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My ESA 3 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

How many airway divisions are there?

A

23

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2
Q

Which are the conducting airway divisions?

A

1-16

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3
Q

Which airway divisions are the respiratory zone?

A

17-23

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4
Q

Define partial pressure of a gas

A

The individual pressure exerted independently by that gas within a mixture. (Each pressure is equal to the pressure it would exert if it were the only gas present)

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5
Q

What determines how much of a gas dissolves in a liquid?

A

The amount of gas dissolved in a liquid is proportional to the pressure of the gas in contact with the liquid

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6
Q

How is partial pressure in alveolar air different to atmospheric air?

A 
More water vapour 
Less O2 (constantly leaving)
More CO2 (constantly entering)
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7
Q

What is the pO2 in capillary blood?

A

13.3KPa

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8
Q

What is the pCO2 in capillary blood?

A

5.3KPa

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9
Q

What is the pO2 in interstitial fluid?

A

6KPa

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10
Q

What is the pCO2 in interstitial fluid?

A

6KPa

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11
Q

What lines the conducting portion of the respiratory tract?

A

Mucous membrane (mucus secreting cells)

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12
Q

Where in the respiratory system are serous membranes found?

A

Lining the pleural sacs that envelope each lung

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13
Q

What are the smallest branches of the conducting portion of the conducting system called?

A

Terminal bronchioles

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14
Q

What histiological cells are in the majority of the conducting portion of the respiratory system?

A

Pseudostratified epithelium with cilia and goblet cells

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15
Q

What hisiological cells are in the terminal bronchioles, and what portion of the respiratory system are they a part of?

A

Simple columnar epithelium with cilia and Clara cells (but no goblet cells)
Conducting portion

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16
Q

What type of cells are in the respiratory portion of the respiratory system, minus alveoli?

A

Simple cuboidal epithelium with Clara cells. Few sparse cilia.
(Respiratory bronchioles and alveolar ducts)

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17
Q

What type of cells are in the alveoli?

A

Simple squamous, types 1 & 2

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18
Q

How do Venus plexuses avoid overdrying?

A

Swell every 20-30mins, alternating airflow thus preventing over drying. Patence maintained by surrounding cartilage/bone.

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19
Q

What is the olfactory system?

A

Your sense of smell

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20
Q

What does the olfactory system look like histiologically?

A

Particularly thick pseudostratified columnar epithelium, without goblet cells.

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21
Q

Where is the olfactory system located?

A

In the posterior, superior regions of each nasal fossa

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22
Q

Describe olfactory cells

A

Bipolar neurones. One dendrite extends to surface to form a swelling from which non-motile cilia extend parallel to surface. These increase surface are and respond to odours

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23
Q

What cells line the vocal cords?

A

Stratified squamous epithelium

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24
Q

What do the vocal cords consist of?

A

A vocal ligament (elastic fibre bundle front to back)

A vocalis muscle (skeletal muscle)

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25
Q

Other than talking, what other functions do the vocal cords have?

A

Help prevent foreign objects from reaching the lungs, close to build up pressure when coughing is required.

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26
Q

What dimensions is the trachea?

A

10cm long

2.5cm wide

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27
Q

Describe the histology of the primary bronchi

A

Hisiologically similar to the trachea, but their cartilage rings/spiral muscle completely encircles the lumen

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28
Q

Describe the histology of the secondary/tertiary bronchi

A

Histiologically similar to primary bronchi, but cartilage arranged as irregular crescent plates/islands rather than rings

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29
Q

What is a bronchiole?

A

Has a diameter of 1mm or less

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30
Q

What do Clara cells secrete, and what does it do?

A

Lipoprotein, which prevents walls sticking together during expiration.
Also Clara fell Protein CC16 (a measurable marker for disease)

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31
Q

What is a terminal bronchiole?

A

Has a diameter of less than 0.5mm

The smallest conducting portion, no goblet cells to prevent ‘drowning’ in own mucous

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32
Q

What can an alveolus open up into?

A

Respiratory bronchiole
Alveolar duct
Alveolar sac
Another alveolus (via an alveolar pour)

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33
Q

Give 4 features of alveolar walls

A

Have abundant capillaries
Are supported by a basketwork of elastic and reticular fibres
Have a covering composed chiefly of type 1 pneumocytes
Have a scattering of type 11 pneumocytes

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34
Q

Other than pneumocytes, what other cell may be in alveoli?

A

Macrophages, to phagocytise particles

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35
Q

What are the name of the 4 facial sinuses?

A

Frontal
Ethmoid
Maxillary
Sphenoid

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36
Q

What are the 3 different types of rib, and which ones are they?

A

True - connect directly to sternum 1-7
False - connect to sternum via cartilage 8-10
Floating - don’t connect to sternum at all 11-12

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37
Q

What are the 2 connections via which the ribs connect to the vertebrae?

A

Superior costotransverse ligament
Costotransverse joint
Joint with ventral body

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38
Q

What are the 3 movements of the chest wall?

A

‘Bucket handle’ - up/down of ribs
‘Pump handle’ - anterior/posterior motion
Diaphragm moves down 1 1/2 intercostal spaces

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39
Q

In which way do the Intercostal muscles pull the ribs?

A

External - pulls ribs up (1st rib is anchored). inhalation

Internal and innermost pull ribs down. Exhalation

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40
Q

In which order is the intercostal neurovascular bundle arranged?

A

Vein
Artery
Nerve
Top—>Bottom

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41
Q

In which direction do the external intercostal muscle fibres run?

A

‘Hands in pocket’ down and medially

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42
Q

In which way do the innermost and internal intercostal muscles run?

A

Perpendicular to the external

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43
Q

Where abouts in the intercostal space does the neurovascular bundle run?

A

Along the bottom of each rib/top of each space

Between the internal and innermost muscles

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44
Q

At what level does the vena cava go through the diaphragm?

A

T8

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45
Q

At what level does the oesophagus go through the diaphragm?

A

T10

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46
Q

At what level does the aortic hiatus go through the diaphragm?

A

T12

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47
Q

What is the diaphragm comprised of?

A

Dome shaped peripheral muscle and central tendon

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48
Q

What does the azygous system do?

A

Collection of veins which collect blood from intercostal spaces taking it to the superior vena cava

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49
Q

Which way do the lungs themselves pull?

A

In and up

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50
Q

Which way does the thoracic cavity itself pull?

A

Out

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51
Q

What way does the passive stretch of the diaphragm pull?

A

Down

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52
Q

When respiratory muscles relax, what happens?

A

Expiration

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53
Q

When respiratory muscles contract in resting breathing, what happens?

A

Inspiration

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54
Q

What are the 4 stages of the respiratory cycle?

A
  1. Inhalation
  2. Rest
  3. Expiration
  4. Pause
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55
Q

When is forced expiration required?

A

Exercise, coughing, singing

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56
Q

What brings about forced expiration?

A

Contraction of internal intercostal muscles/abdominal muscles

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57
Q

How many lobes has the left lung got? What are they called?

A

2

Upper and lower

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58
Q

How many lobes has the right lung got? What are they called?

A

3

Upper, middle and lower

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59
Q

How many fissures has the left lung got? What are they called?

A

1

Oblique fissure

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60
Q

How many fissures has the right lung got? What are they called?

A

2

Oblique fissure, horizontal fissure

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61
Q

What vessels has each lung got at its hilum?

A 
Principal bronchus
Pulmonary artery
2 pulmonary veins
Bronchial vessels
Pulmonary plexus (nerves)
Lymphatics
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62
Q

What is pneumothorax?

A

The integrity of the pleural seal is broken, lungs tend to collapse

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63
Q

What vasculature supplies the parietal pleura?

A

Intercostal arteries/veins

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64
Q

What vasculature supplies the visceral pleura?

A

Bronchial arteries/veins

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65
Q

What are the 3 surfaces of each lung?

A

Costal, diaphragmatic, mediastinal

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66
Q

What are the sympathetic efferents of the lungs?

A

Bronchodilator, vasoconstrictor

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67
Q

What are the two lymphatic plexuses to the lungs?

A

Superficial sub-pleural lymphatic plexus

Deep bronchopulmonary lymphatic plexus

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68
Q

Where is the superficial sub-pleural lymphatic plexus of the lungs found?

A

Deep in visceral pleura.

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69
Q

What does the superficial sub-pleural lymphatic plexus drain?

A

Drains hilar lymph nodes and lung parenchyma and visceral pleura

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70
Q

Where does the deep bronchopulmonary lymphatic plexus drain to?

A

Hilar nodes

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71
Q

What is compliance?

A

The ‘stretchiness’ of the lungs
Volume rover unit pressure change
(Higher compliance - easier to stretch)

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72
Q

What does the pleural seal do?

A

Holds outer surface of the lungs to inner surface of the chest wall, ensuring the 2 move together

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73
Q

When are the elastic forces of lung and chest wall balanced?

A

Functional residual capacity

Lung volume at the end of resting expiration

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74
Q

What is elastic recoil inversely proportional to?

A

Compliance of lung

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75
Q

What muscles may you additionally use for forced expiration?

A

Serratus anterior
Pectoralis maj
Sternocleidomastoid
Scalene

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76
Q

What are the elastic properties of the lung due to?

A

Elastic tissue

Surface tension of alveolar fluid

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77
Q

What does surfactant do?

A

Reduces surface tension by disrupting interactions between surface molecules (breaking up hydrogen bonds)

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78
Q

What is surfactant comprised of?

A

90% phospholipids (60% of which is phosophatidylcholine)
7-15% phosphatidyglycerol
10% protein
Surfactant protein A

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79
Q

What produces surfactant?

A

Type 2 pneumocytes (cuboidal)

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80
Q

What does surfactant do?

A

Reduces surface tension when lungs are deflated, but less so when fully inflated (little breaths easy)

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81
Q

What is Laplace law? (Pressure)

A

Pressure = (2xsurface tension) / radius

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82
Q

Give 3 ways surfactant aids lung function

A

Increases lung compliance by reducing surface tension
Stabilises lungs, preventing small alveoli collapsing into big ones
Prevents surface tension in alveoli creating suction force causing Transudation of fluid from pulmonary capillaries

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83
Q

What is respiratory distress syndrome in premature babies?

A

Babies are born with too little surfactant and few large alveoli

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84
Q

What is poiseuilles law? (Movement through tubes)

A

Resistance = pressure / rate of flow

=(8 x viscosity of fluid x length of tube) / (1 x radius)

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85
Q

What is the key point if poiseuilles law of movement through tubes?

