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Question 1

Define anatomical, alveolar and physiological dead space. Define and calculate pulmonary ventilation rate (the minute
volume) and alveolar ventilation rate

Answer 1

Anatomical dead space = The volume of air in the conducting airways
Alveolar dead space = air in alveoli which do not take part in gas exchange (These are alveoli which are not perfused or are damaged)
Physiological dead space = Anatomical dead space + Alveolar dead space.

Tidal volume = Anatomical Dead space + Alveolar ventilation
• Total Pulmonary ventilation (Minute volume)= Tidal volume x Respiratory Rate
• Alveolar ventilation = (Tidal volume – Dead space) x Respiratory Rate

Question 2

Normal quiet inspiration and expiration and the role of inspiratory muscles of breathing and what can lead to
hypoventilation

Answer 2

Intercostals contract ‘up and out’ • Diaphragm flattens • Intrathoracic volume increases • Intrapulmonary pressure
decreases • Elastic tissue in alveoli is stretched

Air expelled from the airways passively, by relaxing
muscles used in inspiration • Volume of thoracic cavity reduces • Volume of lungs reduces as they return to original
volume • Lungs returning to original volume depends on their
elastic recoil • Intrapulmonary pressure relative to atmosphere
increases and air expelled

Question 3

Explain the changes in alveolar pressure and pleural pressure during respiratory cycle.

Question 4

Forced inspiration/ forced expiration and the accessory muscles of inspiration and expiration

Answer 4

Accessory muscles of inspiration
Sternocleidomastoid
Scalene muscles
Serratus anterior
Pectoralis major

Accessory muscles of expiration (not passive)
Internal intercostals
Abdominal wall muscles

Question 5

Pleural Seal

Answer 5

The surface tension of the pleural fluid creates a film that coats the lungs and thoracic cavity. This film prevents the lungs from collapsing and allows them to expand and contract during breathing.

Question 6

Lung Compliance / Lung Elastic Recoil and this is affected in Emphysema/Pulmonary Fibrosis

Answer 6

Measure of distensibility – change in volume relative to change in pressure

Compliance = ∆𝑣 ∆𝑝

LUNG ELASTIC RECOIL
The tendency of something that has been distended to return to its original size • Directly related to connective tissue surrounding alveoli -
elastin & collagen etc
• Directly related to alveolar fluid surface tension

Emphysema- enlargement of alveoli and walls destroyed. Destruction of elastin by protease. Reduced elasticity.

PULMONARY FIBROSIS - Elastic recoil of the lungs is increased - the resting lung volume is
smaller than normal - lung compliance reduced.

Question 7

Airway resistance in the normal lung and how it is affected in Asthma/COPD

Answer 7

Surface tension within airways
2) Airway diameter - small diameter have higher resistance to flow (Poiseuille’s Law)
i. Individual resistance is high - but altogether is low - tubes connected in parallel. highest resistance in the upper airways.

a) Diameter of the airways also affected by
i. Mucus in airways
ii. Intrapulmonary pressure gradients - inspiration vs expiration
iii. Radial Traction

Asthma
inflammation causes airway narrowing due to bronchial smooth muscle contraction, thickening of airway walls by mucosal oedema and excess mucous production which can partially block the lumen

Question 8

Explain the forces acting on the lung and chest wall at the equilibrium position at the end of a quiet
expiration/Resting Expiratory Level

Question 9

Define the following lung volumes and capacities:
Alveolar ventilation + pulmonary ventilation
Tidal Volume,
Inspiratory Reserve Volume, Expiratory Reserve Volume, Residual Volume;
Inspiratory Capacity, Functional Residual Capacity, Vital Capacity
Forced Vital Capacity
Total Lung Capacity

Answer 9

Alveolar ventilation = volume - alveolar dead space x resp rate
Total Pulmonary ventilation (Minute volume)= Tidal volume x Respiratory Rate

Tidal volume = Anatomical Dead space + Alveolar ventilation

Inspiratory Reserve Volume – vol of air that is the difference between the vol of quiet inspiration and the maximum inspiratory volume possible.

Expiratory Reserve Volume – vol of air that is the difference between the vol of quiet expiration and the maximum expiratory volume possible.

Residual Volume – after forced expiration lungs are not completely emptied - remaining air is residual vol.

Inspiratory Capacity - from end of quiet expiration to maximum inspiration. (i.e. Inspiratory Reserve Volume + Tidal Volume)

Functional Residual Capacity - vol of air in the lungs at the end of a quiet expiration (i.e. Expiratory Reserve Volume + Residual Volume)

Vital Capacity = Inspiratory Capacity + Expiratory Reserve Volume OR Inspiratory Reserve Volume + TV + Expiratory Reserve Volume. Max vol of air that can be expelled after max inspiration.

Total Lung Capacity = Vital Capacity + Residual Volume

Question 10

Surface tension in the alveoli and the role surfactant. Clinical relevance: Neonatal Respiratory Distress
Syndrome

Answer 10

Thin inner lining of water-based fluid whose surface tension exerts a collapsing force on the alveolus.
Surface Tension decreases compliance making it more difficult for alveoli (and therefore lungs) to expand

NRDS - babies younger than 35 weeks don’t produce enough surfactants so alveoli collapse. Surfactant replacement via an endotracheal tube (inserted in the infraglottis)
• Supportive treatment: O2/ assisted ventilation
• Grunting
• Nasal flaring
• Intercostal and subcostal retractions
• (tachypnoea)
Cyanosis

Question 11

Hypoventilation

Question 12

• Explain the concept of the ‘partial pressure’ of an individual gas in a gas mixture

Answer 12

In a mixture of gases, each component gas exerts a ‘partial pressure’ in proportion to its volume percentage in the mixture, and the sum of the partial pressures of all the gases equals the total pressure. Pressure is expressed as kPa.

Question 13

• Calculate the partial pressures of constituent gases in atmospheric air and explain the effects of altitude upon them.

Answer 13

To calculate the partial pressure of a gas in a gas mixture:
multiply the percentage of that gas with the total pressure eg 0.20 x 100kPa = 20kPa partial pressure of gas x.

High altitude = lower atmosphere pressure so lower total pressure of gases so lower partial pressure of gas x.

Question 14

• Explain the effect of saturated water vapour pressure on partial pressure of inhaled gases such as oxygen

Answer 14

air entering our respiratory tract is humidified – water is added to the air.
The added water vaporises and has a pressure -water vapour pressure.
How much water vaporises, and therefore the water vapour pressure, only depends on temperature.
At body temperature (37 C), water vapour pressure = 6.28 kPa.
The percentage of O2 -20.9%. Therefore, the partial pressure of oxygen of the humidified air in our upper respiratory tract = 94.72 kPa (101 kPa – 6.28 kPa ) x 20.9% = 19.8 kPa.

Question 15

• Explain what is meant by “partial pressure of oxygen” in blood, and how it is different from the “content” of oxygen in the blood.

Answer 15

Partial pressure of O2 in blood is the amount dissolved = solubility coefficient of that gas x the partial pressure to which it is exposed - The solubility coefficient of O2 in blood is 0.01 mmol/Litre/kPa.
Therefore, if plasma at 37 C is exposed to alveolar air with a pO2 of 13.3 kPa, the dissolved O2 content of plasma will be= 13.3 x 0.01 = 0.13mmol/Litre.

Total content is 0.13 + O2 bound to Hb which is 8.8 so 8.933 mmol/L oxygen

Question 16

• Calculate the content of oxygen and carbon dioxide in plasma using their solubility coefficients and partial pressures

Question 17

Explain the different partial pressures of O2 and CO2 observed in inspired air, alveolar air, mixed venous blood and arterial blood,
•

Question 18

Be aware of the normal pO2 and pCO2 in alveolar air, arterial blood and mixed venous blood
•

Answer 18

Mixed Venous Blood
pO2 5.3 kPa
pCO2 6.6 kPa

Alveolar Air
13.3 kPa
5.3 kPa

partial pressure of arterial O2 of between 10.5-13.5 kPa

Question 19

Describe the layers making up the diffusion barrier at the air-blood interface
•

Answer 19

1. Fluid film lining inside of alveolus
2. Alveolar epithelial cell membrane
3. Interstitial fluid
4. Capillary endothelial cell membrane
5. Plasma
6. Red cell membrane

Question 20

Describe factors affecting the rate of diffusion across the air blood interface
•

Answer 20

1. Surface area available for exchange - alveolar surface = 70m2
2. Gradient of partial pressure – difference between partial pressure of gas in blood versus alveolar air
   • T – (thickness) i.e. distance molecules must diffuse
   • D- Diffusion coefficient of the individual gas - solubility/ square root molecular weight

Question 21

Explain why gas exchange depends on the partial pressure gradient across the diffusion barrier

Answer 21

Goes from higher to lower partial pressure

Question 22

Describe the role of diffusion coefficient in gas exchange. State and explain the difference in the diffusion rates of O2 and CO2
•

Answer 22

For most of the barrier (the cells, membranes and fluid) the rate of diffusion is affected by the solubility of the gas in water and molecular weight.
CO2 bigger but more soluble so
21 times as fast as oxygen for a given gradient.
Larger difference in partial pressures compensates for slower diffusion of O2

Question 23

Begin to understand and be able to describe the concept of ventilation-perfusion match, and ventilation-perfusion mismatch as a cause of hypoxaemia (low Partial pressure of O2 in arterial blood)
And response to mismatch

Answer 23

Optimal gas exchange occurs when ALVEOLI are ventilated in
proportion to their perfusion-0.9.
Improves to 1 with exercise due to:
increased blood flow/perfusion to the lung apices which increases V/Q match, and also increased recruitment of alveoli in the lung bases.

perfuse an unventilated alveolus - blood entering and leaving (i.e perfusing) unventilated lung areas will remain deoxygenated - no gas exchange- wasting perfusion so some other part of the lung is being under perfused - shunt - V:Q <1

ventilate an alveolus that is not perfused - that bit of air is wasted -hypoxaemia - dead space - V:Q >1
Capillary pO2 falls and pCO2 rises
Lung hypoxic vasoconstriction causes diversion of blood to better ventilated parts of the lung.
However, the haemoglobin in these well-ventilated capillaries will already be saturated so unable to raise pO2
Hyperventilation happens so back to normal pCO2.

