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Resp Flashcards

0
Q

What is charles’s law, what units are required

A

Pressure is directly proportional to temperature

Kelvin

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1
Q

What is boyles law?

A

Pressure is indirectly proportional to volume of a fixed amount of gas

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2
Q

What is the universal gas law?

What is its significance to drs?

A

Boyles and charles combined
Pressure x volume = universal gas constant x temperature
Any testing done outside of the body will generate different results of pressure as temperature changes

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3
Q

What is daltons law?

A

Each gas exerts its own pressure as if no other gases were present which is the same fraction of the total mix pressure as the fraction of the volume the gas.

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4
Q

How can water interact with gasses?

A

Evaporation of water

Dissolving of gas

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5
Q

What effect does evaporation have on inhaled gasses?

A

Water evapourates creating a fixed saturated vapour pressure at a given temperature (6.28kPa in the body) this is always exerted no matter the total pressure so is proportionally more important if total pressure falls

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6
Q

What is the tension of a gas in water? What does it equal at equilibrium?

A

A measure of how readily a gas molecule will leave the liquid
Partial pressure

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7
Q

How is the amount of gas in a liquid calculated?

A

Content = solubility x tension

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8
Q

What is the effect on gases binding to molecules within a liquid on amount and tension?

A

Tension remains the same but amount goes up

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9
Q

In blood plasma what is the oxygen tension, what amount is dissolved in plasma at that tension given oxygens low solubility? How much is carried in whole blood? Why?

A

13.3kPa gives a dissolved content of 0.13mmol/L

Total blood has 8.93mmol/L due to haemoglobin binding

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10
Q

If an abg shows a pO2 of 13.3 is the patient definitely adequately oxygenated?

A

No - there could be a haemoglobin deficiency - anaemia

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11
Q

What is the partial pressure of oxygen in the atmosphere? What about alveolar air? Why the drop?

A

21.1kpa
13.3kpa
Oxygen is being removed and co2 and h2o added

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12
Q

What is the order of the airways?

A 
Trachea
Primary bronchi
Secondary bronchi
Bronchioles 
Terminal bronchioles
Respiratory bronchioles
Alveolar ducts
Alveoli
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13
Q

What causes the alteration in nostril side during breathing?

A

Swelling of the venous plexuses in the lamina propria

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14
Q

What is the laryngeal epithelium?

A

Psudostratified ciliated columnar epithelium with mucous glands for the most part
Stratified squamous covering the vocal ligaments and the vocalis muscle

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15
Q

What is the change in epithelium from trachea to alveoli?

A

Psuedostratified ciliated (trachea, proximal bronchi)
Simple columnar ciliated (distal bronchi, proximal bronchioles)
Simple cuboidal ciliated (terminal bronchioles)

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16
Q

What changes occur to the secretory cells in the lower airways? Where?

A

In terminal bronchioles goblet cells are replaced with clara cells. In respiratory bronchioles clara cells are the predominant cell type.

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17
Q

What are the replacement for goblet cells in the lower airway? What do they produce?

A

Clara cells

Surfactant lipoproteins to prevent walls adhering in expiration

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18
Q

Where is bronchiole smooth muscle found?

A

Between the lamina propria and submucosa

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19
Q

What keeps the small airways open during expiration?

A

Direct pull from elasticity from neighbouring alveoli

Air pressure from the lumen exceeding that of the pleura due to elastic recoil of the alveoli in forced expiration

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20
Q

How does mucus secretion differ from bronchi to bronchioles?

A

Bronchi - mucus from goblet cells and submucosal glands

Bronchioles - no submucosal glands and goblet cells replaced with clara cells distally

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21
Q

Where do alveoli arise in the airways?

A

Other alveoli
Alveolar sacs
Alveolar ducts
Respiratory bronchioles

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22
Q

What are the cell types in the alveoli? What do they do?

A

Type 1 pneumocyte - squamous type that provides. Gas exchange surface
Type 2 pneumocyte - cuboidal type that secretes surfactant
Alveolar macrophages.

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23
Q

Where are the lungs by surface markings?

A

Apex 3cm above medial 1/3rd of pleural cavity
Nearly meet at mid sternal line at 2nd rib
Descend together to the 4th rib
Left moves to left sternal before descending to 6, right decends straight to 6
Both descend to 8 (pleura) / 6 (lung) at MCL
Both descend to 10 p 8 l at MAL
Both descend to 12 p 10 l at medial scapular boder

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24
Q

What are the two fissures of the right lung?

What are their surface markings?

A

Oblique T2 to 6th costal cartilage

Horizontal 4th rib at mid axillary line to anterior edge of lung

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25
Q

Where does the manubrium join the body of the sternum?

A

Sternal angle of louis at level of second costal cartilage

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26
Q

How are the ribs classified?

A

1-7 true
8-10 false
11-12 floating

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27
Q

Which ribs are typical? What are landmarks on their structure?