A

Small tubes have high flow resistance

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86
Q

What helps compensate for the increase of resistance in the lungs as the tubes get narrower?

A

Each branching point increases the number of airways in parallel, this compensates for increase of resistance as air passes down

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87
Q

Where is the highest resistance in the airways?

A

Upper airways - trachea and larger bronchi
Each branching point increases the number of airways in parallel, this compensates for increase of resistance as air passes down

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88
Q

What happens to pressure throughout the lung?

A

Remains constant as surfactant equalises surface tension

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89
Q

What is flicks first law of diffusion?

A

Flux of molecules across a barrier is proportional to the permeability of the molecules times the surface area over which diffusion can occur times the concentration gradient

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90
Q

What is me soluble, CO2 or O2?

A

CO2 (~20 times more soluble)

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91
Q

What is the limiting factor of the rate of gas exchange in the lungs?

A

Rate of O2 diffusion

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92
Q

What compensates for slower O2 diffusion?

A

Larger pressure difference for O2

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93
Q

What is ficks equation for rate of diffusion?

A

D = (Pressure diff. x Area x Solubility) / distance x (root of molecular weight of gas)
Assume 37 degrees C

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94
Q

What are the barriers O2 must cross to get from in the alveolus to the RBC?

A 
Epithelial cell of alveolus
Tissue fluid
Endothelial cell of capillary 
Plasma
Red cell membrane
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95
Q

What is the distance between air and alveolar capillary blood?

A

~0.6um

Decreases during inhalation as lung distends

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96
Q

How is inspired air different in concentrations to atmospheric air?

A

Saturated with water vapour as it passes along moist airways (PH2O ~6%)
Therefore O2 and N2 are slightly diluted

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97
Q

What is the normal value for partial pressure of CO2 in the alveoli?

A

5.3kPa

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98
Q

What is the normal value for partial pressure of O2 in the alveoli?

A

13.3kPa

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99
Q

CO2 reacts with water to form what?

A

Carbonic acid, which then dissociates to form bicarbonate ions CO3- and H+

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100
Q

Where is the bodies CO2 found?

A

5% dissolved in plasma
5% carried as carboxy-haemoglobin on proteins
90% carried as bicarbonate ions in plasma

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101
Q

How does fibrotic lung disease impede gas exchange?

A

Thickened alveolar membrane due to collagen deposition slows gas exchange

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102
Q

How does emphysema impede gas exchange?

A

Destruction of alveoli reduces surface area for gas exchange

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103
Q

How does pulmonary oedema impede gas exchange?

A

Fluid in interstitial space increases diffusion distance

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104
Q

What proportion of air inhaled doesn’t actually partake in gas exchange (only goes to ‘dead space’)

A

1/3

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105
Q

How much air is usually in the anatomical/serial dead space?

A

150ml

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106
Q

What is the respiratory zone of the respiratory pathway?

A

The useful portion (over which gas exchange takes place)

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107
Q

What mathematical equation must you do to calculate alveolar ventilation rate?

A

Subtract dead space volume from tidal volume

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108
Q

What is the approximate usual pulmonary blood pressure?

A

~20-30mmHg

Low

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109
Q

What does the low pulmonary blood pressure result in?

A

Lungs are not perfused evenly (more blood in base of lung)

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110
Q

What does V/Q ratio effect?

A

The concentration of O2 and CO2 in the alveoli and blood during respiration

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111
Q

How would you measure diffusion resistance?

A

Carbon monoxide transfer test

14% He, 0.1% CO inhaled. Hold breath for 10s. Rate of diffusion estimated due to its high affinity for CO

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112
Q

What is spirometry?

A

Lung function test

Subject breathes from a closed chamber over water, chambers volume changes with ventilation

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113
Q

Define tidal volume

A

Volume in and out with each resting breath

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114
Q

Define inspiratory reserve volume

A

Extra volume that can be inhaled at rest

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115
Q

Define expiratory reserve volume

A

Extra volume that can be exhaled at rest

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116
Q

Define residual volume

A

Volume remaining after a maximal expiration (contributes to total lung capacity)

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117
Q

What is a lung capacity?

A

2 or more lung volumes added together

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118
Q

What is inspiratory capacity?

A

TV + IRV

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119
Q

What is vital capacity?

A

IRV + TV + ERV

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120
Q

What is a typical value for tidal volume?

A

0.5l

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121
Q

What is a typical value for expiratory reserve volume?

A

1.5l

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122
Q

What is a typical value for inspiratory capacity?

A

3.0l

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123
Q

What is a typical value for vital capacity?

A

5.0l

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124
Q

What is a typical value for inspiratory reserve volume?

A

2.5l

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125
Q

What is a typical value for residual volume?

A

0.8l

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126
Q

What is a typical value for functional residual capacity?

A

2.3l

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127
Q

What is a typical value for total lung capacity?

A

5.8l

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128
Q

What factors influence vital capacity?

A

Inspiration - compliance of lungs, force of inspiratory muscles
Expiration - airway resistance, increases as expiration proceeds

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129
Q

What is single breath spirometry?

A

Patient fills lungs, then breaths out as far and fully as possible. Volumes measured by detector over time - how much and how fast.

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130
Q

What is FEV 1.0?

A

Forced expiratory volume for the 1st second - volume expired over the 1st second, effected by how quickly air slows down, decreased if airways are narrowed.

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131
Q

What is FVC?

A

Forced vital capacity ~5l

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132
Q

What should the ratio between FVC and FEV 1.0 usually be?

A

More than 70% FVC

If reversible, then suggestive of asthma

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133
Q

What is a vitalograph trace?

A

A plot of volume expired Vs time

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134
Q

Why is peak expiratory reserve rate often used as a screening test for airway narrowing?

A

Can be measured simply using a cheap device

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135
Q

What is a helium dilution test used for?

A

Measuring the volumes of air left in lungs after expiration

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136
Q

How is a helium dilution test carried out?

A

Patient inhales a known volume of gas containing a known concentration of helium. Helium is not metabolised, so as patient breaths, helium conc. changes as it gets diluted as it is in a larger volume. (Adding to air already in lungs)

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137
Q

What test would you use to measure dead space?

A

Nitrogen washout

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138
Q

How would you carry out a nitrogen washout test?

A

The last gas in the airways is the first out. Subject inhalers breath of pure O2, then exhales via a metre measuring the % N2. Initially only O2 expired, then mixture of O2 and air (including N2) from alveoli. Volume expired at transition is serial dead space.

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139
Q

At a pO2 of 13.3 kPa in the alveoli, how much O2 will be dissolved into blood?

A

0.13mmol/l

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140
Q

Describe the structure of haemoglobin

A

Tetramer (2 alpha, 2 beta subunits, each consisting of 1 haem and 1 globin), can hold up to 4 O2 molecules

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141
Q

Describe the structure of myoglobin

A

Monomer, 1 O2 molecule

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142
Q

What is myoglobin used for primarily?

A

O2 store for when O2 gets very low, e.g. In muscle

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143
Q

Why is %saturation a good measure to use?

A

Takes into account the amount of pigment present, independent of pigment concentration

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144
Q

What state is haemoglobin in when pO2 is low?

A

Tense - difficult for O2 to bind

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145
Q

What state is haemoglobin in when pO2 is high?

A

Relaxed - easy for O2 to bind

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146
Q

When is haemaglobin ‘saturated’?

A

Above 9-10kPa

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147
Q

When is haemaglobin unsaturated?

A

Below 1kPa

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148
Q

When in haemaglobin half saturated?

A

3.5-4kPa

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149
Q

What will the effect of pO2 and O2 content in a patient with anaemia?

A

pO2 will be normal (saturation will be normal), but O2 content will be lower

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150
Q

What does tissue pO2 depend on?

A

How metabolically active the tissue is

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151
Q

What is a typical value for tissue pO2?

A

~5kPa

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152
Q

To what level does Hb saturation usually drop to?

A

~65% (~35% O2 given up)

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153
Q

What level can the pO2 not fall below in most cells? Why?

A

3kPa

Must be this high to drive diffusion of O2 to cells

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154
Q

How does capillary density effect how low pO2 can be in tissue?

A

The higher the capillary density, the lower the pO2 can fall (doesn’t have as far to diffuse)
There will be a high capillary density in very metabolically active tissue

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155
Q

How does decreased pH effect haemaglobin?

A

Promotes T-state (O2 dissociation)

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156
Q

How does increased pH effect haemaglobin?

A

Promotes R-state (O2 association)

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157
Q

What is the Bohr effect?

A

pH is lower in more metabolically active tissues (CO2 production), so extra O2 is given up

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158
Q

In which direction does the Bohr effect cause the curve to shift?

A

To the right

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159
Q

High way does increased temperature cause the oxygen disassociation curve to shift?

A

To the right

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160
Q

What effect does temperature have on haemaglobin affinity for O2?

A

Decreased

Metabolically active tissues have slightly higher temperature, so more O2 is given up

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161
Q

When might maximum unloading of haemaglobin occur?

A

In tissues where pO2 can fall to low level and conditions where increased metabolic activity results in more acid environment and higher temperature - up to 70% of bound O2 can be given up

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162
Q

What is the maximum % of bound O2 which can be given up?

A

70%

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163
Q

Over the whole body, what percentage of bound O2 is generally given up?

A

~27%

This will increase during exercise (oxygen reserve)

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164
Q

What effect does 2,3-diphosphoglycerate have on oxygen association curve?

A

Shifts curve to the right

Allows more O2 to be given up at tissues

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165
Q

What happens to 2,3-DPG levels in stored blood?

A

Levels decrease due to refrigeration

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166
Q

What causes 2,3-DPG levels to increase?

A

Altitude, anaemia

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167
Q

When CO binds to Hb, what does it form? What is key about this reaction?

A

COHb
Irreversible reaction
Increases affinity of subunits for O2, so they wont give it up in tissues

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168
Q

At what level does CO poisoning become fatal?

A

If HbCO > 50%

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169
Q

What is cyanosis?

A

Bluish colouration due to unsaturated haemoglobin (deoxygenated Hb is less red than oxygenated Hb)
Can be peripheral or central

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170
Q

What causes peripheral cyanosis?

A

Poor circulation

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171
Q

What causes central cyanosis?

A

Poorly saturated blood in systemic circulation

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172
Q

What does pulse oximetry detect?

A

Hb saturation

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173
Q

How does pulse oximetry detect Hb saturation?