Question 24

Explain why lung disease causing a diffusion defect affects the diffusion of O2 more than the diffusion of CO2

Answer 24

Diseases causing diffusion defects:
1. Interstitial/fibrotic lung disease - excessive deposition of collagen in the interstitial space, with thickening of alveolar walls:
Longer diffusion pathway.
May be idiopathic or secondary to many causes, including inhaled dusts.

2. Pulmonary oedema: The fluid in the interstitium and alveolus increases length of diffusion pathway.
3. Emphysema: destruction of alveoli reduces total surface area for gas exchange.

– CO2 always diffuses much faster than O2
– So, diffusion of O2 affected→pO2 is low
– Diffusion of CO2 not affected→pCO2 normal

Question 25

Define and explain the difference between:
o Oxygen saturation (SaO2, ‘Sats’)
ArterialPaO2(partialpressureofoxygen)
o Oxygencontentofblood

Answer 25

% Oxygen saturation of Hb in arterial blood

Arterial partial pressure of oxygen (PaO2) in the blood is a function of the amount of dissolved oxygen. Note: PAO2 is alveolar partial pressure of O2.

Oxygen content = oxygen bound to haemoglobin and the amount of oxygen dissolved in the blood

Question 26

Draw an oxygen-haemoglobin dissociation curve, label the axes correctly and indicate the normal values of (i) alveolar pO2, and (ii) capillary pO2 in a typical tissue.

Question 27

• List the properties of the haemoglobin molecule which facilitate the transport of oxygen in the blood.

Answer 27

2 alpha & 2 beta subunits
Each subunit has one haem group that can bind one oxygen molecule forming oxyhaemoglobin.

changes shape based on the number of oxygen molecules bound to it.
change in shape also alters its affinity to oxygen - inc binding = inc affinity = cooperativity

No O2 = Tense state (T-state)
Bind = Relaxed state

Question 28

Draw the effects on the haemoglobin oxygen dissociation curve of (i) a fall or increase in pH above the physiological range (ii) a rise in temperature Iii) an increase or fall in 2-3 DPG

Answer 28

Fall pH= right
Inc temp = right
Inc 2-3 DPG = right - 2,3-DPG binds to the beta chains of haemoglobin, so increased 2,3-DPG levels results in it binding to haemoglobin

Question 29

• Understand why anaemia causes tissue hypoxia despite normal arterial paO2 and normal Oxygen saturation (SaO2, ‘Sats’).

Answer 29

Hypoxia – low oxygen levels relative to the need in body or tissues
1Shock - reduces blood flow - peripheral vasoconstriction causes peripheral hypoxia
2Tissues using O2 faster than it is delivered
3Secondary to anaemia

Anaemia - O2 sat and PaO2 will
be normal - Hb levels low. Oxygen content low.

Question 30

PE

Answer 30

pulmonary embolism causes hypoxaemia by causing V/Q mismatch with V>Q at the site of the embolism (the clot blocks perfusion), and also by diverting blood to other alveoli and creating V<Q in those areas other than the clot.

Question 31

Define cyanosis and explain its significance

Answer 31

Bluish colouration due to unsaturated haemoglobin (< 85 or 90%)
Deoxygenated haemoglobin is less red than oxygenated
Can be peripheral (hands or feet) due to poor local circulation
Or central (mouth, tongue, lips, mucous membranes) due to poorly saturated blood in systemic circulation

Can be difficult to detect
• Poor lighting
• Skin colouration - darker skin need to look at nail beds for peripheral cyanosis
• Shoes

Question 32

Describe and explain the basis for carbon monoxide poisoning

Answer 32

Fatal if CO-Hb is > 50%
Does not decrease PaO2

Children at inc risk
Symptoms:
Headache
Nausea
Vomiting
Slurred speech
Confusion

Higher affinity so less O2 transport
Increases affinity of unaffected subunits for oxygen - Left shift in dissociation curve - dec oxygen release to peripheral tissues

Question 33

Understand and explain the methods of pulse oximetry and arterial blood gas testing and their clinical application

Answer 33

Pulse oxi:
Detects level of Hb saturation – non-invasive
Detects difference in absorption of light between oxygenated and deoxygenated Hb
Only detects pulsatile arterial blood levels
Can’t detect tissue oxygen levels or non-pulsatile venous blood
Can’t give information about Hb levels

Less accurate in darker coloured skin

ABG:
Partial pressure of PO2 - depends on dissolved O2.
Also data on PCO2 and pH and bicarbonate
Invasive - blood sample from radial artery

Question 34

Diff between shunt and VQ mismatch

Answer 34

Shunt = 0
VQ mismatch = no. other than 0

Question 35

List the reactions of CO2 in blood.
Describe the buffering action of haemoglobin in red cells.
Describe the function of carbamino compounds.
Haldane effect

All part of CO2/ Bicarbonate buffer system

Answer 35

In plasma:
CO2 + H2O <-> H2CO3 <-> H+ + HCO3-
Slow because little CA in plasma
Negligible amount of bicarbonate formed

In Hb:
CO2+H2O->H2CO3->H+ + HCO3-

H+ + Hb- ->HbH
Happens when Hb in deoxygenated state
CA present so rapid
Mainly bicarbonate produced (H+ taken up by Hb)
Goes into plasma in exchange for Cl-

Carbon dioxide also reacts directly with the protein part of haemoglobin, forming Carbamino compounds. This is at low O2 and high CO2 conc.

The Haldane effect - low O2 conc inc CO2 carrying capacity of Hb because release of O2 from Hb promotes binding of CO2.

Question 36

Describe factors influencing PaCO2 and plasma [HCO3-] - finish card
And ratio that maintains pH

Answer 36

the pH of plasma is determined by the ratio of [HCO3-]: pCO2 which is normally about 20:1.

Question 37

Define the terms hypoxia, hypoxaemia, hypercapnia,
hypocapnia, hyperventilation, and hypoventilation. •

Answer 37

Hypoxia
Hypoxaemia - Falls in arterial pO2 below normal
Hyper and hypocapnia- rise or fall in arterial pCO2
Hypoventilation - Removal of CO2 from lungs is less rapid than its production.
Hyperventilation. Removal of CO2 from alveoli is more rapid than its production.

Question 38

Describe the fundamental principles of neural control of breathing including the associated anatomy

Answer 38

Dorsal respiratory group of neurones - dorsal surface of the medulla - basic rhythm of respiration - inspiratory neuron action potentials to spinal nerves innervating the diaphragm and external intercostal muscles - spontaneously and continuously fire. (Preventing over inflation of lung - Stretch receptors located in the walls of bronchi and bronchioles transmit information via the vagus nerve back to the brainstem.)

the ventral group located on the ventral-lateral surface of medulla - expiration

the pontine - pneumotaxic centre of neurons, located dorsally on the pons - inspiratory off switch. Limits phrenic nerve, dec tidal vol and resp rate.

Question 39

Describe the fundamental principles of chemical control of breathing including the associated anatomy - peripheral and central - where they are, what they detect, what they change
• notion

Answer 39

Peripheral chemoreceptors detect changes in arterial pO2 (also change in pH and arterial pCO2)
Located in carotid and aortic body.
Afferent impulses travel via the glossopharyngeal nerves to the medulla oblongata and the pons in the brainstem.
Changes made:
Respiratory rate and tidal volume are increased
Blood flow is directed towards the kidneys and the brain
Cardiac Output is increased to maintain blood flow, and therefore oxygen supply to tissues

Central chemoreceptors
Located in the ventral medulla oblongata of brainstem.
They detect changes in the arterial partial pressure of carbon dioxide (pCO2).
Receptors send impulses to the respiratory centres in the brainstem that initiate changes in ventilation.
Get reset to higher value in prolonged hypercapnia.

pH Control of CSF
Stimulated by dec pH in CSF
CO2 freely diffuses from the arterial blood supply into the CSF.
CO2 reacts with H2O, producing carbonic acid, which lowers the pH - stimulates respiratory centres to increase ventilation.
However if pCO2 levels stay abnormal for a long period of time, choroid plexus cells within the blood brain barrier allow HCO3– ions to enter the CSF.
Alters the pH which in turn resets the pCO2 to a different value.

Question 40

State the normal range plasma pH
Define the terms ‘
Respiratory Acidosis’, ‘Respiratory Alkalosis’, ‘Compensated Respiratory Acidosis’
‘Compensated Respiratory Alkalosis’.
Full and partial

Answer 40

Normal = 7.35-7.45

Hypoventilation- Removal of CO2 from lungs is less rapid than its production.

Resp acidosis - more CO2 in lungs. The alveolar pCO2 rises, so dissolved CO2 rises more than HCO3- producing a fall in plasma pH

Compensated - kidneys respond to the low pH by reducing excretion of HCO3-.
Full = normal pH
Partial = abnormal pH, but opp process is trying to get it back to normal

Hyperventilation - Removal of CO2 from alveoli is more rapid than its production.

