
Q

What are mucin granules produced in response to?

A
  • airway irritation
  • tobacco smoke
  • infection
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33
Q

How do the cilia move mucus along?

A

Recovery and effective stroke

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34
Q

What are the two layers of airway lining fluid?

A

Mucous layer and periciliary

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35
Q

What inhibits the cilia?

A
  • tobacco smoke
  • inhaled anaesthetics
  • air pollution
  • infection
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36
Q

What are the functions of the airway?

A

Humidification and airway defence

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37
Q

How is humidification by airway lining fluid made more efficient?

A

Heat and moisture exchanger

The moisture and heat added to air during inhalation is returned in exhalation

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38
Q

How does the airway lining fluid aid airway defence?

A

The muco-ciliary escalator works alongside expectoration to remove pathogens from the body

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39
Q

What is cystic fibrosis?

A

Disease in which there is an abnormal transmembrane regulator protein.

It leads to progressive lung infection and destruction

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40
Q

What is the size, deposition site and mechanism of very large particles?

A

> 8um
Nose and pharynx
Inertial impaction

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41
Q

Why is the size of inhaled particles important?

A

It impacts the part of the airway on which they act

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42
Q

What is the size, deposition site and mechanism of large particles?

A

3-8um
Large airways
Inertial impaction

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43
Q

What is the size, deposition site and mechanism of small particles?

A

0.5-3um
Deposited in the bronchioles
Sedimentation

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44
Q

What is the size, deposition site and mechanism of very small particles?

A

<0.5um
Exhaled
Diffusion

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45
Q

What are large particles in inhaled drug delivery used to treat?

A

Hay fever

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46
Q

What are medium particles in inhaled drug delivery used to treat?

A

Asthma and COPD

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47
Q

What is the function small particles in inhaled drug delivery?

A

Absorption into the blood

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48
Q

What are the non-immunological pulmonary defences?

A
  • physical barrier and removal
  • chemical barrier inactivation by lysozymes, protease enzymes and anti microbial peptides
  • alveolar macrophages
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49
Q

What are the humoral pulmonary defences?

A

IgA (nose and large airways)
IgG (small airways)
IgE (allergic responses)

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50
Q

What are the cell-mediated pulmonary defences?

A

Epithelial cells
Macrophages
- neutrophils (infection)
- eosinophils (allergy)

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51
Q

How does CO affect airway physiology?

A

Decreased O2 carriage

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52
Q

How does NO affect airway physiology?

A

Airway irritation and asthma

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53
Q

How does ozone affect airway physiology?

A

Airway irritation and cough

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54
Q

How does particulate matter affect airway physiology?

A

Lung and systemic inflammatory response

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55
Q

what are the 2 pieces of equipment we use to measure compliance and what are they used to measure exactly?

A
  • sprirometry –> measures changes in lung volume

- oesophageal balloon –> measures inter pleural pressure

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56
Q

what is barometric pressure

A

pressure of atmosphere

usually assume is 0

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57
Q

what is recoil pressure

A

tendency for alveoli or lungs to collapse

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58
Q

is inter pleural pressure always negative or positive in comparison to atmospheric pressure

A

negative

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59
Q

what does the lung compliance curve measure

A

difference between alveolar pressure and inter pleural pressure

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60
Q

what does opening the glottis do during breathing?

A

stops air flow and allows alveolar pressure to equilibrate and equal atmospheric pressure (usually 0)

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61
Q

lung compliance curve: during maximal expiration with the glottis open what are the Palv, Ppl values and recoil pressure?

A

Palv = 0
Pb = +3
recoil pressure = +3
NB- compliance wants your lungs to expand

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62
Q

lung compliance curve: during end expiration with the glottis open what are the Palv, Ppl values and recoil pressure?

A

Palv = 0
Pb = -5
recoil pressure = +5

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63
Q

lung compliance curve: during peak inspiration with the glottis open what are the Palv, Ppl values and recoil pressure?

A

Palv = 0
ppl = -30
recoil pressure = +30

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64
Q

chest wall compliance: during maximal expiration, closed glottis and relaxed muscles what are the values fro Pbs, Ppl and recoil pressure?

A

Pbs = 0
Ppl = -30
recoil pressure of chest Wall = -30

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65
Q

chest wall compliance: during maximal expiration, open glottis and relaxed muscles what are the values fro Pbs, Ppl and recoil pressure?

A

Pbs= 0
Ppl = -5
recoil pressure = -5

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66
Q

chest wall compliance: during maximal inspiration, closed glottis and relaxed muscles what are the values fro Pbs, Ppl and recoil pressure?

A

Pbs= 0
Ppl = +3
recoil pressure = +3

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67
Q

what is the significance of FRC

A

relaxation point of respiratory system

point when compliance of lung and chest wall cancel each other out

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68
Q

name 3 diseases associated with reduced compliance

A

pulmonary fibrosis
kyphoscoliosis
circumferential burn

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69
Q

what kind of pulmonary disease is emphysema and how does it affect compliance

A
  • Obstructive pulmonary disease

- increases compliance

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70
Q

why does emphysema cause increased compliance ?

A

increases elastic
= less resistance to stretching
= increasing compliance

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71
Q

how does emphysema effect energy store?

A

reduces the amount of energy needed to stretch the lung so reduces the amount of energy stored when we breathe out

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72
Q

what is closing capacity

A

where alveoli begin to collapse

alveoli at base of lung more prone to collapse as don’t always open as purely ventilated

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73
Q

what does surface tension do?

A

minimises surface area of liquid gas interface, pulls water molcules together - tension directed to centre

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74
Q

what is the affect of the phospholipid surfactant in the alveoli

A
  • reduces the surface tension so increases compliance
  • prevents collapse of alveolar in smaller airways
  • increases the number of active alveoli in inspiration (surfactant reduces pressure needed to open alveolar at bottom)
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75
Q

what are the 2 types of cell in alveoli and what are their functions

A

type1 - specialised, gas exchange

type2 - produce surfactant

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76
Q

why can we get respiratory distress syndrome in neonatal

A

type 2 alveoli cells not matures as mature between 24-28 weeks or later

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77
Q

do smaller or larger alveoli have a larger collapsing pressure

A

smaller

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78
Q

how is pressure equalised between alveoli of different size?

A

the same amount of surfactant used
thinner and more spread in larger alveoli
so neither collapses

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79
Q

what is hysteresis

A

the different paths in one cycle compared to another

more pressure is required to inflate the lungs than to deflate them

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80
Q

what are the causes of hysteresis

A
  • reduced compliance of the lung

- airway calibers

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81
Q

in what way does airway calibre have a major impact on laminar flow?

A

size of the radius is inversely proportional to resistance

as lung expands less pressure needed to change volume = change in resistance causes hysteresis

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82
Q

describe the 2 types of airflow that affect change in pressure

A
  • laminar flow

- turbulent flow

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83
Q

what is laminar flow

A

gas particles moving down parallel to each other

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84
Q

what is tubular flow

A

smaller more branching and air not moving parallel and consistently = lots of collisions
- needs more driving pressure than L flow

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85
Q

what is the relationship between flow resistance and cross sectional area

A

promotional

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86
Q

is the total cross sectional area larger in the larger or smaller airways

A

smaller airways

more of the despite being narrower

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87
Q

in the larger airways, what are the features of the bronchiole breathe sounds

A 
hollow 
tubular 
higher pitch 
louder 
distinct pause between inspiration and expiration 
(if this heard in periphery = abnormal)
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88
Q

in the periphery, what are the features of vesicular breathe sounds?