A

Difference in absorption of light between oxy and deoxy Hb

Only detects pulsatile arterial blood, ignores levels in tissues and non-pulsatile venous blood

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174
Q

When may pulse oximetry give an incorrect reading?

A

If patient is anaemic - doesn’t take into account how much Hb is present

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175
Q

What is a more accurate alternative to pulse oximetry?

A

Arterial blood gas

However more invasive and time consuming

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176
Q

Does blood contain more CO2 or O2?

A

2.5 times more CO2 than O2

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177
Q

Approximately how much CO2 is dissolved in blood?

A

21mmol/l

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178
Q

Approximately how much O2 is dissolved in blood?

A

8.9mmol/l

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179
Q

What is CO2s major role in the blood?

A

Controlling blood pH (maintaining pH 7.35-7.45)

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180
Q

At pCO2 5.3kPa, how much CO2 is dissolved in blood?

A

1.2mmol/l

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181
Q

What is the pH of plasma dependent on normally?

A

How much CO2 reacts to form H+

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182
Q

What determines how much CO2 reacts to form H+ normally?

A

Concentration of CO2 dissolved (pushing reaction to the right, increasing H+)
Concentration of HCO3- (pushing reaction to left, decreasing H+)

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183
Q

What determines how much dissolved CO2 is in the blood normally?

A

Directly dependent on partial pressure of CO2. If pCO2 rises, pH will fall (more H+)
If pCO2 in alveoli is the determining factor, this is controlled by rate of breathing.

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184
Q

What cation is associated with HCO3- in the plasma?

A

Na+

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185
Q

How much bicarbonate is normally in plasma?

A

25mmol/l

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186
Q

What can the Henderson-Hasselbalch equation be used for?

A

Calculating pH from pCO2 and HCO3- conc.

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187
Q

Where is most of the HCO3- found in the blood produced?

A

In RBCs

Contain enzyme carbonic anyhydrase CA

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188
Q

What is the reaction catalysed by carbonic anhydrase in RBCs?

A

CO2 + H2O —> H+ + HCO3-

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189
Q

How is HCO3- removed from RBCs once it has been produced?

A

Via chloride bicarbonate exchanger on their cell surface

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190
Q

What determines how much HCO3- is produced by erythrocytes?

A

How much H+ is bound to haemoglobin

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191
Q

Do RBC control HCO3- concentration in plasma?

A

No

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192
Q

What controls amount of HCO3- in blood?

A

Kidneys via excretion

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193
Q

What determines how much CO2 is in the blood?

A

Rate of breathing

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194
Q

What buffers extra acids in the blood (e.g. Lactic, keto…)

A

Hydrogen carbonate

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195
Q

How does bicarbonate act as a buffer for extra acids produced by the body (e.g. Keto, lactic…)

A

Acids react with HCO3- to produce CO2, therefore decreasing concentration of HCO3-. CO2 produced is removed by breathing and pH changes are minimised.

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196
Q

What determines arterial pCO2?

A

Alveolar pCO2

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197
Q

What does buffering of H+ by haemoglobin depend on?

A

Level of oxygenation (amount bound is dependent on state of Hb molecule)

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198
Q

How does having lots of O2 bound to a Hb molecule effect the amount of H+ ions it binds?

A

More O2 - R state - less H+ bound

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199
Q

How does having not much O2 bound to a Hb molecule effect the amount of H+ ions it binds?

A

Less O2 bound to Hb - T state - More H+ ions bound

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200
Q

What does more H+ ions being able to bind to Hb (in venous blood) incur?

A

More HCO3- can be produced, therefore more CO2 (unreacted) is present in plasma

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201
Q

When in lungs, and Hb gives up O2, returning to relaxed state, what happens to the H+ associated to it?

A

Hb gives up extra H+, which then goes on to react with HCO3- to form CO2, which is then exhaled

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202
Q

What are carbamino compounds?

A

CO2 bound directly to proteins (onto amino groups on globin of Hb)

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203
Q

Does the binding of CO2 to proteins contribute to blood pH?

A

No, but does contribute to CO2 transport

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204
Q

Where are most carbamino compounds formed?

A

At the tissues, because pCO2 is higher and the unloading of O2 facilitates binding of CO2 to Hb (which will then be given up at lungs)

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205
Q

What are the 3 forms by which CO2 are transported? (And what proportion of CO2 transport is via this mechanism)

A

Dissolved (10%)
As hydrogen carbonate (60%)
As carbamino compounds (30%)

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206
Q

What is the approximate value of CO2 in whole arterial blood?

A

~21.5mmol/l

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207
Q

What is hypoxia?

A

O2 deficiency at tissue level. If it persists tissue will undergo ischaemic damage or necrosis

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208
Q

What are the 4 types of hypoxia?

A

Hypoxaemic, or respiratory hypoxia
Anaemic hypoxia
Stagnant, or circulatory hypoxia
Cytotoxic hypoxia

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209
Q

What is hypoxaemic (or respiratory) hypoxia?

A

Poor oxygenation at the lungs, low pO2 and low O2 saturation

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210
Q

What is anaemic hypoxia?

A

Normal pO2, but insufficient Hb to carry the O2, e.g. CO poisoning

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211
Q

What is stagnant, or circulatory hypoxia?

A

Reduced delivery of O2 due to poor perfusion. Could be global (e.g. Shock), or local (e.g. Peripheral vascular disease)

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212
Q

What is cytotoxic hypoxia?

A

O2 delivery is adequate, but tissues unable to utilise O2, e.g. Cyanosis poisoning

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213
Q

What is the normal level of O2 saturation?

A

94-98%

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214
Q

What is the normal pO2?

A

11.1 - 14.4 kPa

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215
Q

At what level of O2 is tissue at serious risk of being damaged?

A

Less than 90%

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216
Q

At what O2 saturation level is tissue at serious risk of being damaged?

A

Less than 8kPa

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217
Q

Describe type 1 respiratory failure (pO2, O2 saturation, pCO2)

A

pO2 of arterial blood low (less than 8kPa)
O2 saturation less than 90%
pCO2 normal or low

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218
Q

Describe type 2 respiratory failure (pO2, O2 saturation, pCO2)

A

pO2 in arterial blood less than 8kPa
O2 saturation less than 90%
pCO2 high, above normal range (4.3-6.4 kPa)

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219
Q

What are the 3 mechanisms for respiratory failure?

A

Ventilators (pump) failure - unable to move sufficient air in/out of the lungs
Poor diffusion across alveolar membrane
Mismatching of ventilation and perfusion

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220
Q

What happens when V/Q ratio is less than 1?

A

Alveolar pO2 falls, pCO2 rises

Type 1 respiratory failure

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221
Q

What might call V/Q ratio to fall below 1?

A

Could be due to reduced ventilation of part of lung, or reduced perfusion of part of lung (increases Q as rest of lung receives excess of what’s available)

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222
Q

What is the treatment for type 1 respiratory failure?

A

Treat cause

Oxygen therapy might help hypoxia

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223
Q

What is the treatment for type 2 respiratory failure?

A

Treat cause

Problems of hypercapnia might require assisted ventilation (particularly if acute)

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224
Q

What are the clinical features of hypoxia?

A

Exercise intolerance
Tachypnoea (may be perceived as breathlessness)
Confusion
Central cyanosis (late/when O2 saturation <85%)

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225
Q

When is cyanosis present?

A

When more than 50gm/l of desaturated Hb is in the blood

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226
Q

What is cyanosis?

A

Purplish decolorisation of skin and mucous membranes due to the colour of desaturated Hb

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227
Q

What does central cyanosis indicate ?

A

Arterial hypoxia

O2 Saturation <85%

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228
Q

What level of O2 saturation does central cyanosis indicate?

A

Less than 85%

229
Q

What are the consequences of chronic hypoxia?

A

Increased number of RBC, containing more 2,3 DPG
Hypoxia vasoconstriction of pulmonary arterioles (usually to aid V/Q ratio in regions) - can cause pulmonary hypertension, corpulomale

230
Q

What changes occur with chronic hypercapnia?

A

CSF acidity corrected by choroid plexus (HCO3- ion pumping)
Central chemoreceptors ‘reset’ to higher pCO2
Peripheral chemoreceptors remain sensitive to hypoxia
Respiration now driven by hypoxia (pO2)

231
Q

Why is O2 administration dangerous in patients with COPD?

A

Hypoxia is now the stimulus driving respiration - correcting this may reduce ventilation.
Reducing hypoxic vasoconstriction in poorly ventilated alveoli may worsen V/Q mismatch

232
Q

List 4 possible causes of hypoventilation

A

Respiratory centre depression e.g. Head injury, drugs
Muscle weakness of respiratory muscles e.g. Damage, disease, nerve damage
Chest wall problems e.g. Scoliosis, morbid obesity
Hard to ventilate lungs e.g. Severe fibrosis

233
Q

List some common flora of the upper respiratory tract

A

Viridian’s streptococci, Neisseria spp, anaerobes, candida spp.
Also (but less common):
Streptococcus pneumoniae, streptococcus pyogenes, haemophillus influenzae

234
Q

List some of the natural defences of the respiratory tract

A

Muco-ciliary clearance mechanisms, nasal hairs, ciliates columnar epithelium of tract
Coughing/sneezing reflex
Respiratory mucosal immune system. Lymphoid follicles of pharynx and tonsils, alveolar macrophages, secretory IgA and IgG

235
Q

List 5 common compromises to the respiratory tract defences

A 
Poor swallowing 
Abnormal ciliary function
Abnormal mucus
Dilated airways
Defects in host immunity
236
Q

What might cause poor swallowing?

A

CVA, muscle weakness, alcohol

237
Q

What might cause abnormal ciliary function ?

A

Smoking, viral infection

238
Q

What might cause abnormal mucous?

A

Cystic fibrosis

239
Q

What might cause dilated airways?

A

Bronchiectasis

240
Q

What might cause defects in host immunity?

A

HIV

Immunosuppression

241
Q

What is the most common causes of upper respiratory tract infection?

A

Viruses

E.g. Rhinovirus, influenza

242
Q

What is the most common causes of lower respiratory tract infection?

A

Bronchitis, empyema, pneumonia, lung abscess, bronchiolitis

243
Q

What is acute bronchitis?

A

Inflammation of medium sized airways, mainly in smokers. Cough, fever, increased sputum production, shortness of breath. CXR normal.

244
Q

What might cause acute bronchitis?

A

Viruses - e.g. S. Pneumonias, H. Influenzae, M. Catarrhalis.

