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LSS Year 1 > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

How many people die from respiratory disease in the UK?

A

1 in 5

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2
Q

What is the biggest cancer killer in the UK?

A

Lung cancer

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3
Q

What might cause breathlessness?

A
  • Lung disease
  • Heart disease
  • Pulmonary vascular disease
  • Neuromuscular disease (e.g. diaphragm weakness)
  • Systemic disorders (e.g. anaemia, hyperthyroidism, obesity)
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4
Q

What nerves provide a sense of smell?

A

Olfactory nerve

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5
Q

Where do the olfactory nerves connect to?

A

Olfactory bulb and then the olfactory tract

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6
Q

What sinus lies above the eyebrows?

A

Frontal sinus

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7
Q

What sinus lies in between the eyes?

A

Ethmoid sinuses

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8
Q

What sinus lies under the eyes?

A

Maxillary sinuses

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9
Q

What is the most posterior sinus?

A

Sphenoidal sinuses

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10
Q

What are the parts of the pharynx, starting superiorly?

A

Nasopharynx
Oropharynx
Laryngopharynx

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11
Q

What is the muscle in the trachea called?

A

Trachealis muscle

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12
Q

What ligaments are found in the trachea?

A

Anular ligaments

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13
Q

What reduces surface tension in bronchioles and alveoli?

A

Surface tension

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14
Q

What are the main areas of the chest?

A

Lungs and mediastinum

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15
Q

How many lobes in the lungs?

A

Left lung: 2 lobes

Right lung: 3 lobes

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16
Q

What are the names of the fissures in the lungs?

A

Left: Oblique fissure
Right: Oblique fissure and horizontal fissure

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17
Q

How many segments are there in each lung?

A

Left lung: 8

Right lung: 10

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18
Q

What is the pressure of oxygen in the air and in the blood?

A

PO2 Air= 100mmHg

PO2 Blood= 40mmHg

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19
Q

Where is the diaphragm? When is it highest?

A

Margin attached to costal margin

Highest in expiration

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20
Q

What nerve provides motor innervation to the diaphragm? Where does it originate in the spine?

A

Phrenic nerve

C3, 4, 5

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21
Q

What is minute ventilation?

A

The volume of air expired in one minute (VE) or per minute

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22
Q

What is respiratory rate?

A

(RF) The frequency of breathing per minute

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23
Q

What is alveolar ventilation?

A

(Valv) The volume of air reaching the respiratory zone

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24
Q

What is respiration?

A

The process of generating ATP either with an excess of oxygen (aerobic) and a shortfall (anaerobic)

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25
Q

What is anatomical dead space?

A

The capacity of the airways nincapable of undertaking gas exchange

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26
Q

What is alveolar dead space?

A

Capacity of the airways that should be able to undertake gas exchange but cannot (e.g. hypoperfused alveoli)
Alveoli without a blood supply

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27
Q

What is physiological dead space?

A

Equivalent to the sum of alveolar and anatomical dead space

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28
Q

What is hypoventilation?

A

Deficient ventilation of the lungs; unable to meet metabolic demand (increased PO2- acidosis)

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29
Q

What is hyperventilation?

A

Excessive ventilation of the lungs atop of metabolic demand (results in reduced PCO2- alkalosis)

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30
Q

What is hyperpnoea?

A

Increased depth of breathing (to meet metabolic demand)

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31
Q

What is hypopnoea?

A

Decreased depth of breathing (inadequate to meet metabolic demand)

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32
Q

What is apnoea?

A

Cessation of breathing (no air movement)

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33
Q

What is dyspnoea?

A

Difficulty in breathing

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34
Q

What is bradypnoea?

A

Abnormally slow breathing rate

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35
Q

What is tachypnoea?

A

Abnormally fast breathing rate

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36
Q

What is orthopnoea?

A

Positional difficulty in breathing (when lying down)

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37
Q

What pleural membrane surrounds the lungs?

A

Visceral pleural membrane

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38
Q

What pleural membrane covers the chest wall?

A

Parietal pleural membrane

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39
Q

What fills the pleural cavity?

A

A protein-rich pleural fluid

fixed volume

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40
Q

What is a haemothorax?

A

Intrapleural bleeding

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41
Q

When are the forces in the lungs equal?

A

At the end of a normal breath out

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42
Q

What is tidal volume?

A

The amount of breathing you are doing to meet metabolic demand (∼500mL - increases with exercise)

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43
Q

What is your inspiratory reserve volume?

A

The amount you can breath in (up to total lung capacity) after a normal tidal breath inhalation
∼3100mL

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44
Q

What is expiratory reserve volume?

A

The amount you can exhale after a normal tidal breath exhalation
∼1200mL

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45
Q

What is risidual volume?

A

The amount of air left in the lungs which you cannot exhale

∼1200

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46
Q

What is total lung capacity?

A

Total lung volume
= IRV+TV+ERV+RV
∼6L

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47
Q

What is vital capacity?

A

Total of the volumes in the lungs we have access to
=IRV+TV+ERV
∼4800mL

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48
Q

What is functional residual capacity?

A

Amount of air in your lungs at the equilibrium point (when forces are equal at the end of normal expiration)
=ERV+RV
∼2400mL

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49
Q

What is inspiratory capacity?

A

From your functional residual capacity how much air can you draw into the lungs, if you put the effort in (air in from equilibrium point)
=IRV+TV
∼3600mL

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50
Q

What factors affect lung volumes and capacities? (5)

A

1) Body size (height, shape)
2) Sex
3) Disease (pulmonary, neurological)
4) Age (chronological, physical)
5) Fitness (innate inheritance, training)

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51
Q

What is negative pressure breathing? When do we do this? What is the relationship between Palv and Patm?

A

Normal healthy breathing- creating a negative pressure in the lungs for the air to be sucked into
Palv is reduced below Patm

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52
Q

What is positive pressure breathing? When so we do this? What is the relationship between Palv and Patm?

A

Occurs when on ventilation or undergoing CPR

Patm is increased above Palv

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53
Q

What is the pressure in the pleural cavity?

A

Ppl=-5cmH2O

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54
Q

What is transmural pressure? What affect does it have on ventilation?

A

The pressure difference (Pinside - Poutside)
A negative transrespiratory pressure will lead to inspiration
A positive transmural pressure leads to expiration

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55
Q

Describe the changes that occur during quiet breathing and the mechanism which allows this to happen

A

1) At equilibrium: No volume change, pressure at equilibrium
2) Chest wall expands and diaphragm pulls down: create negative pressure, volume goes up
3) More air flows in and pressure goes back to equilibrium
4) Recoil forces pull the lungs closed: pressure goes up and volume starts to go down
5) Return to equilibrium

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56
Q

What is the conducting zone in the lungs? What is the volume of this area?

A

Anatomical dead space
Doesn’t participate in gas exchange
16 generations. Typically 150mL in adults at FRC

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57
Q

What is the respiratory zone in the lungs? What is the volume of this area?

A

Alveolar ventilation
Where gas exchange takes place.
7 generations. Typically 350mL in adults

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58
Q

If someone has an obstructive disease, how would this affect their FVC?

A

It would be lower

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59
Q

What percentage of lung capacity can a healthy person expect to exhale for FEV1?

A

75-100%

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60
Q

What percentage of lung capacity can a person with an obstructive disease expect to exhale for FEV1?

A

50%

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61
Q

If someone has a restrictive disease, how would this affect their FVC?

A

It would be lower

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62
Q

What percentage of lung capacity can a person with a restrictive disease expect to exhale for FEV1?

A

75-100%

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63
Q

What are the approximate FEV1/FVC ratios for normal, restrictive and obstructive disease?

A 
Normal= 73%
Restrictive= 87%
Obstructive= 53%

Restrictive = >75%
Obstructive=

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64
Q

What happens to a flow-volume loop with obstructive disease? (mild and severe)

A

Displaced to the left with coving on exhalation
Mild: Flow rate not much lower than normal
Severe: Shorter curve (flow rate) than normal

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65
Q

What happens to a flow-volume loop with restrictive disease?

A

Displaced to the right

Narrower curve

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66
Q

How does obstruction effect a flow-volume loop? What are the different types?

A

e.g. tumour
Extrathoracic: Inspiratory blunting, otherwise normal
Intrathoracic: Expiratory blunting, otherwise normal
Fixed airway obstruction: Inspiratory and expiratory blunting, otherwise normal

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67
Q

What is Dalton’s Law?

A

Pressure of a gas mixture is equal to the sum of the partial pressures of the gases in that mixture

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68
Q

What is Boyle’s Law?

A

At a constant temperature, the volume of a gas is inversely proportional to the pressure of that gas

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69
Q

What percentage of gases make up the air?

A 
Nitrogen: 78.09
Oxygen: 20.95
Argon: 0.93
Carbon dioxide: 0.04
Ne, He, H, Kr etc:
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70
Q 
If inspiring dry air at sea level:
PO2 = 21.3kPa
PCO2 = 0kPa
PH2O = 0kPa
what changes occur to the gas as it passes through the conducting airways to the respiratory airways?
A 
Air is WARMED, HUMIDIFIED, SLOWED and MIXED
Conducting airways:
PO2 = 20kPa
PCO2 = 0kPa
PH2O = 6.3kPa

Respiratory airways:
PO2 = 13.5kPa
PCO2 = 5.3kPa
PH2O = 6.3kPa

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71
Q

How much greater is the affinity for the fourth oxygen molecule binding to haemoglobin, than the first one?

A

300 times greater

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72
Q

What does haemoglobin binding allow the binding of in the centre of a haemoglobin molecule?

A

2, 3-DPG

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73
Q

What is methaemoglobin? What disease is associated with it?