A 
less turbulent flow =more laminar flow 
slower 
less harsh 
soft 
low pitch
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89
Q

what 2 things does a vitalograph measure

A

FVC

FEV1

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90
Q

what is FVC

A

forced vital capacity

volume of air that can be expelled from max inspiration to max expiration

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91
Q

what is FEV1

A

forced expiratory volume in one second

volume of air that can be expelled from max inspiration in the first one second

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92
Q

how does obstructive disease effect FVC and FEV1

A

takes longer to achieve FVC

FEV1 = much less

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93
Q

how can we distinguish between OPD and RPD

A

FEV1/FVC ratio
should be <0.7 for obstructive
and normal or >0.7 for restrictive

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94
Q

what is a Peak Expiratory Flow Rate -PEFR

A

Way of measuring obstruction
only measures expiratory flow rate
patients can use at home for asthma or COPD

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95
Q

how do we distinguish between asthma and COPD

A
  • measurements of FEV1 and PEFR made before and after inhalation of bronchodilator/salbutamol
  • airway constriction =reversible in asthma = improves impressively
  • irreversible airway restriction in COPD = no/little improvement
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96
Q

what’s dynamic airway collapse

A

collapse and narrowing of airway during expiration - no matter hoe hard you expire flow occurs at a predictable expiratory Flow rate

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97
Q

during what 3 points are the airways not collapsed

A

pre-inspiration
during inspiration
end inspiration

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98
Q

how are the airways kept open and not collapsed in pre inspiration

A

Pb = 0 from alveolus
Ppl = -5
Palv = 0
pressure gradient out of airway of +5 keeping airway open

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99
Q

how are the airways kept open and not collapsed in inspiration

A

Pb = 0
Ppl = falls to -7
Palv = -2
outward pressure of +6

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100
Q

how are the airways kept open and not collapsed in end inspiration

A

Pb=0
Ppl = -8
outward pressure of +8

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101
Q

which one does dynamic airway collapse happen and why

A 
forced expiration 
Pb = 0
thoracic pressure = +30
Palv = +38
midpoint of airway = +19
outward pressure. = - 11
causes dynamic airway collapse
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102
Q

what is work of breathing

A
  • work needed to overcome resistive forces
  • the energy used in inspiration used to overcome elastic forces as stored in potential energy which is dissipated in expiration
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103
Q

what 2 forces must we overcome for inspiration

A
  • our chest wall has to overcome force of inertia from elastic forces of tissues
  • frictional/resistive forces of narrow passages - resistance reduces as we expand lungs
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104
Q

why does expiration have low/no energy expenditure?

A

all through natural recoil of elastic tissue of lungs

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105
Q

how does the work of breathing change in severe airway narrowing

A
  • huge amount of energy needed for inspiration and expiration
  • for expiration lungs and chest wall utilise stored energy from inspiration and require additional energy to conclude
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106
Q

how does the work of breathing change in lung stiffness

A

increased work of breathing

reduced compliance so more work needed to overcome elastic forces

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107
Q

how is work of breathing reduced in RPD

A

small rapid breaths in RPD as work very hard for each breath
- when there respiratory rate goes up, cant maintain large volumes and can become exhausted

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108
Q

how is work of breathing reduced in COPD

A

large volumes and slow breathes

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109
Q

What is rate of diffusion proportional to?

A

surface area

pressure gradient

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110
Q

what layers does gas have to cross in the alveoli

A
  • capillary endothelium
  • alveolar epithelium
  • basement layer
  • surfactant layer
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111
Q

what is the pressure gradient of gas exchange dependent on?

A

partial pressures of respective gases in the alveolus and blood

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112
Q

what is the partial pressure of a gas

A

the pressure it would exert if it was the only gas in the container
dependent on the fraction of gas it occupies

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113
Q

what is the % fractional concentration of oxygen,CO2, and nitrogen in the air?

A 
oxygen = 21%
CO2 = 0%
nitrogen = 79%
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114
Q

what is the pp of oxygen,CO2, and nitrogen at sea level?

A 
oxygen = 21.3
CO2= 0
nitrogen = 80
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115
Q

what is the pp of oxygen,CO2, and nitrogen at 5000m altitude?

A 
oxygen = 11.8
CO2 = 0
nitrogen = 44.2
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116
Q

how can low partial pressures of oxygen at high altitudes affect us?

A
  • can run out of breathe faster as less oxygen transported around the body
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117
Q

why is the partial pressure of oxygen lower in the alveoli than in room air

A
  • inspired air is humidified at in upper airway
  • CO2 dilutes gas coming in in alveoli
  • body consumes more oxygen than produces co2 (typically 1.25x)
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118
Q

why is it important to humidify air?

A

as tissues are very moist and we don’t want them to dry up as crisp lungs would perform badly

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119
Q

why do mouth breather often have a dry mouth

A

because air is meant to be humidified in nose , so when humidified through mouth leaves mouth dry

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120
Q

why does the body consume more oxygen than it produces C02

A
  • we need more oxygen to respire fats and proteins compared to carbs = respiratory quotion
  • negative pressure build in body, pulling more oxygen in
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121
Q

what is the pp of water vapour and how does this change the pp of oxygen in fully humidified air ?

A

water vapour = 6.3kPa
101.3(total pp of all gases)-6.3kPa x 0.21(% oxygen in air)
= 19.95kPa

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122
Q

what is the typical value of alveolar pp of CO2

A

5 kPa

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123
Q

if one CO2 molecule was produced for every O2 molecule consumed what would the pp of oxygen be? why is this not the case?

A

19.95(pp O2) - 5 (pp CO2)= 14.95 kPa

because due to respiratory quotation 1.25x O2 molecules consumed for every CO2 = 19.95-6.25 = 13.7 kPa

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124
Q

why does thickening of the diffusion pathway cause major problems?

A

reduces the rate of gas exchange and so oxygen consumption which has a big impact as through normal physiological process we have already reduced the amount of oxygen significantly

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125
Q

does a more soluble gas have a higher or lower PP and why?

A

lower:
dissolves quicker and takes longer to form dynamic equilibrium: more commutable being there so doesnt exert as much pressure to get out

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126
Q

does a less soluble gas have a higher or lower PP and why?

A

higher:

gets to equilibrium faster as wants to get out of solution quicker

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127
Q

why is equilibrium important in pp of gases in solution?

A

once gas gets to equilibrium can exert a pp on the air above solution

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128
Q

does greater or lower solubility mean more molecules can be accommodated for for a given pp?

A

lower solubility

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129
Q

do we use lower or higher solubility gases for anaesthesia and why?

A

lower solubility gases as rapidly equilibrate in lungs and get out of blood to have its effect in the lungs

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130
Q

is CO2 more or less soluble than oxygen?

A

more (x24)

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131
Q

what effect does increased solubility of CO2 have?

A

solution can take more CO2 and release it slower

need a lot more CO2 to exert pp so (that’s why gets into blood more and oxygen gets into tissue faster )

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132
Q

what is the pp gradient of oxygen and CO2 in the lungs?

A

oxygen - 8.3 kPa

CO2 - 6.1 kPa

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133
Q

why does CO2 equilibrate faster in a healthy person at rest?

A

O2 has a much larger diffusion gradient as for the same number of molecules Oxygen has to drop by 8kPa whereas CO2 only needs to drop by 0.8 kPa so oxygen takes longer to equilibrate

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134
Q

what type of respiratory failure is more common in a healthy person at rest and why

A

type 1 as blood only needs 0.8kP of CO2 to release enough molecules to counteract oxygen coming in because its far more soluble

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135
Q

what is type 1 respiratory failure?