245
Q

What is the treatment for acute bronchitis?

A

Physiotherapy +/- antibiotics

246
Q

What is pneumonia?

A

Inflammation of lung alveoli. Patients are unwell - 20-40% admitted to hospital

247
Q

Describe the presentation of a patient with pneumonia

A

Fever, cough, pleuritic chest pain, shortness of breath. Often localising signs and abnormal CXR

248
Q

How is pneumonia classified?

A

Clinical setting (community/hospital acquired)
Presentation (acute/chronic)
Organism (bacterial/viral/fungal)
Lung pathology (lobar, bronchi, interstitial)

249
Q

What is the cellular presentation of pneumonia?

A

Acute inflammatory response - exudation of fibrin-rich fluid. Neutrophil and macrophage infiltration

250
Q

What factors in the patient history might be suggestive of pneumonia?

A

Pre-existing lung disease, immune-compromisation, geography, seasons, epidemics, travel, exposure to animals

251
Q

What is a nosocomial infection?

A

A hospital acquired infection

252
Q

What is a common mechanism of spread for hospital awaited pneumonia?

A

Ventilator associated

253
Q

What are the main causative organisms for community acquired pneumonia?

A 
Streptococcus pneumoniae 
Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus
Klebsiella pneumoniae
254
Q

What are the symptoms of pneumonia?

A

Cough (+/- sputum), shortness of breath, fever, rigours, pleuritic chest pain, malaise, nausea, vomiting

255
Q

What will you find on examination of a patient with pneumonia?

A

Pyrexia, tachycardia, tachypnoea, cyanosis, bronchial breathing, crackles, dullness to percussion, tactile voice fremitus

256
Q

What investigations should you do for a patient with pneumonia?

A 
FBC
U &amp; Es
CRP
Arterial blood gases
CXR
Microbiological samples/investigations
257
Q

What microbiological samples/investigations should you do for a patient with pneumonia?

A 
Sputum (induced if required)
Blood culture 
Bronchodilator alveolar lavage fluid BAL
Nose and throat swabs or NPAs
Urine (antigen test for legionella/pneumococcus)
Serum (antibody test)
258
Q

What could contribute towards points on the CURB 65 score?

A 
Confusion
Urea >7mmol/l
Respiratory rate >30
Blood pressure <90 systolic, <60 diastolic
Over 65yrs
259
Q

What score on the CURB 65 scale constitutes patient to be managed as ‘severe’?

A

2-5

260
Q

What does antibiotic treatment for pneumonia depend upon?

A

Probable infection, personal risk factors, community Vs hospital, severity ect

261
Q

What antibiotics should you give for mild-moderate pneumonia?

A

Amoxicillin

Or doxycycline/clarithromycin

262
Q

What antibiotics should you give for moderate-severe pneumonia?

A

Hospital admission

Co-amoxiclav AND clarithromycin/doxycycline

263
Q

What are the possible complications of acute bacterial pneumonia?

A

Lung abscess, bronchiectasis, empyema

264
Q

What might increase the risk of complications arising from a pneumonia infection?

A

Resistant organism, wrong diagnosis, immunosuppression, proximal obstruction, empyma/abscess.

265
Q

What type of organism is S. Pneumoniae?

A

Gram positive cocci (pairs, diplococci)

266
Q

What sort of pneumonia does S. Pneumoniae cause?

A

Acute onset, severe. Fever/rigours

267
Q

What do you use to treat pneumonia caused by S. Pneumoniae?

A

Benzyl penicillin of amoxicillin

268
Q

What causes atypical pneumonia?

A

Organisms without a cell wall - meaning penicillins (cell-wall active antibiotics)won’t work on them.

269
Q

List some atypical organisms that may cause pneumonia

A

Leigionella, chlamydia, coexiella, mycoplasure

270
Q

What would you use to treat atypical pneumonia?

A

Agents active on protein synthesis - macrolides, tetracyclines

271
Q

What extrapulmonary features might be present in atypical pneumonia?

A

Hepatitis, low Na+

272
Q

What would be a typical CXR for viral pneumonia?

A

Patchy or diffuse ground glass opacity on CXR

273
Q

What can severe viral pneumonia present similarly to?

A

Adult respiratory distress syndrome ARDS

274
Q

What are the features of viral pneumonia?

A

Damage to cells lining airways/alveoli by virus and immune cells. Fluid filled air spaces interferes with gas exchange. Can be mild - severe

275
Q

What accessory muscles are used for additional inspiration?

A

Sternomastoid, scalenus (anterior, medial posterior), pectoralis maj/minor, internal fibres of serratus anterior and posterior, serrated (anterior, posterior)

276
Q

What accessory muscles are used for forced expiration?

A

Abdominal wall muscles, (rectus abdominus, transversis abdominus, external/internal oblique muscles)

277
Q

When is pneumonia classed as hospital acquired?

A

If patient develops symptoms after 48hrs or more in hospital

278
Q

What is aspiration pneumonia?

A

Exogenous material or secretions in respiratory tract

279
Q

When is aspiration pneumonia most commonly seen?

A

In patients with neurological dysphagia (e.g. Strokes), epilepsy, alcoholic. IVDU and nursing home residents at risk

280
Q

How is pneumonia prevented?

A

Immunisation (e.g. flu vaccine)
Chemoprophylaxis (e.g. Oral penicillin) to patients with high risk of lower RTI
Smoking advice

281
Q

What are the most common causative organisms for TB?

A

Mycobacterium tuberculosis
Mycobacterium bovis
Mycobacterium africanum

282
Q

What sort of bacteria are the mycobacterium species, causing TB?

A

Non-motile, rod-shaped, aerobes.
They have long chain fatty (mycolic) acids, complex waxes and glycolipids in their cell wall. This gives structural rigidity, staining characteristics, acid alcohol fast.
Relatively slow growing (generation times 15-20hrs)

283
Q

How is tuberculosis transmitted?

A

Not easy to catch! Prolonged exposure facilitates transmission.
Spread by respiratory droplets. Air remains infectious for 30mins.
Infectious dose 1-10 bacilli, less than 10um particles suspended in droplets.
Reach lower respiratory airway macrophages

284
Q

Describe the pathogenesis of TB

A

Inhaled aerosols
Engulfed by alveolar macrophages
Local lymph nodes
Primary complex (5% forms active TB here)
Initial containment of infection
Latent infection (can either self cure, or go on to form post primary TB)

285
Q

What would the TST test result be for active TB?

A

Positive

286
Q

What would the TST test result be for latent TB?

A

Positive

Also IFN gamma test result positive

287
Q

What would a CXR for a patient with latent TB look like?

A

Normal

288
Q

What would a CXR for a patient with active TB look like?

A

Abnormal

289
Q

What would the result of sputum smears/culture be for a patient with latent TB?

A

Negative

290
Q

What would the result of sputum smears/culture be for a patient with active TB?

A

Positive

291
Q

Would a patient with patent TB have symptoms?

A

No

292
Q

Would a patient with active TB have symptoms?

A

Yes

Cough, fever, weight loss

293
Q

What might stimulate post primary TB?

A

Reactivation or exogenous reinfection

294
Q

When is TB classed as post primary TB

A

When it appears over 5yrs after primary infection

295
Q

Can clinical presentation of post primary TB be extra pulmonary?

A

Yes

296
Q

List some risk factors for reactivation of TB

A

HIV, substance abuse, organ transplants, low BMI, immunosuppression, prolonged therapy with corticosteroids, DM

297
Q

What forms in the lungs of patients with active TB?

A

Caseating granuloma (with caseous necrosis at the centre)

298
Q

List some frequent sites for TB

A

Pulmonary (most cases)
Extrapulmonary - lymph nodes, pleura, kidneys, brain… (found more in immunosuppressed patients/young children)
Military - carried to all parts of the body via bloodstream (rare)

299
Q

List some risk factors for TB

A

Non U.K. Born/recent migrants
HIV/immunosuppression
Homeless, drug users, prison
Close contacts infected

300
Q

What are the symptoms of pulmonary TB?

A

Fever, night sweats, weight loss, anorexia, tiredness, malaise, cough, breathlessness (if pleural effusion)

301
Q

What are the signs on examination of pulmonary TB?

A

Crackles in effected area. Often no chest signs despite CXR abnormality

302
Q

What investigations should you do for pulmonary TB?

A

CXR, sputum (3 early morning samples, min volume 5ml, induced if needed), bronchoscopy

303
Q

What might be visible in a CXR from a patient with pulmonary TB?

A

Cavitation usually develops within consolidation. Healing results in fibrosis

304
Q

What are the limitations of microscopy?

A

Sputum smears only have 60% sensitivity (increased with more samples)
Operator skills dependent

305
Q

What is the ‘gold standard’ for TB diagnosis?

A

Culture

306
Q

What is a tuberculosis sensitivity test TST?

A

Tuberculin injected intradermally, read 48-72hrs later.
Tests if you’ve been exposed, not if you’ve had the disease.
Subject to interpretation, can give false results, but is cheap and doesn’t require a laboratory infrastructure

307
Q

What are interferon gamma releasing assays IGRAs?

A

Detection of antigen-specific IFN-gamma production. No cross reaction with BCG. Can distinguish latent and active TB. Similar problems with sensitivity and specificity

308
Q

What are the 1st line anti TB drugs?

A

Rifampicin, isoniazid, pyrazinamide, ethambutol

Always in combination!

309
Q

What are some second line medications for TB?

A

Quinolones (moxifloxacin), injectables, capreomycin, kanamycin, amikacin, ethionamide, prothionamide…

310
Q

What are some key points for treating TB?

A

Early and adequate treatment, close monitoring of compliance. Check no secondary transmission and cases.

311
Q

Describe the multidrug therapy one would typically give a patient with TB (RHZE), and how it works

A

Rifampicin - raised transaminatse and induces cytochrome P450. Orange secretions (orange urine!)
Isoniazid - peripheral neuropathy (pyridoxine 10mg od). Hepatotoxicity
Pyrazinamide - hepatotoxicity
Ethambutol - visual disturbance
Vitamin D
Surgery?

312
Q

Describe the duration of drugs taken for TB

A

3/4 drugs for 2 months, then rifampicin for 4 months. 18 months if CNS TB. Cure rate 90%

313
Q

How long would a patient be required to take medication if they had CNS TB?

A

18 months

314
Q

What is MDR TB resistant to?

A

Rifampicin and isoniazid

315
Q

What is XDR TB resistant to?

