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ESA 3 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is Boyles Law?

A

Pressure of a gas is inversely proportional to its volume

As long as temperature and number of gas molecule remains constant

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2
Q

How does Boyles law explain inspiration and expiration?

A

Inspiration: diaphragm moves down, volume increases, alveolar pressure drops below atmospheric pressure, air moves in

Expiration: volume decreases, air above atmospheric pressure, air flows out of the lungs

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3
Q

The airway has 23 divisions, which are the conducting zone and the respiratory zone?

A

1-16: conducting zone, no gas exchange, anatomical dead space

17-23: respiratory zone, gas exchange

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4
Q

What is the pO2 in alveolar air and venous blood?

A

Alveolar air: 13.3 kPa
Venous blood: 6.6 kPa

(Hence moves down its conc gradient from alveoli in pulmonary veins)

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5
Q

What is the atmospheric partial pressure in air?

A

101 kPa

Hence partial pressure of a gas is directly proportional to its %,
so pO2 = 101 x 20.9% = 21.1kPa
pCO2 = 101 x 0.03 = 0.03kPa

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6
Q

At body temperature, what is the saturated vapour pressure?

A

6.28 kPa

When water enters inspired air, water molecules enter gas phase until gas phase is saturated with water

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7
Q

How does atmospheric pressure change at altitude?

A

Atmospheric pressure is lower so gas molecules disperse (hence less air molecules available when you breathe).

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8
Q

What is the anatomy within the nasal cavity?

A

Turbinates/ conchae are bony projections (superior, middle, inferior)
Meatuses are in between, and increase SA
Floor of nasa cavity = roof of mouth = hard and soft palates

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9
Q

What are the 4 paranasal sinuses?

A

Frontal (above eyes) maxillary (below eyes), ethmoidal (between eyes), sphenoidal (behind eyes)

Air filled spaces that drain into nail cavity to humidify and warm inspired air

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10
Q

What are the functions of the nasal cavity?

A
  • warm and humidify air
  • drain paranasal sinuses and lacrimal ducts
  • traps pathogens from the air
  • sense of smell
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11
Q

What is the ‘glottis’?

A

The vocal cords and the aperture between them

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12
Q

Are the vocal cords adducted or abducted during respiration, phonation and swallowing?

A

Adducted during swallowing
Partially abducted in phonation
Abducted for respiration

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13
Q

Vocal cord movements are due to which muscles?

A

Intrinsic laryngeal muscles

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14
Q

What is the costodiaphragmic recess?

A

The inferior part of the pleural cavity not occupied by lung

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15
Q

How do the surface markings of the pleural cavity compare the the surface markings of the lungs?

A

Pleura both pass vertically down the sternum to 4th sternal angle, where left pleura deviates laterally (due to heart) to 6th cc, right continues vertically to 6th. Both go lateral and cross mid clavicular line at 8th rib, then mid Axillary at 10th rib and 12th rib at scapular line.

Lungs are 2 ribs higher than pleural cavity so cross mid clavicular at6th, mid Axillary at 8th then cross the 10th rib at the scapular line.

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16
Q

How many lobes do the lungs have and what are the lobes separated by?

A

Left has 2 lobes, separated by oblique fissure

Right has three lobes; upper and middle separated by horizontal fissure, middle and lower separated by oblique fissure

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17
Q

What will be the pO2 in blood exposed to gas with 14% O2 at a total pressure of 101.1kPa, saturated with water vapour at Boyd temperature?

A

(101.1-6.28) x 0.14 = 13.27 kPa

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18
Q

How does the epithelium change along the respiratory tract?

A

URT is pseudostratified with goblet cells and cilia.
Bronchioles is simple columnar will Clara cells but no goblet cells.
Respiratory bronchioles are simple cuboidal with Clara cells.
Alveoli are simple squamous.

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19
Q

How is the arrangement of cartilage different in primary bronchi compared the secondary & tertiary bronchi?

A

In primary bronchi it’s in rings

In secondary bronchi it’s in irregular islands

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20
Q

How do bronchi and bronchioles differ histologically?

A

Bronchioles have no cartilage or glands, unlike bronchi

Surrounding alveoli keep the lumen of bronchioles open

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21
Q

What are alveoli surrounded by?

A

A network of capillaries and elastic fibres. Lot of type 1 pneumocytes and some type 2 pneumocytes.
Lots of macrophages also line alveolar surface.

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22
Q

What is the difference between type 1 and 2 alveolar cells in terms of function and abundance?

A

Type 1 cover 90% of surface area and permit gas exchange with capillaries.