A

hypoxia

normal CO2

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136
Q

what is type 2 respiratory failure?

A

hypoxia

hypocarbia

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137
Q

during exercise does CO2 take more or less time to equilibrate?

A

less time as blood moving past capillaries faster and the oxygen diffusion gradient increases to 9kPa

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138
Q

what type of respiratory failure is more common in someone with pulmonary fibrosis and why

A

type 1 as even though gas exchange is slower due to the ticketing of the alveoli, still have enough time to equilibrate CO2 as more soluble

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139
Q

how can we measure the amount of oxygen in capillaries and why do we use this?

A

use Carbon monoxide diffusing capacity

  • Co binds avidly to Hb and not very soluble
  • so can calc how much going in and out of blood cell and diffusion gradient
  • so can work out amount of oxygen taken up by single breathe
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140
Q

what happens to the alveoli in atelectasis and why?

A

alveolar collapse as wall thickens so gas cant get to bottom of alveoli

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141
Q

why do we get alveolar consolidation in pneumonia ?

A

alveolar filled with pus and fuss do gas coming in cannot get to the bottom of the alveoli and so increases diffusion time and gas exchange

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142
Q

what happens to the alveoli pulmonary edema?

A

frothy secretions

longer gas exchange

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143
Q

what happens to the alveoli in interstitial Edema and why?

A

lots of fluid accumulates between alveoli and capillary due to leaking membrane

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144
Q

what happens to the alveoli in emphysema?

A

alveolar -capillary destruction = bad gas exchange

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145
Q

what happens to the alveoli in alveolar fibrosis?

A

thickening of alveolar wall

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146
Q

what happens to the lungs in atelectasis and what is the major cause for this?

A

lungs collapsed and lungs compressed and pushed closed due to fat on chest wall
heavy, obesity

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147
Q

what are the 4 paranasal sinuses?

A

frontal, ethmoidal, sphenoidal and maxillary

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148
Q

what are the role of the sinuses?

A

with turbulent flow viruses and bacteria can be passed into sinuses and immune response ammounted -> runny nose as they empty into nasal cavity

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149
Q

what is the mediastinum?

A

midline region that encloses heart, major vessels and nerves, trachea, oesophagus

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150
Q

how many lobes doe each lung have?

A

right - 3

left - 2

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151
Q

what are the names for the lobes of the lungs?

A

superior, inferior and middle (only in right)

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152
Q

why does the left lung only have two lobes?

A

position of heart means it is taller and narrower

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153
Q

what is the hilum?

A

where the arteries, veins and bronchi enter the lungs

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154
Q

outline the pathway of the conducting portion

A 
trachea
primary bronchi
lobar (secondary) bronchi
segmental (tertiary) bronchi
terminal bronchi
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155
Q

what is the respiratory portion?

A

branching of terminal bronchioles to to respiratory bronchioles and alveolar sacs

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156
Q

how do pulmonary vessels branch?

A

like the bronchi - to lungs, to lobes, to segments

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157
Q

what are the anatomical divisions of the respiratory system?

A

upper respiratory tract and lower respiratory tract

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158
Q

what is the demarcation point of URT and LRT?

A

larynx

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159
Q

what are the functions of the thoracic cage?

A

protection - bony cage around vital organs

respiratory movements - changes in thoracic volume underlie movement of fresh air into lungs and stale air out

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160
Q

how many bones are in the sternum?

A

3

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161
Q

how many planes of movement are there for breathing?

A

3 - vertical, antero-posterior and transvers

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162
Q

what is the function of the diaphragm?

A
  • muscular sheet that closes off thoracic outlet (has apertures to allow passage of structures)
  • comprises radial muscle fibres inserted into central tendon
  • major role in breathing
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163
Q

what is a typical residual volume?

A

70kg male = 1000ml

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164
Q

what is innervation?

A

nerve provides a stimulus to a muscle

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165
Q

what nerves innervate the diaphragm?

A

phrenic nerves - C3,4,5 in neck region

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166
Q

how many muscle layers are in each intercostal space?

A

3 - external, internal and innermost

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167
Q

what comprises the neurovascular bundle?

A

intercostal nerve, intercostal artery and intercostal vein (VAN)

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168
Q

what are pleura?

A
  • 2 membranous sacs that surround each lung

- pleural cavity contains a thin film of liquid to help lungs slide and create surface tension

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169
Q

what is the visceral pleura?

A

membrane in contact with the lungs

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170
Q

what is the parietal pleura?

A

membrane in contact with the thoracic cavity

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171
Q

how can we divide the parietal pleura?

A

cervical - towards the neck
costal - ribs
diaphragmatic - over the diaphragm
mediastinal - towards mediastinum

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172
Q

why is the division of the parietal pleura important?

A

receive sensory innervation from different nerves

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173
Q

what is breathing?

A

the bodily function that leads to ventilation of the lungs

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174
Q

what is ventilation?

A

the process of moving gases in and out of the lungs

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175
Q

what is the mechanics of breathing?

A

describes the structural and physiological bases of ventialtion

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176
Q

what are obstructive conditions?

A

obstruction to flow in airways

- asthma, COPD, lung cancer

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177
Q

what are restrictive conditions?

A

loss of elasticity of lung tissue or thoracic cavity
intrinsic - pulmonary fibrosis
extrinsic - pneumothorax, thoracic skeleton disorders

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178
Q

during inspiration which pressure is larger?

A

atmospheric>alveolar

but atmosphere always = 0 so need to reduce alveolar

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179
Q

during expiration which pressure is larger?

A

alveolar>atmospheric

need to increase alveolar

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180
Q

what is deltaP dependent on?

A

cycle of pressure changes in the chest

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181
Q

what is the relationship between alveolar pressure and thoracic volume?

A

pressure is inversely proportional to volume

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182
Q

during quiet inspiratory breathing what muscles are working?

A

diaphragm (most important)

external intercostals stabilise rib cage

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183
Q

during increased effort inspiratory breathing what muscles are working?

A

diaphragm
external intercostals lift anf expand rib cage
accessory muscles - neck and shoulder girdle

184
Q

during quiet expiratory breathing what muscles are working?

A

elastic recoil of muscles reliant on energy stored by stretching the muscles

185
Q

during increased effort expiratory breathing what muscles are working?

A

internal intercostals

abdominal wall muscles

186
Q

what nerves innervate the intercostal muscles?

A

segmental thoracic nerves

187
Q

What is tonic activity?

A

When a muscle is contracted all the time to maintain muscle tone

188
Q

What is phasic activity?

A

When a muscle contracts at different stages of the respiratory cycle

189
Q

what is the relationship between thoracic cage expansion and pressure on the intrapleaural space?

A

increasing negative pressure exerted

- draws lungs with it and need surface tension of liquid

190
Q

which is higher - alveolar or intrapleural pressure?

A

alveolar

191
Q

what is a pneumothorax?

A

air in pleural space - lung collapses as loss of surface tension in pleural membrane means lung does not move with thoracic wall

192
Q

what is a pleural effusion?

A

fluid forms between pleura and thoracic wall

193
Q

how can we measure the volume of air moving in and out during ventilation?

A

spirometer

194
Q

what is tidal volume?

A

volume fo air moved in or out of the lungs during normal breathing

195
Q

what is a typical tidal volume at rest?

A

6-7 ml/kG

196
Q

what is a typical tidal volume during exercise?

A

15 ml/kg

197
Q

what is inspiratory reserve volume?

A

maximal inspiratory effort from end expiration (ie after a normal expiration take as deep a breath as possible)

198
Q

what is typical inspiratory reserve volume?