A

Rifampicin and isoniazid

Also fluroquinolones and at least 1 injectable

316
Q

How do you treat drug resistant TB?

A

4-5 drug regimes for longer duration

317
Q

What sort of drugs would you use to treat drug resistant TB?

A

Quinolones, aminoglycosides, PAS, cycloserine, ethionamide

318
Q

What might induce miliary TB?

A

Rupture of caseous pulmonary focus into blood vessel

319
Q

What is miliary TB?

A

Bacilli spreading throughout bloodstream - widespread infection
Can be during primary infection or during reactivation. Lungs are always involved, but few respiratory symptoms

320
Q

What might be some symptoms of miliary TB?

A

Fever, dry cough, very unwell

321
Q

What is done to help reduce spread of TB?

A

All forms of TB are compulsorily notifiable under the public health act 1984. This enables data, to detect and monitor outbreaks, and triggers contact tracing procedures

322
Q

What is the BCG vaccine?

A

A live attenuated virus (M. Bovis strain), given in high prevalence communities only. 70-80% effective

323
Q

What is asthma?

A

A chronic inflammatory disease of the airways, resulting in reversible airway obstruction
Inflammation, bronchoconstriction, mucus

324
Q

Describe the process by which an asthma attack occurs

A

Environmental trigger inhaled
Type 1 hypersensitivity reaction
Airway narrowing (smooth muscle contraction, mucus production, inflammatory cell infiltration)
Remodelling - damaged epithelium, increased smooth muscle thickness

325
Q

What might trigger an asthma attack?

A

Indoor - pets, mould, dust mites, medications (NSAIDs, beta blockers)
Outdoor - cold, pollens, tobacco smoke, pollutants, exercise

326
Q

Is there any standardisation of type, severity, or frequency of symptoms for asthma?

A

No

327
Q

What are the symptoms of asthma?

A 
RECURRENT
Breathlessness
Chest tightness
Wheeze
Cough (worse at night/exercise. Dry)
Tracheal tug, recession, nasal flaring
Accessory muscle use
328
Q

What are the stages of examination of a patient with asthma?

A

Full history, inspection, palpating, percussion, auscultation, peak flow, spirometry

329
Q

What is the management of a patient with asthma?

A

Education - how to use inhaler properly

Prevention - change pillows/bedsheets frequently, fresh air, no smoking…

330
Q

What does SABA stand for?

A

Short acting beta agonist

331
Q

What is SABA used for?

A

Helps relax respiratory smooth muscle, ‘quick relief’ of asthma symptoms

332
Q

When would you step up an inhaler?

A

If used more than 3 times a week, or if nocturnal symptoms

333
Q

What is a steroid used for when treating asthma?

A

Reduces inflammation, inhibits inflammatory cells/mediators

334
Q

When is LABA used?

A

Used in asthma patients who still have asthma symptoms despite steroid. Slower onset of action therefore not for an acute asthma attack

335
Q

What does LABA stand for?

A

Long acting beta agonist

336
Q

What is the criteria for a mild asthma attack?

A 
Sats >92% on air
Pulse <110
RR <25
Speech normal
Minimal wheeze
PEFR >75% predicted
337
Q

What are the criteria for a moderate asthma attack?

A 
Sats >92% in air
Pulse <110
RR <25
Speech normal
Wheeze +++
PEFR 50-75% predicted
338
Q

What is the criteria for a severe asthma attack?

A 
Sats <92% in air
Pulse >110
RR >25
Can't complete sentences
No wheeze (not enough air in lungs)
PEFR 35-50% predicted
Needs to be in hospital (resuss)
339
Q

What is the criteria for a life threatening acute asthma attack?

A 
Sats <92% in air - cyanosis
Silent cheat - poor respiratory effort (tired muscles)
Altered consciousness
Exhaustion
PEFR 35% predicted 
May need to be intubated
340
Q

What treatment would you give for an asthma attack?

A

Oxygen
Salbutamol nebulisers, atrovent nebulisers ‘back to back’
IV access
May need to incubate and ITU admission

341
Q

What is COPD?

A

Chronic obstructive pulmonary disease
Characterised by airflow obstruction that is progressive, not fully reversible and does not change markedly over several months. Predominantly caused by smoking.
Umbrella term encompassing emphysema and chronic bronchitis - patients may have features of either or both

342
Q

What is emphysema?

A

Pathological process in which there is destruction of the terminal bronchioles and distal airspaces. This leads to loss of alveolar surface area, therefore impairment of gas exchange. Process often progresses to the development of larger redundant air spaces within the lung, called bullae.
Emphysema causes the destruction of the supporting tissue surrounding the small airways and therefore their close/collapse during expiration - airflow obstruction of small airways.
In addition, the loss of elastic tissue in the lung causes the lungs to hyperinflate as the lungs are unable to resist the natural tendency of the rib cage to expand outwards.

343
Q

What is chronic bronchitis?

A

Chronic mucus hypersecretion that frequently occurs in smokers. Caused by inflammation in the large airways (often due to cigarette smoke), leading to proliferation of mucus producing cells in the respiratory epithelium.
Resulting chronic productive cough and frequent respiratory infections, frequently persists even after quitting smoking. Results in airflow obstruction due to remodelling and narrowing of airways

344
Q

What, other than smoking, might cause COPD?

A

Alpha-1-antitrypsin deficiency (rare genetic condition)

Pollution (developing countries)

345
Q

What are the symptoms of COPD?

A

Cough/sputum production usually the first signs, although patients usually don’t present until they are breathless.

346
Q

Describe the MRS dyspnoea score system for the grading of breathlessness

A

1 - Not troubled by breathlessness except on strenuous exercise
2 - Short of breath when hurrying or walking up a slight hill
3 - Walks slower than contemporaries on level ground due to breathlessness, or has to stop for breath when walking at own pace
4 - Stops for breath after walking about 100m, or after a few minutes on level ground
5 - Too breathless to leave house, or breathless when dressing

347
Q

What are the signs of COPD?

A

‘Purse lip’ breathing - protective manoeuvre that increases the pressure within airways, causing a reduction or a delay in the closure of the airways
Tachypnoea
Using accessory muscles
Hyperinflation (diaphragm/resp muscles must work harder to ventilate lungs)
Wheeze/quiet breath sounds on ausculation
Cyanosis and CO2 retention, right heart failure (cor pulmonale) with oedema

348
Q

How may COPD be diagnosed?

A

Measurement of airflow obstruction is essential - this is achieved with spirometry

349
Q

What is spirometry?

A

Subjects are asked to perform a forced expiratory manoeuvre (blowing out as hard and fast as possible into a sealed tube), and the volume of expelled air is plotted against time

350
Q

What is the spirometry values for someone with COPD?

A

FEV1<80% predicted

FEV1/FVC ratio <70%

351
Q

What is the NICE guidelines for mild airflow obstruction spirometry value?

A

FEV1 50-80% predicted

352
Q

What is the NICE guidelines for moderate airflow obstruction spirometry value?

A

FEV1 30-49% predicted

353
Q

What is the NICE guidelines for severe airflow obstruction spirometry value?

A

FEV1 <30% predicted

354
Q

What does COPD diagnosis depend on?

A

A combination of suggestive symptoms and signs, together with the presence of airflow obstruction on spirometry (FEV1<80% predicted and FEV1/FVC ratio <70%)

355
Q

What are some suggestive features of COPD?

A

Smoker or ex smoker
Older patient (>40yrs) and onset of symptoms later in life
Chronic productive cough
Breathlessness that is usually persistent and progressive

356
Q

What other investigations might you do for COPD?

A

CXR - not diagnostic, but mandatory to exclude other diagnosis
Arterial blood gas to assess respiratory failure
Alpha -1-antitrypsin blood test for younger patients
High-resolution computed technology (HRCT) scanning, detailed assessment of the degree of alveolar destruction. Helpful in considering surgical intervention, or if doubtful diagnosis - not required for routine assessment

357
Q

What treatment is available for COPD?

A 
Smoking cessation
Pulmonary rehabilitation
Bronchodilation
Antimuscarinics
Steroids
Mucolytics
Diet-supplements/dietician review
Supportive e.g. Flu vaccine
Long term oxygen therapy 
Lung volume reduction
358
Q

What is the treatment for stable COPD?

A 
Bronchodilators
Steroids - inhaled
Antimuscarinics
Mucolytics
Methylxanthines
359
Q

What is the mechanism of action for beta 2 agonists in COPD?

A

Ligand binds to receptor, activating adenylcyclase, increasing cAMP and activating protein kinase (PKA), leading to phosphorylation of downstream targets (myosin light chain kinase MLCK). Leads to relaxation of smooth muscle in airway - bronchodilation.

360
Q

What are possible side effects of using beta2 agonists?

A

Tachycardia (atrial Beta2 receptors, palpitations)
Tremor (skeletal Beta 2 receptors)
Hypokalaemia (skeletal muscle uptake of K+)

361
Q

How do anticholinergics work in COPD?

A

Synergistic with Beta2 agonists
Blocks ACh by blocking the binding of ACh to its receptor in nerve cells thus inhibiting parasympathetic impulses (as that’s its target)

362
Q

Give some examples of anticholinergics

A

Ipratropium (short acting muscarinic)

Tiotropium (longer acting)

363
Q

What are some local adverse effects of anticholinergics?

A 
Dry mouth/cough
Sore throat
Upper respiratory tract infection
Bitter taste
Nausea
364
Q

What are some possible systemic adverse effects of anticholinergics?

A

Supraventricular tachycardia
Atrial fibrillation
Urinary difficulty/retention
Constipation

365
Q

Give some examples of methylxanthines used for COPD

A

Theophylline

Aminophylline

366
Q

Describe the mode of action of methylxanthines, used for COPD

A

Bronchodilation. Increase respiratory drive, anti-inflammatory effects.
Inhibition of phosphodiesterases (which break down cAMP, so inhibition leads to an increase in cAMP - bronchodilation)

367
Q

Why do methylxanthines require blood level monitoring?

A

Toxicity - tachycardia, SUT, nausea, seizures

368
Q

What are the side effects of long term steroids?

A

Thin skin, bruising, cataracts, adrenal insufficiency, osteoporosis, diabetes, increased weight, (fluid retention), mental disturbance, GI symptoms, proximal myopathy

369
Q

What might mucolytics be up for?

A

Can help reduce the thickness of sputum, helping airways clearance

370
Q

Give an example of a mucolytic

A

Carbocysteine

371
Q

What are the key messages for drug therapy in COPD?