A

Haemoglobin with iron in Fe3+ state which does not bind haemoglobin
Methaemoglobinaemia

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74
Q

At what point is haemoglobin 50% saturated?

A

P50

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75
Q

What is a rightward shift of the oxygen dissociation curve associated with?

A

↑ temperature
Acidosis (Bohr effect)
Hypercapnia
↑ 2, 3-DPG

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76
Q

What is a leftward shift of the oxygen dissociation curve associated with?

A

↓ temperature
Alkalosis
Hypocapnia
↓ 2, 3-DPG

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77
Q

What causes a downward shift of the oxygen dissociation curve?

A

Anaemia

Impaired oxygen-carrying capacity

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78
Q

What causes an upward shift of the oxygen dissociation curve?

A

Polycythaemia

Increased oxygen-carrying capacity

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79
Q

What does carbon monoxide do to the oxygen dissociation curve?

A

Causes a downward and leftward shift

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80
Q

What is myoglobin?

A

A monomer that is found in muscles that stores oxygen needed in exercise

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81
Q 
What are the gas values in post-alveolar venular blood?
PO2
SaO2
HbO2
CDO2
CaO2
A 
PO2 = 13.5kPa
SaO2 = 100%
HbO2 = 20.1mL/dL
CDO2 = 0.34mL/dL
CaO2 = 20.4mL/dL
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82
Q 
What are the gas values once the blood has returned to the heart? Why are they different?
PO2
SaO2
HbO2
CDO2
CaO2
A 
Blood supplying the lungs is added to the oxygenated blood so the values drop
PO2 = 12.7kPa
SaO2 = 97%
HbO2 = 20mL/dL
CDO2 = 0.32mL/dL
CaO2 = 20.3mL/dL
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83
Q 
What are the gas values that return to the right side of the heart?
PO2
SaO2
HbO2
CDO2
CaO2
A 
PO2 = 3.5kPa
SaO2 = 75%
HbO2 = 15mL/dL
CDO2 = 0.14mL/dL
CaO2 = 15.1mL/dL
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84
Q

What is the oxygen flux?

A 
△ = -5mL/dL
△ = -250mL O2/min
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85
Q

How is CO2 transported in the body?

A

Dissolves in the plasma

CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3-

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86
Q 
What are the gas values of carbon dioxide in arterial blood?
PaCO2
CO2 as HCO3
HbCO2
CDCO2
CaCO2
pH
A 
PaCO2 = 5.3kPa
CO2 as HCO3 = 43mL/dL
HbCO2 = 2.5mL/dL
CDCO2 = 3.0mL/dL
CaCO2 = 48.5mL/dL
pH = 7.40
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87
Q 
What are the gas values of carbon dioxide in venous blood?
PaCO2
CO2 as HCO3
HbCO2
CDCO2
CaCO2
pH
A 
PaCO2 = 6.1kPa
CO2 as HCO3 = 45.2mL/dL
HbCO2 = 3.8mL/dL
CDCO2 = 3.4mL/dL
CaCO2 = 52.4mL/dL
pH = 7.36
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88
Q

What is the CO2 flux?

A 
△ = +4mL/dL
△ = +200mL CO2/min
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89
Q

What happens to CO2 when it enters a red blood cell?

A

CO2 + H2O ⇌ H2CO3 (carbonic anhydrase) ⇌H+ + HCO3-
HCO3- (bicarb) ⇌ Cl- + H2O (swapped in plasma- Chloride shift)
CO2 + amine end → carbaminohaemoglobin

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90
Q

What are the three roles of haemoglobin?

A

1) Oxygen transport
2) Carbon dioxide transport
3) Buffering (accepts H+ from CO2 reaction)

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91
Q

How is carbon dioxide transported in arterial and venous blood? Include proportions

A 
Arterial = 48mL/dL
HCO3- = 43.0mL/dL
HbCO2 = 2.5mL/dL
Dissolved = 2.5mL/dL
Venous = 52mL/dL
HCO3- = 45.2mL/dL
HbCO2 = 3.0mL/dL
Dissolved = 3.8mL/dL
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92
Q

What are cardiac output and ventilation roughly?

A 
CO = 5L
Ventilation = 6L
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93
Q

What part of the lungs is most perfused?

A

Basal area

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94
Q

How do you calculate alveolar ventilation?

A

= (Tidal volume - dead space) x respiratory frequency

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95
Q

How do you calculate the ventilation perfusion ratio?

A

= Alveolar ventilation / cardiac output

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96
Q

How do the branches of the lungs divide?

A

Dichotomous branching

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97
Q

What is the structure of the cartilage in the trachea?

A

C shaped

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98
Q

What cells make up the surface of the airway?

A

Cilia cells

Goblet cells

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99
Q

What are the contractile cells of the airway?

A

Smooth muscle

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100
Q

What are the secretory cells of the airway?

A

Goblet (epitheliul)

Mucous, serous (glands)

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101
Q

What connective tissue is found in the airway?

A

Fibroblast, interstitial cell (elastin, collagen, cartilage)

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102
Q

How do goblet cells secrete mucus?

A

Upon stimulus granules move to the surface of the cell and fuse. Lots of water is taken into the cell, it expands and explodes out

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103
Q

What are the different types of cells which make up the airway submucosal glands? What do they do?

A

Mucous acini: secrete mucous
Serous acini: secrete antibacterials (e.g. lysozyme) (produce a watery secretion which flushes over the mucous acini)
Glands also secrete water and salts (e.g. Na+ and Cl-)

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104
Q

How many cilia are there per cell?

A

Around 200 per cell

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105
Q

What are the functions of the airway epithelium?

A

1) Secretion of mucins, water and electrolytes (components of mucus)
2) Movement of mucus by cilia (mucociliary mediators
3) Physical barrier
4) Production of regulatory and inflammatory mediators
- NO (by NOS)
- CO (by hemeoxygenase, HO)
- Arachidonic acid metabolites (e.g. prostaglandins COX)
- Chemokines (e.g. IL-8)
- Cytokines (e.g. GM-CSF)
- Proteases

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106
Q

What three things does inflammation of airway smooth muscle cause?

A 
1) Structure
Hypertrophy, proliferation
2) Tone
(airway calibre)
Contraction, relaxation
3) Secretion
Mediators, cytokines, chemokines
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107
Q

What happens when there is inflammation in airway smooth muscle?

A

Smooth muscle cells upregulate NOS, COX and cause inflammatory cell recruitment (cytokine, chemokines and adhesion molecules)
(e.g. asthma causes enlargement of the muscle)

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108
Q

How much of the cardiac output supplies the airway?

A

1-5%

100-150ml/min/100g tissue

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109
Q

What are the functions of the tracheo-broncial circulation?

A

1) Good gas exchange
2) Contributes to warming of inspired air
3) Contributes to humidification of inspired air
4) Clears inflammatory mediators
5) Clears inhaled drugs (good/bad depending on drug)
6) Supplies airway tissue and lumen with inflammatory cells
7) Supplies airway tissue and lumen with proteinacious plasma (plasma exudation)

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110
Q

What is plasma exudation in the airways?

A

Where venules in the airway contract which causes the cells to pull away from each other and form a gap which allows plasma to flow through

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111
Q

What condition is plasma exudation associated with?

A

Asthma

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112
Q

What nerve innervates the airway? What part of the nervous system does this belong to?

A

Vagus nerve

Parasympathetic pathway

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113
Q

What causes relaxation of the airway?

A

Nitric oxide by nitric oxide synthase (NOS)

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114
Q

If there are airborne irritants in the airway what is the cholinergic mechanism in the airway?

A 
Sensory nerves feedback to CNS
Vagus nerve to parasympathetic ganglion
Postganglionic releases ACh on muscarinic receptor to
1) Submucosal gland
2) Smooth muscle
3) Blood vessel
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115
Q

What are the regulatory-inflammatory cells in the airway?

A 
Eosinophils
Neutrophils
Macrophage
Mast cell
T lymphocyte
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116
Q

What three respiratory diseases cause a loss of airway control?

A

Asthma
Chronic obstructive pulmonary disease (COPD)
Cystic Fibrosis

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117
Q

What is asthma?

A

A clinical syndrome characterised by increased airway responsiveness to a variety of stimuli
Airway obstruction: varies over short periods of time and is reversible (spontaneously or with drugs)
Dyspnea, wheezing and cough (varying degrees- mild to severe)
Airway inflammation causes remodelling

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118
Q

What is the pathology of asthma?

A 
Mucus plug
Epithelial fragility
Basement membrane thickening
Vasodilation (congested vessels)
Cellular infiltration of tissue
Airway wall thrown into folds
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119
Q

What is the order of the airways from trachea to alveoli?

A 
Primary bronchus
Secondary bronchus
Tertiary bronchus
Bronchiole
Terminal bronchiole
Alveoli
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120
Q

Where are the vocal cords located?

A

In the larynx

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121
Q

What are the functions of epithelium in the lungs?

A

1) Forms a continuous barrier, isolating external environment from host
2) Produces secretions to facilitate clearance, via mucociliary escalator, and protect underlying cells as well as maintain reduced surface tension (alveolae)
3) Metabolises foreign and host-derived compounds
4) Releases mediators
5) Triggers lung repair processes

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122
Q

What happens to the airway epithelium in COPD?

A

Increased goblet cell numbers (goblet cell hyperplasia) and increased mucus secretion
(causes chronic bronchitis)

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123
Q

How much of the epithelium is made up of goblet cells?

A

Normally 20% of the epithelium

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124
Q

What happens to goblet cells in smokers?