Resp alkalosis - Alveolar CO2 falls - plasma pH rises

Compensated - kidneys respond by excreting HCO3- and plasma pH normal. But buffer base concentration is reduced.

Question 41

Interpret arterial blood gas abnormalities and recognise
respiratory acidosis, respiratory alkalosis, metabolic
acidosis, and metabolic alkalosis.

Interpret arterial blood gas evidence of respiratory or
metabolic compensation in response to alterations in
normal pH levels.

Answer 41

Normal ABG:
pH: 7.35-7.45
PaO2: 9.3-13.3 kPa
PaCO2: 4.6-6 kPa
Bicarbonate(HCO3): 22-26 mmol/L

Information from ABG:
Lung function: pO2, pCO2
Also pH status
through the Henderson-H equation that relates pCO2 to pH.
Acid-base status: If pH is <7.35 the person has acidaemia caused by an acidosis process. And vice versa.
Metabolic status: metabolism, and kidney function, by providing us with the bicarbonate level.

Interpretation:
1. Look at pH. Let’s say it is acidic
2. Look at pCO2. If it is elevated = respiratory acidosis
4. If pCO2 normal and bicarbonate low = metabolic acidosis
5. If pCO2 and bicarbonate are elevated and low pH then metabolic compensation is taking place. If pCO2 low, bicarbonate high and low pH then respiratory compensation.
6. If pH normal and other stuff abnormal then full compensation has happened.

Question 42

Understand the mechanisms of overall acid base control
in the body and the role of the respiratory system in
comparison with the renal system (covered in both the
Urinary and Respiratory system Units).

Question 43

• Describe the effects on plasma pH of hyper and hypo
ventilation.
• Describe the general effects of acute hypo and hyper
ventilation.

Question 44

• Describe the main causes of respiratory alkalosis
• Describe the main causes of respiratory acidosis

Answer 44

Resp alkalosis
High altitude
Central Causes eg Head Injury, Stroke
Anxiety
Hyperthyroidism
Pulmonary Embolism
Pneumonia
Asthma
Pulmonary oedema

Resp acidosis
Conditions that impair CNS respiratory drive (eg, brain stem stroke, medications, drugs, or alcohol)
Conditions that impair neuromuscular transmission and other conditions that cause muscular weakness
Obstructive, restrictive, and parenchymal pulmonary disorders eg COPD

Question 45

• Describe the acute effects upon ventilation of: (i) falling
inspired pO2; (ii) hypoxaemia; (iii) increases in inspired
pCO2 (iv) falls in arterial plasma pH.

Question 46

• Describe the location of peripheral chemoreceptors and
their nerve supply
• Describe the response of peripheral chemoreceptors to
changes in arterial pO2, pCO2 and pH and their role in
the regulation of breathing

Answer 46

Peripheral - carotid bodies and aortic bodies. The impulses are
carried via the glossopharyngeal nerves and vagus nerve respectively. Sends to brainstem resp centres.
Response to O2 - increase in tidal volume and rate of respiration.
More blood to brain and kidneys & increased pumping of blood by the heart.
Response to CO2
Response to pH - low pH results in an increased respiratory rate and tidal volume.

Question 47

Describe the process of transport of CO2 from tissues to lungs, and state the proportion of CO2 traveling in various forms.

Answer 47

10% of transported CO2 travels as dissolved CO2,
60 % as bicarbonate
30% as carbamino compounds

1) Tissues produce CO2.
The increase in pCO2 causes a little more CO2 to dissolve in venous compared with arterial blood
2) When blood arrives at the tissues oxygen is unloaded from haemoglobin. Hb can now bind with H+.
Bicarbonate mostly exported to the plasma.
3) CO2 binds to amino groups on Hb so carbamino products.
This stabilises pH– CO2 is unable to leave the blood cell to contribute to changes in pH
Bohr Effect – it stabilises the T state of haemoglobin
4)When that mixed venous blood reaches the lungs there is oxygenation of Hb.
Less good at holding onto CO2 - Haldane effect
H+ driven off Hb react with the bicarbonate to form CO2 which is breathed out.

Question 48

• Describe the location of central chemoreceptors and
their response to changes in arterial pCO2 and pH in the
regulation of breathing
• Describe the roles of the CSF, brain extracellular fluid,
blood-brain barrier and the choroid plexus in the
response of central chemoreceptors to changes in
arterial pCO2 • Explain the effect of prolonged elevation of pCO2 on the
central chemoreceptors.

Answer 48

Location - ventral surface of the medulla
Responds to brain extracellular fluid. The pH is determined by plasma PaCO2.
Choroid plexus cells pump HCO3- into or out of CSF.
If pCO2 rises, ventilation increases, to lower pCO2 again.
If this does not occur (eg due to disease of lung) choroid plexus cells will pump more bicarbonate ions into CSF.
And vice versa.
Adjustment means higher level of CO2 needed to cause acidosis and

Question 49

• Define hypoxia, hypoxaemia and the difference between
the two terms

Answer 49

Hypoxia is defined as reduced oxygen at the tissue level. Abnormalities occurring at any point on the oxygen supply chain can result in hypoxia.

Hypoxaemia is defined as a decrease in the partial pressure of oxygen (pO2) in the blood. The pO2 of the blood is determined by gas exchange in the lung.

Question 50

Define type 1 respiratory failure (RF) and type 2 respiratory
failure (RF)

Answer 50

Type 1 respiratory failure is characterised by a low pO2 (< 8kPa) with a normal or low PCO2.

Type 2 respiratory failure is characterised by a low pO2 (< 8kPa) and a high pCO2 of > 6.7 kPa

Question 51

• Outline the major causes of Type 1 RF

Answer 51

Low inspired pO2 e.g. high altitude - pO2= FiO2 x total atmospheric pressure -pO2 falls
in alveoli at higher altitude - hypoxaemia - Type 1 respiratory
failure.
Give O2.

V/Q mismatch- alveoli poorly ventilated - caused by pneumonia (exudate), asthma (airway narrowing), COPD (airway narrowing+loss of alveoli) , resp distress syndrome in newborn(alveoli not expanded), PE(perfusion blocked), PO(fluid).
Give O2 and treat underlying.

Diffusion impairment - lung fibrosis(inc distance), emphysema(dec SA). pO2 low and pCO2 normal as it is more soluble.

Intrapulmonary shunts - shunt is perfusion of alveoli that have no
ventilation – V/Q ratio = 0
Alveolar filling with pus, oedema fluid, blood or tumour eg ARDS.

Right to left shunts (e.g. cyanotic heart disease). Blood
from the right side of the heart enters the left side without passing through the lungs and taking part in gas exchange.

Question 52

• Outline the major causes of Type 2 RF

Answer 52

Hypoventilation - entire lung poorly ventilated due to inadequate resp rate or reducing alveolar minute ventilation.
Low pO2 and high pCO2 in the alveolar air.
Hypoxaemia and hypercapnia.

Acute Causes - Opiate overdose, Head injury, severe asthma
Chronic - severe COPD

Central control - opioid OD, hypothyroidism
MN - MND, ALS
Peripheral neuropathy- GBS
Nm junction- MG, Organophosphate toxicity, Botulism

Resp muscle weakness and fatigue- Duchennes, malnutrition, asthma, COPD, RDS

Chest wall disorders - e.g.
Scoliosis, morbid obesity, rib fractures, kyphosis(excessive outward curve of spine).

Severe lung fibrosis, or
widespread severe airway obstruction (life threatening
asthma, late stages of COPD)

Question 53

Explain how Type 1 RF can progress to Type 2 RF

Answer 53

Pump failure - as more and more airways become severely narrowed and exhaustion sets in ,so hypoventilation, it becomes type 2 respiratory failure eg asthma, COPD, fibrosis.

In fibrosis As disease progresses, restrictive lung disease leads to hypoventilation – which
will cause hypercapnia.

Causes
• Idiopathic pulmonary
Fibrosis • Asbestosis • Extrinsic allergic alveolitis • Pneumoconiosis

Question 54

• Explain Acute Respiratory Distress Syndrome (ARDS) and
how it leads to Respiratory Failure

Answer 54

Acute inflammation affecting alveolar-capillary membrane

Inc permeability of membrane

Exudate inactivates surfactant so collapse of alveoli and dec SA. alveolar atelectasis.

Lungs stiff and vol dec.

No hypoxic pulmonary vasoconstriction due to inflammation causing vasodilation.

intrapulmonary shunt - no ventilation with respect
to perfusion

Hypoxaemia

Deoxygenated blood goes to left heart

Eventually type 2 as hyperventilation fails to keep pace with carbon dioxide production.

Question 55

• Explain what cyanosis is and the difference between
central and peripheral cyanosis.

Answer 55

bluish discolouration due to presence of 4 to 6 gm/dl of deoxyhaemoglobin

Central - Seen in oral mucosa, tongue, lips. Indicates hypoxaemia
Peripheral - In fingers, toes

Question 56

• Explain the acute and chronic effects of hypoxaemia/hypoxia and hypercapnia

Answer 56

Effects of Hypoxaemia and/or Hypoxia:
• Impaired CNS function – lethargy, confusion, irritability
• Cardiac arrhythmias and ischaemia
• Hypoxic vasoconstriction of pulmonary vessels
• Central cyanosis
• Initially tachycardia but as condition persists worsens
bradycardia will develop. Tachypnoea.

Effects of Hypercapnia:
• Respiratory acidosis
• Impaired CNS function: drowsiness, confusion, coma,
flapping tremors, seizures, and if severe and persistent
respiratory arrest
• Peripheral vasodilatation –warm hands, bounding pulse
• Cerebral vasodilation – headache – if severe and
persistent will cause cerebral oedema

Question 57

• Describe the pathophysiology of pulmonary embolism - look at Virhow’s triad in path pro

Answer 57

Obstruction of a pulmonary artery or one of its branches, usually by DVT (deep vein thrombosis- venous thromboembolism), which has become dislodged and been carried to the lungs by the blood stream.