A

Bronchodilator therapy may provide symptomatic relief
Steroids can help reduce inflammatory pathways
Mucolytics can reduce sputum thickness
Drugs can help improve quality of life and reduce exacerbation frequency, but do not provide cure or improve survival in COPD
Education on inhaler technique is essential as well as side effects counselling

372
Q

What is reconditioning in COPD?

A

Many patients with COPD avoid exercise/physical activity due to breathlessness……
Viscous cycle of increasing social isolation and inactivity, leading to worsening of symptoms….

373
Q

What is the reconditioning cycle?

A

Feel bad due to illness, so avoid activities that exacerbate feeling such, so do less, so muscles weakens, so feel worse, so feel depressed, so avoid activities……

374
Q

What is the aim of pulmonary rehabilitation?

A

To break the deconditioning cycle!

375
Q

What is pulmonary rehabilitation?

A

6-12wk programme of supervised exercise, advise, education ect.
Aims to break the deconditioning cycle!

376
Q

How long a day must a patient be on oxygen for a survival benefit?

A

At least 16hr a day

377
Q

What can be used to prevent renal and cardiac damage due to extended periods of hypoxia in COPD?

A

Long term oxygen therapy

378
Q

When might long term oxygen therapy be offered to a patient?

A

If pO2 is persistently below 7.3 kPa, or below 8kPa with cor pulmonale
Patients must be non-smokers and not retain high levels of CO2 (checked in hospital on O2 first). Must have home fire risk assessment for safety

379
Q

What must patients be in order to be offered long term oxygen therapy?

A

Patients must be non-smokers and not retain high levels of CO2 (checked in hospital on O2 first). Must have home fire risk assessment for safety

380
Q

What surgical options might be used for treatment of COPD?

A

Lung volume reduction - reduction of hyperinflation is principle aim - gets rid of dead space.
Lung transplant - rare, used in young patients

381
Q

What multidisciplinary people might be involved in the care of a patient with COPD?

A

Physicians, GPs, specialist nurse, physio, pharmacist, occupational therapists, dietician, surgoen

382
Q

What is the treatment of acute exacerbations of COPD?

A

Aim for sats 88-92% by controlled O2 therapy
Nebulisers - bronchodilators
Steroids - oral (possibly IV)
Antibiotics if infective features (WCC, purulent sputum, raised CRP)
Repeat ABG, if no better consider non-invasive ventilation or referral to ITU for invasive ventilation

383
Q

What is non invasive ventilation?

A

The provision of ventilatory support through upper airways via mask/similar device

384
Q

When might non invasive ventilation be used?

A

Used for acute exacerbations of COPD with type 2 respiratory failure and mild acidosis (pH 7.25-7.35)
Patients must be conscious to use it!

385
Q

When must you NOT use non invasive ventilation?

A 
Untreated pneumothorax
Facial injury
Vomiting 
Agitated
Life threatening hypoxia
Lots of upper airway secretions 
Unconscious
386
Q

What are the markers of addiction?

A

Use despite knowledge of harmful consequences
Cravings during abstinence
Failure of attempts to stop
Withdrawal symptoms during abstinence

387
Q

How long does it take for ACh receptors to desensitise after the last cigarette?

A

6-12wks

388
Q

How many puffs of a cigarette does it take to bind 50% of ACh receptors?

A

1-2

389
Q

What receptors does nicotine act upon? What does this stimulate?

A

Nicotinic acetylcholine ACh receptors, stimulating dopamine release

390
Q

What causes the satisfaction associated with smoking?

A

Dopamine release as a results of nicotine binding to nicotinic ACh receptors

391
Q

What happens to ACh receptors following chronic nicotinic exposure?

A

ACh receptors enter up regulated state, increases affinity and functional sensitivity to an agonist

392
Q

What is the quickest method of nicotine delivery?

A

Cigarette (2 x as fast as a spray, 3 x as fast as gum/inhaler/tablet)

393
Q

What is the most effective treatment for tobacco related disease?

A

Quitting smoking!

394
Q

Why is it particularly important to advice patients to quit smoking?

A

2nd most effective way to get people to quit smoking

If don’t condone it, patients may assume it’s acceptable behaviour

395
Q

What are the 3 As for discussing smoking with a patient?

A

Ask - and record smoking status (current, ex, non)
Advice - patient of healthcare benefits (best thing for health is stopping!)
Act - on patients response (build confidence, give info, refer, prescribe, follow up)

396
Q

Why does NRT aid successful quitting of smoking?

A

Nicotine withdrawal causes discomfort, NRT provides temporary nicotine substitution (weaning)
Via therapeutic routes provides relief and encourages complete abstinence.
Doubles success rate of quitting

397
Q

Why is NRT better than just reducing the number of cigarettes gradually?

A

NRT contains nicotine only. Short and long acting agents can be used in combination

398
Q

What does champix - varenicline tartrate do?

A

Reduces craving for nicotine by binding to nicotine acetylcholine receptors in the brain. High affinity and selectivity, act as a partial agonist.
Reduces withdrawal symptoms, reduces the satisfaction a smoker gets from smoking.
Should be taken for ~3mths. Can be combined with NRT prescribing, relatively good success rate.

399
Q

What are some mechanisms of harm reduction for smoking, if patient can’t give up entirely?

A 
Cut down to stop e.g. Using 1 or more NRT
Smoke less (long term reduction)
Stop temporarily (abstain for an agreed length of time)
E-Cigarettes (toxins present, but lower, so fewer risks)
400
Q

What risk factors are there for cancer other than smoking?

A

Asbestos
Radon
Occupational carcinogens (e.g. Cr, Ni, arsenic, coal dust)
Genetic/family factors

401
Q

What is the criteria for a screening test to be successful?

A

Must:
Be for a disease with serious consequences
High prevalence of detectable disease
Test detects little pseudo-disease (no over diagnosis)
Test detects disease before the critical point
Test causes little morbidity
Test affordable and available
Treatment for disease exists
Treatment more effective when applied before symptomatic detection
Treatment not too risky or toxic

402
Q

Is there currently a screening test for cancer?

A

No

Possibly CT in the future?

403
Q

What is the primary reason most lung cancer is untreatable?

A

Found too late (80%)

404
Q

What does a successful screening test do?

A

Decreases disease specific mortality

405
Q

List some common places for lung cancer to spread to

A

Brain, draining lymph nodes, pericardium, lung, pleura, liver, adrenals, bone

406
Q

What staging tests would you perform for lung cancer?

A

CT scan and PET scan
Do PET scan as well as CT as this shows the activity of tissue, suggesting if it is cancer or not. Also picks up some missed by CT scan.

407
Q

What are all the frequently used investigations/staging tests for lung cancer?

A 
CT scan and PET scan (standard procedure)
CXR
MRI
USS
Bone scan
ECHO
408
Q

What possible methods of tissue sampling are there for lung cancer?

A

Bronchoscopy - endobronchial bx, wash, EBUS, radial EBUS, EUS
USS-neck node, lung/chest wall mass, pleural fluid, liver
CT biopsy - lung, pleura
Thorocoscopy - medical
Surgical - mediastinoscopy, VATS pleural box, rigid bronchoscopy, neck and axillary nodal excision, VATS excision bx, brain bx, bone bx

409
Q

What are the symptoms of a primary lung tumour?

A 
No symptoms (most common presentation!)
Cough, wheezing, dyspnoea, haemoptysis, lung infection, chest/shoulder pain, weight loss, lethargy/malaise
410
Q

What is haemoptysis?

A

Coughing up blood

411
Q

What is dyspnoea?

A

Shortness of breath

412
Q

What might the symptoms of regional metastases of lung cancer be?

A

Bloated face (SVC obstruction), hoarseness (left recurrent laryngeal nerve palsy), dyspnoea (anaemia, pleural or pericardial effusions), dysphagia (oesophageal compression), chest pain (parietal pleural involvement), post obstructive pneumonia (tumour blocks airway, sputum collects, bacteria infect)

413
Q

What might be some symptoms of distant metastases of lung cancer?

A 
Bone pain/fractures
CNS symptoms (headache, double vision, confusion)
Metabolic - thirst and constipation (hypercalcaemia), seizures (hyponatraemia)
414
Q

What are some possible signs of lung cancer?

A

Cachexia, pale conjunctiva, cervical lymphadenopathy, horners syndrome, consolidation, signs of pleural effusion, muffled heart sounds, liver enlargement, skin metastases, neurological long tract signs, enlarged veins (vena cava obstruction)
Or… no signs

415
Q

What are the endocrine paraneoplastic syndromes that might be seen in lung cancer?

A

Hypercalcaemia
Cushing’s syndrome
Inappropriate ADH secretion (SIADH)

416
Q

What are the haematological paraneoplastic syndromes that might be seen in lung cancer?

A

Anaemia

Thrombocytosis

417
Q

What are the cutaneous paraneoplastic syndromes that might be seen in lung cancer?

A

Dermatomyositis

418
Q

What are the neurological paraneoplastic syndromes that might be seen in lung cancer?

A

Encephalopathy
Peripheral neuropathy
Eaton-Lambert syndrome

419
Q

What are the skeletal paraneoplastic syndromes that might be seen in lung cancer?

A

Finger clubbing

420
Q

When would you carry out a biopsy in lung cancer?

A

If patient is well enough to sustain it, and results might change your management plan

421
Q

What is a carcinoma?

A

An invasive malignant epithelial tumour

422
Q

What are the main types of cancer present in lung cancer?

A 
Non-small cell:
- Squamous cell carcinoma
- Adenocarcinoma 
- Large cell carcinoma
Small cell carcinoma
423
Q

What molecular markers might you look for in lung cancer?

A

EGFR mutations
ALK mutations
KRAS mutations
PD1 mutations

424
Q

Describe the stages in the performance status of a patient with lung cancer

A

0 - No symptoms, normal activity level
1 - Symptomatic, but able to carry out normal daily activities
2 - Symptomatic, in bed or chair less than half the day. Needs some assistance with daily activities
3 - Symptomatic, in bed or chair more than half the day
4 - Bedridden
5 - Dead

425
Q

What are the different treatment options for lung cancer?

A

Surgery - mostly for non-small cell carcinoma
Radiotherapy - ‘radical’ (curative intent), or ‘palliative’
Combination chemotherapy - survival increase, symptom control, neoadjuvant or adjuvant therapy (potentially curative in small cell)
Combination therapy - chemo-radiotherapy (potentially curative)
‘Biological (targeted)’ therapies - based on mutational analysis (EGFR, ALK, RAS, PD1)
Palliative care - active symptom control e.g. Analgesia, radiotherapy, airway stents, anxiolytics, nutritional support, patient support groups

426
Q

What is an X-ray?

