Respiratory Flashcards
(531 cards)
1
Q
What does the respiratory system develop from?
A
The diverticulum of the pharynx - outgrowth of the embryonic pharynx, which bifurcates multiple times.
2
Q
What is the conducting part of the airways?
A
Trachea, primary (main) bronchi, secondary (lobar) bronchi, tertiary (segmental) bronchi, bronchioles and terminal bronchioles.
3
Q
What is the respiratory part of the airway?
A
The alveolar bronchioles and alveoli.
4
Q
What are the borders of the thorax?
A
Anteriorly - the costal cartilages and sternum.
Laterally - ribs.
Posteriorly - vertebral column.
Inferiorly - diaphragm.
5
Q
How are the ribs shaped and articulate with the vertebral column, and how does this correlate to the movement formed?
A
They are wedge-shaped, with their superior and inferior facts articulating with two vertebra to facilitate rotational movements.
6
Q
What two specific movements can the thoracic wall perform?
A
Lateral movement - bucket handle movement.
Anterior, elevation movement - pump-handle movement.
7
Q
How far can the diaphragm move during expiration, from flat?
A
It can elevate 2 intercostal spaces in distance.
8
Q
What is the origin of the diaphragm and what does it converge to form?
A
Originates from the rib cage and costal cartilages to form a central tendon.
9
Q
What are the 3 layers of the intercostal muscles, and what movements do each of them cause? State the direction of their fibres.
A
External intercostal - passive inspiration, inferomedial direction.
Internal intercostal - forced expiration, superomedial direction.
Innermost intercostal - forced expiration, superomedial direction.
10
Q
What are the 3 perforations of the diaphragm and at what level do they pass through?
A
Vena cava - T8.
Oesophagus - T10.
Aortic hiatus - T12.
11
Q
What are the accessory muscles of inspiration?
A
Pectoralis major, sternocleidomastoid, scalenes, and serratus anterior.
12
Q
What are the intercostal neurovascular bundle, and what happens to them?
A
The intercostal vein - drains into the azygous system.
The intercostal arteries - formed from the aorta.
The intercostal nerves - at the level of each of the spinal nerves.
13
Q
What is the azygous system supported by, what does it drain into, and what is its importance in a critical situation?
A
It is supported by the hemi-zygous and accessory hemi-zygous veins.
It drains into the superior vena cava.
If the superior vena cava becomes blocked then the zygous system can save this.
14
Q
What is the diaphragms innervation, and why can it have referred pain?
A
It is innervated by the phrenic nerves, which is supplied by C3, 4 and 5.
This means that pain can be felt in the dermatome of C3, 4 and 5.
15
Q
What are the lobes and fissures of the lungs?
A
The right lung has the superior, middle and inferior lobes - the superior and middle lobes are separated by the horizontal fissure, with the upper and middle lobes being separated from the inferior lobe by the oblique fissure.
The left lung has a superior and inferior lobe, which is separated by the oblique fissure.
16
Q
What is the relevance of the fissures?
A
Pleural fluid accumulation can occur in them.
17
Q
What is the difference between the two main bronchi, relating to potential pathology?
A
The right main bronchi is more vertical, meaning that foreign bodies entering the lungs will be more likely to enter this.
18
Q
What is the hilum of the lung and what are the contents locations?
A
The bronchus is posterior.
The branches of the pulmonary arteries are supero-medial.
The branches of the pulmonary veins are inferior.
19
Q
What is the difference between the left and right bronchus?
A
The right bronchus has a branch that supplies the superior lobe and one that supplies the middle and inferior lobes.
20
Q
What is the costodiaphragmatic/ costophrenic recess, and what is it called when fluid enters this?
A
It is the space inferior to the lungs that the lungs expand into.
When fluid enters it, it is called pleural effusion.
21
Q
What is the difference between the sizes of the left and right lungs, and what effect does this have on the diaphragms position?
A
The right lung bigger and heavier, and is shorter and wider, meaning that the right dome of the diaphragm sits higher.
22
Q
Where does the parietal and visceral pleura meet, and what does this form?
A
They meet at the hilum, forming the pulmonary ligament to the mediastinum.
23
Q
Explain the tracheobrachial tree.
A
The trachea splits into the primary bronchi at the sternal angle.
The primary bronchi split into the secondary lobar bronchi, of which there are 3 on the right and 2 on the left.
The secondary lobar bronchi split into tertiary bronchi which supply the brachiopulmonary segments.
The tertiary bronchi split into bronchioles, which further split into terminal and then alveolar bronchioles.
The alveolar bronchioles split into alveolar sacs, which contain alveoli.
24
Q
Explain the pulmonary supply to the lungs.
A
The pulmonary trunk splits into the pulmonary arteries at the sternal angle.
The pulmonary arteries split into secondary lobar arteries, and then into intermediate arteries.
These split into middle and inferior lobar arteries, and then into tertiary segmental arteries.
25
Describe the bronchial circulation and is function.
There are two left bronchial arteries and one right bronchial artery, which supply the tissues of the lung and visceral pleura.
26
What are the 3 nervous supplies to the lungs?
Sympathetic - post-synaptic neurons.
Parasympathetic - from the vagus nerve.
Visceral afferent fibres.
27
What is the function of the sympathetic innervation of the lungs?
Bronchodilation, vasoconstriction and decreased glandular secretion.
28
What is the function of the parasympathetic innervation to the lungs?
Bronchoconstriction, vasodilation and increased glandular secretions.
29
What are the two different types of visceral afferent fibres and what does they travel with?
Reflective - travel with parasympathetic fibres.
Nocioceptive - travel with sympathetic fibres.
30
What two different nervous supplies does the parietal pleura have?