A

3-9
Two articular facets on head to articulate with body of vertebra or spine and vertebra above (i.e. 3rd rib with T2 and T3)
One articular facet to articulate with the transverse process of the vertebra
An inferior costal groove for vessels and nerves

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28
Q

Which ribs only have one facet on their head?

A

1,10,11,12

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29
Q

What makes rib 2 atypical?

A

Poorly marked costal groove

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30
Q

When the ribs elevate how does the shape of the chest change?

A

Upper ribs cause increase in sagittal diameter and lower ribs transverse diameter

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31
Q

What are the different intercostal muscles? Where are they and which way do they run?

A

External - costoverterbral junction to start of costal cartliage, runs down and anteriorly
Internal - sternal edge to just before costoverterbral junction, runs down and posteriorly
Innermost - only found laterally, run as with the internals

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32
Q

What muscles are used in normal inspiration and expiration?

A

Insp - diaphragm and external intercostal

Exp - none

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33
Q

What muscles are used in forced inspiration?

A

Sternocleidomastoid
Scalenes
Pectoralis minor
Serratus anterior

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34
Q

Which muscles are used in forced expiraiton?

A

Internal and innermost intercostals
Rectus abdomins
External and internal obliques
Transvers abdominus

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35
Q

What is the order superior to inferior, of the contents of the costal groove?
What about those vessels running on the superior surface?

A

Vein
Artery
Nerve

Reversed

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36
Q

Where do the intercostal nerves arise? Where do they run?

A

Anterior rami of t1-12

Between the internal and innermost intercostals

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37
Q

Where do the intercostal arteries arrise?

A

Anterior branch from internal thoracic

Posterior branch from thoracic aorta

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38
Q

Where do the intercostal veins drain?

A

Anteriorly to the internal thoracic vein

Posteriorly to the azygos system (azygos vein on the right, hemizygos and accessory azygos on left)

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39
Q

What are the levels of the openings through the diaphragm?

A

Vena cava t8
Oesophagus t10
Aortic hiatus t12

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40
Q

What does the phrenic nerve supply?

A 
Sensation of the 
Pericardium
Mediastinal parietal pleura
Diaphragmatic parietal pleura
Both sides of the diaphragm (except the margins supplied by the intercostal nerve)

Motor
Diaphragm

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41
Q

What are the various regions of the parietal pleura?

A

Cervical
Mediastinal
Costal
Diaphragmatic

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42
Q

What are the functions of the serous fluid?

A

Allows sliding of the pleura

Creates the pleural seal

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43
Q

At what level is the carina?

A

t4/t5

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44
Q

Which bronchi is more susceptable to obstruction, why?

A

Right

Shorter, wider, more verticle

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45
Q

What follows the main bronchi?

A

Lobar bronchi

Segmental bronchi

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46
Q

What do segmental bronchi supply? What is special about this?

A

A bronchopulmonary segment

Each has its own bronchi, pulmonary artery and pulmonary vein. Thus can be isolated and surgically removed

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47
Q

What are the three surfaces of the lung?

A

Costal
Mediasteinal
Diaphragmatic

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48
Q

What is the equivalent of the middle lobe in the left?

A

The lingula

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49
Q

How can the left and right hilum be distinguished?

A

Right - arteries are anterior to the bronchus
Left - arteries superior to bronchus
RALS

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50
Q

What is the lymphatic drainage of the lungs?

A

Hiliar nodes
Trachobronchial nodes (right and lower left up the right, upper left up the left)
Bronchiomediasteinal trunk to subclavian veins

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51
Q

What structures are associated with the hilum besides the obvious?

A

Phrenic nerve anteriorly
Left recurrent laryngeal nerve superiorly
Aorta on the left
Svc and azygos on the right

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52
Q

To what level do the bronchial arteries provide oxygen?

Where does the rest get o2 and nutrients from?

A

Terminal bronchioles

Gas exchange and pulmonary arteries for nutrients

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53
Q

How is the mediasteinum divided?

What is in each bit?

A

Anterior - between sternum and pericaridum
Middle - between anterior and posterior! Fibrous pericardial contents
Posterior - between vertebral bodies and pericardium
Superior - above line from sternal angle and t4

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54
Q

What is the pO2 and pCO2 of pulmonary arteriolar blood?

A

6

6.5 kPa

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55
Q

What influences the rate of diffusion across the alveolar membrane?

A

Area
Gradient
Resistance (nature of barrier and gas)

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56
Q

What 6 layers must an oxygen molecule travel from mid alveoli to inside a rbc?

A 
Through the gas
Alveolar cells
Intersitial fluid
Endothelial cells
Plasma
Red cell membrane
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57
Q

Which gas moves through gas easier?

A

Oxygen - it has a lower molecular weight

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58
Q

What gas diffuses faster through liquids (including phospholipid bilayer)? What is the result of this?

A

co2

As a result a problem with diffusion nearly always selectively effects O2

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59
Q

Why do small changes in diffusion resistance not affect concentration of blood gasses in the pulmonary veins?