A

An electromagnetic wave of high energy and very short wavelength, which is able to pass through many material opaque to light.
A photographic of digital image of the internal composition of the body, produced by X-rays being passed through the body part and being absorbed to different degrees by different tissues.
This is displayed as levels of contrast on a grey scale (black to white)

427
Q

What is the most common orientation for an X-ray?

A

Posterior to anterior (PA)

Assume it is such unless written otherwise on X-ray

428
Q

Why are anterior to posterior (AP) X-rays not so useful?

A

Heart is closer to the receptor, and therefore is magnified. Can’t make judgement of heart on AP. Generally AP only done if patient can’t stand up.

429
Q

What must be included in a chest x-ray?

A

1st rib, lateral margin of ribs, costophrenic angle

430
Q

Where would you look for rotation in a CXR?

A

Look at medial ends of clavicle (but slight rotation is not important)

431
Q

In which phase of respiration is a CXR usually done?

A

Inspiratory phase (patient holds breath)

432
Q

What is the normal inspiratory lung volume visible on a CXR?

A

5th-7th anterior ribs at MCL

Look at diaphragm, if curved cool, if flattened then increased lung volume

433
Q

What might cause problems with incomplete inspiration visible on a CXR?

A

Big heart, increased lung markings

434
Q

What might cause exaggerated expansion visible on a CXR?

A

Obstructive airway disease

435
Q

What is penetration with regards to an X-ray?

A

The degree to which the X-rays have penetrated the body. Adequate penetration - vertebrae just visible through heart, complete left hemidiaphragm is visible. Digital manipulation often negates this

436
Q

What is an artifact with regards to an X-ray?

A

External (iatrogenic) material which obstructs view, e.g. clothes (buttons!), hair, surgical/vascular lines, pacemaker

437
Q

What are the different zones of a lung? (As used to describe an X-ray)

A 
Left/right
Upper (above hilar)
Middle (Hilary level)
Lower (below hilar)
Zonesssss
438
Q

Describe the systematic process you would go though to evaluate a chest x-ray

A 
Patient demographics 
Projection
Adequacy
Airway
Breathing
Circulation
Diaphragm (/dem bones)
Review areas
439
Q

What does the AABCD stand for when analysing a CXR?

A

A - adequacy (RIP - rotation, inspiration, penetration)
A - airway (trachea, bronchi, hilar)
B - breathing (lungs (whole?), pleural spaces, lung interfaces)
C - circulation (mediastinum, aortic arch, pulmonary vessels (hilar), right heart border, right atrium, middle lobe interface, left heart border, left ventricle, lingual interface)
D - Diaphragm/Dem bones (free gas, nodules, fracture/dislocation, mass)

440
Q

List some areas commonly missed when analysing a CXR

A 
Apices - pneumothorax
Thoracic inlet - mass
Paratracheal stripe - mass/lymph nodes
AP window - lymph nodes
Hila - mass/collapse 
Behind heart - mass 
Below diaphragm - pneumoperitoneum/mass
Bones (all of them) - fracture, mass, missing
Edge of films
441
Q

What is a silhouette sign?

A

Adjacent structures of differing density form a crisp ‘silhouette’, e.g. Heart nest to lung, white next to black. Loss of this contour can suggest/locate pathology.

442
Q

What can the right heart border be referred to in a CXR?

A

RML

443
Q

What can the left heart border be referred to in a CXR?

A

Lingula

444
Q

What does a paratracheal stripe in a CXR suggest?

A

Mediastinal disease

445
Q

Where is the aortic knuckle located?

A

Anterior mediastinum/upper lobe

446
Q

What do you look for when analysing the chest wall in a CXR?

A

Lung/pleura/rib lesion

447
Q

How do you look for a mediastinal shift in a CXR?

A

Check adequately centred image. Then look at trachea, cardiac shadows pushed or pulled?

448
Q

What would a mediastinal push look like on a CXR?

A

Increased volume or pressure

449
Q

What would a mediastinal pull look like on a CXR?

A

Decreased volume or pressure

450
Q

List some specific CXR findings

A

Pneumothorax, pleural effusion, consolidation, space occupying lesion within lung, lobar collapse, estimate the cardiac index

451
Q

What is pneumothorax?

A

Air trapped in the pleural space

452
Q

What can cause pneumothorax?

A

Can be spontaneous, or as a result of underlying lung disease

453
Q

What is the most common cause of pneumothorax?

A

Trauma, with laceration of the visceral pleura by a fractured rib

454
Q

When is a pneumothorax said to be ‘large’?

A

If lung edge measures more than 2cm from the inner chest wall at the level of the hilum

455
Q

What is a tension pneumothorax?

A

Tracheal or mediastinal shift away from pneumothorax and depressed hemidiaphragm

456
Q

What are the signs of a tension pneumothorax?

A

Visible pleural edge (lung markings not visible beyond this edge)

457
Q

What is pleural effusion?

A

Collection of fluid in the pleural space.

458
Q

What would a pleural effusion look like on a CXR?

A

Uniform white area. Loss of costophrenic angle. Hemidiaphragm obscured. Meniscus at upper border.
Beware supine CXR (laying down)

459
Q

What is lobar lung collapse?

A

Volume loss within lung lobe

460
Q

What might cause lobar lung collapse?

A

Luminal - aspirated foreign material, mucous plugging, latrogenic
Mural - bronchogenic carcinoma
Extrinsic - compression by adjacent mass

461
Q

What are some generic findings of lobar lung collapse?

A

Elevation of the ipsilateral hemidiaphragm
Crowding of the ipsilateral ribs
Shift of the mediastinum towards the side of atelectasis
Crowding of pulmonary vessels

462
Q

What is consolidation?

A

Filling of small airways/alveoli with stuff

463
Q

If the lungs are filled with pus, what does this suggest the cause of consolidation is?

A

Pneumonia

464
Q

If the lungs are filled with blood, what does this suggest the cause of consolidation is?

A

Haemorrhage

465
Q

If the lungs are filled with fluid, what does this suggest the cause of consolidation is?

A

Oedema

466
Q

If the lungs are filled with cells, what does this suggest the cause of consolidation is?

A

Cancer

467
Q

What does consolidation look like on a CXR?

A

Dense opicification. Volume preserved/increased. Air bronchogram

468
Q

What is a space occupying lesion?

A

Nodule >3cm
Mass >3cm
Single or multiple

469
Q

What could be the cause of a space occupying lesion?

A

Malignant (primary, metastases), benign mass lesion, inflammatory, congenital, mimics (bone lesion, cutaneous lesion, nipple shadow)

470
Q

What is a normal cardiac index?

A

Usually less than 50% width of chest wall

471
Q

What’s a key point to remember when analysing cardiac index?

A

Must be a PA image!

472
Q

What is interstitial disease?

A

Disease effecting acini, alveolar lumen, bronchiolar lumen, bronchioles…
Broad discriptive term

473
Q

What cells might be involved in interstitial disease?

A

Epithelial, endothelial, mesenchymal, macrophage, recruited inflammatory cells

474
Q

What symptoms might be present for interstitial lung disease?

A

SOB, cough, chronic onset.

Clubbing, right heart failure, cyanosis, tachycardia, tachypnoea, decreased chest movement, course crackles

475
Q

What might cause interstitial lung disease?

A

Occupational, treatment related, connective tissue disease, immunological, idiopathic (mostly)

476
Q

What is IPF? (With regards to respiratory disease)

A

Idiopathic pulmonary fibrosis

477
Q

What is the prognosis of idiopathic pulmonary fibrosis?

A

Bad - mean survival 3yrs.

478
Q

How is idiopathic pulmonary fibrosis usually diagnosed?

A

CT

479
Q

What therapies are available for treatment of IPF idiopathic pulmonary fibrosis?

A

Pirfenidone and ninedanib - slows decline inf FVC, but some drug toxicity (only used if have to)

480
Q

What is asbestosis?

A

Interstitial lung disease associated with asbestos

481
Q

What can asbestos plaques cause?

A

Diffuse pleural thickening (benign asbestos pleural effusions BAPE)

482
Q

What are some diseases associated with asbestos?

A

Mesothelioma, bronchogenic lung cancer, rounded atelectasis

483
Q

What happens to the asbestos fibres?

A

They are needle like, and can lodge in pleura, causing disease

484
Q

What treatment would you give for drug induced ILD?

A

Stop drug and give steroid instead (methotrexate, bleomycin, amiodarone, nitrofurantoin)

485
Q

List some connective tissue diseases that have manifestations in the lung

A 
Dermatomyositis/polymyositis
Sjögren's syndrome
Systemic lucid erythematosis
Scleroderma
Rheumatoid arthritis (lung symptoms may present before joint!)
486
Q

What is sarcoidosis?

A

Often asymptomatic, or cough/rash. PFTs normal, restrictive, obstructive, mixed. Onset 20-80yrs.
Biopsy non-caseating granuloma

487
Q

What is the treatment for sarcoidosis?

A

None, or steroids (but these have many side effects), methotrexate

488
Q

What are the functions of the pleural space?

A

Allow movement of lung and chest wall
Coupling of chest wall and lung - inward lung recoil, outward chest wall recoil
Pleural fluid circulation

489
Q

What is the innervation of the parietal pleura of the chest wall?

A

Somatic, sympathetic, and parasympathetic. Phrenic and intercostal nerves

490
Q

What is the innervation of the visceral pleura of the chest wall?

A

No somatic innervation

Sympathetic and parasympathetic

491
Q

How might a patient describe pleuritic chest pain? (Parietal)

A

‘Knife like’

Worse with inspiration

492
Q

What is the average turnover of pleural fluid?

A

~15ml a day

Can increase to 300ml a day

493
Q

How is pleural fluid produced?

A

Capillary filtration (starling forces), parietal pleura only

494
Q

Where is pleural fluid reabsorbed?

A

Lymphatic drainage, parietal pleural lymphatic vis stomata on parietal pleural surface (mainly mediastinal, diaphragmatic regions)

495
Q

What might cause pleural fluid accumulation?

A 
Increased production/decreased absorption:
Lung interstitial fluid increase
Hydrostatic pressure increase
Permeability increase
Oncotic pressure decrease
Peritoneal fluid
Thoracic duct disruption
Lymphatic blockage
Elevated systemic venous pressure
496
Q

What is the criteria for which, if one or more is met than fluid is classed as exudate?