Type 2 cover 10% of surface area and secrete surfactant.

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23
Q

Emphysema destroys alveolar walls. How does this affect bronchioles?

A

Alveoli hold bronchioles open so that air can leave on exhalation.
Emphysema will cause bronchial collapse, and hence make it difficult for the lungs to empty (hence the hallmark sign of pursed lip breathing).

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24
Q

How does the diaphragm move in inspiration?

A

Moves down

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25
Q

What are the muscles between the ribs?

A

External intercostal muscles
Internal intercostal muscles
Innermost intercostal muscles

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26
Q

At what spinal level does the vena cava pass through the diaphragm?

A

T8

8 letters!

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27
Q

At what spinal level does the oesophagus pass through the diaphragm?

A

T10

10 letters

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28
Q

At what spinal level is the aortic hiatus in the diaphragm?

A

T12

12 letters!

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29
Q

When performing a chest drain, should the needle be inserted at the upper or lower border of the rib and why?

A

Insert needle at the upper border, to avoid injury to the neurovascular bundle (intercostal nerve, artery and vein) which lies below each rib?

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30
Q

The azygos venous system collects blood from between the intercostal veins and drains it into where?

A

SVC

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31
Q

Why do foreign bodies usually go to the right lung and not the left?

A

Right main bronchus has a less acute angle (is more vertical) than the left, and is also slightly larger

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32
Q

Is inspiration and expiration active or passive?

A

Inspiration is active

Expiration to resting expiratory level is passive,
But forced expiration is active

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33
Q

How does volume and pressure change during inspiration and expiration?

A

Inspiration: volume increases, pressures decreases, air moves in

Expiration: volume decreases, pressure increases, air moves out

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34
Q

Forced expiration requires which muscles?

A 
Abdominal muscles 
(& internal intercostal muscles)
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35
Q

Is the pressure in the intrapleural space negative or positive?

A

Negative

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36
Q

Forced inspiration uses which muscles?

A

External intercostal muscles, sternocleidomastoid, scalene, serratus anterior and pectoralis major

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37
Q

What is the compliance of the lungs?

A

Aka the stretchiness of the lungs
(Volume change per unit pressure change)
Higher compliance = easier to stretch

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38
Q

How would emphysema affect a patients compliance?

A

More compliance due to a loss of elasticity

  • elastic recoil is inversely proportional to compliance *
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39
Q

How would lung fibrosis affect a patients compliance?

A

Less compliance due to stiffening and hardening of the lungs

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40
Q

Does a higher surface tension make it harder or easier to stretch the lungs?

A

Higher surface tension makes it harder to stretch the lungs, as more force is needed to exceed the elastic recoil

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41
Q

What substance reduces surface tension in the lungs?

A

Surfactant, breaks up H-bonds to disrupt interactions between surface molecules so they’re easier to inflate.

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42
Q

What is surfactant composed of?

A

Mainly phospholipids, specifically surfactant protein A.

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43
Q

What is surfactant produced by?

A

Type 2 alveolar cells (pneumocytes)

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44
Q

Does surfactant reduce surface tension more when lungs are deflated or inflated?

A

Reduces surface tension more when lungs are deflated, so little breaths are easy but big breaths (forced inspiration) is difficult.

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45
Q

If a big bubble is connected to a small bubble, what will happen to the air flow inside them?

A

Smaller bubbles have higher pressure inside than big bubbles.
So, the air would move from the higher pressure in the smaller bubble, to the lower pressure in the larger bubble and the smaller bubbles would collapse. Surfactant is needed to equalise the pressure between different sized alveoli so they do not collapse into each other.
Hence “big bubbles eat smaller bubbles”

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46
Q

What are the roles of surfactant?

A
  • reduce surface tension
  • increase compliance
  • prevent alveoli collapsing into each other
  • prevent atelectasis (parts of the lung collapsing) at the end of expiration
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47
Q

What is acute respiratory distress syndrome?

A

Infants born with too little surfactant, lungs are very stiff with few and large alveoli hence breathing and gas exchange is compromised.

  • different to adult respiratory distress syndrome which is not due to loss of surfactant *
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48
Q

What are the divisions of the mediastinum?

A

?

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49
Q

What is the innervation of the diaphragm?

A

Phrenic nerve: c3,4,5

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50
Q

How does the blood supply to the visceral and parietal pleura differ?

A

Visceral pleura supplied by bronchial arteries

Parietal pleura supplied by intercostal arteries and internal thoracic arteries

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51
Q

How does the nerve supply of the parietal and visceral pleura differ?