A

Goblet cell number at least doubles
Secretions increase
Secretions are more viscoelastic
Cigarette smoke particles are trapped but also harbours microorganisms, enhancing chances of infection

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125
Q

What airways are goblet cells found in?

A

Large, central and small airways

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126
Q

What airways are ciliated cells found in?

A

Large, central and small airways

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127
Q

How much of the epithelium is made up of ciliated cells?

A

Normally 80% of the epithelium

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128
Q

How do cilia beat?

A

Metasynchronously

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129
Q

What happens to the cilia in smokers and smokers with bronchitis?

A

Ciliated cells are severely depleted
Cilia beat asynchronously
Ciliated cells found in bronchioles (further down respiratory tract)
Cilia unable to transport thickened mucus
Reduced mucus clearance leading to respiratory infection and bronchitis. Airways obstructed by mucus secretions

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130
Q

What happens in COPD?

A

Small airways disease and emphysema

  • Decreased elasticity of supporting structure
  • Plugging, inflammatory narrowing and obliteration of small airways
  • Destruction of peribronchiolar support
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131
Q

What cells are found in the respiratory bronchiole?

A

Bronchiolar ciliated cells

Clara (club) cells

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132
Q

What are clara cells? How much of the bronchiole is made up of them?

A

∼20% of epithelial cells (lower in smokers)
Secretory cells
Detoxification
Repair/ progenitor cells

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133
Q

What cells make up the alveoli?

A

1) Type I epithelial cells
2) Type II epithelial cells
3) Stromal cells (myo) fibroblasts

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134
Q

What are type I epithelial cells?

A

95% of the alveolar surface
Large cells (∼80μm)
Very thin to allow gas exchange
0.2-0.5μm thin

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135
Q

What are type II epithelial cells?

A

Cuboidal (∼10μm)
Secrete surfactant
Repair/progenitor cells
Precursor of type I cells
Outnumber type I cells but are much smaller
Contain lamellar bodies which store surfactant prior to release onto the air-liquid interface

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136
Q

What are stromal cells?

A

(Myofibroblasts)
Make ECM- the lung’s cement
Collagen, elastin, to give elasticity and compliance
Divide to repair

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137
Q

What is the ratio between type I and II cells and what percentage of the surface of the alveoli are made up of each?

A

Type I : Type II
1 : 2
95% : 5%

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138
Q

What is the function of surfactant?

A

Lowers surface tension and prevents alveolar collapse on expiration

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139
Q

What happens during alveolar repair?

A

Increased type II cells (ie repair)
Increased fibroblasts
Increased collagen deposition

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140
Q

What is xenobiotic metabolism?

A

Process and detoxify foreign compounds such as carcinogens in cigarette smoke

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141
Q

How do the number of leukocytes differ in smokers?

A

Increases 10 fold

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142
Q

What is the function of leukocytes in the airway?

A

Phagocytosis
Antimicrobial defence
Synthesise antioxidants e.g. glutathione
Xenobiotic metabolism

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143
Q

What is the difference in leukocytes in the primary bronchus between a healthy individual and a smoker?

A

Healthy
30% Neutrophils
70% Macrophages

Smokers
70% Neutrophils
30% Macrophages

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144
Q

In the periphery of the lung what percentage of the leukocytes are macrophages?

A

80-90%

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145
Q

What proteases are produced by neutrophils and macrophages?

A

Neutrophil: serine proteinases (e.g. neutrophil elastase NE)
Macrophage: Metalloproteinases (e.g. MMP-9)

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146
Q

What effect do macrophage metalloproteinases and neutrophil elastase have on emphysema?

A

If you can’t produce MMP or NE you can’t produce emphysema

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147
Q

What do proteases do?

A

Substrates: proteins; connective tissues, elastin, collagen
Actiate other proteinases (e.g. NE degrades and activates MMP), inactivates antiproteases (e.g. MMP degrades and inactivates α-1 antitrypsin)
Activate cytokines/chemokines and other pro-inflammatory mediators

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148
Q

What is the function of oxidants produced by leukocytes?

A 
Antimicrobial
Generate highly reactive peroxides
Interact with proteins and lipids
Inactivate α-1 anti-trypsin
Fragment connective tissue
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149
Q

What mediators do leukocytes secrete?

A

1) Chemokines
- IL-8 (neutrophil)
- MCP-1 (monocytes)
2) Cytokines
- IL-1β, IL-6, TNFα (inflammation)
3) Growth factors
- VEGF, FGF, TGFβ (cell survival, repair and remodelling)

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150
Q

What percentage os patients diagnosed with lung cancer die within 1 year? How many is this?

A

80%

40,000

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151
Q

What are the main causes of lung cancer?

A

SMOKING
Radon
Asbestos

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152
Q

What is p53?

A

Housekeeping gene- causes apoptosis (cell death) when cells threaten to become cancerous

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153
Q

What housekeeping genes prevent cancer?

A

pRB
p53
bax

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154
Q

How does smoking cause cancer?

A

Disrupts the housekeeping genes

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155
Q

What are the clinical features of lung cancer?

A

Haemoptysis (coughing up blood)

>3 weeks of: cough, chest/shoulder pains, chest signs, dyspnoea, hoarseness, finger clubbing

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156
Q

What are the two types of lung cancer?

A

Non-small cell cancer

Small cell lung cancer

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157
Q

What is the staging of lung cancer?

A 
TNM classification
Tumour (T1-4):
T1: 30mm and in periphery
T3: Close to other organs
T4: Close to mediastinum
Nodes (N0-3):
N1: Hila nodes same side
N2: Mediastinal nodes same side
N3: Nodes on contralateral (other) side
Metastases (M0 or 1):
M1a: Metastases in same tissue
M1b: Metastases in bone or brain etc
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158
Q

What treatment is used on small cell cancer?

A

Localised with fit patient: aggressive treatment of chemo and radio
Widespread: chemo
Widespread or weak: Palliate them

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159
Q

What treatment is used for non-small cell lung cancer?

A

Early detection: Surgical resection (if no metastases)

If metastases: Chemo or palliation

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160
Q

On average how long has lung cancer been present before detection?

A

13 to 15 years

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161
Q

What type of samples are used for cytology?

A
  • Sputum
  • Bronchial washings and brushings
  • Pleural fluid
  • Endoscopic fine needle aspiration of tumour/enlarged lymph nodes
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162
Q

What type of samples are used of histology?

A
  • Biopsy at bronchoscopy
  • Percutaneous CT guided biopsy
  • Mediastinoscopy and lymph node biopsy (staging)
  • Open biopsy at time of surgery (frozen section)
  • Resection specimen
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163
Q

What is the difference between benign and malignant lung tumours?

A

Benign (e.g. chondroma):
Do not metastasise, can cause local complications (e.g. airway obstruction)
Malignant:
Potential to metastasise, but variable clinical behaviour from relatively indolent to aggressive. Commonest are epithelial tumours

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164
Q

What are the different types of non-small cell carcinoma?

A
  • Squamous cell carcinoma (20-40%)
  • Adenocarcinoma (20-40%)
  • Large cell carcinoma (uncommon)
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165
Q

What percentage of lung cancers are small-cell carcinoma?

A

20-25%

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166
Q

What type of lung cancer is squamous cell carcinoma? Where does it normally arise?

A

Non-small cell carcinoma

Arise in the airways

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167
Q

What causes squamous cell carcinoma in smokers?

A

Smoking causes irritation to ciliated cells
Cells adapt to squamous cells which are “tougher”
Prevents mucus from being clear
Carcinogens become trapped in mucus which cannot be cleared from the airway. Repeated exposure to carcinogen causes mutations to cells, leading to carcinoma
As tumours develop they acquire more and more mutations

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168
Q

What type of lung cancer is adenocarcinoma? Where does this normally arise? How does it progress?

A

Non-small cell carcinoma
Arises in the periphery of the lung
Moves along the surface of the alveolar walls until it acquires the mutation to become invasive

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169
Q

Who is adenocarcinoma most common in?

A

Far east, females and non-smokers

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170
Q

What is the progression of a lung cancer?

A

Mutation caused by carcinogen
Carcinoma-in-situ
Invasive carcinoma

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171
Q

What type of cancer is large cell carcinoma? What is the most likely cell type?

A

Non-small cell carcinoma

Probably very poorly differentiated adeno/squamous cell carcinoma

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172
Q

Where are small cell carcinomas typically located? Who are these type of cancer normally present in?

A

Often central near bronchi

Almost always seen in smokers

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173
Q

What treatment is typically used in small cell lung carcinoma? What is the prognosis?

A

Chemoradiotherapy (surgery very rare as has usually spread by diagnosis)
Survive 2-4 months untreated
10-20 months with current therapy

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174
Q

What treatment is typically used in non-small cell lung carcinoma? What is the prognosis?

A

Not as chemosensitive as SCC
20-30% have end-stage tumours suitable for surgical resection
Early stage 1: 60% 5 year survival
Late stage 4: 5% 5 year survival

175
Q

Why is it important to differentiate between adenocarcinoma and squamous cell carcinoma?

A

Some adenocarcinomas respond well to anti-EGFR drugs (Tarceva)
In contrast some patients with squamous cell carcinoma develop fatal haemorrhage with Bevacizumab

176
Q

What are the complications of bronchial obstruction?

A

1) Collapse of distal lung

2) Impaired drainage of bronchus

177
Q

What are the local effects of bronchogenic carcinoma?

A

1) Bronchial obstruction
2) Invasion of local structures
3) Extension through pleura or pericardium
4) Diffuse lymphatic spread within lung

178
Q

What are the systemic effects of bronchogenic carcinoma?