Consequences:
Hypoxaemia due to V/Q mismatch

Rise in pulmonary artery pressure - right ventricular strain - drop in the cardiac output - vasoconstriction of pulmonary vessels to maintain BP so even more strain on right heart.
Can lead to death because of cardiogenic shock with circulatory failure / cardiac arrest due to arrhythmias.
If they have patent foramen ovale then shunting then hypoxia. Also paradoxical embolization – clot passes into left heart & systemic circulation -> stroke

Pulmonary infarction - alveolar
haemorrhage & infarction
Causes haemoptysis, pleuritis, small pleural effusion

Question 58

• Describe the risk factors, clinical features, investigation,
and principles of treatment and prevention of pulmonary
embolism

Answer 58

Risk factors:
Immobility
• Recent long distance travel
• Malignancy,
• Inherited hypercoagulable states,
• Pregnancy,
• Obesity
• Recent surgery
• Hormone replacement therapy or oral contraceptives

Symptoms - pleuritic chest pain, • coughing • dyspnea, syncope, Haemoptysis, Unilateral leg pain/swelling

Signs - Tachypnoea and tachycardia, fever up to 39, cyanosis, crackles

Investigation
Imaging - Detection in CT pulmonary angiography (CTPA) (V/Q scan for pregnant), Chest x-ray - might have peripheral wedge shaped opacification due to infarction

Arterial blood gas shows respiratory alkalosis with low pO2, low CO2

D-dimer levels can rule out PE if -ve in low risk patients.

ECG = sinus tachycardia

Treatment:
O2
Anticoagulants - LMW heparin (Heparin-Induced Thrombocytopenia - antibodies form and platelets activate and clump. Thrombi form. Stroke, MI, limb ischaemia).
Thrombolytic agents or thrombectomy, resp and haemo support for massive PE.
Vena cava filters if high bleeding risk or recurrent PE.

Prevention:
Early mobilisation post-surgery or during long airplane flights DVT prophylaxis in high-risk patients
Postoperative anticoagulation
Avoid certain medications (e.g., OCPs) in patients with
thrombophilia (e.g., factor V Leiden) or smokers (elevated risk
DVT).
Falls prevention
AES stockings

Question 59

Other emboli

Answer 59

Fat Embolism Syndrome
traumatic fracture of femur, pelvis, tibia. pelvic and knee arthroplasty.
massive soft tissue injury, severe burn, bone marrow biopsy etc
acute pancreatitis, fatty liver etc

Triad - petechial rash, decreased level of consciousness, and shortness of breath.

Amniotic fluid embolism - presents as sudden maternal collapse associated with hypotension, hypoxaemia, and DIC.
It occurs when amniotic fluid or other debris enter the maternal circulation.
Most cases occur during labour or immediately after delivery.

Air emboli

Question 60

Compensatory mechanisms to hypoxia

Answer 60

Inc EPO secreted by kidney - raised Hb (Polycythaemia)

Increased 2,3, DPG – shifts Hb/O2 saturation curve to the right so oxygen released more freely

Increased capillary density

Chronic hypoxic vasoconstriction of pulmonary vessels results in-
• Pulmonary hypertension • Right heart failure • Cor pulmonale

Question 61

Why treatment of hypoxaemia may worsen hypercapnia in type 2

Answer 61

1. Correction of hypoxia removes pulmonary arteriole hypoxic
   vasoconstriction
   a. leads to increased perfusion of poorly ventilated alveoli - more CO2 in blood.
   b. diverting blood away from better ventilated alveoli – i.e worsens V:Q mismatch (V<Q) - less CO2 expiration.
2. Haldane mechanism – oxygenated Hb has low affinity for CO2.
   CO2 dissociates from Hb into blood.

Question 62

What is COPD

Answer 62

COPD is a disease state characterised by: airflow limitation that is not fully reversible
Persistent respiratory symptoms

It encompasses both emphysema and chronic bronchitis
The airflow limitation is usually progressive
Associated with an abnormal inflammatory response of the lungs to noxious particles or gases.

Question 63

Aetiology of COPD

Answer 63

Tobacco smoking = 90%

Air pollution and occupational exposure

Alpha-1 antitrypsin deficiency (anti protease so deficiency means destruction of alveolar walls and emphysema)

Question 64

Be able to describe COPD features that have emphysema and chronic bronchitis and pulmonary hypertension

Answer 64

Host response to noxious substance
Chronic inflammatory process:

• Enlargement of mucus-secreting glands of the central airways
• Increased number of goblet cells (which replace ciliated respiratory epithelium)
• Ciliary dysfunction
These are all chronic bronchitis

• Elastin breakdown leading to destruction of alveolar walls
and structure, and loss of elastic recoil - emphysema
• Formation of larger air spaces with reduction in total surface area available for gas exchange
• Loss of capillaries with loss of the alveolar-capillary membrane secondary to destruction of elastin

• Vascular bed changes leading to pulmonary hypertension.

Question 65

Describe the pathophysiology of COPD (including the nature of airflow obstruction)
Look at CVS hypoxia pulmonary vasoconstriction

Answer 65

1. Luminal airflow obstruction due to secretions due to airway inflammation and there is airway fibrosis so inc airway resistance
   AND
   Narrowing of bronchioles that are kept open by radial traction (exerted on their walls by outward pull of elastin in surrounding alveoli).
2. Elastase break down so destruction of alveolar walls so less lung recoil
3. Less expiration force
4. Hyperinflation of lungs
5. Dec gas exchange as old air trapped in lungs so dec con gradient of O2
6. Air trapping flattens the diaphragm and thus reduces its force upon contraction – dec inspiration force.
7. Hypoxia causes pulmonary vasoconstriction so pulmonary hypertension and R heart failure. Also, thickening of vascular smooth muscle.
8. Hypercapnia

Question 66

Describe the symptoms and signs of COPD and understand how they arise and how they differ

Answer 66

Clinical signs

History - gradual, older people with long history of smoking, occupation, pollution

Physical:
Tachypnoea: to compensate for hypoxaemia and hypoventilation.
Use of accessory muscles of respiration
Barrel chest (increased antero-posterior diameter of the chest) is due to hyperinflation
Purse lip breathing

Hyper- resonance on percussion due to hyperinflation and air trapping
Reduced intensity breath sounds caused by hyperinflation and loss of lung parenchyma.
Dec air entry - secondary to loss of lung elasticity
Wheezing on auscultation

Late:
Central cyanosis – hypoxaemia and tissue hypoxia
Flapping tremors - hypercapnia
Signs of right-sided heart failure (distended neck veins, hepatomegaly, and ankle oedema).

Symptoms
Cough - morning but becomes constant, productive but not purulent (not green or yellow)
Dyspnoea on exertion then rest

Question 67

Outline the treatment of COPD

Answer 67

Lifestyle
• Smoking cessation
• Pulmonary rehabilitation: many COPD patients avoid exercise because of breathlessness = muscle weakness =worsening symptoms. Need exercise, disease education and nutritional advice.
• Patient weight, nutrition, physical activity– obesity also impairs lung function.

First
• Pneumococcal, Influenza, Covid19 vaccination
• Bronchodilators
• Inhaled corticosteroid

Second
• If severe- long acting anti-muscarinic agent inhalers
Long term oxygen treatment
Surgical interventions: such as removal of large bullae, lung volume reduction, and lung transplant).

Question 68

Define acute exacerbations of COPD
Management

Answer 68

Event characterised by acute worsening of resp symptoms eg dysponea, cough, sputum. Result in additional therapy.

Monitoring for hypoxaemia and hypercapnia, using Pulse oximetry and ABG analysis.

Acute infectious exacerbations = severe dysponea, fever, chest pain, purulent sputum.

Give antibiotics, bronchodilators, oral steroids, O2, ventilation.

Question 69

COPD investigations

Answer 69

Spirometry shows an obstructive pattern with FEV1/FVC ratio <70%.

CXR: Hyper inflated lungs may result in flattened diaphragm,
hyperlucent lungs and an increased antero-posterior diameter of the chest (seen on lateral chest x-ray only).
May show complications of COPD, such as pneumonia and pneumothorax
Mandatory to exclude other diagnoses.

Lung function tests

ABG analysis for hypoxaemia and hypercapnia for suspicion of resp failure.

Alpha-1 antitrypsin level - atypical history

Question 70

• Describe the complications of long-standing COPD - 4

Answer 70

• Recurrent pneumonia
• Pneumothorax: Occurs because of lung parenchyma
damage with sub-pleural bulla formation and rupture
• Respiratory Failure – acute (higher risk for this) or chronic
• Cor pulmonale (Right heart failure)

Question 71

What is bronchiectasis
Causes (diff between oedema and lymphoedema)

Answer 71

Chronic, irreversible dilatation of bronchi due to destruction of the elastic and muscular components of the bronchial wall.