A

Visceral pleura has no somatic innervation, only autonomic

Parietal pleura has somatic innervation including pain fibres from intercostal and phrenic nerves, as well as autonomic innervation

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52
Q

Why does CO2 diffuse much faster then O2?

A

As CO2 is 20 times more soluble than O2.

Although this is usually compensated for because O2 has a larger partial pressure than CO2

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53
Q

What factors affect diffusion rate of a gas in fluid?

A
  • solubility of the gas
  • pressure difference
  • molecular weight of gas
  • surface area
  • disunion distance
  • temperature
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54
Q

What are the layers of the diffusion barrier from the alveolus to the blood?

A

Alveolus membrane, tissue fluid, capillary endothelium, plasma, red cell membrane

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55
Q

What happens to carbon dioxide when it enters RBCs as a waste product from cells?

A

Reacts with water to form carbonic acid, which breaks down to bicarbonate and H+.
Bicarbonate enters plasma and H+ is buffered by Hb in RBCs.

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56
Q

In normal lungs what is the PO2 and PCO2 of alveolar air?

A 
PO2 = 13.3 kPa
PCO2 = 5.3 kPa
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57
Q

How would fibrotic lung disease, emphysema and pulmonary oedema each affect diffusion of gases in the lungs?

A

Fibrosis: increases diffusion distance due to thickened alveolar wall

Oedema: increases fluid in interstitial space increases diffusion distance

Emphysema: reduces SA

  • all cause low arterial pO2
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58
Q

What is the difference between the anatomical, distributive and physiological dead space?

A

Anatomical is conducting zone of the airways not involved in gas exchange.

Distributive is portion of airways eg damaged alveoli that aren’t involved in gas exchange.

Physiological is combined anatomical + distributive dead space.

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59
Q

How do we account for dead space when calculating alveolar ventilation rate?

A

Subtract resp rate x dead space volume from pulmonary ventilation rate = AVR

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60
Q

What is the ideal V/Q ratio?

A

1

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61
Q

What is tidal volume?

A

Volume breathed in and our with each breath

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62
Q

What is inspiratory reserve volume?

A

Extra volume that can be breathed in over that at rest

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63
Q

What is expiratory reserve volume?

A

Extra volume that can be breathed out over that at rest

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64
Q

What is residual volume?

A

Volume remaining in the lungs after maximum expiration

So CANNOT BE MEASURED BY SPIROMETRY

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65
Q

What is a lung capacity?

A

Two or more volumes added together

Capacities are fixed but volumes can change over the cycle

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66
Q

What is vital capacity?

A

Biggest breath that can be taken, measured from maximum inspiration to maximum expiration (usually about 5L)

= IRV + TV + ERV

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67
Q

What is inspiratory capacity?

A

Biggest breath that can be taken from resting expiratory level, usually about 3L

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68
Q

What is functional residual capacity?

A

The volume of air in the lungs at resting expiratory level, usually about 2L

= ERV + RV

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69
Q

What is total lung capacity?

A

Volume of air in the lungs at the end of maximum inspiration, usually about 5.8L

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70
Q

What is a vitalograph trace?

A

Plots volume expired against time, measureS FVC

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71
Q

What is FEV1?

A

Volume expired in the first second, will decrease if airway is narrowed

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72
Q

What should the FEV1 to FVC ratio be?

A

> 70% in healthy patients

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73
Q

How will an obstructive deficit affect FEV1 and FVC?

A

Lungs narrowed so increased resistance in airways when breathing out, although they can still full normally.
So reduced FEV1 but normal FVC

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74
Q

How will a restrictive deficit affect FEV1 and FVC?

A

Lungs cannot fill as well so start less full but air comes out normally
So, both FEV1 and FVC reduced although FEV1:FVC still >70%

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75
Q

How would obstructive and restrictive deficits present differently on a flow volume loop?

A

Obstructive would show as more scooped out upon expiration due to the increased resistance.

Restrictive would generally show the same shape but a narrowed curve (less volume expired as lungs less full to start)

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76
Q

How can the anatomical dead space be measured?

A

Nitrogen washout test

  • subject takes breath of pure O2
  • breathes out via meter measuring nitrogen %
  • initially only O2 expired (as last air in is first air out)
  • then air mixed with nitrogen will be breathed out
  • volume of air that was pure O2 is the anatomical dead space
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77
Q

How can we measure the residual volume?

A

Via the helium dilution test and calculation

Helium is not metabolised by the body
Patient breathes in a known volume of gas with a known volume of helium
Starts at FRC
Can measure the change in helium concentration as it becomes diluted in a larger volume of air in the lungs

78
Q

How many oxygen molecules can haemoglobin transport compared to myoglobin?