A

70 kg male = 3000 ml

199
Q

what is expiratory reserve volume?

A

maximal expiratory effort (after normal inspiration breath out as deeply as possible)

200
Q

what is typical expiratory reserve volume?

A

70 kg male = 1500 ml

201
Q

why does air remain in the lungs after maximal expiration?

A

rigid nature of thorax and the pleural attachments of lungs to chest wall prevent complete emptying

202
Q

what is residual volume and can it be measured by spirometry?

A

volume of air in lungs after maximal expiration

203
Q

what is a typical residual volume?

A

70kg male = 1000ml

204
Q

how many lung volumes are there?

A

4 - tidal, inspiratory reserve, expiratory reserve and residual

205
Q

what is a lung capacity?

A

combination of volumes

206
Q

what is total lung capacity?

A

TV+IRV+ERV+RV

207
Q

what is vital capacity?

A

volume that can be shifted in and out (after maximal inspiration make a maximal expiration)
TV+IRV+ERV

208
Q

what is functional residual capacity?

A

volume of air in lungs after normal breathing

ERV+RV

209
Q

what is a typical vital capacity?

A

70 kg male = 5000ml

210
Q

how do restrictive lung diseases affect lung volumes?

A

reduced RV, FRC, VC and TLC

211
Q

how do obstructive lung diseases affect lung volumes?

A

increased RV
COPD = reduced TLC
emphysema = increased TLC and FRC

212
Q

How is oxygen carried in the blood?

A

Dissolved in blood

Bound to haemoglobin

213
Q

How is the volume of oxygen carried in the blood at 37 degrees calculated?

A

0.0232 x partial pressure of oxygen

214
Q

How many molecules of oxygen can one molecule of haemoglobin carry?

A

4

215
Q

How is the oxygen saturation of haemoglobin calculated?

A

(HbO2) / (HHb + HbO2)

HbO2 = oxygenated haemoglobin
HHb = deoxygenated haemoglobin
216
Q

How is the volume of O2 bound to haemoglobin calculated?

A

SO2 x [Hb] x 1.39

SO2 = oxygen saturation
1.39 = Hüfner constant
217
Q

what are the basic units that control respiratory function ?

A

medulla

pons

218
Q

what feeds into the medulla and pons to act on respiratory function?

A

cerebellum
pituitary
thalamus

219
Q

what are the 4 major centres in the medulla that control breathing ?

A

dorsal respiratory group
ventral respiratory group
Apneustic center
pneuomotaxic center

220
Q

what is the basic respiratory group that is needed to ventilate the lungs?

A

dorsal respiratory group

all the others input into DRG

221
Q

what does the DRG (Dorsal respiratory group) do

A

contains neurones which fire during inspiration

222
Q

what does the VRG (ventral respiratory group) do

A

contains mixed neurones- some which fire during inspiration, some which fire during expiration

223
Q

does the inspiratory nerve activity change during breathing?

A

yes goes up and down

224
Q

does the expiratory nerve activity change during breathing at rest?

A

no as its a passive process at rest

225
Q

does the expiratory nerve activity change during breathing in exercise ?

A

yes as it involves active expiration sue to harder and faster breathing - VRG involved

226
Q

do the VRG and DRG influence each other?

A

yes - negative feedback each other - as VRG fires = inhibits DRG and visa versa

227
Q

how is VRG involved in expiration

A
  • activation of internal intercostal muscles on expiration = increased rate of expiration = shrinks thoracic wall = air out faster
228
Q

what does the apneustic centre do?

A

stimulates inspiratory neurones - kicks in when you need to. breathe harder

229
Q

what does the pneuomotaxic centre do?

A

inhibits inspiratory neurones

230
Q

how can inspiratory activity be depressed?

A

hypoxia
therapeutic drugs
inhibition of blood supply

231
Q

what has voluntary control over breathing and where is this located?

A

higher brain centres

in cerebral cortex

232
Q

what kind of stimuli act through hypothalamus?

A

pain and emotional stimuli

233
Q

where are stretch receptors located ?

A

in the lungs

234
Q

where are irritant and cough receptors located

A
  • lungs - throughout airways
  • upper airways
  • nose
235
Q

what do chemo receptors do?

A

stimulate breathing

236
Q

what are the 2 higher brain centre influences ?

A

cortical and hypothalamic

237
Q

what does the cortical centre of the higher brain centre influence control ?

A
  • voluntary hyperventilation > hypocapnia > alkalosis

- voluntary breath holding > hypoxia > unsustainable

238
Q

what does the hypothalamic centre of the higher brain centre influence control ?

A
  • emotions >anger, anxiety >hyperventilation

- sensory reflexes > pain, cold > gasping (use up oxygen reserves in lungs), hyperventilation

239
Q

why does alkalosis happen in hyperventilation?

A

breathe off more CO2

= drop in carbonic acid

240
Q

what is the function of the pulmonary stretch receptor?

A

prevents over expansion of lungs and so damage

241
Q

how do pulmonary stretch receptors communicate info to medulla?

A

afferent fibres fro smooth muscle of bronchi and trachea run in vagus nerve to respiratory centre in medulla

242
Q

do the lungs ever expand to their full potential?

A

no - confounded by thoracic wall = prevents damage

243
Q

when inspiration progresses what impulse do we get from VRG, DRG?

A

more impulses from VRG

less impulse from drug

244
Q

what is the hering-Breuer lung inflation reflex?

A

limits breathing frequency (f) x tidal volume (VT)

245
Q

how do irritant and cough receptors send information to medulla?

A

afferent fibres from these receptors run in vagus nerve and into repository centre - parasympathetic pathway (not much control over this)

246
Q

what do stimulation of these irritant receptors result in?

A

leads to hyperpnoea/deep inhalation and airway constriction = explosive cough and may contribute to sneeze

247
Q

where muscles are rich in muscle fibres?

A

diaphragm

intercostals

248
Q

how are muscle/joint receptors and proprioreceptors activated?

A

by stretch associated with contraction of breathing

NB- increased activation in excersise to

249
Q

how can proprioreceptors influence ventilation?

A

relay info about activity induced motion which can influence ventilation
- feedback from excersise = breathe harder

250
Q

what stimulus do baroreceptors respond to?

A

BP

251
Q

what influence do baroreceptors have?

A

can influence ventilation

- increase BP= decrease ventilation- visa era

252
Q

why may we get a drop in BP during moderate exercise?

A

veins and arteries open up for more blood flow

may increase ventilation

253
Q

what are J receptors and where are they located?

A

juxtacapillary

lie close to capillaries around alveolar walls

254
Q

what activates J receptors?

A

traumas:

  • pulmonary oedema
  • inflammatory agents
  • pneumonia
255
Q

what does the activation of J receptors cause?

A

increases ventilation - breathe harder

256
Q

what are the 2 types of chemoreceptors?

A

central and peripheral chemoreceptors

257
Q

where are central chemoreceptors found ?

A

specialised regions close to medulla respiratory centres

also close to rich blood supply

258
Q

what are central chemoreceptors sensitive to?

A

CO2 and H+

pick up from ventral surface of medulla

259
Q

is the CO2 sensor of the central chemoreceptor a direct or indirect sensor and why

A

indirect

CO2 dissolves out of capillary into CSF and combines with water = carbonic acid = dissociated into H+ and bicarb

260
Q

what affect does H+ ions on the central surface of medulla have on the chemorecpetor?

A

feeds this into medullary respiratory centre and increase respiratory rate/ventialtion and tidal volume

261
Q

what does a rise in CO2 or [H+] cause

A

fall in pH= acidosis
stimulates the central chemoreceptors
increases ventilation

262
Q

can both H+ and CO2 cross blood brain barrier?