Causes:
Post infective:
whooping cough, TB, measles

Immune deficiency: Hypogammaglobulinaemia

Genetic / Mucociliary clearance defects:
o Cystic fibrosis
o Primary ciliary dyskinesia,
Young’s syndrome(triad of bronchiectasis, sinusitis,
reduced fertility)
o Kartagener syndrome (triad - bronchiectasis, sinusitis, situs inversus)
o Yellow Nail Syndrome - triad of yellow nail, pulmonary problems and lower limb lymphoedema

Obstruction eg tumour

Question 72

Bronchiestais
Symptoms
Risk factors
Investigate - notion
Management

Answer 72

Cough
Sputum production (can be bloody)
Crackles, high pitched inspiratory squeaks and ronchi
Dyspnoea
Fever

Risk - Cystic fibrosis, immunodeficiency, previous infections, IBD, alpha1-antitrypsin def

Investigate:
High resolution CT scan - bronchus is more dilated than the adjacent blood vessel and bronchial wall thickening.
Classically show the ‘Signet Ring sign’ - a very dilated bronchus and smaller pulmonary artery are seen in close association.

Treat underlying cause
• Physiotherapy – daily mucus clearance
• Antibiotics according to sputum cultures
• Supportive – vaccine, bronchodilators
• Pulmonary Rehab

Question 73

• Describe how to differentiate bronchiectasis from COPD
• Describe the common pathogens affecting people with COPD and Bronchiectasis

Answer 73

Sounds:
Diminished in COPD
Rhonchi, inspiratory squeaks and crackles in B

Chest CT:
May be normal or show emphysema in COPD
Thickened, dilated airways with or without air fluid levels in B

Pathogens:
Haemophilae influenzae, Strep pneumoniae and moraxella catarrhalis in COPD

HI, MC, Pseudomonas aeruginosa, fungi (aspergillus, candida), non-tuberculous mycobacteria, Staphylococcus aureus in B

However, patients with COPD may also develop bronchiectasis.

Question 74

• Describe what, diagnosis, management of cystic fibrosis

Answer 74

What = common cause of bronchiectasis, autosomal recessive where CFTR is mutated.

Diagnosis = history of CF in sibling or +ve newborn screening test result
AND
Inc NACL in sweat
2 CF mutations
Or abnormal nasa epithelial ion transport

Management = No smoking
Avoid people with colds
Avoid Jacuzzis (pseudomonas)
Avoid stables,compost–riskof aspergillus fumigatus inhalation
o influenza vaccine
o strep pneumoniae vaccination
oNaCl tablets in hot weather/exercise

Question 75

CF Pathophysiology

Answer 75

Defect on Long arm of Chromosome 7
Leads to Cystic Fibrosis Transmembrane Conductance Regulator mutation
Leads to ineffective cell surface
chloride transport
Leads to thick, dehydrated body fluids in organs which have CFTR

Question 76

CF presentation

Answer 76

1. Meconium ileus: in CF infants the bowel is blocked by the sticky secretions.
   Signs of intestinal obstruction soon after birth with bilious vomiting, abdominal distension and delay in passing meconium.
2. Intestinal malabsorption - The main cause is a severe deficiency of pancreatic enzymes.
3. Recurrent Chest infections, Pneumothorax, Respiratory failure, Cardiac failure
4. Osteoporosis
5. Male infertility

Question 77

CF complications

Answer 77

Complications:
1.Respiratory Infections
Treatment = antibiotics and lung physio
Prophylactic antibiotics to maintain health

2. Low Body Weight
   o if needed give pancreatic enzyme replacement therapy
   o high calorie intake + extra supplements
   o may need NG or PEG feeding
3. Distal Intestinal Obstruction Syndrome (DIOS)
   o DIOS vs constipation–faecal obstruction in ileo- caecum vs whole bowel
   o Due to intestinal contents in the distal ileum and proximal colon (thick, dehydrated faeces)
   o Due to insufficient pancreatic enzymes or salt deficiency
   o Palpable right iliac fossa mass (faecal)
   o Do abdominal XR demonstrating faecal loading at junction of small and large bowel
4. CF Related Diabetes
   o exocrine pancreatic duct inflammation affects the endocrine portion thus destroying insulin producing beta cells.

Question 78

Describe the underlying molecular defects that cause to cystic fibrosis

Question 79

Describe the microbiology of mycobacterium tuberculosis

Answer 79

TB bacilli are aerobic, rod-shaped, non-motile
Can be demonstrated on smears stained by the Ziehl-Nielsen method
2-6 weeks to form colonies on cultures
Long chain fatty acids and glycolipids in cell wall = structural rigidity, acid alcohol fast bacilli (resist decolorisation by acids).

Question 80

Describe the pathophysiology of TB infections and the host
response to TB infection

Answer 80

Transmission = infected droplets formed from sputum with MTB being released into the air. Need long periods of contact - more than 8hrs so more likely to get from co-worker or family

1. Alveolar macrophages infected as deposition of TB bacilli in the alveoli.
2. Phagocytose MTB
3. T helper cells (Th1 cells or CD+4 cells) activate macrophages enabling them to become bactericidal with enhanced ability to kill MTB. 4-6 weeks
4. Interferon – (IFN-gamma) produced by lymphocytes is
   critical to activating macrophages
5. Granuloma with central caseous necrosis (tubercles) surrounded by epithelioid macrophages, Langhans giant cells, lymphocytes (eg dendritic cells), neutrophils, foamy macrophages.
6. Development of tubercles called Ghon’s focus.
   Occurs in subpleural airways in the lower part of the upper lung or the upper part of the lower lobes.
7. MTB bacilli drain from the
   Ghon’s focus into the hilar lymph nodes. Ghon’s focus and draining lymph nodes = primary Gohn complex.

Possible host response:
1) Immediate clearance of the organism through mucosal barriers
2) Complete clearance of infection via innate immunity
3) Complete clearance of infection via innate and adaptive immunity: no MTB + immune system remembers the infection
4) Primary infection contained to latent infection
5) Primary (active) disease - immediate symptoms
6) Post-Primary TB (or Secondary TB) - The onset of an active disease years after a period of latent infection.

Question 81

Explain what is meant by the terms primary infection, primary TB, post primary TB

Answer 81

Primary infection - first exposure to MTB.

Primary active TB - immediate onset of active disease in the individual. 5%

Post primary TB - disease in a previously infected host. Can occur due to re-activation of latent infection, re-exposure with weakened host immunity or large inoculum. 5%.
Cavity formation: liquefaction of the caseous material discharged into bronchus results in cavity formation. Fibrous tissue forms around periphery.
Haemorrhage - extension of caseous process into vessels in the cavity →causes haemoptysis
Spread to involve rest of the lung
Pleural Effusion: Seeding of TB bacilli in the pleura can result in this.

Question 82

• Explain what is meant by the terms extra pulmonary TB and Miliary TB.

Answer 82

Extra pulmonary TB - Haematogenous spread of primary TB or reactivation of latent TB in sites other than the lungs. Eg lymph nodes, bones (osteomyelitis), CNS (tuberculous meningitis), GI tract, urinary tract and adrenal glands (addison’s).

Miliary TB - MTB draining through the lymphatic system enter venous blood and circulate back to the lung. Small foci of infection (resembling millet seeds) are visible throughout the lungs.

Question 83

• Explain the difference between Latent TB and Active TB

Answer 83

Latent TB -Primary infection contained to latent infection. dormant bacteria present in body but no symptoms

Active TB - have symptoms

Question 84

• Describe the typical symptoms and signs of respiratory TB

Answer 84

The onset of active TB is gradual over weeks or months.
Tiredness, malaise, weight loss, fever, sweats and cough.
The cough may be dry or productive of mucoid sputum, and haemoptysis may occur.
Crackles may be present. Cavitation, fibrosis or a pleural effusion present.

Question 85

• Describe and recognise the typical findings of pulmonary TB on a chest x-ray

Answer 85

CXR shows pulmonary shadowing,
which may be patchy solid lesions, cavitated solid lesions,
streaky fibrosis with flecks of calcification
hilar adenopathy.

Question 86

• Describe how the diagnosis of Active pulmonary TB is established as opposed to latent TB

Answer 86

ACTIVE lung disease = acid-fast smear and cultures of sputum should be obtained (for drug susceptibility).
May have false -ve skin/IGRA test.

LATENT TB, or screening for TB = IFN-gamma assays (IGRA) or tuberculin skin test.
Positive tests = T cell mediated immunity to mycobacterial antigens
BUT does not differentiate between infection and active disease.

Question 87

• Describe the principles of management of TB /Describe why combination therapy is used in the treatment of TB

Answer 87

TB is treated using a combination of antibiotics over several months.

4 drugs - rifampicin, isoniazid (INAH), pyrazinamide, ethambutol - wild MTB strain has drug resistant organisms arising from mutations. However, the likelihood of such organisms being resistant to all 4 drugs is highly unlikely.

To prevent peripheral nerve damage pyridoxine (vitamin B6) must be given along with INAH.

Question 88

• Describe the role of BCG vaccination

Answer 88

Anti MTB antigens present. Adaptive immunity.
Will be +ve in tuberculin skin test.

Question 89

• List groups at high risk of TB in the UK.

Answer 89

People who have come from countries with a high rate of TB – may be related to immigration, work, tourism

Children of parents whose country of origin has a high rate of TB

People with weakened immune system due to disease or treatment eg HIV

People who are homeless or living in overcrowded conditions

People who are undernourished

People have been in prison
People who are addicted

Question 90

Describe the relationship between TB and HIV infections

Answer 90

HIV = weakened immune system = risk factor for TB

Interferon γ producing CD4-T cells are key components of the immune response against MTB.
HIV infection causes CD4 T-cell depletion = increased susceptibility to TB disease.

Question 91

Describe in broad terms the public health issues
surrounding a case of TB

Question 92

1) asthma definition
, including key differences between asthma and COPD and how to differentiate amongst these conditions and how
management approaches vary between these key respiratory conditions
2) Describe general preventative health measures in asthma, COPD, and bronchiectasis.