A

1) Physical effects of metastatic spread
- brain (fits)
- skin (lumps)
- liver (pain, deranged LFTs)
- bones (pain, fracture)
2) Paraneoplastic syndromes
Tumour expresses factor (e.g. hormones and other factors) not normally expressed

179
Q

What is paraneoplastic syndrome?

A

When a tumour has abnormal expression of factors (e.g. hormones and other factors) not normally expressed by the tissue where the tumour arose

180
Q

What are the different types of paraneoplastic syndrome? What do they secrete and what lung cancer is this associated with?

A

1) Endocrine
- ADH (causes hyponatremia; small cell carcinoma)
- ACTH (Cushing’s syndrome; small cell carcinoma)
- Parathyroid hormone- related peptides (hypercalcaemia; squamous carcinoma)
- Calcitonin, gonadotrophin, serotonin
2) NON-endocrine
- Haematologic/ coagulation defects, skin, muscular, miscellaneous disorders

181
Q

How does the metabolic centre control breathing?

A

Metabolic centre in the brain sends a specific number of impulses down the nerves which stimulate the respiratory muscles (mainly diaphragm).
Strength of contraction is proportional to the frequency of the impulses coming from the phrenic nerve
Frequency of impulses = strength of contraction = faster the contraction = greater inspiratory flow
Inspiration is switched off and as is expiration

182
Q

How does COPD affect breathing rate and tidal volume?

A

Breath faster with a smaller tidal volume

Worse in chronic bronchitis than emphysema

183
Q

What and where is the involuntary breathing centre? What can influence it?

A 
Metabolic
In the medulla
Can be influenced by:
- emotional responses
- sleep via the reticular formation
184
Q

What and where is the voluntary breathing centre?

A

Behavioural

In the motor area of cerebral cortex

185
Q

What does the metabolic centre (breathing) respond to?

A

Metabolic demands for and production of CO2 (pH)

Can be influenced by the limbic system (hunger, suffocation) and frontal cortex (emotion) and sensory input (pain)

186
Q

What does the behavioural centre (breathing) control?

A

Breath holing

Singing etc

187
Q

Where is the metabolic centre (breathing)?

A

Automatic bulbopontine controller

In the brainstem

188
Q

Where is the behavioural centre (breathing)?

A

Behavioural suprapontine control

Widely distributed

189
Q

Where is the diaphragm control in the brain?

A

In the motor homunculus in the cortex (between trunk and shoulder)

190
Q

How does the metabolic controller detect brain pH?

A

It has a H+ receptor which measures ECF

Also has feedback from carotid bodies which have a H+ receptor detecting arterial blood

191
Q

What complex is known as the gasping centre?

A

pre-Botzinger complex in the ventro-cranial medulla

192
Q

What do irritant receptors do?

A

Defensive

Lead to coughing and sneexing

193
Q

What are the irritant receptors? Where are they located

A

Vth nerve: afferents from nose and face
IXth nerve: from pharynx and larynx
Xth nerve: from bronchi and bronchioles

194
Q

What two locations for the metabolic controller process information from?

A

1) Central part in medulla which responds to H+ ion of ECF

2) Peripheral part at carotid bifurcation, the H+ receptors of the carotid body

195
Q

What effect does PCO2 have on minute ventilation? How is PO2 involved in this relationship?

A

As PCO2 increases so does minute ventilation

Minute ventilation increases more at higher PACO2 levels

196
Q

What is more tightly controlled? PaO2 or PaCO2?

A

PaCO2

197
Q

What happens to blood gases when there is a fall in ventilation?

A

↓ PaO2; ↑ PaCO2
↓ PaO2 causes ↑ sensitivity of carotid body to PaCO2 and H+
↑ ventilation; ↑ PaO2
↓ PaCO2 by negative feedback

198
Q

In chronic bronchitis does the diaphragm do the same amount of work as in a healthy patient?

A

No, it works much harder

199
Q

What are the causes of hypoventilation?

A

1) Central
- Acute (metabolic centre poisoning: drugs, anaesthetics)
- Chronic (vascular/neoplastic disease, congenital central hypoventialtion syndrome, obesity hypoventialtion syndrome, chronic mountain sickness)
2) Peripheral
- Acute (muscle relaxant drugs, myasthenia gravis)
- Chronic (neuromuscular with respiratory muscle weakness)
3) COPD (mixture of central (won’t breathe) and peripheral (can’t breathe)

200
Q

What are 4 types of hyperventilation condition?

A

1) Chronic hypoxaemia
2) Excess H+ (metabolic)
3) Pulmonary vascular disease
4) Chronic anxiety (psychogenic)

201
Q

What causes air hunger?

A

A mismatch between minute ventilation required (signal by metabolic controller) and minute ventilation achieved (lungs and chest wall; carotid body)

202
Q

What scale is used to measure dyspnoea during exercise?

A

Borg CR-10 scale

or Clinical Dyspnoea scale

203
Q

What test measures the strength of behavioural versus metabolic controller?

A

Breath holding time (BHT)

204
Q

What are the three types of breathlessness?

A

1) Tightness (airway narrowing)
2) Increased work and effort
3) Air hunger

205
Q

What are the different types of acid in the body? Give examples

A 
1) Respiratory acid
CO2
2) Metabolic acid
Pyruvic acid
Lactic acid
206
Q

What type of acid affects pH more?
Respiratory acid
Metabolic acid

A

Respiratory acid (99%)

207
Q

What is pK?

A

The dissociation contant

Tells you how many of the molecule are dissociated or bound (CO2 and HCO3-)

208
Q

What is the Sorensen equation?

A

pH= -log10[H+]

209
Q

What is the rate of carbon dioxide production?

A

200mL/min

210
Q

What is the rate of oxygen consumption?

A

250mL/min

211
Q

48nmol/L is how many hydrogen ions?

A

0.000000048

212
Q

What is base excess?

A

A comparison of what the base should be versus what it is

213
Q

What does pH show on an arterial blood gas measure?

A

If it is acidotic or alkalotic

214
Q

Why look at pO2 on an arterial blood gas measure?

A

It indicates if the patient has any respiratory problems

215
Q

What are the basic guidelines for PaO2?

A

> 10kPa is normal
8-10 is mild hypoxaemia
6-8 is moderate hypoxaemia

216
Q

If you have an acid-base disturbance what modifications will the body make and are they rapid or slow?

A

Lungs- RAPID:
Ventilation= Change CO2 elimination and therefore alter pH
Kidneys- SLOW:
Changes HCO3- and H+ retention/secretion in the kidneys in response to ↑/↓pH

217
Q

pH: ↓
PaCO2: ↑
BE: normal
What is the evaluation?

A

Uncompensated respiratory acidosis

218
Q

pH: ↑
PaCO2: normal
BE: ↑
What is the evaluation?

A

Uncompensated metabolic alkalosis

219
Q

pH: ↓
PaCO2: ↑
BE: ↓
What is the evaluation?

A

Uncompensated mixed acidosis

220
Q

pH: ↑
PaCO2: ↑
BE: ↑
What is the evaluation?

A

Partially compensated metabolic alkalosis

221
Q

pH: ↑
PaCO2: ↓
BE: ↓
What is the evaluation?

A

Partially compensated respiratory alkalosis

222
Q

What is the function of cough?

A

A crucial defence mechanism protecting the lower respiratory tract from
- inhaled foreign material
- excessive mucous secretion
Usually secondary to mucociliary clearance (important in lung disease when mucociliary function is impaired and mucous production is increased
Expulsive phase
-generates high velocity airflow facilitated by bronchoconstriction and mucous secretion

223
Q

Where are the cough receptors located?

A

Most numerous on the posterior wall of the trachea
Also found at branching points of large airways, pharynx, external auditory meatus, eardrum, paranasal sinuses, diaphragm, pleura, pericardium and stomach

224
Q

What do cough receptors respond to?

A

Chemical and mechanical stimuli

225
Q

What are the different types of cough receptor?

A

1) Slowly adapting stretch receptors
2) Rapidly adapting stretch receptors
3) C- fibre receptors

226
Q

Where are C-fibre receptors found? What do they respond to and release?

A

Small unmyelinated fibres
In the larynx, trachea, bronchi and lungs
Respond to chemical irritant stimuli and inflammatory mediators
Release neuropeptide inflammatory mediators (substance P, neurokinin A, calcitonin gene related peptide)

227
Q

Where are rapidly adapting stretch receptors found? What are they?

A

In the naso-pharynx, larynx, trachea and bronchi
Small, myelinated nerve fibres
Mechanical, chemical irritant stimuli, inflammatory mediators

228
Q

Where are the slowly adapting stretch receptors located? What are they?

A

Located in airway smooth muscle, predominantly in trachea and main bronchi
Myelinated nerve fibres
Mechanoreceptors- respond to lung inflation

229
Q

What are the most common causes of acute cough (

A

Common cold

  • Cough
  • Post nasal drip
  • Throat clearing
  • Nasal blockage
  • Nasal discharge
230
Q

What are the causes (and percentages) or chronic persistent cough (>3 weeks)

A
  • Asthma and eosinophilic-associated (25%)
  • Gastro-oesophageal reflux (25%)
  • Rhinosinusitis (postnasal drip) (20%)
  • Chronic bronchitis (8%)
  • Bronchiectasis (5%)
  • Drugs e.g. ACE inhibitor (1%)
  • Post-viral (3%)
  • Idiopathic (10%)
  • Other causes (3%)
231
Q

What can cause a change in plasticity of neural mechanisms, causing a chronic cough?

A

1) Excitability of afferent nerves is increased by chemical mediators (e.g. prostaglandin E2)
2) Increase in receptor numbers (e.g. TRPV-1)
3) Neurotransmitter increase (e.g. neurokinins) in brainstem

232
Q

What nerve innervated the pharynx, larynx and lungs?