A

Because blood passes next to alveoli for 1s but only takes 0.5s to reach equilibrium thus there is plenty of leaway

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60
Q

How does the body keep the concentrations of alveolar gasses constant during respiration?

A

Pulmonary ventilation only reaches the terminal bronchioles. From there gas diffuses into and out of the alveoli not fluctuating with the respiratory cycle. This is alveolar ventilation

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61
Q

What are the lung volumes?

A

Inspiratory reserve volume - 3.3L
Tidal volume - 0.5L
Expiratory reserve volume - 1.2L
Residual volume - 0.8L

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62
Q

What are the lung capacities?

A

Vital capacity - 5L
Inspiratory capacity - 3.8L
Functional residual capacity - 2L
Total capacity 5.8L

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63
Q

Why do we measure lung capacities?

A

Volumes change with patterns of breathing so are not fixed for an individual. As a result tests would vary time to time (poor consistency)
Capacities are all measured from fixed points in the cycle - max inspiration, max expiration, end of passive expiration

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64
Q

What is the term for the volume of air moved in a breath times the respiratory rate?
What is it typically?

A

Pulmonary ventilation rate

16x500ml = 8000ml/min

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65
Q

What are the dead spaces? Typical values?

A

Serial - conducting airway volume (0.15L
Distributive - non perfused alveoli volume (0.02L)
Physiological - serial + distributive (0.17L)

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66
Q

What is alveolar ventilation rate?

Typical values

A 
AVR = pulmonary ventilation rate - dead space ventilation rate
AVR = (16x500)-(16x170)
AVR = 8000 - 2720 = 5280
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67
Q

What is the consequence of dead space in the lungs?

A

Rapid breathing is less efficient as dead space becomes proportionately more important.

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68
Q

What is the term for the connection between the two layers of pleura that means the lungs pull out with chest expansion?

A

Pleural seal

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69
Q

Why do we expire by relaxing after inspiration? Why does it stop?

A

At the end of inspiration we relax our muscles. Consequently the inward elastic pull of the lungs becomes greater than the outward pull of diaphragm and chest so they are pulled inwards. At the end of passive expiration the inward elastic pull equals the outward recoil of the chest and diaphragm so there is no movement.

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70
Q

What happens during forced expiration?

A

Muscles augment the inwards elastic pull of the lungs and pleural pressure exceeds atmospheric pressure (the only time this occurs) forcing the lungs to contract.

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71
Q

What is lung compliance?

A

A measure of the volume change per unit pressure change. A highly compliant lung has big volume changes for small pressure changes, a poorly compliant lung has the reverse.

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72
Q

What causes the elastic recoil of the lungs?

A

Elastin in the walls/interstitium

Surface tension

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73
Q

What is surface tension?

A

The tendency of a liquid to contract to its minimal volume as molecules on the surface are being pulled into the centre (attractive forces with other water molecules but not the air - thus pulled in)

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74
Q

Why do small alveoli tend towards collapse? How does surfactant prevent alveolar collapse?

A

Pressure required to keep alveoli open = (2x surface tension) / r
Thus small alveoli require a larger pressure to stay open than big
Surfactant reduces surface tension more when compact, thus reduces surface tension more in small alveoli so the pressure needed to stay open reduces more in these.

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75
Q

Functions of surfactant

A

Stopping alveolar collapse

Reducing compliance

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76
Q

Diseases with high compliance

A

Emphysema

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77
Q

Diseases with low compliance

A

Fibrosis

Respiratory distress syndrome of the newborn

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78
Q

Will FRC increase or decrease in a disease which increases compliance like emphysema? Why?

A

It will increase
The point at which FRC is reached is the point when inward pull of the lung is matched to outwards pull of the chest. As lung compliance has increased then at this volume inward pull will be less. For the forces to balance the volume must be greater - the new equilibrium is at a greater volume!

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79
Q

What will be the effect on FRC of a disease that decreases lung compliance like fibrosis?

A

Decreased frc.
Frc depends on an equilibrium between inward pull of the lung and outward pull of the chest wall. At a healthy FRC the stiff lung will be generating greater force than the outward pull - as a result FRC must reduce to reach equilibrium with outward pull.

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80
Q

What is hysteresis? How does it apply to the lungs?

A

The energy expanded increasing surface tension when surface area is increased is not all recovered when surface area reduces. Practically this means as pressure increases on inspiration the volume will increase as it overcomes surface tension - however, on expiration for each given pressure the lung volume will be greater.

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81
Q

During inspiration order atmospheric pleural and alveolar pressures from high to low

A

Atmospheric
Alveolar
Pleural

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82
Q

During expiration order atmospheric pleural and alveolar pressures from high to low

A

Alveolar
Atmospheric
Pleural

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83
Q

During forced expiration order atmospheric pleural and alveolar pressures from high to low

A

Pleural
Alveolar
Atmospheric

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84
Q

What law is relevant to the size of alveoli and pressure?