Answer 92

Definition: Asthma is a chronic inflammatory disorder of the airways.
Asthma is characterized by a triad of bronchial smooth
muscle contraction, airway inflammation, and increased secretions.
Result in Airflow obstruction and an increase in airway responsiveness.

Question 93

Explore the pathophysiology, of asthma notion

Answer 93

• Genetic susceptibility
• Often associated with atopy
• Sensitisation to an allergen

Macrophages present antigens to T lymphocytes.
Activates Th2 cells (CD4+).
Th2 cells release cytokines, which activate inflammatory cells.
Th2 cells also activate B cells, which produce IgE.

2-phase response:
Immediate response (20 mins)- type 1 hypersensitivity. It is caused by interaction of the
allergen (eg pollen, Fumes,
NSAIDS and beta blockers) & specific IgE antibodies.
Lead to mast cells degranulation and release of mediators (histamine, prostaglandin, leukotriene) which cause
bronchoconstriction.

2. The Late Phase Response - type IV.
   It involves inflammatory cells, eg eosinophils (release Leukotriene C4 and causes shedding of epithelial cells), mast cells, lymphocytes, & neutrophils, which release mediators and cytokines, which cause airway inflammation.

Question 94

9 Effect of airway inflammation on airways

Answer 94

The airway inflammation causes reduced airway calibre due to:

• Mucosal swelling (oedema) due to vascular leak

• Thickening of bronchial walls due to infiltration of by
inflammatory cells

• Mucus over production; the mucus is also abnormal - slow-moving- dry,white sputum cough. Airways can have mucus plugs.

• Smooth muscle contraction

• The epithelium is shed and is incorporated into the
thick mucus

hyper-responsiveness of airways - non- allergic stimuli like cold air & fumes can also trigger attacks.

Long-term asthma can lead to airway remodelling. The irreversible changes include:
• hypertrophy & hyperplasia of smooth muscle,
• hypertrophy of mucus glands
• thickening of the basement membrane.

Question 95

Effect on gas exchange clinical features, investigation, microbiology, and treatment of asthma

Answer 95

Type 1 resp failure due to hyperventilation so dec CO2 and O2.
increasing pCO2 is a sign of life-threatening Asthma - complete blockage of some airways and exhaustion - require mechanical ventilation.

Dec ventilation of the affected alveoli → ventilation / perfusion mismatch in the affected area.

Question 96

Investigate + Treatment

Answer 96

Investigation:

Peak flow and spirometry(shows obstructive pattern)

Treatment:
• Patient education
• Drug treatment using the BTS stepwise approach. Bronchodilators and steroids
• Up to date vaccinations

Exacerbations:
• Oxygen – keep sats 94-98%
• Bronchodilators inhaler - Salbutamol, Ipratropium and anti-inflammatory inhaler (Steroids)
• If severe- Magnesium sulphate IV, Aminophylline IV
• antibiotics

Question 97

Differentiating between asthma and COPD and how management approaches vary - finish

Answer 97

Onset of asthma is typically in early life. COPD older.
A personal or family history of allergy, rhinitis, and eczema is often present. COPD history of smoking.
Symptoms may be episodic with obvious triggering factors. COPD - gradual worsening.
Wheezing and lung function tests responds to bronchodilators. after bronchodilators the airway Obstruction in COPD is not fully reversible.

Both can have Tachypnoea and Use of accessory muscles of respiration

COPD - chronic bronchitis + emphysema so narrowing of airways and destruction of alveoli. There is hyperinflation so barrel chest and signs of right sided heart failure.

Question 98

clinical features

Answer 98

Recurring/variable symptoms
• Wheeze
• Cough
• Chest tightness
• Breathlessness
Dry cough

Atopic features • Eczema, Rhinitis, Nasal polyps

Periods of increased symptoms - exacerbations
Examination:
Tachypnoea
• Tachycardia
• Hypoxia
• Unable to speak full sentences • Accessory muscle use
• Silent chest
• Altered conscious level

Can mimic other conditions:
• Psychosocial factors - Anxiety, panic disorder

• Inducible Laryngeal Obstruction - Abnormal closing of vocal cords

Breathing Pattern Disorder (BPD)

Question 99

Describe general preventative health measures in asthma, COPD, and bronchiectasis.

Answer 99

:

Question 100

• Understand the principles of collection of specimens for
laboratory diagnosis of pneumonias

Question 101

Describe the basic radiological principles used to evaluate
the quality of a chest x-ray

Answer 101

RIPE (for image quality)
Rotation
The medial aspect of each clavicle should be equidistant from the spinous processes
The spinous processes should also be vertically orientated against the vertebral bodies.

Inspiration
5-6 anterior ribs, the lung apices, both costophrenic angles and lateral rib edges should be visible

Projection
AP vs PA film
Tip- if there is no label, then assume it’s a PA. Also, if the scapulae are not projected within the chest, it’s PA.

Exposure
Left hemidiaphragm should be visible to the spine.
vertebrae visible behind heart

Question 102

Describe the basic radiological principles of a chest x-ray
and recognise anatomical landmarks in a normal chest x-
ray.

Answer 102

INTERPRETATION (ABCDE)

Airway
Is the trachea significantly deviated from its normal position? If so is anything pushing or pulling? Pushing eg pleural effusion or tension pneumothorax. Pulling eg consolidation with lobar collapse
Paratracheal
masses / lymphadenopathy
• The trachea is normally located centrally or just slightly
off to the right
Look at Carina and bronchi, Hilar structures

Breathing
Lungs, Pleura

Cardiac
Heart size Heart borders

Diaphragm
Costophrenic angles
Location diaphragm in relation to ribs/chest

Everything else
Bones, Soft tissues
Air beneath the diaphragm Pacemaker, Wires/ Central access devices

Question 103

• Describe pathological changes in a chest x-ray and the
differential diagnoses of such changes
Indications

Answer 103

Shadowing/ opacification in lung field = pneumonia

Evaluating symptoms (cough, chest pain, etc), signs (hypoxemia or pulmonary exam), lines, tubes and pacemakers, effects of treatment

Question 104

• Outline the distribution and composition of the normal
flora of the respiratory tract

Answer 104

Common
Viridans streptococci, Neisseria spp, Anaerobes Candida
Less common
Streptococcus pneumoniae Streptococcus pyogenes Haemophillus influenzae
Other
Pseudomonas, Escherichia coli

Lungs are not sterile
Alveolar microbiota
Aspiration
Blood stream spread
Direct spread

Question 105

• List the main infectious diseases of the lower respiratory
tract and state the organisms commonly causing these
infections
See notion for air fluid level on x-ray

Answer 105

Acute bronchitis: infections causing inflammation in the bronchial airways - virus, smokers, usual symptoms, CXR normal

Bronchiectasis: Bronchiectasis is a permanent dilatation and thickening of the airways associated with chronic cough, sputum production, bacterial colonisation, and recurrent infection

Bronchiolitis: Bronchiolitis is a viral infection of the bronchioles, commonly caused by respiratory syncytial virus and commonly occurs in children younger than 12 months

Empyema: Empyema is a collection of pus in the pleural
cavity, usually with pneumonia but also after thoracic surgery or trauma

Lung Abscess: localised collection of pus within
lung that leads to cavity formation with a thick wall.

Commonly when microbial infection causes necrosis of the lung parenchyma; if they communicate with an airway they may lead to purulent cough.

imaging typically demonstrates the presence of air-fluid levels in the cavity ( air rises above a fluid in a contained space + flat surface at the “air-fluid”
interface).

Question 106

• Define the term ‘pneumonia’; distinguish between acute
‘lobar pneumonia’ and ‘bronchopneumonia’

Answer 106

Pneumonia is a general term denoting inflammation of the lung parenchyma due to infection.
The common feature of pneumonias is a cellular exudate in the alveolar spaces.
localized to a particular lobe/s of the lungs –”lobar pneumonia”
diffuse and patchier –”bronchopneumonia”.

Question 107

• Describe the infectious aetiology of acute community
acquired

Answer 107

Community acquired Pneumonia (CAP)
symptoms and signs consistent with a lower respiratory tract infection. no other explanation for the illness.

commonest causative organism = Streptococcus Pneumoniae - split immunoglobin (IgA)

Others:
• Haemophilus influenzae,
• Moraxella catarrhalis,
Above 2 common with COPD
• group A streptococci,
• Staphylococcus aureus.

Atypical:
• Mycoplasma pneumoniae (commonest, lacks a peptidoglycan bacterial cell wall)-shear off cilia
• Chlamydia pneumoniae (obligate intracellular pathogen) - ciliostatic factor
• Legionella pneumophila (intracellular pathogen) - contaminated water sources

Question 108

Nosocomial Pneumonia

Answer 108

Hospital acquired pneumonia:
occurring > 48 hours after admission and was not incubating at the time of admission.
Causative organisms include aerobic gram-negative bacilli, such as:
• Pseudomonas aeruginosa,
• Escherichia coli,
• Klebsiella pneumoniae,
• Acinetobacter species
Gram-positive bacteria = Staph aureus(MRSA)

Patients with poor immune response are susceptible to a range of organisms, such as Pneumocystis jiroveci, Aspergillus, Cytomegalovirus.

Question 109

• Describe the symptoms and signs of pneumonia
Investigation
Complications
Pathology
Prevention

Answer 109

cough with mucopurulent sputum, dyspnoea, pleuritic chest pain, myalgia

Signs in community - Crackles, Decreased breath sounds, Dullness to percussion, Wheeze, Increased vocal resonance over area consolidation, Tachypnoea, Fever

Chest x-ray - shadowing in lung field.
in patients at risk for malignancy - obtain an initial chest x- ray. Then, request a repeat chest x-ray during recovery for patients with persisting symptoms or higher risk of underlying malignancy (smokers, ex-smokers, age >50 years).
Microbiology: Gram stain and culture of sputum, blood culture, nose and throat swabs for viral PCR, urine antigen test for strep p and legionella).
FBC, U & E, CRP, ABG

Complications of pneumonia include: • Pleural effusion, Empyema, Lung abscess formation.