A

Vagus nerve

233
Q

At what point do touch nerves move to the opposite side of the spinal cord/brain?

A

At the brain stem (medulla)

234
Q

At what point do pain receptors move to the opposite side of the spinal cord/brain?

A

At the vertebral level in which they enter the spine- immediately

235
Q

What are the treatment options for dyspnoea?

A

Treat the cause (e.g. lung or cardiac)
Therapeutic options
- Add bronchodilators (e.g. anticholinergics or β- adrenergic agonists
- Drugs affecting the brain (e.g. morphine, diazepam)
- Lung resection (e.g. volume reduction surgery)
- Pulmonary rehabilitation (improve general fitness, general health, psychological well-being)

236
Q

What are the bacterial strategies to avoid clearance from the airways?

A

1) Exoproducts impair mucociliary clearance
2) Enzymes: break down local immunoglobulins
3) Exoproducts: Impair leukocyte function
4) Adherence: increased by epithelial damage and tight junction separation
5) Avoid immune surveillance: Surface heterogeneity, biofilm formation, surrounding gel and endocytosis

237
Q

What are the most common clinical features of pneumonia?

A 
Cough
- Sputum
Fever
Dyspnoea
Pleural pain
Headache
238
Q

What are the causes of chronic bronchial sepsis?

A

1) Congenital
2) Mechanical obstruction
3) Inflammation pneumonitis
4) Fibrosis
5) Post-infective
6) Immunological
7) impairs mucociliary clearance
8) Immune deficiency

239
Q

How much of a healthy lung is sterile?

A

From the first bronchial division onwards

240
Q

What is the structure of cilia?

A

Consists of 9 doublets and 2 central microtubules, which slide up and down each other to cause ciliary movement
ATP in the dynein arms provides the energy for movement

241
Q

What is PCD?

A

Primary Ciliary Dyskinesia

Cilia don’t beat properly so mucociliary clearance doesn’t work

242
Q

What are the two groups of bacterial pathogen of the lung and what infections do they cause?

A

1) Virulent species: causes pneumonia (e.g. Strep. oneumonia)
2) Less virulent species: causes bronchitis, are equipped to chronically infect airways in which the host defences have been compromised (e.g. unencapsulated haemophilus influenza)

243
Q

What is the most common cause of airway infection? How does it evade host defences?

A

Haemophilus influenza
1/4 of smokers have this bacterium chronically infecting their airways
Bacteria have fimbriae which anchor the bacterium to stop them being moved by cilia

244
Q

What part of the lungs does pneumonia infect?

A

The alveoli

245
Q

What toxin is produced by pneumonia? What does this do?

A

Pneumolysin

Punches holes into the cell membrane, killing the cell

246
Q

What is obstructive lung disease? What volumes are the lungs operating at? What are some chronic and acute causes of this?

A 
The flow of air into and out of the lungs is obstructed
Lungs are operating at HIGHER volumes
Chronic:
COPD (emphysema, bronchitis)
Acute:
Asthma
247
Q

What is restrictive lung disease? What volumes are the lungs operating at? What are some pulmonary and extrapulmonary causes of this?

A 
Inflation/deflation of the lungs or chest walls is restricted
Lungs are operating at LOWER volumes
Pulmonary:
Lung fibrosis
Interstitial lung disease
Extrapulmonary causes:
Obesity
Neuromuscular disease
248
Q

During tidal breathing what requires muscular effort?

A

Inspiration requires muscular effort

Expiration is a passive process so does NOT!

249
Q

What happens to the mechanics of ventilation (pressure-volume relationship) in someone with restrictive lung disease? What are they like compared to a healthy individual?

A

Volumes are much lower than a healthy individual.

They have a low functional residual capacity and also require higher pressures to reach maximum capacity

250
Q

What happens to the mechanics of ventilation (pressure-volume relationship) in someone with restrictive lung disease? What are they like compared to a healthy individual?

A

Volumes are much higher than for a healthy individual.
They require lower pressures to reach maximum capacity- much more complient.
They have a smaller vital capacity

251
Q

What is compliance? How do you calculate it?

A

The tendency to distort under pressure
Compliance = △V/△P
A more compliant structure would distort easier with pressure

252
Q

What is elastance?

A

The tendency to recoil to its original volume

Elastance = △P/△V

253
Q

What is the relationship between compliance and elastance?

A

Compliance is inversely proportional to elastance

254
Q

How does surface tension affect the alveoli?

A

Water molecules are spread across the alveolar surface, with intermolecular bonds between them. Only molecules that do not have intermolecular bonds is the uppermost layer. This means they are pulled downwards towards the other water molecules
The even pull of water molecules downwards causes the alveoli to be spherical

255
Q

What is the composition of surfactant?

A

80% polar phospholipids
10% non-polar lipids
10% protein

256
Q

How are the smaller alveoli prevented from collapsing?

A

Smaller alveoli have more surfactant increasing surface tension, preventing collapse

257
Q

How do the number of airways in the lungs affect the resistance?

A

There are so many airways in the periphery of the lung that the air doesn’t “flow” it diffuses. For this reason the resistance actually decreases the further into the lungs you get.

258
Q

What is conductance?

A

How much the airways are willing to let the air flow through them.

259
Q

What happens to the airways as the lungs fill? How does this affect the resistance?

A

The airways dilate as the lungs fill with air. This means the resistance decreases as you reach higher lung volumes

260
Q

How do you work out the airway transmural pressure?

A 
It is the pressure inside (alveoli pressure) minus the pressure outside (interpleural pressure)
At rest (tidal expiration) = 0 - -5 = +5
261
Q

What is the pressure of oxygen as it enters the lungs and moves further into the airways?

A

PlO2: 21.3kPa bronchus
PO2: 20.0kPa bronchioles
PAO2: 13.5kPa alveoli

262
Q

What is Fisk’s law? (describe)

A

Flow rate (of diffusion) is proportional to the pressure gradient

263
Q

How does inspiring hypoxic gas affect the oxygen cascade?

A

It reduces the gradient between air and cells and so reduces the flow

264
Q

How does structural disease affect the oxygen cascade?

A

It reduces the surface area where gas exchange can take place, therefore reducing the diffusion of oxygen from air to cells

265
Q

How does fluid in the lungs affect the oxygen cascade?

A

It increases the thickness the gas much diffuse through and therefore reduces the flow into cells

266
Q

What are the stages of the oxygen cascade?

A

1) Breath in air (21.3kPa)
2) Humidification in upper airways (20.0kPa)
3) Mixing with air already in the capillaries (13.5)
4) Moves into blood- equilibrates (13.5)
5) Mixes with venous blood supplying the bronchioles (13.3kPa)
6a) At rest (5.3kPa)
6b) Exercising (1.3kPa)

267
Q

What disease states can affect the oxygen cascade?

A

Alveolar ventilation
Ventilation/perfusion matching
Diffusion capacity
Cardiac output

268
Q

What fibres signal the brain to increase oxygen intake during exercise?

A

Proprioceptive muscle fibres

269
Q

During exercise what part of breathing changes first?

A

Tidal volume increases first

270
Q

What are the challenges of altitude?

A

1) Hypoxia
2) Thermal stress
3) Solar radiation
4) Hydration
5) Dangerous

271
Q

What is the process of acclimatisation?

A 
↓ atmospheric O2
↓PAO2
↓PaO2
Activation of peripheral chemoreceptors
↑ Sympathetic outflow
↑ Ventilation
↓ PaCO2
↓ Ventilation
↑ pH
Alkalosis detected by carotid bodies
↑ HCO3- excretion
↑ H+ in blood
↑ Erythropoietin
272
Q

What is acclimation?

A

Different to acclimatisation as it is stimulated by an artificial environment

273
Q

What is acetazolamide?

A

Used for altitude sickness

A carbonic anhydrase inhibitor- accelerates the slow renal compensation to hypoxia-induced hyperventilation

274
Q

What are the innate/developmental adaptations to altitude?

A

‘Barrel chest’
Increased haematocrit
Larger heart
Increased mitochondrial density

275
Q

What is chronic mountain sickness? What are the symptoms and treatments?

A

Secondary polycythaemia increases blood viscosity, which sludges through systemic capillary bed impeding O2 delivery (despite more than adequate oxygenation)
Symptoms: Cyanosis, fatigue
Causes ischaemic tissue damage, heart failure and eventual death
Treatment: move to lower altitude

276
Q

What is acute mountain sickness? What are the symptoms and treatments?

A

Caused by a maladaptation to the high-altitude environment. Usually associated with recent ascent. Onset within 24 hours and can last more than a week
Associated with a mild cerebral oedema.
Symptoms: Nausea, vomiting, irritability, dizziness, insomnia, fatigue and dyspnoea
Can develop into HAPE or HACE
Treatment: Stop ascent, monitor, analgesia, fluids, medication (acetazolamide) o hyperbaric O2 therapy

277
Q

What is HACE?

A

High-Altitude Cerebral Oedema
Caused by rapid ascent or inability to acclimatise
Vasodilation of vessels in response to hypoxaemia, more blood going into the capillaries increases fluid leakage
Symptoms: confusion, ataxia, behaviour change, hallucinations, disorientation. Can cause irreversible neurological damage, coma and death
Treatment: immediately descend, O2 therapy, hyperbaric O2 therapy, dexamethasone

278
Q

What is HAPE?

A

High Altitude Pulmonary Oedema
Caused by rapid ascent or inability to acclimatise
Vasoconstriction of pulmonary vessels in response to hypoxia, increased pulmonary pressure, permeability and fluid leakage from capillaries, fluid accumulates once production exceeds the maximum rate of lymph drainage
Symptoms: dyspnoea, dry cough, bloody sputum, crackling chest sounds. Causes impaired gas exchange and impaired ventilatory mechanics
Treatment: Descend, hyperbaric O2 therapy, nifedipine, salmeterol, sildenafil

279
Q

What is type I respiratory failure?