A

Laplaces

Pressure = 2 ST / r

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85
Q

What law is relevant to flow through tubes?

A

Poiseulles
Flow is directly proportional to:
(Pressure gradient x radius squared x radius squared) / (viscosity x
length)

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86
Q

Where is the highest resistance in the airways during normal respiration?

A

Trachea! Smaller airways are in parallel so their radius is actually greater!

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87
Q

Where is the highest resistance to airflow in forced expiration?

A

The small airways - they narrow as interpleural pressure increases

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88
Q

Why do you get airway obstruction in empysema?

A

On forced expiration inter-pleural pressure increases. Due to the lack of elasticity of the lungs there is less alveolar pressure. As a result the airways are compressed

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89
Q

What does spirometry show?

A

Inspired and expired volume with time

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90
Q

What is an issue with spirometry in determining vital capacity? What can effect both

A

Is a lowered value due to low max inspiration or low max expiration?
Low max insp - chest wall defect, chest muscle weakness (restrictive defect)
Low max exp - narrowed airways (obstructive defect)

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91
Q

How can we differentiate between restrictive and obstructive defects of the lung?

A

A vitalograph trace

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92
Q

What does a vitalograph trace involve? What values are derived from it?

A

Taking a single maximal inspiration then expiring into a spirometer as fast as possible
Forced Vital Capacity (FVC)
Forced Expiratory Volume in one second (FEV1)

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93
Q

What vitelograph reading would suggest an obstructive lung defect?

A

A FEV1 <70% of FVC

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94
Q

What suggests a restrictive defect on vitalograph?

A

A low FVC with a FEV1 >70% (note actual value of FEV1 will be lowered but it is the ratio that is important)

95
Q

How can more information be gained from a vitelograph over and above fvc and fev1?

A

Conversion into a flow volume loop.

96
Q

At what point of forced expiration does an individual produce PEFR?

A

Almost immediately as lungs are stretched so resistance is least

97
Q

What is seen on an flow volume curve in obstructive airway disease? What is the advantage of this test over vitalograph?

A

A rapid decrease from maximal flow with increasing volume scooping out the curve

98
Q

Why do we use PEFV is asthma?

A

Very cheap and simple to use. It is measuring large airway resistance but in severe asthma will become effected by small thus indicates a severe issue

99
Q

How can we measure residual volume?

A

Breath in helium at a known concentration starting from end of passive expiration
Monitor how concentration of expired helium has reduced to determine volume of air already in the lungs

100
Q

How can we measure serial dead space?

A

Perform a nitrogen washout
Breath pure O2
Measure percentage of nitrogen against volume on expiration
Initial expiration will have no nitrogen (as large airways replaced with o2 first)
Mid expiration will have increasing nitrogen from alveolar air diffusion
End expiration will have normal nitrogen
Draw a line midway down the curve - area to left represents serial dead space

101
Q

How can we measure diffusion over alveoli?

A

Give carbon monoxide

Measure the amount on haemoglobin in blood

102
Q

Why do we use CO to measure alveolar diffusion?

A

It binds fully to haemoglobin so exerts no partial pressure thus gradient is always (given concentration : 0)

103
Q

What is a flaw with oxygen saturation measurements when considering amount of oxygen reaching the tissues?

A

Doesnt consider pigment concentration thus not amount of oxygen

104
Q

What is the typical concentration (!) of o2 in pulmonary venous gas

A

Conc Hb = 2.2mmol/L
Each Hb can hold 4 O2 thus conc O2 is 8.8mmol/L
Add disolved O2 of 0.13mmol/L gives 8.93mmol/L

105
Q

If 100% saturated blood in the lungs has a O2 concentration of 8.8mM what is the concentration in 65% saturated tissue?

A

0.65x8.8=5.8

106
Q

How are active tissues adapted to get the most O2?

How much extra of the norm of 3mM drop in concentration can active tissues achieve? What does this mean?

A

High capillary density allowing lower pO2 with all cells still recieving sufficient
H+, co2 and temp high

Can double amount released to. 6mM
This means that an increased O2 demand can be matched with half the increase by the CVS

107
Q

What is the concentration of CO2 in arterial blood? How does it change in venous?
What is the implication of this?

A

21.5mM
Raises by 2mM
The vast majority of CO2 in blood is nothing to do with respiration!

108
Q

How is CO2 carried in blood? Percentages please

A

8% dissolved
12% as carbaminocompounds (mainly carboxyhaemoglobin)
80% reacts with water forming H+ and bicarbonate ions from carbonic acid

109
Q

What happens to CO2 as it leaves a producing cell

A

Enters plasma. No CA in plasma so little reaction occurs
Enters RBC. CA converts it to carbonic acid
Carbonic acid to H and bicarbonate ion
H binds to Hb (HbH) causing stabilisation of T state releasing O2
Bicarbonate ion shunted into plasma in exchange for Cl-
Removal of products from RBC favours continued forward reaction

110
Q

What is the consequence of high bicarbonate concentration in plasma?