A

Hb can bind 4 molecules as its a tetramer

Myoglobin can bind 1 as it is only a monomer

79
Q

What factors shift the Hb dissociation curve to the right (Bohr shift)?

A

Acid
Increased temperature
Increased 2,3-DPG (anaemia or altitude)

80
Q

What is pulse oximetry?

A

An easy and non-invasive method to measure saturated Hb levels in pulsation arterial blood

but doesn’t say how much Hb is present (Ie wouldn’t detect anaemia) and ignores levels in tissues and venous blood

81
Q

What is the Henderson Hasselbalch equation?

A

pH = 6.1 + log[HCO3-]/(pCO2 x 0.23)

Must be 20 x as much bicarbonate as CO2 for pH to be in range

82
Q

How is high HCO3- established in red blood cells?

A

CO2 reacts with water to produce bicarbonate and H+ (catalysed by carbonic anhydrase)

Bicarbonate enters plasma and H+ are mopped up by Hb, so reaction proceeds in forwards direction

83
Q

Via which channel does bicarbonate leave RBCs to enter plasma?

A

Chloride bicarbonate exchanger

84
Q

Do H+ bind more easily to Hb in the T or R state?

A

In the T state (as at tissues, so then more H+ mopped up so more bicarbonate can be produced which means more CO2 is present in plasma as the bicarbonate pushes the plasma reaction to the left)

85
Q

By what methods can CO2 be transported?

A
  • dissolve in plasma
  • as hydrogen bicarbonate
  • as carbamino compounds
86
Q

If hypoxia is corrected by ventilation, what can this lead to?

A

Could lead to hypocapnia

(But the plateau at the end of the Hb dissociation curve shows that a considerable drop in O2 can be tolerated before having an affect)

87
Q

What can a low and a high pH outside the normal range cause?

A

Low pH can denature enzymes

High pH causes a drop in free Ca levels and can lead to tetany

88
Q

Which are more sensitive to changes in pCO2: peripheral or central chemoceptors?

A

Central chemoceptors

Can then increase or decrease ventilation by negative feedback based on pCO2

89
Q

Central chemoceptors respond to changes in the pH of which fluid?

A

CSF

90
Q

Which cells control the CSF concentration of HCO3-?

A

Choroid plexus cells

So can correct pH

91
Q

What is type 1 respiratory failure?

A

Type 1 affects only 1 (oxygen)

So low O2 and normal/ low CO2

92
Q

What is type 2 respiratory failure?

A

Type 2 affects 2.

So, low O2 AND high CO2

93
Q

How can oxygen levels in the blood be measured?

A
  • pulse oximetry (measures saturated Hb in arterial blood)

- arterial blood gas (can measure pCO2, pO2 and pH of arterial blood)

94
Q

What can cause type 2 respiratory failure?

A

Ventilatory (pump) failure unable to move sufficient air into and out of lungs
Eg: kyphoscoliosis, flail segments, COPD, myopathy of resp muscles, head injury (affect resp centre), severe obesity, lung fibrosis, pneumothorax, Guillain Barre syndrome

95
Q

What can cause type 1 respiratory failure?

A
  • diffusion defects across the alveolar membrane
    (Eg fibrosis causing membrane thickening, or emphysema reducing SA)
  • v/q mismatch
    (V/q <1 causes O2 to fall and CO2 to rise.)
    Due to problems with ventilation of part of lungs eg pneumonia, COPD, asthma, RDS of newborn.
    Or, due to reduced perfusion of part of lungs eg pulmonary embolism, which diverts blood to other parts of the lungs so they’re more perfused
96
Q

Which receptors does hypoxia stimulate?

A

Peripheral chemoreceptors (stimulates hyperventilation)

97
Q

How can respiratory failure be managed?

A

In type 1 oxygen therapy can treat hypoxia

In type 2 may require assisted ventilation for the hypercapnia

98
Q

What are some clinical features of hypoxia?

A
  • exercise intolerance
  • central cyanosis
  • tachypnoea
  • confusion (cerebral hypoxia as brain very sensitive to low O2)
99
Q

What is cyanosis?

A

Purple discolouration of skin and mucous membranes due to the colour of desaturated Hb

100
Q

What is the difference between peripheral and central cyanosis?

A

Central seen in tongue and oral mucosa, these areas are very well perfused so not usually affected by perfusion problems, is due to low arterial pO2

Peripheral is seen in the extremities and can occur without central cyanosis due to poor perfusion eg peripheral vascular disease

101
Q

What is the effects of chronic hypercapnia?