A

Hypoxic respiratory failure

PaO2

280
Q

What is type II respiratory failure?

A

Hypercapnic respiratory failure
PaCO2>6.7kPa
Causes: Increased CO2 production. Decreased CO2 elimination
Decreased CNS drive, Increased work of breathing, pulmonary fibrosis, neuromuscular disease, increased physiological dead space, obesity

281
Q

Who is likely to suffer from acute hypoxia?

A

Myocardial infarction
Severe haemorrhage
Pulmonary embolus

282
Q

Who is likely to suffer from chronic hypoxia?

A

Diabetes
Respiratory failure
Anaemia
COPD

283
Q

What allergic airway disease affects the upper airways?

A

Allergic rhinitis

Hayfever

284
Q

What allergic airway disease affects the bronchi?

A

Asthma

285
Q

What allergic airway disease affects the alveoli?

A

Allergic alveolitis

286
Q

What is the difference between intolerance and allergy?

A

Intolerance is not immunologically mediated

287
Q

What is atopy? Give examples of atopic diseases

A

Hereditary predisposition to produce IgE antiboidies against common environmental pathogens.
Characterised by infiltration of Th2 cells and eosinophils
e.g. allergic rhinitis, asthma and atopic eczema

288
Q

What interleukin cytokines are released by Th2 cells?

A

IL-4
IL-5
IL-9
IL-13

289
Q

What does IL-4 do?

A

IgE synthesis

290
Q

What does IL-5 do?

A

Eosinophil development

291
Q

What does IL-9 do?

A

Mast cell development

292
Q

What does IL-13 do?

A

IgE synthesis
Airway hyperresponsiveness
Goblet cell hyperplasia

293
Q

How much of the population is affected by allergic rhino-conjunctivitis?

A

11-17% of the adult population

12-15% of children

294
Q

What is perennial allergic rhinitis? What are the most common causes?

A 
Allergies all year round
Horses
Dogs
Cats
Dust mite
295
Q

How much of the population is affected by asthma?

A

8-12%

296
Q

What happens to the airways in asthma?

A

Airways become narrowed due to inflammation:

1) Constriction of smooth muscle
2) Oedema of small airways
3) Plugging of small airways (LEADS TO DEATHS)

297
Q

What are the different types of asthma?

A 
Early-onset allergic
Late onset-eosinophilic
Exercise-induced
Obesity-related
Neutrophilic
298
Q

What are the symptoms of anaphylaxis?

A 
Dizziness/seizures/loss of consciousness
Lip/tongue swelling
Laryngeal oedema
Bronchoconstriction
Tingling limbs
Anxiety
Arrhythmia
Vomiting/diarrhoea
299
Q

What drug is required for anaphylaxis?

A

Adrenaline

300
Q

What is the mechanism of extrinsic allergic alveolitis?

A

Allergen (spores) are inhaled, they undergo an immune complex reaction
The interstitium becomes inflamed and oedematous and gas exchange becomes impaired

301
Q

What is the “Hygiene Hypothesis”?

A

For allergic disease
Loss of species diversity (“biome depletion”)
Origins in sanitation rather than hygiene
Does not involve personal hygiene

302
Q

What are the risk factors for allergic disorders?

A 
"Westernised" countries
Small family size
Affluent, urban homes
Intestinal micro-flora-stable
High antibiotic use
Low or absent helminth burden
Good sanitation, low orofaecal burden
303
Q

What are the principles of treatment of allergic diseases?

A

1) Allergy avoidance
2) Anti-allergy medication
3) Immunotherapy (desensitisation)

304
Q

What is immunotherapy? What are the advantages and disadvantages?

A 
Injecting or ingesting very small amounts of allergen and increasing the dose to desensitive the patient
Advantages:
- Effective
- Produces long lasting immunity
Disadvantages:
- Occasional severe allergic reaction
- Time consuming
- Standardisation problems
305
Q

How does immunotherapy work?

A

Down-regulates Th2 cells

Up-regulates Th1 and Treg cells

306
Q

What is the embryonic phase of lung development? What weeks does this occur in?

A

0-7 weeks
Lung buds
Main bronchi

307
Q

What is the pseudoglandular phase of lung development? What weeks does this occur in?

A

5-17 weeks
Conducting airways
Bronchi and bronchioli

308
Q

What is the canalicular phase of lung development? What weeks does this occur in?

A

16-27 weeks
Respiratory airways
Blood gas barrier

309
Q

What is the saccular/alveolar phase of lung development? What weeks does this occur in?

A

28-40 weeks

Alveoli appear

310
Q

In terms of lung development, what changes occur during growth and maturity to adolescence?

A

Alveoli multiply and enlarge in size with chest cavity

311
Q

What is Scimitar syndrome?

A

Anomalous pulmonary venous drainage of the right lung to the IVC, usually close to the junction of the right atrium
Associated right lung and right pulmonary artery hypoplasia
Dextrocardia (dextropsition)
Anomalous systemic arterial supply

312
Q

How do the lungs develop during the embryonic phase? (weekly)

A

4 weeks: Bronchial buds (left and right)
5 weeks: Clear bifurcation with left and right secondary bronchus
6 weeks: Hint of lobular structure
7 weeks: 3 right lobes and 2 left lobes of the lungs are visible- main bronchus formed

313
Q

What are malacic cartilage rings?

A

Soft cartilage rings- do not harden correctly
Generalised: laryngotracheomalcia
Localised: Malacic segment

314
Q

What is laryngomalacia?

A

Where the cartilage is soft/floppy. Can cause the airway to close whilst breathing. Can require a tracheostomy

315
Q

What are the inductive growth factors for lung development?

A

FGF: branching morphogenesis, subtypes found in epithelium and mesenchyme
EGF: epithelial proliferation and differentiation

316
Q

What are the inhibitory growth factors for lung development?

A

TGFβ: matrix synthesis, surfactant production, inhibits proliferation of epithelium and blood vessels
Retinoic acid: inhibits branching

317
Q

What is CPAM?

A

Cystic Pulmonary Airway Malformation
Occurs: 1/8300 to 1/35000- mostly diagnosed on antenatal USS
Defect in pulmonary mesenchyma, abnormal differentiation 5-7 weeks. Normal blood supply, but can be associated with sequastrion

318
Q

What is typically seen in type 2 CPAM? What does this typically present with? What are the histological symptoms?

A

Multiple small cysts
May be associated with renal agenesis, cardiovascular defects, diaphragmatic hernia and syryngomyelia
Histologically bronchiolar epithelium with overgrowth, separated by alveolar tissue which was underdeveloped

319
Q

What is congenital lobar emphysema? What is it also known as? Who is it most common in?

A 
CLHL (Congenital Large Hyperlucent Lobe)
Progressive lobar overexpansion
Underlying cause: weak cartilage, extrinsic compression, one way valve effect, alveoli expand (not disrupted)
LUL>RML>RUL
Males>females
CHD association
320
Q

What is intralobar sequestration?

A

When part of the lung has an abnormal blood supply (e.g. branch off the aorta) which forms a cystic area. Usually blocked off surgically and does not cause problems.
75% of pulmonary sequestrations
No communication to tracheobronchial tree
Lower lobe predominance L>R
Possibly due to chronic bronchial obstruction and chronic postobstructive pneumonia

321
Q

What are different types of lung growth anomaly that can occur?

A

Agenesis: Complete absence of lung and vessel
Aplasia: Blind ending bronchus, no long or vessel
Hypoplasia: Bronchus and rudimentary lung are present, all elements are reduced in size and number
Intralobular sequestration
CPAM

322
Q

How common is lung agenesis? What is it?

A

Rare
Formation of only one lung. Cuased by abnormal flow in the 4th week.
Commonly associated with other pathology
Mediastinal shift towards an opaque hemithorax

323
Q

What is lung hypoplasia? How common is it?

A 
Lung underdevelopment
Common (relatively) and usually secondary
Lack of space: intrathoracic or extrathoracic
- Hernia (L=75-90%)
- Chest wall pathology
- Oligohydramnios
- Lymphatic or cardiac mass
Lack of growth
- CTM
324
Q

What growth factors control early blood vessel growth?

A

VEGF: produced by epithelial cells throughout gestation in humans
Flk-1: VEGF receptor on endothelium (Flk deficient mice have no blood vessel development)
IGF and IGFR: identified in man from 4 weeks, blocking prevents capillary development
eNOS: stimulates proliferation and tube formation
Angiopoietin: (receptor Tie) important in wall differentiation

325
Q

How developed are the lungs at the end of the pseudogladular period?

A

All airways and blood vessels to the level of the terminal bronchiolus are present
the appearance of the lung changes as the lung enters the canalicular stage

326
Q

What occurs in the canalicular stage of lung development?

A

The airspaces at the periphery enlarge
Thinning of the epithelium by underlying capillaries allows gas exchange
Blood gas barrier required in post-natal life
Epithelial differentiation into type I and II cells
Surfactant first detectable at 24-25 weeks

327
Q

When is surfactant first detectable?

A

24-25 weeks

328
Q

At full term, how many alveoli do you have compared to a fully grown adult?

A

1/3 to 1/2 the alveoli of an adult

329
Q

What is the mechanism for formation of alveolar walls?