A

Pushes the CO2 and Water to H and HCO3- to the left stopping the creation of H+ in the plasma

111
Q

Why is venous pH not higher than arterial? There is more CO2 after all?

A

Less o2 thus H+ can bind more to Hb and thus more HCO3- in plasma
Also higher caboxyhaemoglobin

112
Q

What. Happens in the lungs to cause CO2 exhalation?

A

High. O2 = HbH to Hb and H
H and HCO3- to CO2 and H2O
CO2 breathed out

113
Q

What is the dilemma with respiratory control?

A

Compensating for hypoxia alone would cause hypocapnia and vica versa. Only works if hypoxic and hypercapnia

114
Q

How is low oxygen detected? At what level?

A

By peripheral chemoreceptors

At 8kPa prior to significant fall in sats

115
Q

What feature of peripheral chemoreceptors allows them to respond to oxygen conc. changes?

A

Very well supplied with blood so only become hypoxic if ppO2 drops below 8kPa

116
Q

What is the response of the body to hypoxia?

A

Increased resps
Increased heart rate
Diversion of blood to the brain

117
Q

What can increase the sensitivity of peripheral chemoreceptors to hypoxia?

A

Hypovolemia - become hypoxic more easily

118
Q

What would a biochemical profile of resp acidosis look like?

A

Low ph
High co2
High bicarb (over several days - compensation)

119
Q

Differentiate compensation and correction of acidosis/alkalosis

A

Compensation - other system trying to return ph to normal

Correction - effected system altering to oppose changes

120
Q

What would a metabolic alkalosis look like biochemically?

A

High pH
High bicarb
High CO2

121
Q

How would a resp alkalosis appear biochemically?

A

High pH
Low CO2
Low bicarb

122
Q

How would a metabolic acidosis appear biochemically?

A

Low ph
Low bicarb
Low CO2

123
Q

Why does compensation help stabilise pH?

A

Because its ratios that matter not actual componenets. Circa henderson hasselbach

124
Q

Where and how are changes in pCO2 detected?

A

Mainly central chemoreceptors in medulla

Respond to pH changes in CSF

125
Q

How does change in CO2 effect CSF pH?

A

Co2 diffuses freely into CSF whilst bicarbonate cannont
Thus acute rise in CO2 causes acidosis in CSF and increased respirations
But CSF doesnt like being acidic so choroid plexuses increase import of bicarbonate normalising pH in chronic high CO2 and resps return to normal thus CO2 builds up.

126
Q

What is type 1 resp failure?

When does it normally occur?

A

Low O2, normal or low CO2

Usually from v/q mismatch or diffusion problems

127
Q

Examples of vq mismatch resulting in type 1 resp failure

A

PE
Pneumonia
Early acute asthma

128
Q

Why does poor perfusion of an alveoli lead to type 1 resp failure?

A

Alveoli still equally ventilated but more blood passing by some.
Alveoli with low V/Q (not effected) has lower pO2 due to more blood passing so lower pO2 in blood. CO2 removal can be increased however.
Alveoli with high V/Q (effected) cant raise pO2 as either no exchange at all if no blood, or, if some blood passing then already at maximum O2

129
Q

Why does poor ventilation of some alveoli cause type 1 resp failure?

A

In alveoli with low V/Q (effected) alveolar pO2 falls and pCO2 increases. Passing blood becomes hypercapnic and hypoxic
Air is diverted to healthy alveoli:
In alveoli with high V/Q (not effected) blood cannot receive more O2 as already fully saturated, however, CO2 removal can increase

130
Q

Examples of diffusion problems causing type 1 resp. Failure. How does this occur?

A

Fibrotic lung disease
Pulmonary oedema
Emphysema (early)
By increasing diffusion resistance, distance or reducing surface area oxygen is primarily effected as CO2 can diffuse more easily

131
Q

What is type 2 resp failure?

Cause?

A

Decreased o2 and increased CO2
Cause is ventilation failure
- chest wall defect eg kyphosis or trauma
- resp depression eg opiates or stroke
- decreased compliance eg fibrosis
- increased airway resistance eg asthma or COPD

132
Q

How can someone with type one resp failure be acidotic?

A

Decreased O2 means increased anaerobic resp means lactic acid

133
Q

Long term complications of t2rf

A

Hypoxic drive
Resp acidosis
Cor pulmonale due to pulmonary htn
Increased Hb

134
Q

Characteristics of asthma

A

Reversible airway obstruction
Increased airway responsiveness to stimuli
Airway inflammation and remodelling

135
Q

What occurs in airway remodelling in asthma?

A

Increased sumbmucosa
Epithelial metaplasia increasing goblet cells
Epithelial damage increasing vulnerability to infection
Deposition of collagen in lamina reticularis causing BM thickening
Increased smooth muscle mass and responsivness

136
Q

What causes airway remodelling in asthma?