A
  • warm hands flapping tremors
  • CSF acidity corrected by choroid plexus cells so central chemoceptors reset to the new higher pCO2 but peripheral chemoceptors do not adapt and remain sensitive to hypoxia, hence respiration is driven by hypoxia
102
Q

What is the effects of chronic hypoxia?

A
  • increased oxygen delivery by increased Hb levels due to increase erythropoietin production
  • increased 2,3-DPG in RBCs
  • pulmonary vasoconstriction of pulmonary arterioles can lead to right sided heart failure, pulmonary hypertension, cor pulmonale
103
Q

Why may oxygen administration worsen hypercapnia? (So cannot give oxygen to COPD patient)

A

As the central chemoceptors reset to the higher pCO2. If oxygen is administered, the respiratory drive to the peripheral chemoceptors is lost and so they reduce ventilation which will cause CO2 to rise even more

104
Q

What is bronchitis?

A

Inflammation of medium sized airways

105
Q

What are some causative organisms of ACUTE bronchitis?

Chronic bronchitis is not primarily infective

A

Streptococcus pneumoniae

Haemophilius influenzae

106
Q

How would acute bronchitis present?

A

Cough, increased sputum production, breathlessness, fever, normal CXR

107
Q

How could acute bronchitis be treated?

A

Physiotherapy/ antibiotics/ bronchodilators

108
Q

What is pneumonia and how does it present?

A

Inflammation of the lung alveoli

Presents as fever, cough, shortness of breath and pleuritic chest pain with an ABnormal CXR (unlike bronchitis)

109
Q

What are some typical and some atypical causative organisms of community acquired pneumonia?

A

Typical:
Streptococcus pneumonia, Haemophilius influenzae, staphlococcus pneumoniae

Atypical:
Legionella, mycoplasma, coxiella

110
Q

How would a patient with pneumonia show on examination?

A 
Tachycardia
Tachypnoea 
Dullness on percussion
Pyrexia
Cyanosis
Bronchial breathing
Crackles
111
Q

What is the CURB-65 score?

A 
Basis of where to manage a patient
C: confusion
U: urea > 7mmol/L
R: resp rate > 30
B: blood pressure (<90 systolic or <60 diastolic)
65 years or older
112
Q

Why do penicillins not work for atypical pneumonias?

A

Atypical pneumonia is caused by organisms without a cell wall (eg chlamydia, legionella), so cell wall active antibiotics like penicillins will be ineffective.

Need antibiotics that will work on protein synthesis eg macrolides (erythromycin, clarithromycin) or tetracyclines (doxycycline).

113
Q

What antibiotics can be used for atypical pneumonias?

A

Need antibiotics that will work on protein synthesis eg macrolides (erythromycin, clarithromycin) or tetracyclines (doxycycline).

114
Q

What are some preventative measures for lower respiratory tract infections?

A
  • stop smoking
  • flu vaccine for at risk patients
  • chemoprophylaxis for at risk patients ie asplenia, immunodeficiency (give penicillin/ erythromycin)
115
Q

What is an example of an obligate anaerobe?

A

Clostrodia

Cannot survive in presence of oxygen unless spores have formed

116
Q

If hypoxia is corrected by ventilation, what can this lead to?

A

Could lead to hypocapnia

(But the plateau at the end of the Hb dissociation curve shows that a considerable drop in O2 can be tolerated before having an affect)

117
Q

What can a low and a high pH outside the normal range cause?

A

Low pH can denature enzymes

High pH causes a drop in free Ca levels and can lead to tetany

118
Q

Which are more sensitive to changes in pCO2: peripheral or central chemoceptors?

A

Central chemoceptors

Can then increase or decrease ventilation by negative feedback based on pCO2

119
Q

Central chemoceptors respond to changes in the pH of which fluid?

A

CSF

120
Q

Which cells control the CSF concentration of HCO3-?

A

Choroid plexus cells

So can correct pH

121
Q

What is type 1 respiratory failure?

A

Type 1 affects only 1 (oxygen)

So low O2 and normal/ low CO2

122
Q

What is type 2 respiratory failure?

A

Type 2 affects 2.

So, low O2 AND high CO2

123
Q

How can oxygen levels in the blood be measured?

A
  • pulse oximetry (measures saturated Hb in arterial blood)

- arterial blood gas (can measure pCO2, pO2 and pH of arterial blood)

124
Q

What can cause type 2 respiratory failure?