A

no only CO2 not acid

263
Q

does the central chemoreceptor respond to metabolic acidosis and if not what does?

A

no as this is will be a lactate or bacterial event, not CO2 related
this will be picked up by peripheral chemoreceptors

264
Q

where are the peripheral chemoreceptors located?

A

carotid and aortic bodies

265
Q

what are peripheral chemoreceptors sensitive to?

A

hypoxia, hypercarbia and acidosis

266
Q

how do peripheral chemoreceptors send information to respiratory center in the medulla?

A

sensation at peripheral chemo receptor feeds in from sensory afferent (glossopharyngeal nerve or vagus nerve) and into respiratory centre

267
Q

what stimulus does the gloms cell respond to and how does it send this info to the respiratory centre in the medulla

A

po2 or CO2 or acidity to signal which then goes along afferent nerve and stimulates medullary centre for respiratory control

268
Q

what is the primary sensor for hypoxia

A

glomus cell

269
Q

how does hypoxia trigger the gloms cell and how does this cause excitation of the nerve ?

A
  • triggers Ca2+ influx into glomus cells via depolarization

- Ca2+ triggers release of transmitters which initiate action potentials in the afferent nerve

270
Q

which NTs are released from glomus cella= and which ones causing w e excitation of the nerve

A

dopamine, ATP, acetylcholine

ATP and acetylcholine cause excitation of the nerve

271
Q

In the lung what structure does the endoderm form

A

Epithelial linning of lungs

‘C’ shape trachea

272
Q

In the lung what structure does the mesoderm form

A

Connective structures, eg. Trachea, cartilage smooth muscle

273
Q

What is the respiratory divaticulum, where does it appear and what will it form

A

Apouchlikestructurethat appears in ventral wall of foregut and will form respiratory system- the lung buds-trachea and larynx

274
Q

At what stage does the respiratory divaticulum start growing and in what direction

A

Day 22

Grows venterocaudally

275
Q

How does the respiratory divaticulum Seperate from the foregut and what structure is exempt from this separation

A

Tracheosophageal ridges develop and meet and so Seperate

Laryngeal inlet is exempt

276
Q

What do the lung buds go onto form

A

Develop centrally + causally to form bronchioles

277
Q

What is a fistula

A

Abnormal communication between trachea toesophagus

278
Q

Why do we get fistula’s

A

Incomplete division of foregut into oesophageal and respiratory portions

279
Q

What is the main abnormality associated with tracheoosophageal fistuals

A

Esophageal atresia (closed /absent)

280
Q

What are the main problems with an oesopnageal fistula

A

Abdomen distension as stomach can fill with air

Stomach contents can go back up into the trachea-enzymes and acid respiratory not adapted to or food

281
Q

What are the signs associated with oesophageal fistula

A

Baby choking

Infection from food in trachea

282
Q

What is a h-type traceoospnageal fistula

A

Abnormal connection between desopnagous and

Trachea

283
Q

In a h-type TOF what is a common problem and why

A

Infection as due to the force of gravity breast milk more likely end up in respiratory system than oesophagus

284
Q

What other congenital malformations are associated with TOF (acronym)

A 
V- vertebral defects
A-anal atresia
C-cardiac defects
T-tracheosophageal fistula
E-Eosophageal atresia
R-renal abnormalities
L- limb defects
285
Q

What lines the respiratory divaticulum as it matures

A

Overlying mesoderm

286
Q

What tissue forms the capillaries

A

Visceral mesoderm

287
Q

What drives branching of respiratory divaticulum

A

Signalling between mesoderm + endoderm

288
Q

During week 5 and 6 what do the primary bronchiole form.

A

Main bronchi secondary bronchi (3r, 2l)

6th week-ternary bronchi

289
Q

What do the tertiary bronchi supply

A

Bronchopulmonary segment

290
Q

What is the final branching of respiratory system

A

Terminal bronchiole and respiratory bronchiole in week 16

291
Q

When do the first alveoli develop

A

36 weeks

292
Q

What is pulmonary agenesis

A

Longs fail to form as lung buds fail to Seperate

293
Q

What are the 2 types of pulmonary agenesis

A

Unilateral (one lung missing) or bilateral

294
Q

What pulmonary agenesis Is incompatible with life

A

Bilateral

295
Q

What are the problems caused by unilateral pulmonary agenesis

A

Respiratory distress

lower respiratory tract infection

296
Q

What is pulmonary hypoplasia

A

All components present but not developed properly

297
Q

What is pulmonary hypoplasia found in association with and what does it cause

A

Congenital diaphragmatic hernia

Intestinal contents petruded into thorax

298
Q

What are the 4 stages of lung maturation

A

Pseudoglandular
Canalicular
Saccular / terminal sac
Alveolar

299
Q

What point does Pseudoglandular stage a take place and what happens

A

5-7 weeks-branching of respiratory tree to form terminal bronchiole

300
Q

Is respiration possible in Pseudoglandular phase

A

No only connective tissues formed

301
Q

What point does Canalicuiar stage take place and what happens

A

16-25 weeks
Respiratory bronchiole formed and give rise to alveolar ducts
Mesodermal tissue becomes highly specialised

302
Q

What point does terminal sac stage take place and what happens

A 
26-birth weeks
 further development of alveoli
Epithelium thins
Capillaries come into contact with epithelium
Blood air-barrier formed
303
Q

What 2 types of cell do the epithelium give rise to

A

Type 1 pneumocytes - for gases exchange

Type 2 pneumocytes - recreate surfactants

304
Q

Can a premature feotus of befor 25 weeks survive

A

Given intensive care
Dependent on amount of surfactant
May suffer respiratory distress

305
Q

When does the alveolar period stop

A

Age 10

95% develop after birth

306
Q

What are the treatments used for insufficient surfactant of baby

A

Glococortitoid - to mother

surfactant therapy temporary to baby

307
Q

What are the two states of haemoglobin?

A

Relaxed state - the oxygen binding sites in a crevice are easier to access
Tense state - the oxygen binding site is harder to access and oxygen molecules are pushed out

308
Q

Why is haemoglobin described as being cooperative?

A

When one molecule of haemoglobin it alters the tertiary structure of the protein, making it easier for further molecules of oxygen to bind.

Ie once one molecule of oxygen binds, the affinity of haemoglobin to oxygen increases.

309
Q

What is the structure of haemoglobin?

A

4 protein chains - 2 alpha and 2 beta

4 haem groups based around an iron ion (Fe2+). This means one molecule of haemoglobin can bind 4 molecules of oxygen.

141-146 amino acids per chain

310
Q

How can the cooperativity of haemoglobin be demonstrated?

A

Oxygen dissociation curve has a sigmoid (S) shape

311
Q

What factors affect the oxygen dissociation curve?

A

pH
Temperature
Level of 2,3 diphosphoglycerate

312
Q

How does pH affect the oxygen dissociation curve?

A 
Increased = shifts left
Decreased = shifts right
313
Q

How does temperature affect the oxygen dissociation curve?

A 
Increased = shifts left
Decreased = shifts right
314
Q

How does 2,3 diphosphoglycerate affect the oxygen dissociation curve?

A 
Decreased = left shift 
Increased = right shift
315
Q

What is P50?

A

When the oxygen saturation is 50%.

316
Q

What is the PO2 and SO2 of arterial blood?

A

PO2: 12.5 kPa
SO2: 97%

317
Q

What is the PO2 and SO2 of venous blood?