A

Pleural fluid protein divided by serum protein is >0.5 (or protein is >30g/l)
Pleural fluid lactate dehydrogenase LDH divided by serum LDH is >0.6
Pleural fluid LDH >2/3 the upper limit of laboratory normal value for serum LDH (LDH>200)

497
Q

How would you get some pleural fluid to test?

A

Thoracocentesis (ultrasound/CT guided)

498
Q

What would you do with the sample following a thoracocentesis?

A

Analyse appearance, then get cell count and differential, protein, LDH, pH, glucose, cytology

499
Q

If pleural fluid is transudate, what might be causing it?

A

Heart failure, cirrhosis, hypoalbunaemia

500
Q

If pleural fluid is exudate, what might be causing it?

A

Infection, malignancy, RA, pulmonary embolism, asbestos

501
Q

What is empyema?

A 
pH <7.2
Glucose <3.4mmol
CT/USS - septations
May or may not be 'unwell'
Inflammatory markers may/may not be raised.
502
Q

What are risk factors for empyema?

A

Risk factors - alcoholism, immunocompromise

503
Q

What is the treatment for empyema?

A

Antibiotics +- drainage (surgical chest drain)

504
Q

What usually causes haemothorax?

A

Usually traumatic or iatrogenic

505
Q

What might be required for treatment of haemothorax?

A

Chest drain or surgical drain

506
Q

What is chylothorax?

A

Milky appearance. Lymphatic interruption. lymphoma, iatrogenic

507
Q

What is the commonest metastatic cancer to spread to the lungs?

A

Breast, renal, colon

508
Q

What is the commonest primary malignancy of the lungs?

A

Mesothelioma (classic symptom = chest pain)

509
Q

What are the symptoms of mesothelioma?

A

Chest pain (classic symptom)
Pain, breathlessness
CXR effusion, mediastinal pleural enlargement
History of asbestos exposure

510
Q

What is primary pneumothorax?

A

In otherwise healthy people

‘Spontaneous’

511
Q

What is secondary pneumothorax?

A

Underlying lung disease e.g. Cancer, COPD

512
Q

What is iatrogenic pneumothorax?

A

Due to procedures e.g. Central lines

513
Q

What are the symptoms of pneumothorax?

A

Pleuritic chest pain, dyspnoea

514
Q

When is a pneumothoax small?

A

<2cm

515
Q

When is a pneumothorax large?

A

> 2cm between lung margin and chest wall

516
Q

What investigations might you do for a pneumothorax?

A

Plain CXR

517
Q

What is the treatment of a patient with a small pneumothorax and no SOB?

A

Discharge and early outpatient review

518
Q

What is the treatment of a patient with pneumothorax and SOB?

A

Intervention regardless of size of pneumothorax

519
Q

What are the treatment options for a patient with pneumothorax and SOB?

A

Aspiration
Chest drain
Chemical pleurodesis (surgically glue peritoneum to wall) if recurrent
Open thoracotomy and pleuroectomy - lowest reoccurrence rate

520
Q

When might you use aspiration to treat pneumothorax?

A

1st line treatment for primary pneumothorax requiring intervention
Used for small secondary pneumothorax in minimally breathless patients

521
Q

When might you use a chest drain to treat a pneumothorax?

A

If aspiration fails to control symptoms, insert intercostal tube.
Recommended treatment for secondary pneumothorax

522
Q

How is tension pneumothorax diagnosed?

A

Clinically

523
Q

What are the signs of tension pneumothorax?

A

Cardiovascular compromise - tachycardia, hypotension
Decreased expansion with hyper resonance and absent breath sounds on side of pneumothorax
Shift of mediastinum to opposite side - trachea, apex beat
Hypoxaemia

524
Q

What is the treatment of tension pneumothorax?

A

Don’t wait for CXR! Cannula into affected side. O2. Intercostal chest drain. Respiratory/thoracic surgical referral - do not want to have a chance of it happening again (surgical pleurodesis)

525
Q

How does having a pneumothorax effect flying?

A

Must wait at least 1 wk before can fly

526
Q

When can you go diving, if you’ve had a pneumothorax?

A

Only if you have had a bilateral surgical pleuroectomy

527
Q

Should you admit a patient with a secondary pneumothorax?

A

Yes for at least 24hrs

528
Q

List some congenital forms of chest wall disease

A

Pectus deformities
Scoliosis
Kyphosis
Muscular dystrophy

529
Q

List some aquired forms of chest wall disease

A

Trauma
Latrogenic
Ankylosing spondylitis
Motor neurone disease

530
Q

What could cause tracheal shift - push to opposite side of diseased lung?

A

Massive effusion, large or tension pneumothorax

531
Q

What could cause tracheal shift - pulled to same side as diseased lung?

A

Central collapse, unilateral fibrosis (e.g. Previous TB infection)

532
Q

List some lung diseases which do not cause tracheal shift

A

Pneumonia, COPD, asthma, diffuse fibrosis

533
Q

What could hyper resonant percussion be a sign of?

A

Pneumothorax

534
Q

What could stony dull percussion be a sign of?

A

Pleural effusion

535
Q

What could dull/impaired percussion be a sign of?

A

Consolidation

536
Q

How would one describe normal breath sounds?

A

Normally vesicular

537
Q

What could bronchial breath sounds be due to?

A

Consolidation (lobar pneumonia)

538
Q

What could reduced intensity/absent breath sounds be due to?

A

Air (pneumothorax) or fluid (effusion) between chest wall and lung

539
Q

When is vocal resonance increased?

A

When bronchial breathing is present (e.g. Lobar pneumonia)

540
Q

When would vocal resonance be decreased?

A

Pneumothorax/pleural effusion

541
Q

List the signs on examination of a patient with consolidation

A

Trachea: not shifted
Chest movements: reduced on effected side
Percussion: dull
Breath sounds: bronchial breath sounds. Conducted through consolidated lung to chest wall (sounds from large airways)
Vocal resonance: increased
Added sounds: crackles +- pleural rub

542
Q

Describe the signs on examination of a patient with pleural effusion

A

Trachea: if large, shifted to opposite side (pushed by effusion)
Chest movements: reduced on effected side
Percussion: stony dull over effusion
Breath sounds: vesicular - reduced intensity/absent on affected side
Vocal resonance: reduced
Added sounds: none

543
Q

Describe what you would find on examination of a patient with pneumothorax

A

Trachea: if large or tension, trachea shifted to opposite side (away from PNX)
Chest movements: reduced on effected side
Percussion: hyper resonant on affected side
Breath sounds: vesicular, reduced intensity. (Air between chest wall and lung)
Vocal resonance: decreased
Added sounds: none

544
Q

What is a lobar collapse?

A

Due to an obstruction of a large airway, air in that part of lung is gradually absorbed/diffuses away - ‘central’ cause of lung collapse. Lung is tethered to pleura, so is pulled towards it, bringing the trachea/mediastinum with it.

545
Q

Describe what you would find on examination of a patient with lobar collapse

A

Trachea shift: towards effected side. Subatmospheric pleural pressure pulls collapsed lung and mediastinum to affected side
Chest movements: reduced on effected side
Percussion: normal (or dull) over affected lobe
Breath sounds: reduced or absent over effects lobe
Vocal resonance: reduced
Added sounds: none

546
Q

Describe what you would find on examination of a patient with localised lung fibrosis

A

Trachea: pulled by contracting fibrous tissue towards effected side
Chest movements: reduced on effected side
Percussion: normal
Breath sounds: vesicular
Added sounds: crackles
Vocal resonance: normal/increased

547
Q

Describe what you would find on examination of a patient with diffuse lung fibrosis

A 
Trachea: central
Chest movements: reduced on both sides symmetrically
Percussion: normal
Added sounds: (fine) crackles
Vocal resonance: normal/increased
548
Q

Describe what you would find on examination of a patient with COPD or asthma

A

May find a barrel chest on inspection
Trachea: central
Chest movements: reduced symmetrically on both sides
Percussion: resonant
Breath sounds: vesicular
Added sounds: prolonged expiration and wheezes
Vocal resonance: normal

549
Q

What is COPD?

A

Loss of elastic tissue
Airways obstruction and reduced elastic recoil - hyperinflated lung (barrel chest)
FEV1/FVC <70%
FVC not reduced much
Low diffusion capacity (due to less surface area)

550
Q

How does fibrosis effect lungs?

A

Increase of fibrous tissue
Less compliant - harder to stretch, smaller lungs
No airway obstruction
FEV1/FVC >70%
FVC markedly reduced
Low diffusion capacity (due to thickened membrane)

551
Q

What might cause pleuritic chest pain?

A

Lobar pneumonia, pulmonary embolism, infarction, pneumothorax

552
Q

What is dyspnoea?

A

An awareness that it is taking an abnormal amount of effort to breath (see MRC dyspnoea scale to gauge how bad it is)

553
Q

What might a cough lasting <3wk be due to?

A

Upper/lower respiratory tract infection,

554
Q

What might a cough lasting >3wk be due to?

A

COPD, asthma, cancer, medication (e.g. ACE inhibitors)

555
Q

What is haemoptysis?

A

Coughing up blood (from lungs)

556
Q

What is haematemesis?

A

Throwing up blood (from GIT)

557
Q

What might cause haemoptysis?

A

Bronchitis, bronchial carcinoma, pneumonia, pulmonary infection, tuberculosis

558
Q

What might cause a wheeze?

A

Asthma, COPD, foreign body…

559
Q

Is strider normally on inspiration or expiration?

A

Inspiration

560
Q

Is wheeze normally on inspiration or expiration?

A

Expiration

561
Q

What might cause hoarseness of voice?

A

Transient infection of vocal cords, vocal cord tumour, recurrent laryngeal nerve palsy (left side has a particularly long course, could be damaged by bronchial carcinoma)

562
Q

What drugs might cause a cough?

A

ACE inhibitors

563
Q

What drugs might cause a wheeze?

A

Beta blockers

564
Q

What drugs might cause a pulmonary embolism?

A

Oestrogens

565
Q

What drugs might cause fibrotic lung changes?

A

Amiodarone

566
Q

What is a barrel chest?

A

Increased AP diameter

567
Q

What is a pigeon chest?

A

Prominent sternum/costal cartilage

568
Q

What is a funnel chest?

A

Depression of lower end of sternum

My ESA 3 (6 decks)

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