A

Ventilatory (pump) failure unable to move sufficient air into and out of lungs
Eg: kyphoscoliosis, flail segments, COPD, myopathy of resp muscles, head injury (affect resp centre), severe obesity, lung fibrosis, pneumothorax

125
Q

What can cause type 1 respiratory failure?

A
  • diffusion defects across the alveolar membrane
    (Eg fibrosis causing membrane thickening, or emphysema reducing SA)
  • v/q mismatch
    (V/q <1 causes O2 to fall and CO2 to rise.)
    Due to problems with ventilation of part of lungs eg pneumonia, COPD, asthma, RDS of newborn.
    Or, due to reduced perfusion of part of lungs eg pulmonary embolism, which diverts blood to other parts of the lungs so they’re more perfused
126
Q

Which receptors does hypoxia stimulate?

A

Peripheral chemoreceptors (stimulates hyperventilation)

127
Q

How can respiratory failure be managed?

A

In type 1 oxygen therapy can treat hypoxia

In type 2 may require assisted ventilation for the hypercapnia

128
Q

What are some clinical features of hypoxia?

A
  • exercise intolerance
  • central cyanosis
  • tachypnoea
  • confusion (cerebral hypoxia as brain very sensitive to low O2)
129
Q

What is cyanosis?

A

Purple discolouration of skin and mucous membranes due to the colour of desaturated Hb

130
Q

What is the difference between peripheral and central cyanosis?

A

Central seen in tongue and oral mucosa, these areas are very well perfused so not usually affected by perfusion problems)

Peripheral is seen in the extremities and can occur without central cyanosis due to poor perfusion

131
Q

What is the effects of chronic hypercapnia?

A
  • warm hands flapping tremors
  • CSF acidity corrected by choroid plexus cells so central chemoceptors reset to the new higher pCO2 but peripheral chemoceptors do not adapt and remain sensitive to hypoxia, hence respiration is driven by hypoxia
132
Q

What is the effects of chronic hypoxia?

A
  • increased oxygen delivery by increased Hb levels due to increase erythropoietin production
  • increased 2,3-DPG in RBCs
  • pulmonary vasoconstriction of pulmonary arterioles can lead to right sided heart failure, pulmonary hypertension, cor pulmonale
133
Q

Why may oxygen administration worsen hypercapnia? (So cannot give oxygen to COPD patient)

A

As the central chemoceptors reset to the higher pCO2. If oxygen is administered, the respiratory drive to the peripheral chemoceptors is lost and so they reduce ventilation which will cause CO2 to rise even more

134
Q

What is bronchitis?

A

Inflammation of medium sized airways

135
Q

What are some causative organisms of ACUTE bronchitis?

Chronic bronchitis is not primarily infective

A

Streptococcus pneumoniae

Haemophilius influenzae

136
Q

How would acute bronchitis present?

A

Cough, increased sputum production, breathlessness, fever, normal CXR

137
Q

How could acute bronchitis be treated?

A

Physiotherapy/ antibiotics/ bronchodilators

138
Q

What is pneumonia and how does it present?

A

Inflammation of the lung alveoli

Presents as fever, cough, shortness of breath and pleuritic chest pain with an ABnormal CXR (unlike bronchitis)

139
Q

What are some typical and some atypical causative organisms of community acquired pneumonia?

A

Typical:
Streptococcus pneumonia, Haemophilius influenzae, staphlococcus pneumoniae

Atypical:
Legionella, mycoplasma, coxiella

140
Q

How would a patient with pneumonia show on examination?

A 
Tachycardia
Tachypnoea 
Dullness on percussion
Pyrexia
Cyanosis
Bronchial breathing
Crackles
141
Q

What is the CURB-65 score?

A 
Basis of where to manage a patient
C: confusion
U: urea > 7mmol/L
R: resp rate > 30
B: blood pressure (<90 systolic or <60 diastolic)
65 years or older
142
Q

Why do penicillins not work for atypical pneumonias?

A

Atypical pneumonia is caused by organisms without a cell wall (eg chlamydia, legionella), so cell wall active antibiotics like penicillins will be ineffective.

Need antibiotics that will work on protein synthesis eg macrolides (erythromycin, clarithromycin) or tetracyclines (doxycycline).

143
Q

What antibiotics can be used for atypical pneumonias?

A

Need antibiotics that will work on protein synthesis eg macrolides (erythromycin, clarithromycin) or tetracyclines (doxycycline).

144
Q

What are some preventative measures for lower respiratory tract infections?