A 
PO2 = 6.3 kPa
SO2 = 75%
318
Q

What is the PO2 and SO2 at P50?

A 
PO2 = 3.5 kPa (normally)
SO2 = 50%
319
Q

What are examples of haemoglobin abnormalities?

A
  • absent globin chain in thalassemia
  • defective globin chain in HbS (sickle cell disease)
  • defective Fe atom in methaemoglobin
  • wrong ligand in CO Hb
320
Q

Why are buffers important?

A

Proteins in the body’s cells are extremely pH sensitive. If the cell is not at the correct pH, it will stop functioning. Therefore, buffers exist to compensate for any change in pH.

321
Q

What is a buffer?

A

A buffer is a solution that can minimise changes in the free H+ conc and so the pH

They are usually weak acids dissolved in solution.

322
Q

How do you calculate pH?

A

pH = -log10[H+]

323
Q

What are examples of buffers in the blood?

A

Proteins (carboxyl and amine groups on end of the chain)
Basic/acidic side chains of amino acids

Specific examples include plasma proteins, haemoglobin, bicarbonate and phosphate

324
Q

what is present within the lamina propria of the olfactory mucosa?

A
  • lymphatic vessels
  • unmyelinated olfactory nerves
  • myelinated nerves
  • olfactory glands
325
Q

When is haemoglobin a more effective buffer?

A

When it loses oxygen

326
Q

How is carbon dioxide carried in the blood?

A
  • dissolved in blood
  • as carboamino compounds
  • as carbonic acid/bicarbonate
327
Q

What is the concentration of CO2 in the blood at 37 degrees?

A

3 ml per dl of blood

328
Q

How is CO2 carried in the blood as carboamino compounds?

A

Bound to R-NH2 groups on proteins eg terminal amino acids and side chains of lysine and arginine

329
Q

What concentration of CO2 does carriage by carboamino compounds account for?

A

4ml per dl of blood

330
Q

What concentration of CO2 in blood does the carriage as carbonic acid/bicarbonate account for?

A

45 ml of per dl of blood

331
Q

How is carbon dioxide converted into carbonic acid?

A

Reaction with water catalysed by carbonic anhydrase

332
Q

What is the hamburger shift?

A

A HCO3- ion is pumped out of the red cell in exchange of a chloride ion

333
Q

What is the Haldane effect?

A

The ability of deoxygenated blood to carry more CO2 than oxygenated blood

334
Q

What is the Henderson-Hasselbach equation?

A

pH = pK + log10([HCO3-]/[CO2])

335
Q

How does the respiratory system compensate to maintain the acid base balance?

A

The blood pH regulates ventilation and so controls PCO2

This is a rapid response

336
Q

How does the renal system compensate to maintain the acid base balance?

A

Excretion of H+ in urine controlled by pH

This is a slow response

337
Q

What is alkalosis?

A

An increased pH

338
Q

What happens in respiratory alkalosis?

A

Decreased PCO2

Normal [HCO3-]

339
Q

What is respiratory alkalosis a result of?

A

Hyperventilation eg due to allergy or iatrogenesis

340
Q

What happens in metabolic alkalosis?

A

Normal PCO2

Increased [HCO3-]

341
Q

What causes metabolic alkalosis?

A

Abuse of antacid remedies which causes the body to rid itself of H+ by vomiting

342
Q

What is acidosis?

A

A decrease in pH

343
Q

What happens in respiratory acidosis?

A

Increased PCO2

Increased [HCO3-]

344
Q

What causes respiratory acidosis?

A

Ventilatory failure

345
Q

What happens in metabolic acidosis?

A

Decreased PCO2

Decreased [HCO3-]

346
Q

What causes metabolic acidosis?

A

Renal failure such as diabetes, ketoacidosis or shock (tissue perfusion)

347
Q

why is it important to cough

A
  • protective mechanism
348
Q

what is the most common symptom of respiratory disease?

A

cough

349
Q

what is a useless cough? in what diseases do we see them? should it be suppressed?

A
  • persistant and unproductive - dry cough
  • asthma, oesophageal reflux, sinusitis
  • yes - use suppressants = antitussives
350
Q

what is a useful cough? in what diseases do we see them? should it be suppressed?

A
  • expels secretions, produce sputum
  • chest infections
  • shouldn’t be suppressed
351
Q

is there an exception where a useful cough can be suppressed

A

yes if its exhausting and dangerous

352
Q

highlight the steps in the stimulation of a cough

A
  • cough receptors or lung irritant receptors respond to chemical and mechanical stimulation/forgein bodies in upper airways
  • send info via afferent pathways to cough centre in medulla
  • vagal stimulation initiates cough reflex to muscles involved
353
Q

how do dry cough- cough suppressants effect the afferent side?

A

reduce the stimuli - stimulate tracheal epithelium to produce more mucous and form a protective layer around the larynx

354
Q

how do dry cough- cough suppressants effect the efferent side?

A
  • suppress it through the medullary cough centre

- use antitussives

355
Q

which dry cough- cough suppressants do we use for: above larynx and below larynx?

A
  • above the larynx- Linctuses (cough syrup)

- below the larynx - steam inhalation (increase mucous secretion)

356
Q

what antitussives do we use, how effective are they? give examples of some of the drugs for these

A
  • opiods: very effective- in cough syrups –> codeine, methadone, pholcodeine
  • non opiods: less respiratory depression compared to codeine–> dextromethorphan
    sedatives: dont effect cough, make secretions thicker –> diphenhydramine
357
Q

for a productive cough what are the 2 categories of drugs we use and what are there effects ?

A
  • expectorants –> increase volume of secretion (remove mucous more often)
  • mucolutics –> decrease viscosity so easier for cilia to clear ( break disulphide bonds in mucous
358
Q

what is the most common symptom complaint in OPD?

A

chronic cough

359
Q

what are the common causes for a chronic cough?

A
  • upper airways cough syndrome (post nasal drip/ nasal decongestiers)
  • bronchial asthma (most in morning)
  • COPD
  • gastroesophageal reflux disease
360
Q

what are the 3 main factors associated with chronic lung disease and what are their effects ?

A
  • inflammation of airway lining = swelling of airway = narrowing of lumen
  • bronchoconstriction = constriction of smooth muscle lining airway = further narrowing
  • secretions = form mucus plugs, decreasing diameter of lumen
361
Q

what are the 4 different types of bronchial asthma?

A
  • asthma associated with allergies reactions (type 1 hypersensitivity)
  • asthma not associated with specific allergen (intrinsic asthma)
  • exercise induced asthma
  • asthma associated with COPD
362
Q

highlight the steps involved in allergen mediated asthma which leads to bronchoconstriction

A
  • exposure of antigen to APC
  • IgE production from B cell
  • Mast cell activation
    -release of mediators
    = bronchoconstriction
363
Q

what are the main things we can target to treat asthma?

A
  • prevention of Ag:Ab reaction (avoidance of antigen)
  • dilation of narrowed bronchi
  • prevention of release of transmitter (mast cell stabilisers)
  • antagonism of released transmitter (leukotriene receptor antagnosis’s)
  • non specific reduction of bronchial hypersensitivity (when antigen arrives at bronchial epithelium does not reach with antigen same way)
364
Q

what are the main ways we prevent AG:Ab reaction?

A
  • avoidance of allergen

- avoidance of tobacco/ weight reduction

365
Q

what are the 2 main ways we reduce bronchial hypersensitivity non specifically?

A

1) corticosteroids –> anti-inflammatory

2) reduced bronchial reactivity

366
Q

how do anti inflammatory’s work?