Phrenic nerves.
Intercostal nerves (pain).
31
What is the neural control of ventilation?
Neurons in the respiratory centres of the brain, specifically the medulla.
32
How does the oxygen and carbon dioxide partial pressure, and pH affect respiration?
Chemoreceptors in the brain stem and periphery sense the levels of them.
If there is low oxygen, this is sensed by the peripheral chemoreceptors.
If there is high carbon dioxide or a low pH, this is sensed by the brain stem chemoreceptors.
The respiratory centres are then stimulated to increase the depth and rate of breathing.
33
What is the tidal volume, inspiratory reserve volume, expiratory reserve volume, and residual volume?
TV - quiet breathing, the volume of air that enters and leaves the lungs with each breath.
IRV - the volume of air forcefully inhaled.
ERV - the volume of air forcefully exhaled.
RV - the volume of air that cannot be exhaled.
34
What is the inspiratory capacity, vital capacity, functional residual capacity and total lung capacity?
IC - tidal volume + inspiratory reserve volume.
Vital capacity - tidal volume + inspiratory reserve volume + expiratory reserve volume.
FRC - expiratory reserve volume + residual volume.
TLC - tidal volume + inspiratory reserve volume + expiratory reserve volume + residual volume.
35
What is anatomical, alveolar and physiological dead space?
Anatomical dead space is the volume of air in the conducting section of the respiratory tract, that does not take place in gas exchange.
Alveolar dead space is the volume of air in the alveoli that gas exchange does not occur in, due to damage or lack of perfusion.
Physiological dead space = anatomical dead space + alveolar dead space.
36
What is total pulmonary ventilation and alveolar ventilation?
Pulmonary ventilation is the normal volume of air that enters the lungs per minute - tidal volume x respiratory rate.
Alveolar ventilation is the volume of air that enters gas exchange per minute - (tidal volume - dead space) x respiratory rate.
37
What is the resting expiratory level?
This occurs at rest, at the end of expiration, where the lungs elastic recoil and surface tension is equal to the elastic recoil of the rib cage - due to the muscles and tissues.
38
What is ventilation?
The volume of air that enters and leaves the lungs.
39
What does Boyle’s law state, in relation to the lungs?
If volume increases in the lungs, then the pressure exerted by a gas will decrease and air will flow into the lungs.
40
How does Boyle’s law explain the respiratory cycle?
As the pleural seal ensures that the lungs follow the rib cage, when the diaphragm contracts, the volume in the lungs increases. This decreases the pressure in the lungs, causing the air to flow in.
Due to the elastic recoil of the lungs and the surface tension in the alveoli, the lungs collapse back to their original position, decreasing the volume of the lungs. This increases the intrapulmonary pressure, causing the air to flow out.
41
What does the parietal and visceral pleura adhere to?
Parietal is to the hemi-thorax - thoracic cage, diaphragm and mediastinal surfaces.
Visceral pleura - the outside of the lungs.
42
What is the pleural seal?
The small volume of fluid between the parietal and visceral pleura has a high surface tension. This means that the intra-pleural pressure is negative compared to the lungs and atmosphere, leading to the lungs moving with the chest wall.
43
What is the trans pulmonary pressure?
The intrapulmonary pressure - pleural pressure.
44
What is compliance?
The distensibility of the lungs - the change in volume / the change in pressure.
45
What is surfactant, what is it secreted by and what is its job in respiration?
It is a mixture of phospholipids and proteins with the hydrophilic heads projecting into the alveolar fluid and the hydrophobic parts projecting into the alveolar gas.
It is secreted by type II pneumocytes.
In respiration, the surfactant comes between the alveolar fluid, decreasing the surface tension.
46
What are the benefits of having surfactant?
Surfactant reduces surface tension more as the alveolar shrink as the surfactant is more closely packed together.
This means that the pressure within the small and large alveoli are equal, preventing the small alveoli from collapsing.
It also prevents surface tension in the alveoli from creating a suction, pulling transudation in from the capillaries.
47
When is surfactant synthesised?
It begins to be synthesised from week 24-26.
48
Which part of the lungs has the greatest resistance, and why?
The upper respiratory tract, as the lower respiratory tract has branching to increase the surface area.
49
What are interstitial lung diseases?
Thickening of the alveolar septa, fibroblast proliferation and collagen deposition.
50
What is the end result of interstitial lung disease?
Pulmonary fibrosis.
51
What is the pathophysiology of interstitial lung disease?
Due to collagen being an elastic fibre that is laid down by the fibroblasts, the elastic recoil of the lung increases.
The compliance of the lung will decrease due to increased deposition of collagen fibres, which are less elastic than elastin fibres.
Due to the increased elastic recoil, the lungs are smaller, with chest expansions reduced, and all of the lung volumes are decreased.
It is a restrictive lung disease.
52
Outline the different types of interstitial lung diseases.
53
How does interstitial lung diseases effect gas exchange?
The thickening of the alveolar walls means that it is harder for gases to diffuse across.
54
What are the signs and symptoms of interstitial lung diseases?
Signs - tachypnoea, tachycardia, reduced chest movement, ‘Velcro crackles’.
Symptoms - breathlessness, decreased exercise tolerance, malaise and fatigue.
55
What is respiratory distress syndrome?
This is where premature babies are unable to produce sufficient surfactant, meaning that the surface tension is high, making it difficult to expand the lungs and alveoli, with some of the alveoli remaining collapsed.
56
What are the signs and treatment for babies with respiratory distress syndrome?
Signs - cyanotic, grunting, intercostal and subcostal recession (looks like gaps due to contraction of the muscles).
Treatment - supportive is to give oxygen and assisted ventilation, with specific being to give surfactant using an endotracheal tube.