Pathology:
Acute inflammatory response
Exudation of fibrin rich fluid - consolidation on CXR
Neutrophil and macrophage infiltration

Prevention - vaccine, chemoprophylaxis

Question 110

• List the aetiological clues for the common respiratory tract
pathogens;

Answer 110

Persistent dry cough that does not resolve with time = atypical pneumonia caused by Mycoplasma pneumoniae or Chlamydophila pneumoniae

Pneumonias may be of very rapid onset, particularly if pneumococcal or staphylococcal

Question 111

• Understand the spectrum of clinical features of acute
community acquired and acute hospital acquired
pneumonias and how to assess severity

Answer 111

Assessing severity of pneumonia in hospital setting:
CURB 65 score - presence of 2 or more of the features is an indication for hospital treatment.
C – New mental confusion
U – Urea > 7 mmol/L
R – Respiratory rate > 30 per minute
B – blood pressure (SBP < 90 or DBP <60) Age > 65 years

In community to decide whether to hospitalize:
C – New mental confusion
(no U)
R – Respiratory rate > 30 per minute
B – blood pressure, Age > 65 years

Question 112

• Understand and be able to describe the differences
between typical and atypical community acquired
pneumonia with regards to presentation and
management.

Answer 112

Presentation Atypical - more prolonged prodromal period with symptoms lasting for several weeks.
Factors to consider to find organism = age, community or hospital, chronic lung disease, smoking, immunosuppression, pet.

Management for both:
General measures: maintain good oral fluid intake to avoid dehydration.
Anti-pyretic drugs (e.g. paracetamol) with analgesics for pleural pain.
More severe illness may require intravenous fluids and oxygen.

Treatment:
community-acquired - target is Pneumococcus which is usually sensitive to Amoxycillin.

Atypical - do not respond to ‘cell wall antibiotics’. So antibiotics that act on protein synthesis such as macrolides (erythromycin/clarithromycin/azithromycin) or tetracyclines (doxycycline).

hospital acquired pneumonia - gram negative so e.g. IV Co-Amoxiclav.

Question 113

• Outline the natural defences of the respiratory tract
against infection

Course of infection

Answer 113

mucins lining the surface of the airways trap micro-organisms that are then cleared by ciliary
movement, up respiratory tract; expelled as cough or swallowed- mucociliary escalator.
ciliated epithelial cells and mucus-secreting goblet cells.

Secretory IgA

surfactant has some anti-microbial activity

alveolar macrophages -
neutrophils migrate out of capillaries into the airspaces and phagocytose.

Lymphoid follicles of the pharynx and tonsils,

Lungs infection
1. alveolar macrophage fails to stop the pathogen
2. cytokines recruit more macrophages
3. inflammation = increased permeability
4. more neutrophils/lymphocytes/antibodies to aid macrophages

• Outside the lungs
1. cytokines/chemokines
into systemic circulation
2. activates bone
marrow /more cardiac output /raised body temp
3. dysregulation - signs of tissue injury/organ injury caused by pathogen, Host factors, Drugs

Question 114

Aspiration Pneumonia

Answer 114

Aspiration of food, drink etc can lead to pneumonia.
due to anaesthesia
alcohol or drug abuse
swallowing-related problems due to neuromuscular or oesophageal disease or after a CVA with loss of the gag reflex.

Causative organisms include oral flora & anaerobes, though in-hospital aspiration increases risk for pseudomonas aeruginosa infection.

Common with neurological dysphagia - epilepsy, alcoholics etc

Co-amoxiclav

Question 115

explain how simple spirometry is carried out

Answer 115

nose clip is worn so that
breathing is through the mouth

sterile mouthpiece attached to the spirometer is used for
breathing.

With the mouth forming a tight seal around the
mouthpiece, the patient is instructed to perform various
breathing manoeuvres by inhaling and exhaling.

few cycles of quiet inspiration and expiration. Then forced vital capacity is performed. Involves taking a maximal inspiration followed by breathing out as hard and fast as possible.

Question 116

• Explain and demonstrate to a patient how to use a peak
flow meter

Answer 116

Peak Flow Meters (in L/s) - measures the highest velocity of airflow that can be achieved during forced expiration

Normal: ≥ 80% of the predicted average value based on:
height, gender & age, ethnic group.

Baseline determined when patient is asymptomatic

Useful in monitoring people with asthma

Question 117

• Recognise Diffusing Capacity for Carbon Monoxide (DLCO) test and significance of an abnormal DLCO

Answer 117

Diffusing Capacity Carbon Monoxide
Test lets us determines how much oxygen travels from alveoli of lungs to bloodstream by measuring CO diffusion
Provides information on alveolar-capillary membrane
Can be decreased in Emphysema, Pulmonary fibrosis, idiopathic pulmonary arterial hypertension, chronic thrombo-embolic disease of lung

Question 118

Describe the measurement of

Forced Vital Capacity
Forced expiratory volume in the first second (FEV1.0)
FEV1/FVC ratio.

Answer 118

Forced expiratory volume in 1 second (FEV1): maximum volume of air can be forcefully expired within 1 second after maximal inspiration

Forced vital capacity (FVC): total amount of air exhaled after maximal inspiration during entire FEV test – occurs over 6 seconds

FEV1/FVC: represents proportion of patient’s forced vital capacity that they can expire in first second of forced expiration

Question 119

• Describe and explain the FVC, FEV1, and FEV1/FVC ratio
findings in obstructive and restrictive disease.
Notion for time- volume graphs

Answer 119

Obstructive defect:
During expiration (esp forced) the small airways are compressed, increasing flow resistance, until no more air can be driven out of the alveoli.

If airways are narrowed then expiratory flow is compromised EARLIER in expiration - ‘obstructive’ deficit.
Eg COPD, bronchiectasis, asthma

This means FEV1 will be reduced markedly
FVC is nearly normal though may
decrease as disease progresses if there is air trapping.
FEV1/FVC ratio is <0.7

Restrictive defect:
Total lung capacity is reduced - defined by this
FVC is reduced
FEV1 is reduced proportionately FEV1/FVC ratio is normal or higher (due to reduced compliance)
Eg diffuse lung fibrosis, muscle weakness dec inspiratory
effort

Question 120

• Explain the volume-time graph and the characteristic
changes seen in obstructive and restrictive disease

Purpose of PFTs

Answer 120

Volume of air moved as a function of time - Volume-time plot
Rate of airflow as a function of volume of air in lungs – Flow-volume loop

Measures:
Lung volumes
Rate of airflow
Gas exchange (alveolar/vascular membrane)
• Diagnose patients with respiratory symptoms
• Establish severity and progression of lung disease
• Assess treatment response
• Monitor patients on meds with lung toxicity

Question 121

• Explain expiratory and inspiratory flow volume loops and the changes seen in obstructive and restrictive disease

Answer 121

expiratory flow rate is plotted against lung volume.
Obstructive:
Start of expiration lungs are expanded and airways are open - expiratory flow is max - Peak Expiratory Flow Rate (PEFR)

When small airways are narrowed there is early fall in expiratory flow rate so dec PEFR and SCALLOPING of curve (this is main consequence- more severe means more scalloping, not dec PEFR).

Restrictive:
Reduction in FVC and TLC so narrow flow volume loop
PEFR is not significantly reduced as there is no airways obstruction.
Narrow & tall flow volume loop.

Question 122

• Describe and interpret different values obtained from PFTs

Answer 122

Restrictive:
Reduced TLC
Normal or Reduced FEV1
Reduced FVC
Ratio FEV1:FVC normal

Parenchymal lung diseases - restrictive pattern on spirometry AND abnormal DLCO eg pulmonary fibrosis
Lung diseases related to abnormalities in chest wall – restrictive pattern on spirometry, normal DLCO, abnormal CXR eg kyphoscoliosis
Lung disease related to neuromuscular disease – restrictive pattern on spirometry, normal DLCO eg myasthenia gravis

Pulmonary hypertension – normal spirometry, normal CXR, but abnormal DLCO

Obstructive:
– Reduced FEV1
– FEV1:FVC ratio <0.7
– In late/severe COPD FVC also falls – but still less than the fall in FEV1
– Asthma reversible + response to bronchodilator; COPD not

Question 123

Incidence of lung cancer

Answer 123

leading cause of cancer-related deaths worldwide. Lung cancer is the commonest male cancer
2nd most common in women

Question 124

Aeteological factors

Answer 124

Around 90% of lung cancers in men and 80% in women are caused by smoking. Other
aetiological factors include exposure to asbestos and radon. Genetic and dietary factors also influence individual susceptibility.

Question 125

Symptoms

Answer 125

Primary tumour:
Cough: 3-week cough
Dyspnoea - central tumours may occlude airways resulting in lung collapse. pleural effusions may also present with dyspnoea.
Haemoptysis: occurs typically because of tumour erosion into an airway.
Wheeze: may occur secondary to partial airway obstruction caused by a lung tumour.
• Weight Loss
• Lethargy/Malaise

Regional metastases
Hoarse voice: mediastinal nodal or tumour invasion resulting in compression of the recurrent laryngeal nerve (RLN), left RLN more often.
• Chest / shoulder pain - parietal pleural involvement
Dysphagia (oesophageal compression)
Bloated face (SVC obstruction)

Distant metastases
• Bone pain/fractures
• CNS symptoms (headache,
double vision, confusion etc.)