A
  • inhibition of influx of inflammatory cells after exposure
  • reduced micro vascular leakage: decreased oedema
    inhibition of release of mediators. ie. cytokines/APC
  • inhibition of cycloxygenase enzyme = decrease production of prostaglandins
367
Q

does non specific mechanism of reduced bronchial reactivity relax bronchiole smooth muscle?

A

no as it is has already been constricted therefore has no role in asthmatic attack and just decreases exasperation’s

368
Q

what drug is contained in the brown inhaler

A

inhaled corticosteroids

369
Q

what kind of asthma severity are the inhaled corticosteroids useful for?

A
  • first line regular therapy: mild to moderate asthma

- not useful in severe asthma/asthma attack

370
Q

what kind of asthma severity are the oral corticosteroids useful for?

A

severe asthma

371
Q

what are the adverse side effects of corticosteroids

A
  • iatrogenic Cushing’s syndrome (diabetes, hypertension, peptic ulcer, psychosis, delayed puberty)
  • inhibition of hypothalamic pituitary axis
  • oropharyngeal candidiasis (fungal infection of mucous membrane of mouth)
  • hoarseness- direct effect on vocal chords
372
Q

how are the risks of corticosteroids reduced?

A
  • inhalation route
  • administration in early morning
  • gargle and spit after every treatment: reduce oropharyngeal candidiasis and hoarseness
  • cyclesonide: prodrug (only activated in bronchial epithelium)+ when absorbed tightly bound to proteins and so little effect elsewhere/side effects
373
Q

what are mast cell stabilisers, how are they admitted and what are their effects on bronchial smooth muscle?

A
  • inhibit release of mast cell mediators
  • inhalation (poorly absorbed)- only valuable if taken prophylactically
  • no effect on bronchial smooth muscle = no use in acute bronchospasm as cant do anything against mediators already released
374
Q

what are the main uses of mast cell stabilisers?

A

allergic rhinitis, allergic conjunctivitis

375
Q

what are the side effects of mast cell stabilisers?

A

throat irritation, cough (due to left over drugs in mouth), dermatitis, myositis, gastroenteritis

376
Q

what are the 2 leukotriene pathway inhibitors and what do they inhibit?

A

1) leukotriene synthesis inhibitors –> inhibit enzyme 5 lipoxygenase cycloxygenase
2) leukotriene receptor antagonists –> impair binding of already formed leukor=trine

377
Q

give and example of leukotriene synthesis inhibitor and receptor inhibitor drugs. which has been discontinued and why?

A
  • inhibitors of leukotriene synthesis- Zileuton: discontinued due to liver toxicity
  • inhibitors of leukotriene receptors - montelukast, zafirlukast
378
Q

how are leukotriene receptor antagonists administered and what are they effective in?

A
  • given orally
  • allergen induced asthma and exercise ionic asthma -= reduce frequency of exacerbations
  • not effective in acute asthma
379
Q

what are the side effects of leukotriene receptor antagonists?

A

headaches, gastritis, flu-like symptoms

380
Q

what is control of bronchial tone dependent on?

A

muscle tone of smooth muscle present in walls of bronchi

381
Q

what are the 3 drugs that promote bronchodilator and what do they act on?

A
  • beta agonists –> increase adenylcylase = increase cAMP
  • Theophyline –> inhibit PDE enzyme AND inhibit Adenosine action
  • Muscarinic antagonists –> acetylcholine inhibition
382
Q

What do the blue inhalers consist of ?

A

sympathomimetic agents

383
Q

how do sympathomimetic agents act and what are the 2 classes?

A

via B2 adrenoreceptors

  • selective B2 agonist agents
  • non selective
384
Q

what are the 2 different types of selective B2 agonist agents? give examples of some of these 2 types of drugs

A
  • short acting (3-6hrs)- SABA: salbutamol, terbutaline

- long acting (12-24hrs)- LABA: salmetrol, foametrol

385
Q

give an example of a non selective B2 agonist agent drug

A

adrenaline - used in emergency (as given as subcutaneous injection)

386
Q

what is the most commonly used sympathomimetic agent? how is it administered?

A

salbutamol

inhalation, nebulisation, oral or intravenous

387
Q

are selective or non selective B2 agonists considered 1st line of therapy? what does this mean?

A

selective

have direct affect on smooth muscle-immeidate onset

388
Q

what are the side effects of using selective B2 agonists ? why do we get these side effects?

A
  • heart palpitations, tachycardia, cardiac arrhythmias
  • muscle tremor
    restlessness
  • nervousness
    = due to there being B2 receptors in the heart, muscle and other tissues
389
Q

how do methylxanthines work (what do they inhibit)?

A

inhibit action of:

  • PDE- phosphodiesterase
  • Adenosine
390
Q

how are methylxanthines administered?

A

orally

intravenously

391
Q

what are the adverse effects of methylxanthines?

A
  • palpitations
  • cardiac arthymias
  • hypotension
  • gastrointestinal irritation ( increased acid production)
  • diuresis
  • anxiety
  • headaches
  • seizures
392
Q

what are the two different types of methylxanthines, how are they administered and how are they activated in the body?

A
  • theophylline –> oral, metabolised (saturable metabolism- plasma conc rises rapidly after metabolised), rapid and complete absorption
  • aminophylline –> intravenous, loading dose then leads to infusion
393
Q

how do anticholinergic agents act and what does this cause?

A

inhibiting muscarinic receptors -M3 (subtype of acetylcholine receptors)
inhibit effects of vagus nerve stimulation

394
Q

what are the 2 catogories of muscarinic antagonist agents? give an example of a drug for these

A
  • LAMA- long acting Muscarinic Antagonists
  • selective muscarinic antagonist agents
  • tiotropium - both selective and LAMA
395
Q

what colour inhaler are anticholinergics in what a what are they used for?

A

blue inhaler

- acute severe asthma (COPD)

396
Q

what are the adverse effects of anticholingerics?

A
  • airway irritation
  • anticholingeric effects
  • GI upset
  • urinary retention
397
Q

what can we use to inhibit binding of IgE to mast cells? what is the downside to this method?

A

Anti IgE monoclonal antibody - Omalizumab

V expensive

398
Q

what kind of therapy we use to reduce the production and survival eosinophils? what is the downside to this method?

A

Anti-IL-5 monoclonal antibody

V expensive

399
Q

why do we use Mg in patients who fail to respond to inhaled bronchodilators? why does this work? how do we administer this?

A

intravenous infusion

  • Mg has direct action
  • not specific to bronchi smooth muscle, effects all of the muscles
400
Q

in what severity of asthma do we use ketamine and why?

A

sevre life threatening asthma

has bronchodilator properties

401
Q

in newly diagnosed asthmatic patients what are the drug recommendations? what do we use if this method does not control?

A
  • newly diagnosed: short acting B2 agonist- SABA
  • then… low dose Inhaled corticosteroid/ICS
  • if still uncontrolled… LABA and ICS inhaler therapy
402
Q

how does a tension pneumothorax form?

A
  • tissue where the injury is forms sort of valve, allowing air to enter pleural space but prevents its escape
403
Q

what happens in a tension pneumothorax

A

valve created = progressive build up of air within pleural space = air can escape into pleural space but not return back = progressive build up of pressure in pleural space = pushes mediastinum to opposite side = results in obstruction to venous return to heart = affects BP and CO2 = life threatening

404
Q

symptoms of tension pneumothorax

A
  • chest pain
  • chest wall tenderness
  • breathlessness
  • dizzy/ lightheaded (as bP low)
405
Q

signs of tension pneumothorax

A
  • tachypnoea = breathing fast
  • localised bruising
  • tenderness over ribs (some may be broken)
  • trachea deviated away from pneumothorax - to left
  • surgical emphysema
  • decreased expansion
  • increased percussion note (empty drum sounds)
  • decreased breathe sounds
  • raised central venous pressure
406
Q

what is surgical emphysema ?