A

Chronic inflammation releasing
- cytokines, leukotrienes, growth factors (for repair)
From inflammatory cells and epithelium

137
Q

What is poiseuilles law? What does it mean for asthmatics?

A

Flow = (P x pi x r^4) / (8 x v x L)

Decrease in radius means marked decrease in flow or increase in pressure gradient to maintain flow

138
Q

What can trigger the hyperresponsive smooth muscle in asthma?

A 
Allergens (dust mites, pollen,  pollution, smoke) 
Cold air
Exercise
NSAIDS
Beta blockers
Emotion
Infection
139
Q

Causes of asthma

A

Genetic (family risk)

Environment (hygiene hypothesis, pre/post natal smoke)

140
Q

2 types of asthma

A

Atopic (other allergies, circulating IgE, +ve skin prick tests)
Non-atopic (drug induced, viral induced wheeze, occupational)

141
Q

How does asthma present?

A 
Wheeze
Breathless
Dry cough
Chest tightness
Variable airflow obstruction
142
Q

Diagnostic tests used in asthma

A

Spirometry (pre and post bronchodilator)
CXR
PEF
Allergy testing

143
Q

Non pharmacological management of asthma

A 
Stop smoking
Breast feeding
Decreased exposure to allergens 
Fresh air
Weight loss
144
Q

What is copd?

A

A progressive non reversible ariflow obstruction that does not change markedly over several months. It is caused primerally by smoking

145
Q

What is the pathological mechanism behind emphysema?

A

Destruction of terminal bronchioles and distal airspace leading to a loss of surface area and the formation of bullae (large redundant airspaces)
Destruction of supporting tissue causes decreased elasticity thus collapse of airways on forced expiration and decreased recoil so hyperinflation

146
Q

Pathological mechanism of chronic bronchitis

A

Chronic mucosal hypersecretion due to inflammation
Chronic productive cough
Remodelling, metaplasia and narrowing of the large airways

147
Q

How is copd graded?

A 
MRC score
1 not troubled
2 breathless on hurrying
3 slower than contemporaries
4 stops for breath after 100m
5 too breathless to leave house
148
Q

Signs of copd

A 
Pursed lip breathing
Tacyponea
Accessory muscle use
Hyperinflation of chest
Wheeze
Cyanosis 
Heart failure
Co2 retention flap
149
Q

If there is a good history, what test will confirm copd? What will it show? What is the cut off for severe

A

Spirometry
Low fev1:fvc ratio. (Severe <30%)
Decreased fvc

150
Q

Other than spirometry what tests are useful in copd? Why?

A

Cxr to exclude other pathology
Ct if considering surgery
Abg for checking for resp failure
Alpha one antitrypsin test if young

151
Q

Management of COPD

A 
Stop smoking
Bronchodilators
Steroids
Mucolytics
Flu vaccine
O2 if pO2 consistently below 7.3kPa
Surgery 
Pulmonary rehabilitation
152
Q

What is copd pulmonary rehabilitation

A

Encouraging light exercise to stop cycle of breathless, sedentary, breathless, sedentary

153
Q

How are exacerbations of copd managed?

A 
O2
Nebs
Steroids
Abx
Aninophylline
NIV
ITU
154
Q

Contraindications of NIV

A 
Pneumothorax
Gcs under 8
Facial injury 
Life threatening hypoxia
Vomiting 
Agitated 
Excessive upper airway secretions
155
Q

Why is tb on the risk in uk?

A

Immigration
Aids
Immunosuppressive meds

156
Q

What can happen on initial tb exposure?

A

Containment with langerhans giant cells then granulomas with epitheloid macrophages.
Adaptive response over 3-8 weeks
Granuloma sealed off
Usually sub clinical but can cause vague illness

157
Q

What happens if the immune response to TB infection was inadequate? How does it present?

A

Primary TB with tiredness, malaise, anorexia, weight loss, fever, night sweats, wheezing, lymphadenopathy, clubbing, haemoptysis.

158
Q

Other than direct progression causing primary tb with inadequate response how can typical symptomatic tb develop?

A 
Post primary tb
Contained tb remains latent then reactivated by:
Immunosuppression (meds, aids)
Reinfection
Malnutrition
Malignacy
159
Q

What is the location of the initial tb infection called? What about when it spreads locally (to what tissues)?

A 
Primary focus (or ghons focus)
Spreads to nearby lymph nodes forming primary complex
160
Q

Where can tb spread? What are the infections at different places called?

A 
Pleura - effusion
Meningies - meningitis
Diffuse intravascular - millary
Spine - potts 
Skin - lupus vulgaris
161
Q

What tests are appropriate in suspected tb? What test has a NPV of 100%?

A

CXR - NPV
3 x speutum ziehl neelsen stain
Culture

162
Q

Treatment regime for TB with side effects

A

2 months of all followed by 4 of rif and iso
Rifampicin - liver, red secretions
Isoniazide - liver, peripheral neuropathy
Pyrizinamide - liver, gout
Ethanbutol - optic neuritis

163
Q

Other than treating active tb when might anti. Tb. Antibiotics be used?