57
What is emphysema?
This is where elastases break down the elastin in the lungs, increasing compliance and decreasing elastic recoil, leading to narrow airways.
58
Why are the arterioles in emphysema narrowed?
This is because there is decreased elastin fibres so there is less outward pull on the alveoli - the radial traction is decreased. Alveoli effectively tether the bronchioles open.
In addition, due to the decreased elastic recoil, there is a decrease in intrapulmonary pressure, meaning there is less force exerted on the inside of the arteriole.
59
What can be seen on X-ray and examination of an emphysematous patient?
On X-ray hyperinflation can be seen. On a lateral X-ray there can also be an increased antero-posterior width seen.
On examination, there is a barrel chest appearance.
60
What are two causes of emphysema?
Alpha-1 antitrypsin deficiency.
Smoking - emphysematous COPD.
61
What type of ventilatory defect is emphysema, and what effect will this have on the lung function tests?
It is an obstructive ventilatory defect.
The expiratory reserve volume and tidal volume will decrease.
However, the inspiratory reserve volume and the residual volume will increase.
Total lung capacity and vital capacity will be increased.
62
What are the symptoms of emphysema patients?
Shortness of breath, reduced exercise tolerance and cough.
63
What is the pathophysiology of asthma, and when is airflow most impeded?
It is a chronic inflammatory process, with (non-)allergic triggers.
There is bronchoconstriction, excess mucous production and thickening of the airway walls due to mucosal oedema.
The decreased lumen size means that the airflow is most impeded during expiration (does not dilate like in inspiration).
64
What is pneumothorax?
A disorder where air enters the pleural space, decreasing the pleural pressure, leading to the lungs no longer being adherent to the chest wall.
65
What is atelectasis?
Incomplete expansion of the lungs, producing areas of airless pulmonary parenchyma.
66
Explain the two types of atelectasis.
Compression - increased pressure exerted on the lung, leading to alveolar collapse.
Resorption - complete obstruction of an airway, leading to the alveoli being resorbed.
67
What are risks and complications of post-operative atelectasis?
Risks are obesity, age, chest or abdominal surgery, pain leading to shallow breaths, and underlying lung diseases.
Complications are an increased risk of hypoxia and pulmonary infections.
68
What is hypoventilation?
Poor expansion of the thoracic cavity or lungs, leading to hypercapnia.
69
What can inhalation of food molecules lead to?
Airway obstruction.
Infection - aspiration pneumonia.
70
What is the glottis?
The vocal cords and aperture (hole) between the cords - laryngeal inlet.
71
How do the vocal cords become adducted, and what nerve innervates this?
Intrinsic laryngeal muscles, innervated by the recurrent laryngeal nerve.
72
What is the concave aspect of the manubrium called?
Jugular notch.
73
What do the intercostal neurovascular bundle supply?
Intercostal muscles, parietal pleura and overlying skin.
74
What do the peripheral muscle fibres of the diaphragm arise from?
Inner aspects of the 7-12 costal cartilages.
Arcuate ligaments.
Crura of the diaphragm.
Xiphoid process.
75
Why does the right dome of the diaphragm lie slightly higher, and where do each of the domes lie?
The right is slightly higher due to the liver.
Right - 5th rib.
Left - 5th intercostal space.
76
What abdominal organs are protected by the ribs?
Liver, spleen, stomach and upper kidneys.
77
What is the hemi-thorax made up of?
Thoracic rib cage, diaphragm and mediastinal surfaces.
78
What is the angle between the left and right main bronchi called?
Carina - the distal aspect of the trachea.
79
What can bronchoscopy be used for?
Visualisation of lung tumours.
Obtaining samples of tissue for histological interpretation.
Removing foreign bodies.
Obtaining lung secretions for identification of infective organism.
80
What are alveolar ducts and alveolar sacs?
Alveolar ducts are structures that are completely lined with alveoli budding off.
Alveolar sacs are air spaces in which many alveoli open.
81
What nerve fibres are involved in the stimulation of the cough reflex?
The vagal afferent fibres.
82
What is the surface marking for the horizontal fissure?
The 4th rib, starting at the 4th costochondral junction.
83
How much further down does the pleural cavity extend from the lungs?
2 ribs lower.
84
What nerves can be compressed by enlarged hilar lymph nodes?
Phrenic nerve.
Recurrent laryngeal nerve.
85
What are the terms for blood and lymphatic fluid accumulation within the pleural space?
Blood = haemothroax.
Lymphatic fluid = chlyothorax.
86
Where does fluid accumulate when standing up, in pleural effusion, and what is seen on X-ray?
Costo-diaphragmatic space.
This shows a blunting of the costo-phrenic angle.
87
What are type 1 pneumocytes connected to each other by?
Tight junctions.
88
Where are the tracheal glands and bronchial glands located, and what is the difference between the two?
They are both located in the submucosa.
In the trachea, the glands are distinct from the epithelium, whereas in the bronchi, they are formed from the invagination of the epithelium.
89
What are the secretions from the trachea and bronchi?
Mucin and water, forming mucous.
IgA.
Antiproteases.
Lysozyme.
Serum proteins.
90
How are bronchioles kept open?
They have elastic muscle fibres within the walls.
The alveoli surround the bronchioles, tethering them open - radial traction.
91
Where are Clara cells found in the respiratory tract, and what do they secrete?
They are found in the terminal bronchioles and alveoli.
They secrete lipoprotein factors that make up surfactant.
92
What is the alveolar interstitium formed of?
Predominantly elastin fibres with some collagen fibres.
93
What is the distance between the alveoli and its capillary?
0.2 um.