A

1) Saccule wall forms: epithelium on both sides with double capillary network. Myofibroblast and elastin fibres at intervals along wall
2) Secondary septa develop from wall led by elastin produced by myofibroblast. Capillary lines both sides with matrix between
3) Capillaries have coalesced to form one sheet alveolar wall, thinner and longer with less matrix. Muscle and elastin still at tip

330
Q

What changes occur in blood vessels after birth?

A

1) Decrease in pulmonary vascular resistance
2) 10 fold rise in pulmonary blood flow
3) Arterial lumen increases and wall thins rapidly
4) Change in cell shape and cytoskeletal organisation not loss of cells
5) Once thinning has occurred, arteries grow and maintain a relatively thin wall
Low pressure, low resistance pulmonary vascular system

331
Q

What are the possible mechanisms to increase flow after birth?

A

1) Expansion of alveoli dilates arteries- direst physical effect
2) Expansion stimulates release of vasodilator agents (NO, PGI2)
3) Inhibition of vasoconstrictors present during foetal life (ET)
4) Direct effect of oxygen on smooth muscle cells

332
Q

How do the airways grow between childhood and adolescence?

A

Lung volume increases 30 times (max vol. 22 years in male)
Airways increase in length and width x2-3 by symmetrical growth
Dysanaptic growth during the early period (alveoli grow more than airways)
Structural elements of the wall increase

333
Q

How do the alveoli grow between childhood and adolescence?

A

Alveoli increase in number up to 2-3 years (maybe up to adulthood)
Alveoli increase in size and complexity to increase surface area until body growth complete after adolescence
Arteries, veins and capillaries increase alongside the alveoli

334
Q

How many alveoli does an adult have?

A

300-600 million

335
Q

What is the pulmonary circulation?

A

Blood that collects oxygen from the lungs

DOES NOT SUPPLY THE LUNG WITH OXYGEN!

336
Q

How is the pulmonary circulation different from the systemic circulation?

A

Arterial walls are thinner, less smooth muscle, wider lumen (low pressure circuit)
In the heart the left ventricle is much larger. Right is less powerful
Systemic: high pressure circuit
Pulmonary: low pressure circuit

337
Q

Where does blood leave the heart at the highest pressure and where does it return at the highest pressure?

A

Leaves left venticle at the highest pressure

Returns to the heart at the highest pressure to the left atrium

338
Q

What is the cardiac output on both sides of the heart?

A

5L on both sides

339
Q

What is the volume in the systemic and pulmonary circulation?

A

Systemic: 4.5L
Pulmonary: 0.5L

340
Q

What are the functions of the pulmonary circulation

A

1) Gas exchange (oxygen delivery and carbon dioxide)
2) Metabolism of vasoactive substances (Angiotensin, bradykinin)
3) Filtration of blood (trapping emboli so they don’t trap in the body)

341
Q

What is the difference in MAP in the pulmonary and systemic circulation?

A

Systemic: 93
Pulmonary: 13

342
Q

What is the difference in pressure gradient in the pulmonary and systemic circulation?

A

Systemic: 92
Pulmonary: 9

343
Q

What is the difference in resistance in the pulmonary and systemic circulation?

A

Systemic: 18.4
Pulmonary: 1.8

344
Q

What is a pulmonary shunt?

A

Something bypassing the respiratory exchange surface
1) Bronchial circulation
Blood coming from aorta through the bronchial veins and back to the left atrium and to the aorta
2) Foetal circulation
Foramen ovale- shunt from right to left ventricle- bypasses pulmonary filtration which would trap emboli. Mixes blood, can require surgey
3) Congenital defect
Ventricular-septal defect: hole between ventricles- causes mixing, reduced PaO2

345
Q

What effect does increasing cardiac output have on pulmonary vascular resistance?

A

1) ↑Q (CO)
2a) ↑ pulmonary artery distension
2b) ↑ perfusion of hypoperfused beds (higher up lungs- evenly distributed)
3) Negligable change in MAP
4) Minimal fluid leakage
5) No onset of pulmonary oedema
No detriment to pulmonary function

346
Q

What is the mechanism for pulmonary response to hypoxia?

A

1) Hypoxia
2) Closure of O2-sensitive K+ channels
3) ↓ K+ efflux
4) ↑ membrane potential
5) Membrane depolarisation. Opening of voltage-gated Ca2+ channels
6) Vascular smooth muscle constriction

347
Q

When in the pulmonary response to hypoxia beneficial?

A

During foetal development

  • Blood follows the path of least resistance
  • High-resistance pulmonary circuit means increased blood flow through shunts
  • First breath increases alveolar PO2 and dilates pulmonary vessels
348
Q

When in the pulmonary response to hypoxia detrimental?

A

In COPD

  • Reduced alveolar ventilation and air trapping
  • Increased resistance in pulmonary circuit
  • Pulmonary hypertension (Cor pulmonale)
  • Right ventricular hypertrophy
  • Congestive heart failure
349
Q

What forces affect the pulmonary fluid balance?

A
  • Plasma hydrostatic pressure (capillary to interstitial) 9mmHg out
  • Plasma oncotic (interstitial into capillary) 25mmHg in
  • Interstitial oncotic (capillary to interstitial) 17mmHg out
    TOTAL=1mmHg out
350
Q

How does mitral valve stenosis affect pulmonary fluid balance?

A

Increased plasma hydrostatic pressure
More fluid forced into interstitium
Lymph clearance exceeded
Causes pulmonary oedema

351
Q

How does hypoproteinaemia affect pulmonary fluid balance?

A 
Plasma oncotic pressure reduced
Less fluid drawn into capillary
Fluid accumulates in interstitium
Lymph clearance exceeded
Pulmonary oedema
352
Q

How does infection affect the pulmonary fluid balance?

A 
Increasing interstitial oncotic pressure
More fluid drawn out of capillaries
Large net fluid movement out of capillary
Lymphatic clearance exceeded
Causes pulmonary oedema
353
Q

How does cancer affect the pulmonary fluid balance?

A

Blocked lymphatic vessels causes oedema

354
Q

Is blood more compliant in the pulmonary or systemic circulation?

A

Systemic

355
Q

Is venous return higher in the left or right atrium?

A

Left atrium

because of bronchial shunt

356
Q

Is blood flow greater apically or basally?

A

Basally

357
Q

How long is a sleep cycle?

A

90 minutes

358
Q

What stage of the sleep cycle are you in most of the time during sleep?

A

deep sleep (stage 4)

359
Q

What is REM sleep?

A

Rapid eye movement

360
Q

What part of the sleep cycle to you dream?

A

REM

361
Q

What are the stages of the sleep cycle?

A 
REM
Stage 1- lighter sleep
Stage 2
Stage 3
Stage 4- deep restorative sleep
362
Q

Where is the automatic control of breathing?

A

In the Pre-Bötzinger region in the brain stem

On the edge of the medulla close to the CSF where concentration changes can be detected

363
Q

What is Locked In syndrome?

A

Full sensory input but no capacity to move, except for ocular control

364
Q

What happens to minute ventilation when you fall asleep?

A

Goes down by about 10%

365
Q

What causes breathing to decreases when you go to sleep?

A

Your tidal volume decreases

366
Q

What happens to SaO2 (O saturation) when you go to sleep? What happens to paCO2? What is the significance of this?

A

SaO2: Goes down
PaCO2: Goes up by 0.5kPa (2-4mmHg)- due to reduction in minute ventilation.
This is essential to keep breathing during sleep to stimulate the chemoreceptors to keep breathing

367
Q

What happens to SaO2 in a patient with COPD? Why is this a problem?

A

Goes down. They start to accumulate CO2

368
Q

What is essential to maintain breathing during sleep?

A

Hypercapnia

369
Q

What is the level called over which your CO2 has to go to maintain breathing?

A

Apnoeic threshold

370
Q

What happens to CO2 sensitivity during sleep?

A

Goes up (becomes less sensitive to CO2)

371
Q

What happens to the upper airway muscles during sleep? How can this cause obstructive sleep apnoea?

A

They relax and the extra luminal pressure and negative intraluminal pressure can result in acclusion of the phalangeal airway during sleep

372
Q

What causes snoring?

A

Turbulent air flow over the vocal chords

373
Q

What is the cycle of obstructive sleep apnoea?

A

1) Fall asleep- Muscles relax, CO2 increases
2) Upper airway muscle relaxes
3) Airway occludes- oxygen decreases, CO2 increases and increased effort to try and breath
4) One of these changes will wake you up
5) Hyperventilate due to low CO2
6) Fall back to sleep

374
Q

What si the difference between central apnoea and obstructive apnoea?

A

Both of them have low air flow.
Central apnoea there if no effort to breath- it is caused by low chemosensitivity
Obstructive displays paradoxial breathing due to mechanical blockage

375
Q

What is Congenital Hyperventialation Syndrome (CCHS)?

A

Babies born with low chemosensitivity, have to be ventilated all their life

376
Q

In what condition is central sleep apnoea common? In what percentage of patients? Why?

A

30-40% of heart failure patients
Heart failure causes pulmonary oedema which stimulates (J) receptors causing over breathing. This lowers CO2. Low CO2 when sleeping stops breathing
CO2 is below the apnoeic threshold. (These patients tend to die earlier)

377
Q

What are the principle muscles associated with inspiration? What is the mechanism?

A 
The diaphragm
The accessory muscles:
- External intercostals
- Scalene
- Sternocleidomastoid
Diaphragm contracts and pulls down. External intercostals contract and pulls ribs out.
378
Q

What are the principle muscles associated with expiration? What is the mechanism?

A 
Internal intercostals (infero-lateral direction)
The internal and external oblique
Rectus abdominis
Internal intercostals, oblique muscles and rectus abdominis contract moving ribs in and down
Diaphragm relaxes pushing up
379
Q

What are the additional non-respiratory actions of the muscles associated with breathing?