A
  • air traps under skin in connective tissue = swelling
407
Q

procedure for tension pneumothorax?

A
  • put chest drain in ( relives pressure = lung expands)

- if no chest drain = use needle

408
Q

in who does the risk of a tension pneumothorax recurrence increase? when does this risk of recurrence normally go down in an average person?

A
  • those with co -existing lung conditions

- risk doesn’t significantly decrease until one year later

409
Q

what are the risk factors for a primary spontaneous pneumothorax?

A
  • smoking

- fam history

410
Q

what are the risk factors for a secondary spontaneous pneumothorax?

A
  • COPD
  • CF
    ect.
411
Q

what do spontaneous pneumothorax’s arise from?

A

rupture of small sub-pleural bebs = weaknesses in actual lung

412
Q

what is the risk of recurrence after 1st and 2nd spontaneous pneumothorax?

A
  • after 1st = 10%

- after 2nd + 40%

413
Q

what 2 regions is the nasal cavity divided into?

A

respiratory region

olfactory region

414
Q

what type of mucosa lines the respiratory and olfactory regions of the nasal cavity?

A

respiratory mucosa

olfactory mucosa

415
Q

what does the olfactory mucosa consist of?

A

lamina propria

olfactory epithelium

416
Q

what type of epithelial cells are the olfactory epithelium

A

pseudo-stratified columnar epithelium

417
Q

what do the olfactory epithelium consist of?

A
  • olfactory receptor cells
  • sustentacular (supporting) cells
  • basal cells
418
Q

what are bowman’s glands and what do they secrete ? why is this secretion useful

A

branched tubulalveolar serous glands which secrete protein rich mucous onto olfactory surface via ducts - acting as solvent for scent molecules in inspired air

419
Q

what kind of epithelium is the nasopharynx lined with?

A

pseudo-stratified columnar epithelium

420
Q

what kind of epithelium is the oropharynx and laryngopharynx lined with? why is this type of epithelium advantageous?

A
  • non-keratinised stratified squamous epithelium
  • as oro and laryngopharyx ahem are shared passages for air, food and water multiple layers of flat cells means the epithelium can withstand the loss of the superficial layer without damage to the integrity of the epithelial layer
421
Q

what 2 types of epithelium line the larynx ? where are these epithelium in the larynx and does the location explain their structure?

A
  • stratified squamous epithelium - overlying vocal folds = subject to extreme vibrations = adapted to cope with attrition of its surface
  • pseudo-stratified ciliated columnar epithelium= above vocal folds = not have to cope with attrition to surface
422
Q

what is ventilation?

A

movement of gases in and out of the lungs through the airways (L/min)

423
Q

what is perfusion?

A

blood flow through blood vessels through any organ (mL/min)

424
Q

in which area of the lung are the alveoli largest?

A

apical alveoli 4 times larger than basal due to gravity

425
Q

which alveoli can expand more?

A

basal alveoli (think of slinky)

426
Q

which region of the lung has better ventilation?

A

basal

427
Q

what is the functional supply of pulmonary circulation?

A

oxygenation of venous blood - main blood supply to the lungs

428
Q

what is the structural supply of pulmonary circulation?

A

nutrition to the lung (also bronchial circulation)
bronchial artery from thoracic aorta
2% of cardiac output

429
Q

is pulmonary circulation at lower of higher pressure compared to systemic circulation?

A

very low pressure

walls are thinner with less elastic tissue and muscles but can stretch to hold lots of blood

430
Q

what are extra-alveolar vessels?

A

pulmonary artery splits into smaller branches following division of airway - extra-alveolar are in the lung parenchyma

431
Q

where does gas exchange start?

A

smaller arterioles/ bronchioles

432
Q

how many pulmonary veins are formed from the pulmonary venules?

A

4

433
Q

how is perfusion in the lungs affected by emphysema?

A

widespread destruction and dilation of distal airway
regional destruction of vascular beds
poor gas exchange and hypoxia

434
Q

where is the highest hydrostatic pressure in the lungs?

A

basal - fastest flow

435
Q

how is the diameter of extra-alveolar vessels controlled?

A

affected by lung volume and pull of lung parenchyma

436
Q

what is starlings resistor?

A

a sealed box with a rigid tube entering (P us) and exiting it (P ds), with a collapsible segment inside (P out)

437
Q

would there be flow when Pout>Pus>Pds?

A

no as P us < P out so the collapsable segment is compressed

438
Q

would there be flow when Pus>Pout>Pds?

A

yes as Pus>Pout, but still a little bit of compression of collapsable segment

439
Q

would there be flow when Pus>Pout

A

yes as Pus>Pout - less compression of collapsible segment due to larger Pds

440
Q

when applying starlings resistor to the lungs, what would each bit represent?

A

Upstream tube = P aterial (hydrostatic pressure at end of capillary)
Pressure in box = P alveolar (gaseous pressure inside)
Downstream tube = P venous
Collapsible segment = alveolar vessel

441
Q

what happens in zone 1 of the lungs?

A

towards the top (very small area in healthy people)

  • alveolar dead space
  • good ventilation but no perfusion as blood vessels collapse
442
Q

what are the differences in pressure in zone 1?

A

P alveolar> P arterial> P venous

443
Q

what happens in zone 2 of the lungs?

A

recruitment zone - lower down the lung

  • higher P arterial due to higher hydrostatic pressure
  • recruitment of more alveolar unit especially in systole
444
Q

what are the differences in pressure in zone 2?

A

P arterial> P alveolar> P venous

445
Q

what change in pressure does a haemorrhage cause?

A

drop in P arterial –> lower than P alveolar

446
Q

what change in pressure does positive pressure ventilation cause?

A

rise in P alveolar –> higher than P arterial

447
Q

what happens in zone 3 of the lungs?

A

distension zone - lung bases

  • hydrostatic forces raise P arterial and P venous above P alveolar
  • continuous blood flow, determines by difference in P arterial and P venous
448
Q

what is the differences in pressure in zone 3?

A

P arterial> P venous> P alveolar

449
Q

what is the ventilation perfusion mismatch?

A

V/Q ratio - ideally would be 1 as ventilation and perfusion are equal
varies from 3.3 at apex to 0.6 at base

450
Q

what is a normal average V/Q ratio?

A

0.8

451
Q

what is dead space and its V/Q?

A

Part of each breath that does not participate in gas exchange

  • good ventilation
  • no/ poor perfusion
  • V/Q is infinite or very high
452
Q

what is physiological dead space equal to?

A

anatomic dead space + alveolar dead space

453
Q

what is anatomic dead space?

A

conducting airways where no gas exchange takes place

454
Q

what is alveolar dead space?

A

unperfused or poorly perfused alveoli

455
Q

what is a pulmonary embolism and its effect on dead space?

A

blood clot from deep veins travels to pulmonary arteries

  • causes severe hypoxia
  • lack of blood supply to that part of lung
  • enlarged alveolar dead space
456
Q

what is a shunt?

A

deoxygentaed blood reaching left side of the heart by bypassing lungs or failing to get oxygenated
- eg in pneumothorax or with age

457
Q

what is the V/Q of a shunt?

A

no/poor ventilation
good perfusion
V/Q = 0 or very low

year 1 flash cards (23 decks)

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