94
Outline the positioning of the structures entering the hilum of the lung.
The pulmonary arteries form the anterosuperior aspect of the hilum.
The pulmonary veins are located anteroinferior to the arteries.
The main bronchus enters posteriorly.
95
What is a lung bleb, and what can it lead to?
A collection of air (<1cm) between the lung and the visceral pleura.
Should it rupture, it will lead to a pneumothorax, and the lung collapsing away from the chest wall.
96
Between which layers of the intercostals are is the neurovascular bundle located?
Between the inner and innermost intercostal muscles.
97
What proportion of the inspired air in tidal volume reached the alveoli?
2/3rds.
98
What accounts for the decrease in partial pressure of oxygen from the nose and mouth, to the trachea?
Humidification - the addition of water to the air breathed in.
Some of this water at 37 degrees Celsius vaporises. This then exerts a pressure - saturated vapour pressure - decreasing the partial pressure of oxygen.
99
What is the partial pressure of oxygen in the alveoli and partial pressure of oxygen in the arterial blood referred to?
In the alveoli - pAO2.
In the arterial blood - paO2.
100
What two things affect the amount of dissolved gas?
How are these two things linked?
The partial pressure of the gas above the liquid that it is in contact to.
The solubility of the gas with that liquid.
The amount of the gas dissolved = the partial pressure of the gas multiplied by the solubility of the gas for that liquid.
101
How does the partial pressure of oxygen in the alveoli relate to the partial pressure of oxygen in the capillaries?
The partial pressure equilibrates as, meaning that they will be equal.
102
What is the total content of oxygen a combination of?
The amount of oxygen dissolved within the plasma.
The amount of oxygen bound to haemoglobin.
103
Why is the partial pressure of oxygen within the alveoli lower than the partial pressure within the trachea?
What two things can also influence the gradient between the two?
The residual volume within the alveoli cannot be breathed out and has a lower partial pressure of oxygen, which mixes with the newly inhaled air, decreasing its partial pressure.
The diffusion of oxygen across the alveolar membrane, into the capillaries.
The amount of carbon dioxide being breathed out - the more carbon dioxide being delivered from the pulmonary veins, the greater the partial pressure it exerts, decreasing the oxygen partial pressure.
104
What are the determinants of alveolar oxygen partial pressure?
The rate at which oxygen is taken up by the blood from the alveoli and the rate at which it is replenished by alveolar ventilation.
105
What are the steps to diffusion from the alveoli to the red blood cell, and how thick is this barrier?
Fluid film lining the alveoli.
Epithelial alveolar cell.
Interstitial space.
Endothelial cell of the capillary.
Plasma.
Red blood cell membrane.
It has a thickness of 0.4 micrometers.
106
What proportion of the time that the blood spends in the alveolar capillaries is needed for gas exchange to take place, and what does this mean?
It takes 1/3rd of the time for the blood in the capillaries to become oxygenated, that it is in there for.
This means that there can be a decrease in transit time (faster) when required, without affecting the gas exchange, seen in exercise.
107
What factors affect the diffusion coefficient, and how does this relate to carbon dioxide and oxygen?
The solubility of the gas.
The molecular weight.
The solubility of the gas is much more important in determining rate of diffusion as despite the smaller molecular weight of oxygen than carbon dioxide, the rate of diffusion is 20x greater for carbon dioxide than oxygen.
108
What conditions can affect the thickness of the diffusion membrane, and how does this affect the ability for O2 and CO2 to diffuse?
If there is an increase in fluid within the alveoli, such as in pneumonia or pulmonary oedema (e.g. left sided heart failure).
Pulmonary fibrosis due to there being an increase in elastic fibres being laid down.
Due to the diffusion abilities of the gasses, carbon dioxide will be relatively unaffected until end-stage, whereas oxygen diffusion will be reduced.
109
How can emphysema affect O2 and CO2 diffusion?
The elastase breaks down elastin fibres in the lungs, leading to the collapse of smaller alveoli into larger ones, decreasing surface area.
This means that the ability for oxygen to diffuse across the membrane is impaired. The ability for carbon dioxide to diffuse across is relatively unchanged, until end-stage emphysema.
110
What is ventilation/perfusion matching?
The ratio between the ability of the oxygen to be delivered to the alveoli - ventilation (V) - and the ability of the pulmonary arteries to deliver blood to the alveoli - perfusion (Q).
111
What is considered a normal V/Q - why?
0.8
This is because, due to gravity, there is a greater supply of blood the the base of the lungs, meaning that the alveoli here are hyperperfused and underventilated. There is a greater supply of oxygen to the apices of the lungs, meaning that the alveoli here are hyperventilated and underperfused.
112
In what state does the V/Q reach closer to 1, and why?
During exercise, there is an increase in cardiac output.
This leads to a vasodilation of the arteries supplying the apices of the lungs.
This means that the blood supply to the lungs is more equal throughout the lungs.
There is also an increase in recruitment of alveoli in the base of the lungs, increasing ventilation there.
113
State some conditions where V:Q < 1.
Fibrosis of the lungs.
Pneumonia.
Asthma.
COPD.
Cystic fibrosis.
Pulmonary oedema - left sided heart failure.
114
State some conditions where the V:Q > 1.
Right sided heart failure.
Pulmonary embolism.
Hypovolaemia.
115
What is a shunt in respiration?
Where there are alveoli that are not supplied with oxygen, but are being perfused, so no gas exchange occurs.
116
What does the body do for a ventilation:perfusion mismatch, and how does this compensate?
There will be an increase in ventilation, leading to a very small amount of additional oxygen being dissolved in the blood, when there is V:Q < 1.
There is vasoconstriction of blood vessels supplying poorly ventilated alveoli, when there is V:Q > 1.