A

Control air movement during other behaviours such as speech, laughter, coughing, sneezing and vomiting
Diaphragm is an essential muscle in childbirth

380
Q

What muscle is involved in movement of the head?

A

Sternocleidomastoid

381
Q

What muscle is used during quiet breathing?

A

Diaphragm

382
Q

What muscles are used on increased breathing demand?

A

External intercostals

383
Q

What muscles are used during exercise and on high demand breathing?

A

Scalene
Sternocleidomastoid
Accessory Expiratory Muscles

384
Q

How do you measure RV, FRC and TLC?

A

Inert gas dilution technique

385
Q

During exercise what lung capacities change and which ones cannot change?

A

Mainly tidal volume increases
ERV, IRV, FRC and IC all change
RV, TLC and VC cannot be changed

386
Q

In a patient with chronic obstructive disease what would happen to their lung capacities?

A

VC would decrease or remain constant
TLC would decrease based on VC changes
FRC and RV would increase

387
Q

In a patient with chronic residual disease what would happen to their lung capacities?

A

RV no change
VC and TLC would decrease
FRC would significantly reduce

388
Q

What two methods can be used to evaluate airway resistance?

A

Forced expiratory volume (FEV1) using a vitalograph

Peak expiratory flow rate (PEFR) using a peak flow meter

389
Q

What is FVC?

A

Forced vital capacity

The maximum volume of air expired as forcefully and rapidly as possible following a maximum inspiration

390
Q

What happens to FEV1 in obstructive and restrictive lung disease? Why?

A

Reduced in both
Restrictive: Low compliance so the vital capacity is compromised
Obstructive: Airway narrowing results in high resistance which slows expiration

391
Q

What is the significance of the FEV1/FVC ratio? What is a normal value?

A

Estimates airway resistance

Ratio should normally be around 1 as normal/healthy should be able to breath all air out in 1 second

392
Q

What happens to the FEV1/FVC ration in obstructive lung disease?

A

Vital capacity may be normal but FEV1 is reduced due to airway resistance and so the ratio decreases

393
Q

What happens to the FEV1/FVC ration in restrictive lung disease?

A

Vital capacity is greatly reduced but airway resistance is normal so both values decrease but the ratio stays the same

394
Q

In what circumstances do FVC, FEV1, FEV1/FVC and PEFR change?

A

Increase with subject size (height)
Decrease with age after peaking at 20
Generally lower in females, then males of the same age and height

395
Q

What changes can increase airway resistance?

A

1) Bronchoconstriction
- Smooth muscle contracts the airway walls
- Frequently the case in asthmatics
2) Physical blockage
- e.g. increased mucus secretion
- Leads to more viscous mucus, more difficult to remove and forms a mucus plug
3) Loss of radial traction (outward pull)
4) Change to the airway wall structure
- Lumen can narrow
- Frequently the case with asthmatics
5) Airway inflammation
- Leads to swelling of tissue and reduction in luminal diameter

396
Q

What happens to PO2, PCO2 and SaO2 during breath holding?

A 
PaO2 decreases
PaCO2 increases
SaO2 falls
- less oxygen for haemoglobin to carry
- CO2 now binds to the haemoglobin to be carried back to lungs to be removed
397
Q

What happens to PO2, PCO2 and SaO2 during over-breathing of room air?

A

PaO2 increases
PaCO2 decreases
SaO2 remains constant

398
Q

What happens to PO2, PCO2 and SaO2 during normal breathing of oxygen?

A

PaO2 increases greatly
PaCO2 decreases
SaO2 remains constant

399
Q

What happens to PO2, PCO2 and SaO2 during over-breathing of oxygen?

A

PaO2 increases hugely
PaCO2 decreases
SaO2 rises slightly

400
Q

Why do changes in PaO2 and PaCO2 during a breath hold lead to an inability to hold breath?

A

Increased PaCO2 and decreased PaO2 stimulated the central and peripheral chemoreceptors, which instigate nervous impulses from the respiratory centre that overcome voluntary suppression by the apneustic centre
This forces the subject to stop the breath hold and take a breath of air to bring oxygen and carbon dioxide levels back to normal

401
Q

How is breath holding time changed if PaCO2 and PaO2 are altered prior to the breath hold?

A

If PaCO2 is reduced immediately before the breath hold, stimulation of the chemoreceptors will occur in the required degree at a later time, therefore allowing breath to be help for longer
There is little effect if the PaO2 is changed

402
Q

What other factors other than PaO2 and PaCO2 influence breath-holding time?

A

Neural stimuli from the chest wall and lung receptors induce chest expansion and thus influence breath holding time

403
Q

What factors affect PAO2 and PACO2?

A

1) Composition of inspired air
2) Alveolar ventilation
3) Metabolic rate (O2 use and CO2 production

404
Q

What is hyperpnoea?

A

Rapid ventilation appropriate for a metabolic acidotic state, as observed in exercise

405
Q

How does anaemia affect PaO2 and PaCO2

A

A reduction in haemoglobin concentration does not affect PaO2 of PaCO2
Anaemia does drastically decrease oxygen content
Hyperventialtion with oxygen-rich gas will improve PaO2 but it will not cause a significant rise in oxygen content

406
Q

What three pathological conditions make up COPD?

A

1) Bronchitis
2) Emphysema
3) Small airway disease

407
Q

What level of the respiratory tract is affected by bronchitis?

A

The bronchi mainly and generally not the bronchioles (the cartilaginous part of the airway)

408
Q

What level of the respiratory tract is affected by emphysema?

A

Mainly the respiratory bronchioles, especially of smokers
Leads to the loss of connective tissue scaffold, basement membrane and normal cell organisation
Loss of surface area and elastic recoil of alveoli, which comprises gas exchange

409
Q

What level of the respiratory tract is affected by small airway disease?

A

The bronchioles and other non-cartilaginous regions of the airways

410
Q

What would a bronchoalveolar lavage in a patient with COPD show compared to normal?

A

In healthy lungs the inflammatory cells of a peripheral wash would be 70% macrophages and 30% neutrophils
In COPD there are 70% neutrophils and 30% macrophages

411
Q

In COPD what would a high resolution CT scan show?

A

Much more detail than a normal CT
Bronchitis: Small airways denser in number
Emphysema: Holes in the small airways of the lungs

412
Q

What happens to the structure of the lung in emphysema?

A

Holes in the small airways of the lungs (due to endogenous immune response)
Macrophages and neutrophils contain proteases released during inflammatory phase
Protease secretion overload damages host tissue

413
Q

Why is emphysema far more prevalent in smokers?

A

Due to a deficiency in α-1-antitrypsin, which circulates in the blood and mops up all the excess porteases

414
Q

What are the changes in epithelial cells that occur in bronchitis?

A

Decreased ciliated cells, increased goblet cells and therefore increased mucous production.
Trapped particles cannot be removed by cilia and they beat asynchronously.
Coughing only way to shift mucus “smokers cough”
Mucus traps particles/microbes and inflammatory cell number increases

415
Q

Why does a protease inhibitor help treat COPD?

A

Inhibits the action of secreted proteases

Only given to non-smokers as smoking inhibits protease inhibitors

416
Q

Why don’t endogenous inhibitors work in COPD?

A

e.g. tissue inhibitor of metalloproteinases (TIMP)
Do not work as there is proteolytic overload. An endogenous inhibitor woul not remove any of the protease already present

417
Q

What is a dual inhibitor for COPD?

A

Use of a protease inhibitor to inhibit already present protease and an endogenous inhibitor to prevent the release of more protease

418
Q

How can mucus be removed in COPD?

A

Use of a mucolytic or massage therapy

419
Q

How does a bronchodilator help in COPD?

A

Makes breathing easier as it dilates the airways

420
Q

What is metaplasia?

A

The reversible change in differentiation from one fully differentiated cell type to another

421
Q

What is dysplasia?

A

An abnormal pattern of growth in which some of the histological features of malignancy are present

422
Q

What is hyperplasia?

A

An increase in size of a tissue or organ resulting from an increase in the number of cells

423
Q

What is hypertrophy?

A

An increase in size of a tissue or organ resulting from an increase in size of individual cells

424
Q

What is a lobectomy?

A

Removal of a lung lobe

425
Q

What is a pneumonectomy?

A

Complete removal of a lung

426
Q

What is pleural effusion?

A

Accumulation of fluid in the pleural space, possibly causing pleurisy

427
Q

What is atelectasis?

A

Incomplete expansion of the lung or portion of the lung due to airway obstruction, lung compression or inadequate pulmonary surfactant

428
Q

What is haemoptysis?

A

Coughing up blood

429
Q

What test can be conducted to test breatlessness?

A

Shuttle walk test

430
Q

What is the difference between central and peripheral cyanosis?

A

Central: Poor oxygenation of the blood- assessment of tongue colour. Bluish tongue indicated low PaO2 of 7-8kPa
Peripheral cyanosis: Bluish colour of the hands- can also indicate poor peripheral circulation

431
Q

What are the symptoms of hyperinflation of the lungs?

A
  • Prolonged exiratory phase
  • Expanded, barrel-shaped chest
  • Reduced overall movement of ribcage
  • Apex beat of the heart not palpable
  • Increased activity of the sternocleidomastoid
432
Q

What causes a wheeze with breath sounds?

A

Airways narrowing

Asthma, COPD, pulmonary oedema or localised tumour

433
Q

What causes a crackle with breath sounds?

A

Equalisation of the intra-luminal pressure of the collapsed small airways during inspiration
Acute respiratory distress syndrome (ARDS), pulmonary fibrosis and bronchiectasis

LSS Year 1 (4 decks)

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