A
  • stop smoking
  • flu vaccine for at risk patients
  • chemoprophylaxis for at risk patients ie asplenia, immunodeficiency (give penicillin/ erythromycin)
145
Q

What is an example of an obligate anaerobe?

A

Clostrodia

Cannot survive in presence of oxygen unless spores have formed

146
Q

What are some facts about mycobacterium tuberculosis?

A 
Obligate aerobe
Non-motile bacilli
Long chain fatty acids in cell wall (hence cannot use gram staining)
Relatively slow growing
Spread via droplet
147
Q

What is the pathogenesis of tuberculosis?

A

Bacteria inhaled and engulfed by leveller macrophages
Can form a primary infection, or often lies dormant as a latent infection for many years. Latent TB can then self-cure or reactivate to post-primary TB.

148
Q

What are some differences between latent TB infection and TB disease?

A

Latent TB is inactive, has no symptoms, will show positive on TST and IFN gamma, normal CXR, negative sputum smears, not infectious, not a case of TB

TB disease is active, will show positive on TST and bloods, positive sputum smears, has symptoms, is active, CXR abnormal, infectious, case of TB

149
Q

What are some risk factors for reactivation of TB?

A

HIV, low body weight, substance abuse, immunosuppression, organ transplant, malignancy, diabetes Mellitus

150
Q

How would TB appear histologically?

A

Caseating granulomas with Langhans giant cells

151
Q

Where can TB occur?

A

Most cases are pulmonary

Can become extra pulmonary at kidneys, brain, lymph nodes, bones and joint, pleura, larynx

Military TB when spread throughout the body via the bloodstream

152
Q

What are some risk factors for catching TB?

A

Non-UK born, HIV positive, homeless, drug users, Immunocompromised

153
Q

What are some signs and symptoms of pulmonary TB?

A

Fever, malaise, abnormal CXR, weight loss, night sweats, anorexia, tiredness, cough, haemoptysis

154
Q

What is the TST?

A 
Tuberculin sensitivity test
Tuberculin injected intradermally and measure 3 days later
Subjective!!
Easy and cheap
Positive in latent and active
155
Q

How can TB be investigated?

A

CXR
Sputum smears -> analyse in lab or culture (gold standard)
Detect antigen specific IFN-gamma production (but cannot distinguish latent and active)

156
Q

What drugs are used in TB?

A

RIPE
Rifampicin, isoniazid, pyrazinamide, ethambutamol

3/4 drugs for 2/12 then R and I for 4/12

157
Q

What is a side effect of Rifampicin?

A

Orange secretions

158
Q

How can TB be prevented?

A 
PPE, negative pressure isolation
BCG vaccine (live M bovis strain)
159
Q

What are some triggers of asthma?

A 
Indoor allergens (dust mites, mold, pets)
Outdoor allergens (pollen, smoke, pollutants)
Cold air, exercise, medications (NSAIDs, beta blockers)
160
Q

Is asthma obstructive or restrictive?

A

Obstructive

161
Q

What are some symptoms of asthma?

A

Wheeze, dry cough, breathlessness, chest tightness

Worse after exposure to triggers, at night or early morning

162
Q

How can asthma be diagnosed?

A

Examination (assess RR, tracheal tug, accessory muscle use)
History (aggregating triggers, family history, medication)
PEFR and spirometry (can do before and after bronchodilators)

163
Q

How can asthma be managed?

A

Use inhalers (correct education!)
Change bedding every few years
Stop smoking
Fresh air

164
Q

What is the difference between a blue, brown and green inhaler?

A

Blue inhaler: SABA (short acting beta agonist), relaxes smooth muscle for quick relief

Brown: prevention, steroid to reduce inflammation

Green: LABA (long actin beta agonist), used if still have asthma symptoms despite steroid, not for acute attacks due to slow onset

165
Q

How could a severe asthma attack be treated?

A 
Oxygen
Nebulised salbutamol (IV if mucus blocks it getting in)
166
Q

COPD is an umbrella term for which two conditions?

A

Emphysema and chronic bronchitis

Both causing airflow obstruction

167
Q

What is emphysema?

A 
Destruction of terminal bronchioles and alveoli
So less SA for gas exchange
Develop bullae (large redundant air spaces)
168
Q

What is chronic bronchitis?

A

Inflammation of the large airways and mucus hypersecretion

169
Q

What causes COPD?

A
  • smoking!!!
  • also alpha 1 antitrypsin deficiency (1%)
  • occupational exposure eg coal dust
  • pollution
170
Q

What are some signs and symptoms of COPD?