As the haemoglobin at the well ventilated alveoli is already saturated, there will be only a small increase in the partial pressure of oxygen within the blood as haemoglobin that wouldn’t have been perfused now are. This can lead to hyperventilation.
117
What factors are required for oxygen carrying?
The oxygen must be able to be taken up at the lungs.
The binding to the carrier must be reversible.
The oxygen must be able to dissociate from the carrier at the tissues.
118
How does the binding of oxygen to haemoglobin affect its cooperativity?
The binding of the oxygen causes a conformational change of the haemoglobin.
This causes the rate at which the oxygen is taken up to increase.
It also increases the affinity for oxygen, for the haemoglobin, stabilising the R-state.
The greater the amount of oxygen-bound to the haemoglobin, the further these increase by - positive cooperation.
119
How does the affinities of haemoglobin change within the arterial and venous circulation?
Arterial circulation - increased affinity for oxygen, with a decreased affinity for carbon dioxide, hydrogen and chloride ions.
Venous circulation - this is reversed.
120
What is the Bohr effect?
The allosteric binding of H+ or CO2, which are both seen in high concentrations at metabolically active tissues, decreases the affinity of oxygen by causing a conformational change. Once the first oxygen dissociates, it becomes easier for the others to do so.
2,3-BPG and an increase in temperature also decreases the affinity of haemoglobin for oxygen.
121
What is the Haldane effect at the tissues?
The binding of carbon dioxide to haemoglobin is much greater in deoxygenated conditions than in oxygenated conditions.
This is due to allosteric modulation of carbon dioxide binding sites, increasing the affinity for carbon dioxide and decreasing the affinity for oxygen.
122
How does haemoglobin act as a pH buffer?
Haemoglobin can bind to hydrogen ions, particularly in deoxygenated conditions, at the tissues.
At the lungs, where the partial pressure of oxygen is higher, the hydrogen ions are released and combine with bicarbonate ions.
The carbonic acid then converts to water and carbon dioxide, which is breathed out, in the presence of carbonic anhydrase.
123
What is the normal oxygen-haemoglobin concentration?
Each haem group of the haemoglobin can account for 2.2mmol/L.
As there are 4 haem groups, the oxygen content in haemoglobin is 8.8mmol/L.
124
What are some conditions that use oxygen faster than it is delivered?
Peripheral arterial disease.
Raynaud’s - vasoconstriction of the vessels supplying the extremities.
Congestive heart failure - low cardiac output.
125
What is mixed venous blood and how will this affect the affinity of haemoglobin for oxygen?
Blood returning to the lungs from various tissues.
This will have a lower partial pressure of oxygen, decreasing the affinity for it.
126
What is the maximum unloading of oxygen, and what is normal oxygen extraction?
Maximum = 70%.
Normal = 30%.
127
Why does central cyanosis give a blue-ish tinge, where and when is it seen?
There is haemoglobin saturation less than 85-90%.
As deoxygenated haemoglobin is less red than oxygenated haemoglobin, the mouth, tongue, lips and mucous membranes appear this colour.
128
What are the symptoms of carbon monoxide poisoning?
Headache.
Nausea.
Vomiting.
Slurred speech.
Confusion.
Initially few respiratory symptoms.
129
Why is carbon monoxide pathological?
Haemoglobin has a 200 times greater affinity for it than for oxygen, meaning that it displaces oxygen.
This also means that it stabilises the R-state and so the haemoglobin gives up the oxygen less easily.
130
How does mechanical ventilation work to relieve hypoxaemia, and how does this affect the V:Q ratio?
Air is forced into the lungs, opening the alveoli, causing oxygen to enter the alveoli, pushing carbon dioxide out.
Due to the high partial pressure of oxygen being delivered to the lungs, there is a ventilation perfusion mismatch of V:Q > 1.
131
How does acute respiratory syndrome affect the V:Q?
It inhibits the ability of the lungs to effectively vasoconstrict the poorly ventilated alveoli, leading to a V:Q mismatch of < 1.
Shunt occurs here as some of the haemoglobin supplying the poorly ventilated alveoli will not become saturated.
132
What is the main factor that affects the ability of the tissue to survive with a low partial pressure?
The capillary density at that tissue.
133
In arterial blood gas analysis, what can be used to determine the binding of different gasses to haemoglobin?
Co-oximeter.
134
What effect does vasodilation of capillaries to alveoli have, on gas exchange?
Increased perfusion, increasing the number of red blood cells, thus the amount haemoglobin at the alveoli to be oxygenated, and to remove their CO2.
However:
- There is a decrease in surface area of the capillary for diffusion.
- There is an increase in velocity of the red blood cells passing the alveoli, decreasing the time for diffusion to occur.
135
What is Farmer’s lung?
An interstitial lung disease.
136
Why may there be an increase in ketones and glucose in the blood, with a low oxygen saturation, with nasal cannulae?
There is a chest infection that has caused diabetic ketoacidosis to occur.
Indicative of a chest infection as there is a diffusion barrier, decreasing the ability for oxygen to saturate haemoglobin.
137
What is the complication with very low blood pH?
Phosphofructokinase is pH sensitive, meaning that it is inhibited with a low pH.
This means that glycolysis is impaired, decreasing the energy formed for the brain.
This leads to drowsiness, stupor (near-unconsciousness), coma and death.
138
What does the rate of the reaction depend on?
Law of mass action states that the rate of the reaction is determined by the amount of reactants and products.
Presence of carbonic anhydrase.
139
Why does an increase in carbon dioxide decrease pH when it eventually dissociates into bicarbonate ions?
The dissociation of carbonic acid forms one hydrogen ion and one bicarbonate ion.