Metabolic
• Thirst (hypercalcaemia)
• Constipation (hypercalcaemia)
• Seizures (hyponatraemia– SIADH, small cell)

Question 126

Signs

Answer 126

SVC Obstruction: dyspnoea and/or difficulty swallowing, stridor and a swollen and oedematous face, plethora, neck venous congestion and dilated veins on the upper chest and arms.
Caused by tumour or enlarged lymph nodes compressing or invading the SVC. Medical emergency.

Brachial plexus nerve and/or sympathetic nerve chain compression: Pancoast tumours – tumours occurring in the lung apex (superior sulcus) of the lung- may invade the brachial plexus causing C8/T1 palsy with small muscle wasting in the hand and weakness, as well as pain radiating down the arm.
If the sympathetic chain is also compressed then an ipsilateral Horner’s syndrome may occur( miosis, ptosis and anhidrosis).

Recurrent lung infections: related to partial airway obstruction and resultant post-obstructive pneumonias – post-pneumonia chest X-ray in high-risk patients.

Cachexia
• Pale conjunctiva
• Cervical lymphadenopathy
• Liver enlargement
• Skin metastases

Question 127

parneoplastic syndrome

Answer 127

Paraneoplastic Syndromes:
Arise from secretion of functional peptides or hormones from the tumour, or inappropriate immune cross-reaction between host cells and tumour cells.

Humoural hypercalcaemia by squamous cell carcinoma of the lung - PTH-related protein (secreted from tumour) or Ectopic PTH production.
Or
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) by small cell lung cancer. Also can cause Cushing’s syndrome.

Paraneoplastic neurological syndromes: lung cancer associated myasthenic syndrome.

Haematological
- Anaemia
- Thrombocytosis

Question 128

Describe the histological types and classification of common
lung tumours

Answer 128

Histology - divided broadly into non-small cell lung cancer (more common) or small cell lung cancer.

For NSCLC, adenocarcinomas + squamous-cell carcinomas are most common.

Question 129

Describe in outline the behaviour of different histological
types and their relationship to prognosis and treatment

Describe in outline the different treatments available and how
they may affect survival

Answer 129

Treatments include surgery, chemotherapy, radiotherapy, and palliative therapy.

Prognosis 5-year survival for patients with stage I NSCLC is roughly 80%, and patients with stage II to stage III disease have a 5-year survival of 13–60%.

The standard of care for patients with stage I, stage II, and some stage IIIA NSCLC disease is surgical resection.

Question 130

Understand the imaging techniques used in the diagnosis and
staging of the disease

Answer 130

All
Chest Xray
Staging chest CT

Some:
PET-CT
Head CT
Pelvic CT
MRI -various Bone Scan Ultrasound

Question 131

Describe the common methods used to obtain material for
histological diagnosis

Answer 131

Tissue for diagnostic purposes is usually obtained by bronchoscopy and needle biopsy of the lung or pleura.

• Cervical lymph node fine needle aspiration (FNA)
• Can do biopsy of various structures such as Adrenal, • Skin • Bone • Brain • Lymph nodes

Question 132

Causes of cough

Answer 132

irritation of cough receptors. vagus nerve to medulla. efferent signal down vagus, phrenic, and spinal motor nerves to musculature.
deep breath in, closure of the glottis, inc intra-thoracic pressure. Glottis suddenly opens, so excursion of air. Muscles of expiration are required.

duration:
Acute – less than 3 weeks
Sub-acute - cough persisting for 3-8 weeks
Chronic- more than 8 weeks

Productive, where and when it occurs.

Most common cause = URTI - maybe has sputum, is tired and has fever. Pain and discharge localised to ENT or sinus.

Acute:
Covid
Acute bronchitis - with wheeze
Pneumonia
Pneumothorax- sudden pleuritic pain
PE

Sub-acute:
Post-infectious

Chronic:
Upper airway cough syndrome
ACEi cough
Asthma
GORD

Question 133

Dyspnoea

Answer 133

COPD - History: progressive dyspnoea. Pursed lip breathing, prolonged exhalation.
Asthma - episodic wheezing,
prolonged expiratory phase.
attack may include: severe
breathlessness.
Investigations: peak expiratory flow rate (PEFR): may be reduced; FEV1/FVC ratio dec

Pneumonia
o Exam: crackles
asymmetric chest expansion, bronchial breathing for consolidation signs
focal dec breath sounds, increased vocal resonance for signs of effusion

Pulmonary embolism
o History: sudden-onset dyspnoea and chest pain;
o Exam: tachypnoea

• Pleural effusion
o Exam: asymmetrical chest expansion, decreased tactile fremitus, decreased vocal resonance and absent breath
sounds

Pulmonary tumours
o History: hoarseness;
o Exam: may be unilateral wheeze and decreased breath sounds in large airway lesions.
crackles and rhonchi may be present in post-obstructive pneumonia.

• Bronchiectasis
o Exam: prolonged expiratory phase, crackles,
rhonchi, and wheeze
o Investigation: pulmonary function tests: obstructive ventilatory deficit”

Question 134

Chest pain, Sputum
production, Haemoptysis, Wheeze

Question 135

• Define the terms: simple pneumothorax, tension
pneumothorax, primary pneumothorax, secondary
pneumothorax, spontaneous pneumothorax, iatrogenic
pneumothorax

Answer 135

Pneumothorax is the presence of air in the pleural space -pleura has a hole - air moves down pressure gradient. Pleural seal is broken and lungs collapse due to inward elastic recoil.

Simple • Not expanding pneumothorax • Air goes in and out

Primary spontaneous pneumothorax - most commonly in young, tall, thin males with no predisposing lung disease or history of trauma.
Rupture of an underlying sub pleural bleb (small air- containing spaces) or bulla (permanent, air-filled space at least 1 cm in size) is thought to be responsible.
Risk factor - smoking

Secondary spontaneous pneumothorax occurs
secondary to an underlying lung problem e.g., COPD or Asthma.

Iatrogenic - caused by invasive medical procedures
e.g. - central vein cannulation

Tension pneumothorax - any pneumothorax causing mediastinal shift and cardiovascular collapse.

Question 136

• Explain the pathophysiology, symptoms and signs of a
pneumothorax

• Explain how a tension pneumothorax is produced

Answer 136

Tension:
Air can enter pleural cavity during inspiration but cannot leave during expiration.
Inc in intrapleural pressure.
Cause the mediastinum to shift and compress other lung + cardiac venous return.
Veins of the body rely on the low intrathoracic pressure to return blood to the heart. Dec preload.
impaired gas exchange (from the loss of lung volume).
reduced cardiac output results in the hypoxaemia and haemodynamic compromise.
Tachycardia to inc CO.
Also, tachypnoea, tracheal shift, elevated JVP, and hypotension for tension.

• History:
sudden onset of pleuritic stabbing chest pain and dyspnea. Worse on breathing deeply. One side.
• Examination:
on the affected side, chest movement are reduced, percussion is hyper resonant and breath sounds are reduced in intensity. Vocal resonance is also reduced.

Question 137

Describe and the radiological findings of a simple
pneumothorax

• Describe clinical features and radiological features which
suggest a tension pneumothorax

Answer 137

Loss of lung markings. Pleura moved away from lungs.

Question 138

• Describe principles of treatment of a pneumothorax,
including the placement of an intercostal tube and why
an underwater seal is used.

• Describe an emergency treatment of a tension
pneumothorax including the site of insertion of an
emergency chest drain

Answer 138

Investigations:
Obs
ECG
FBC
CXR

If air is in the pleural space that should not be there Let it out by:
▪ Needle aspiration -2nd intercostal space, mid clavicular
▪ Intercostal chest drain

Where do chest drains go in?
▪ THE TRIANGLE OF SAFETY - lateral borders of pec major, lattismus dorsi and 5th intercostal space, mid-axillary

Reduced chance of damage
Above the rib
How do we prevent air entering the drain? - Water Seal, Hickman Valve

Question 139

• Define ‘pleural effusion’ and explain the terms
haemothorax, chylothorax, empyema and a simple
effusion.

Answer 139

Pleural fluid is secreted by the parietal pleural and drained through the lymphatics of the parietal pleura.
maintained via a balance of hydrostatic and oncotic pressures and lymphatic drainage.
keeps the visceral and parietal pleura connected, lubricant.
may result from disruption of the balance between hydrostatic and oncotic pressures, or disrupted lymphatic drainage.
collection of extra fluid in the pleural space = pleural effusion.
If blood = haemothorax;
if chyle (from the lymphatic system) = chylothorax
if pus = empyema.

Question 140

• Explain the difference between a pleural effusion which is
an exudate and one which is transudate, and know the
causes of each type of pleural effusion

Answer 140

Simple effusion categorised on protein content

Transudates – have a low protein content
Causes
1. Due to increased pleural capillary hydrostatic pressure –
Congestive cardiac failure
2. Due to decreased capillary oncotic pressure- low serum
albumin levels – cirrhosis; nephrotic syndrome

Exudates - have a high protein content

Due to increased capillary permeability (e.g., inflammation, malignancy)
1. Bronchial Carcinoma
2. Pneumonia
associated with three types of pleural effusion:
Simple parapneumonic effusion→complicated parapneumonic effusion→empyema
3. Tuberculosis
4. Pulmonary infarction from pulmonary embolism
5. Metastases (most common) – Cancers that very commonly metastasise to the lung include bladder, colon, breast, prostate, germ cell tumours and head and neck squamous carcinomas.
require drainage by therapeutic pleural aspiration or intercostal chest tube drainage.