A

Prophylaxis in patients about to undergo immunosuppression who have had tb before

164
Q

What forms of tb is the vaccine good against?

A

Menigeal

Milliary

165
Q

What skin test is used for tb? What might cause problems with it?

A

Mantoux - if infected then stimulates inflammation of the skin.
Inflammation

166
Q

When would you consider directly observing tb meds. Being taken?

A 
Homeless
Alcoholics
Mental illness
Immigrants
Drug resistance
167
Q

What is MDR tb resistant too?

A

Rifampicin and isoniazide

168
Q

What is externsivly drug resistant tb resistant too?

A

Rifampicin
Isoniozid
Quinolones
And anther second line

169
Q

How is lung cancer incidence changing?

A

Falling in men and rising in women mimicing smoking habits 15 years delayed

170
Q

What percentage of lung cancer patients are due to cancer?

A

90% in males 80% in females

Many of the remaining due to passive

171
Q

What are causes of lung cancer other than smoking

A 
Copd
Assbestos
Radon
Occupational
Genetic
172
Q

Symptoms from local tumour effects of lung cancer

A 
Cough 
Dysponea
Wheeze
Haemoptysis 
Chest pain 
Weith loss
Lethargy
173
Q

Symptoms from regional lung cancer mets?

A

Svc obstruction
Horse voice
Dysponea
Dysphagia

174
Q

Paraneoplastic symptoms of lung cancer

A 
Hypercalcemia
SIADH
Cushings
Anaemia
Clubbing
Encephalopathy
175
Q

Where does lung ca commonly metastisise?

A

Bone

Brain

176
Q

What are the histological differentiations of lung cancer? How do they appear?

A

Small cell carcinoma (small cells, little cytoplasm, necrosis)
Squamous cell carcinoma (angulated, keritinised, desmosome bridges)
Adenocarcinoma (glandular)
Large cell carcinoma (large rounded cells)

177
Q

Which type of lung cancer is most common?

A

Squamous cell carcinoma

178
Q

What lung cancer type isnt usually aminiable to surgery?

A

Small cell?

179
Q

Which lung cancer type may be curable with chemo?

A

Small cell

180
Q

How can radiotherapy be used in lung cancer?

A

Alone or in combo with chemo

181
Q

Diagnositic techniques used in lung cancer

A 
Chest xray
Ct 
Mri
Pet ct
Isotope bone scans
Bronchoscopy 
Endobronchial ultrasound with biopsy
182
Q

Prognosis of lung cancer

Why is it like this

A

10-15% 10 yr survival
Tends to present late in high stages
Caught very early then 10 year survival is 40%

183
Q

Other than late presentation why might lung cancer survival be so poor?

A

Professional nihilism
Variable standard of care
Lack of public pressure for campaign
Presents to Gp not specialist

184
Q

What is the. Average survival post dx of untreated small cell lung cancer? What if chemo is given?

A

3 months

1 year

185
Q

Examples of types of urti? What is the usual cause?

A 
Pharyngitis
Rhinitis
Tracheitis
Epiglottitis 
Laryngitis 
Sinusitis

Viral

186
Q

Usual cause of pneumonia? What other LRTIs are possible?

A

Bacterial
Bronchiolitis
Bronchitis

187
Q

Normal cause of bronchiolitis?

A

Respiratory syncytial virus

188
Q

In what ways can pneumonia be classified?

A

Community vs hospital
Acute vs subacute vs chronic
Bacteria vs virus vs fungi
Lobar vs broncho vs interstitial

189
Q

Typical bacteria that cause community pneumonia

A

Haemophillus influenza
Streptococcus pneumonia
Kleibesella pneumonia

190
Q

Who is more at risk of community aquired haemophillus influenza infection?

A

Copd

191
Q

Who is more at risk of community aquired strep pneumonia pneumonia?

A

Elderly

192
Q

Common bacteria for hospital acquired pneumonia

A

Staphylococcus aureus inc MRSA
Psuedomonas aeruginosa
Gram neg enteric bacteria

193
Q

What raises risk of hospital acquired staph aureus pneumonia?

A

Post viral infection

194
Q

Common viral causes of pneumonia

A

Influenza
Parainfluenza
Respiratory syncytial virus

195
Q

Atypical causes of pneumonia with risk factors

A

Legionella (air con / travel)
Chlamydia (birds)
Mycoplasma (young people)

196
Q

Opportunistic causes of pneumonia?

A 
Candida
Aspergillus
Pneumocystis jirovecii
Cytomegalovirus
HSV
197
Q

What is the most common cause of lobar pneumonia?

A

Streptococcus pneumonia

198
Q

What is the most common causes of bronchopneumonia?