To maintain physiological pH, the ratio of hydrogen ions to bicarbonate ions should be 1:20, so this ratio is altered.
140
What are the 3 methods of carbon dioxide transport, and their proportions?
Carbamino compounds - 30%.
Bicarbonate ions - 60%.
Dissolved in plasma - 10%.
141
How is carbon dioxide transported bound to haemoglobin, and what are the two goals of this?
It binds to amine groups on the globin chain of haemoglobin.
The goals are:
- Stabilising pH; bound CO2 does not dissociate to affect pH, it is unable to leave the RBC.
- Binding to the Hb stabilises the T state, promoting the release of oxygen. The increase in binding of CO2 occurs in metabolically active tissues, leading to sufficient oxygen dissociation where required. The binding of oxygen in high partial pressures at the lungs leads to more carbon dioxide released and exhaled.
142
How does carbon dioxide entering red blood cells act as a buffer to low pH?
There is a high concentration of carbonic anhydrase within the red blood cells.
The carbon dioxide is therefore converted to carbonic acid, which dissociates into H+ and HCO3-.
The H+ binds to haemoglobin and so is not released into the plasma.
The HCO3- is released into the plasma by the anion exchanger.
143
When are H+ ions released from the haemoglobin and what is the buffering effect of this?
In high partial pressures of oxygen, such as at the lungs, there is an increased binding of oxygen to haemoglobin.
Oxygen binding to the haemoglobin stabilises the R-state. This conformational change releases the hydrogen ions.
The hydrogen ions can then bind to bicarbonate ions and be converted into water and carbon dioxide, for the CO2 to be exhaled.
144
What are some metabolic substances that can be produced that can affect CO2 levels? Explain how this occurs.
Lactic acid, keto acid and sulphuric acid.
The H+ ions released from these acids combine with HCO3-, which favours the backwards reactions, increasing the formation of carbon dioxide.
145
Where does the production and control of bicarbonate ions occur?
Red blood cells are the site of bicarbonate ion production.
Bicarbonate ion concentration is controlled by the kidneys through reabsorption/ secretion and production.
146
Why is the conversion of carbon dioxide into carbonic acid and then into hydrogen ions and bicarbonate ions slow in the plasma?
There are low concentrations of carbonic anhydrase within the plasma.
147
When looking at a full compensated pH, how can you determine whether it was an acidosis or alkalosis? Why is this the case?
Acidosis = pH between 7.35 and 7.40.
Alkalosis = pH between 7.40 and 7.45.
If it is exactly 7.40 then it is driven by acidosis.
This is because the body never overcompensates.
148
What are the 3 main groups of neurons involved in respiration, and what do they control?
Ventral respiratory group - forced expiration.
Dorsal respiratory group - inspiration.
Pontine respiratory group - rate and pattern of breathing.
149
What is the neural cause of passive expiration?
The ceasing of action potential firing from the neurons, leading to muscular relaxation.
150
How do the dorsal respiratory group neurons act to cause inspiration?
They spontaneously, continuously fire.
They do not need to receive sensory information.
They are the central pattern generator for respiration.
151
Where are the dorsal respiratory group of neurons located?
On the dorsal surface of the medulla oblongata of the brainstem.
152
Where are the pontine respiratory group of neurons located?
On the ventral-lateral surface of the pons of the brainstem.
153
Where is the ventral respiratory group of neurons located?
In the medulla oblongata of the brainstem.
154
What are the two centres within the pontine respiratory group, and what is each of their function?
Pneumotaxic centre - limiting inspiration, providing an inspiratory off-switch.
Apneustic centre - promoted inhalation and delays the inspiratory off-switch.
155
How does the penumotaxic group act to limit inspiration?
It limits the bursts of action potential and so the volume of action potentials sent in the phrenic nerve, decreasing tidal volume and regulating respiratory rate.
156
How does the apneustic centre act to promote inhalation? How is it controlled?
It constantly stimulates the neurons within the medulla oblongata.
It is inhibited by pulmonary stretch receptors and by the pneumotaxic centre.
157
How is voluntary respiration controlled?
The primary motor cortex in the pre-central gyrus of the cerebrum, which receives inputs from the limbic system and hypothalamus.
158
Where are the peripheral chemoreceptors, and what do they send their sensory information through, respectively?
Aortic bodies - sensory information is sent through the vagus nerve.
Carotid bodies - sensory information is sent through the glossopharyngeal nerve.
159
What is the primary function of peripheral chemoreceptors, and how do they work?
They detect large changes in partial pressure of oxygen.
In hypoxaemia, afferent impulses travel via the glossopharyngeal and vagus nerves to the medulla oblongata and pons of the brainstem to restore the partial pressure of oxygen.
160
What is the outcome of stimulation of the peripheral chemoreceptors, in hypoxaemia?
Respiratory rate and tidal volume increases.
Blood flow to the kidneys and brain increases.
Cardiac output is increased.
161
Which cells within the peripheral chemoreceptors detect the partial pressure of oxygen? State what they are formed from and how they work.
Glomus cells.
They are formed from ectoderm and depolarise when the partial pressure of oxygen is low (<8kPa).
This stimulates neurotransmitters and ATP to be released, which activates afferent fibres that stimulate respiration.
162
What other substances do peripheral chemoreceptors respond to, and what can influence this?
High partial pressures of carbon dioxide in the arteries and low pH also stimulates the glomus cells to increase alveolar ventilation.
Hypoxaemia increases peripheral chemoreceptors’ sensitivity to acidosis and hypercapnia.
163
Where are the neurons located in central chemoreceptors, and what fluid do they sense changes within?