A

Signs: pursed lip breathing, use of accessory muscles, tachypnoea, hyperinflated barrel chest, if serious cyanosis and right sided heart failure, wheeze

Symptoms: progressive breathlessness (graded by MRC dyspnea score 1-5 with 5 being worse), cough and sputum

171
Q

How would COPD present on spirometry?

A

FEV1 < 80% predicted

FEV1/FVC <70%

172
Q

How should COPD be managed?

A
  • smoking cessation
  • pulmonary rehabilitation
  • bronchodilators
  • steroids
  • mucolytics
  • antimuscarinics
  • long term oxygen therapy
  • lung volume reduction or lung transplant if young
173
Q

How does a beta 2 agonist eg salbutamol work?

A 
Salbutamol binds to Gs receptor
Activates adenylyl cyclase
Activates PKA
Phosphorylates MLCK
Causes smooth muscle relaxation
174
Q

How does pulmonary rehabilitation work?

A

6-12 week exercise and education programme

Aims to break the cycle of deconditioning for patients (ie when symptoms prevent them from doing activities so they do less and in effect worsen their condition)

175
Q

How can lung cancer be staged?

A 
TNM staging
(T= tumour size 1-4, N= node involvement 0-3, M= metastases 0 or 1)
176
Q

What are the main types of lung cancer?

A

Non small cell carcinoma
(Squamous cell carcinoma, adenocarcinoma, large cell carcinoma)

Small cell carcinoma

177
Q

What are some treatments for lung cancer?

A 
Surgery (mostly for non small cell)
Chemotherapy
Radiotherapy
Combination therapy
Palliative care
178
Q

What are some paraneoplastic features that may be associated with lung cancer?

A

Squamous cell -> PTHrp -> raised plasma calcium

Small cell -> ACTHrp -> occasionally Cushing’s
Small cell -> ADHrp -> occasionally dilutional hyponatraemia (SIADH)

179
Q

Where in the CNS is a cough coordinated?

A

Medulla oblongata

180
Q

Why are patients with sickle cell disease at increased risk of bacterial infections?

A

Have small splenic infarctions
Spleen is important for removal of encapsulated bacteria (by splenic macrophages) and also produce antibodies IgM and IgG

181
Q

How would hyperinflation of the chest appear on x Ray?

A

More than 6 ribs anteriorly
Flattened diaphragm
Ribs may appear more horizontal
Narrow heart

182
Q

What is the difference between a transudate and exudate?

A

Exudate has high protein content, often due to infection or malignancy

Transudate has low protein content, may be due to heart failure, nephrotic syndrome, hypoalbuminaemia

183
Q

How would someone with interstitial lung disease present on a lung function test?

A

Restrictive pattern
Reduced FEV1 and FVC
But FEV1/FVC ratio often >70% (as airway resistance does NOT increase)

184
Q

How does ILD affect perfusion of O2 and CO2?

A

Increases the diffusion pathway between alveolar air and blood so impairs gas exchange
O2 affected before CO2 as its less soluble
Hence T1 resp failure then T2 may follow

185
Q

What are some causes of interstitial lung disease?

A 
Asbestos
Silicosis
Rheumatoid arthritis
Radiation
Methotrexate 
Chemotherapy
Lupus
Nitrofurantoin 
Sarcoidosis
186
Q

What is primary malignancy of the pleura called?

A

Mesothelioma

187
Q

What is pleurisy?

A

Sharp pain worse with large breathing movements

Involvement of diaphragmatic pleura may cause shoulder pain on the same side

188
Q

What is a haemothorax?

A

A pleural effusion of blood

189
Q

When would pleural fluid volume increase?

A
  • Increase in permeability of pulmonary capillaries (inflammation or malignancy)
  • rise in pulmonary intra vascular pressure (heart failure)
  • fall in plasma osmotic pressure (eg liver failure)
  • obstruction to lymphatic flow in lungs
190
Q

What is fibrosing alveolitis?

A

Unknown causes
Progressive inflammatory condition of lungs, possibly triggered by pollutant or infection
This increases number of alveolar macrophages which attract neutrophils and cause local tissue damage and fibrosis due to ROS and proteases
Can be strained by steroids in early stages until fibrosis occurs

191
Q

If a lung function test showed a reduced TLCO, what would this mean?

A

Reduced carbon monoxide transfer factor

Means reduced diffusing capacity for gases across the alveolar capillary membrane

192
Q

Which are the true ribs, false ribs, and floating ribs?

A

True ribs 1-7 attach to the sternum
False ribs 8-12 don’t attach to sternum
Floating ribs 11 and 12

ESA 3 (6 decks)

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