A

Streptococcus pneumonia
Haemophillus influenza
Staph aureus
Coliforms

199
Q

On investigation of a pneumonia multiple organisms are cultured? What could be the cause? What sort of pneumonia is it likely to be?

A

Aspiration

Bronchopneumonia

200
Q

How can severity of pneumonia be assessed?

A

C - confused (AMT 7
R - resps >30
B - BP <90
65

201
Q

How is mild to moderate pneumonia treated prior to cultures return?

A

Amoxicillin

202
Q

How is severe pneumonia treated prior to culture?

A

Coamoxiclav

203
Q

Indications for pneumonia onto ICU

A

Resp failure
Progressive acidosis
Shock
Hypercapnia

204
Q

Complications of pneumonia in the long term

A

Fibrous scarring
Abcess
Bronchiectasis
Empyema

205
Q

Risk factors for acquiring pneumonia in hospital

A 
Itu 
Ventilated
Suppressed immunity
Atelectasis (post chest injury/surgery)
Immobile
206
Q

Signs of pneumonia

A

Wheeze
Crackles
Dull percussion
Low resonance

207
Q

Symptoms of pneumonia

A 
Fever
Chills
Sweats
Productive cough
Dysponea 
Pleuritic chest pains
208
Q

What tests are performed in pneumonia?

A

Speutum culture and gram stain
Cxr
Fbc, urea, lft, crp

209
Q

What special tests are performed in legionella pneumonia?

A

Legionella antibodies in urine

210
Q

Things to check at the start of a chest xray

A

Field of view (1st rib to costophrenic angle)
Penetration (vertebra behind heart)
Rotation (spinous processes in midline between clavicles)
Volume (on inspiration with 5-7 ribs visible)
No artefact
Demographics!

211
Q

What should you look for assessing airway on a CXR.

A

Trachea central

Clear angle at hila with left higher than right

212
Q

What should you look for on breathing on a cxr?

A

Lungs equal both sides
No visible pleural space
No consolidation or masses

213
Q

What should you look for on circulation onCXR?

A

Heart less than 50% of chest diameter

Aortic notch present

214
Q

What should you. Look for on diaphragm/dem bones on CXR

A

No free gas
Not flattened
No bony fractures

215
Q

What is sail sign? What else might indicate this pathology?

A

Double heart boder due to left lower lobe collapse
Also presents with lowered pressure causing mediastinal shift towards pathology and elevation of ipsolateral hemidiaphragm

216
Q

What can cause consolidation on a cxr?

A

Pus
Blood
Fluid
Cells

217
Q

What are the overall efffects of interstitial lung disease?

A

Loss of compliance
Increased alveoli to capillary diffusion distance
Destruction of alveoli and capillaries causing v/q mismatch

218
Q

Signs and symptoms of interstital lung disease

A 
Gradual onset sob 
Dry cough
Diffuse crackles
Clubbing
Cynosis 
Right heart failure (cor pulmonale)
Tachycardia and tachyponea
219
Q

How does a ct show interstitial lung disease

A

Honeycombing

220
Q

Hw does a cxr show interstitial lung disease?

A

Increased lung markings

Blurred boarders

221
Q

Causes od interstitial lung disease

A 
Idiopathic
Treatment related
Connective tissue disease
Immunological
Occupational
222
Q

What are the two commonest causes of interstitial lung disease?

A

Idiopathic

Immunological

223
Q

Examples of immunological causes of interstitial lung disease

A

Sarcoidosis

Hypersensitivity pneumonitis

224
Q

Examples of connective tissue diseases causing interstitial lung disease

A

Sle

Ra

225
Q

Examples of occupational exposures leading to interstitial lung disease

A

Asbestosis
Coal workers pneumoconiosis
Silicosis

226
Q

Examples of treatments that cause interstitial lung disease

A

Amiodarone
Methotrexate
Bleomycin
Radiation therapy

227
Q

How does the visceral pleura receive its blood supply?

A

Via the bronchials

228
Q

How does the parietal pleura receive its blood supply

A

Costal - intercostals
Mediastinal - bronchials
Apex - subclavian

229
Q

What can cause increased plural fluid production?

A

High hydrostatic pressure (eg chf)
Increased permeability (eg sepsis)
Decreased oncotic pressure (eg liver failure)
Increased Interstitial fluid

230
Q

What can cause decreased pleural fluid absorption?

A

Lymph blockage

Elevated venous pressure

231
Q

Other than pleural fluid what else can cause a pleural effusion?

A

Empyema (pus)
Haemothorax (blood)
Chylothorax (lymph)

232
Q

What are complications of pleural effusion?

A

Fistula with bronchi or skin
Trapped lung
Functional restriction
Fibrothorax

233
Q

Give some examples of congenital chest wall disease

A

Scoliosis and kyphosis
Pectus carinatum
Pectus excavatum

234
Q

Other than congenital what sorts of chest wall diseases are there?

A

Traumatic

Iatrogenic (eg post tb surgery

PPE (12 decks)

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