Within the medulla oblongata, on the brain side of the blood brain barrier, sensing changes in cerebrospinal fluid.
164
What can central chemoreceptors detect changes in, and what is their sensitivity?
PaCO2 - highly sensitive.
Arterial pH - less sensitive.
165
What is the pH of the cerebrospinal fluid determined by?
The partial pressure of carbon dioxide in there.
This is because CO2 can freely diffuse across the blood brain barrier.
The concentration of bicarbonate ions is much more stable as active transport is required to move HCO3- into the fluid.
166
What moves the bicarbonate ions into the CSF, and what does that mean for the buffering of decreases in pH?
The choroid plexus.
This requires energy to do so and recovering pH changes takes a prolonged period of time - 8 to 24 hours.
167
What happens in prolonged hypercapnia of the cerebrospinal fluid?
The levels for elevated CO2 are re-set to higher levels, due to the function of the choroid plexus cells.
168
How do stretch receptors in the lung act during large inspirations?
The excessive stretch activates the receptors.
Action potentials are sent through the vagus nerve to the dorsal respiratory group in the medulla and the apneustic centre of the pons.
169
What is the effect of stimulating the stretch receptors?
Slowing of the respiratory frequency.
Increases production of pulmonary surfactant.
Prevent over inflation of the lung.
170
What are rapidly adapting pulmonary stretch receptors stimulated by, and what do they cause?
They are stimulated by noxious gases, cold and inhaled dust.
They send action potentials via the vagus nerve, leading to bronchoconstriction and increased respiratory rate.
171
What two muscles does the dorsal respiratory group send action potentials to?
Diaphragm and external intercostal muscles.
172
Where is the majority of the bicarbonate ions reabsorbed and synthesised in the nephron?
Reabsorbed - PCT.
Synthesised - collecting duct and PCT.
173
What is the pathophysiology of acute respiratory distress syndrome?
It is often secondary to infection.
The infection damages the type II pneumocytes, leading to decreased surfactant synthesis. This leads to a decrease in lung compliance.
Hypoxia vasoconstriction is lost due to the the decreased lung compliance being so extensive (greater area).
Intra-pulmonary shunt occurs, leading to deoxygenated blood.
174
What is a mucous plug?
An increased mucous production, with thickening of the mucous, leading to the lumen of a bronchi or respiratory tube of a ventilator becoming blocked.
175
What drug can be given to mothers to increase surfactant production in pre-term infants?
Corticosteroids.
176
Why can hypoxaemia eventually lead to hypercapnia?
There is an increased respiratory rate to attempt to compensate for the decrease in partial pressure of oxygen.
This leads to fatigue of the respiratory muscles, and hypoventilation occurs.
177
What ECG changes can be seen on a patient with a pulmonary embolism?
Sinus tachycardia.
Right bundle branch block.
S1, Q3, T3.
178
What may be seen on X-ray due to an occluding pulmonary embolism?
Wedge-shape infarction.
Hampton hump.
179
Why may a patient with severe asthma no longer be wheezing?
Asthmatic fatigue.
180
Define respiratory failure.
Impairment of gas exchange causing hypoxaemia with or without hypercapnia.
It can be an acute or chronic condition.
181
What are the causes for type II respiratory failure?
Reduced ventilatory rate - pump failure:
- Chest wall collapse.
- Respiratory muscles failing.
- Loss or damage to lung parenchyma.
- Block or damage to the respiratory control centres.
An inability to overcome the resistance to ventilation of the lung.
182
What are the effects of hypoxaemia on the entire body?
Impaired CNS function - confusion, irritability or agitation.
Cardiac arrhythmias & ischaemia.
Hypoxic vasoconstriction of pulmonary vessels.
Central cyanosis - 40-60g/L of unsaturated Hb.
Tachypnoea and tachycardia.
183
What are the causes of hypoxaemia?
Low inspired FiO2 (fraction-inspired) - high altitude.
V/Q mismatch.
Diffusion defect - alveolar capillary membrane.
Intra-lung shunt.
Hypoventilation.
Extrapulmonary shunt - blood shifts from right to left side of the heart.
184
What is the broad cause of type I respiratory failure?
Issue with gas exchange, causing oxygenation of the haemoglobin to decrease.
185
What is an intrapulmonary shunt?
Pulmonary arterial blood that does not participate in gas exchange as it passes through the lung.
186
What common condition increases the alveolar dead space?
Pulmonary embolism.
187
What physiological changes does a loss of surfactant cause?
Alveolar atelectasis - alveoli collapsing.
Less lung compliance - don’t open as easily due to the increase in surface tension.
188
How do you initially treat a loss of surfactant, in an acute setting?
Give positive pressure ventilation to keep the alveoli open.
189
What are some causes of acute hypoventilation, and how can it be treated?
Causes:
- Opiate overdose, respiratory depression decreasing rate.
- Head injury affecting the respiratory centres of the brain.
- Very severe asthma.
- Medullary stroke.
Treated with artificial ventilation.
190
What are some parts of the body in which defects here can cause hypoventilation?
Motor neurone.
Intercostal or phrenic nerve dysfunction - Guillan-Barre syndrome.
Neuromuscular junction problems - myasthenia gravis.
Muscular disease - duchenne’s muscular dystrophy/ ALS.
Chest wall problems - kyphoscoliosis.
Severe lung fibrosis/ airway obstruction.
Respiratory centre depression.
191
What is the Henderson-hasselbach equation for CO2?
192
What are some causes of motor disorders?
Tetanus.
ALS.
Motor neurone disease.
Spinal cord lesions at C3.
193
What are some issues at the neuromuscular junction?
Myasthenia gravis.
Organophosphate toxicity.
Botulism.
194
What is kyphoscoliosis, and what is the problem with it?
Abnormal rounding of the upper back with a sideways curvature of the spine.
It can cause hypoventilation due to the reduction in compliance of the chest wall, and lung - microatelectasis.
195
Why can oxygen treatment of type II respiratory failure have negative impacts on the patient?
196
What 3 pathophysiology factors increase the risk of a pulmonary embolism?
Virchow’s triad:
- Hypercoagulability.
- Vessel wall damage.
- Stasis/ turbulence.
197
State some causes of stasis, vessel wall damage and hypercoagulability.
198
Why does a pulmonary embolism cause acute right ventricular overload?
Blockage in a pulmonary artery increases the pressure proximal to the blockage.
This causes right ventricular dilation and strain, leading to right sided heart failure.
199
Why is cardiac output decreased in pulmonary embolism?
Less blood returning to the left side of the heart.
The left side of the heart cannot expand sufficiently due to the dilation of the right ventricle.
This means that there is a decrease in filling of the left ventricle, decreasing the stroke volume.
200
What is done by the body to maintain systemic blood pressure, due to the decrease in cardiac output?
What is the problem with this?
Adrenaline and noradrenaline are released:
- Increased force of contraction to try to maintain CO.
- Vasoconstriction of the pulmonary arterial system.
This increases the pressure that the right side of the heart has to work against, worsening the heart failure.
201
Why can acute right ventricular overload lead to death?
Cardiogenic shock with circulatory failure.
Cardiac arrhythmias, due to damage to the right ventricular wall and conduction problems, leading to arrest.
202
Why can pulmonary emboli cause respiratory failure?
Low right ventricle output.
V/Q mismatch, as some alveoli not perfused.
203
What are the clinical history/examination signs of a pulmonary infarction?
Haemoptysis - coughing up blood in the alveoli.
Pleuritis - blood irritating the pleura.
Small pleural effusion.
204
When is a D-dimer used?
It is only useful to rule out a PE.
When it is low, with a low-risk patient, then a PE can be ruled out.
205
What are different imaging done with a suspected pulmonary embolism, and when are they used?
Chest X-ray - rule out other pathologies, such as infection.
CT pulmonary angiogram (CTPA) - gold standard.
V/Q scan - only done if they cannot have a CTPA, such as a in pregnant patients or those with poor renal function that cannot have contrast.
206
How can a PE be interpreted on a CTPA?
207
What are some thrombolysis used for treatment of PE’s?
Fibronolytics - streptokinase or tPA.
208
What is percutaneous catheter thrombectomy?
The mechanical removal of a thrombus using a wire.
209
What are the treatments of severe pulmonary emboli?
Haemodynamic support.
Respiratory support.
Thrombolysis/ surgical intervention.
210
What is the time length for anticoagulant use after discharge based off of?
If the identifiable factor can be removed.
If it can be removed then they are given oral anticoagulants for 3 months.
If there is no known identifiable risk factor, or if cannot be removed (such as having had cancer) then it is lifelong.
211
What are some prophylactic mechanisms regarding virchows triad?
212
What is the oxygen supply chain?
213
If there is a PE in the left lung, what can the effects be on the right?
V/Q mismatch.
This is because there will be more blood being pumped to the right lung due to the increased pressure from the left.
214
What is the symptomatic triad associated with fat embolism syndrome?
Petechial rash.
Decreased levels of consciousness.
Shortness of breath.
215
What are some causes of fat embolism syndrome?
Long bone fractures.
Intramedullary nailing in surgery.
Massive soft tissue injury.
Corticosteroid therapy.
Fatty liver and pancreatitis.
Lymphography.
Fat emulsion infusion.
Haemoglobinopathies.
216
What is the ABG of somebody with a PE?
Respiratory alkalosis.
Low paO2.
Low paCO2.
217
What are the categories of results for a Wells Two test?
PE unlikely if 4 or less.
PE likely if greater than 4.
218
How do you define a bronchiectasis exacerbation?
A person with bronchiectasis with deterioration within 48 hours, of at least 3 of the following symptoms:
- Cough.
- Sputum volume/ consistency.
- Sputum purulence.
- Breathlessness.
- Fatigue.
- Heamoptysis.
219
When can cavitation lesions be seen on X-ray?
Primary or post-primary TB.
Last-stage lung cancer.
220
What are B-/ constitutional symptoms?
Non-specific symptoms to a disease - fever, weight loss, lethargy, etc.
221
Why is TB cultured?
To see antibiotic susceptibility.
Gold-standard for TB diagnosis, but not done for everyone.
222
What two drugs can make the urine turn orange?
Rifampicin.
Nitrofurantoin.
223
What should be given to a patient with a latent TB infection?
One of rifampicin or isoniazid.
224
What is emphysema?
The breakdown of elastic tissue around the alveoli, leading to formation of bulla and a decreased surface area, with hyperinflation.
225
Why is there an obstruction of ventilation in chronic bronchitis?
Inflammation of the walls of the airway narrows the lumen.
Increased mucous production also narrows the lumen.
226
What are the causes of COPD?
Smoking.
Biomass exposure - chronic bronchitis.
Alpha-1 anti-trypsin deficiency.
Air pollution.
Illicit drug use - heroine and cannabis accelerates emphysematous changes.
227
What childhood factors can predispose to COPD?
Low birthweight.
Childhood respiratory infections.
228
What are some signs of COPD, at rest or on examination?
At rest, often none but can have:
- Pursed lip breathing.
- Hyperinflation or barrel-shaped chest.
- Prolonged expiratory phase.
On examination:
- Expiratory wheeze on auscultation.
- Cyanosis.
- Cor pulmonale.
229
What are the measures in spirometry?
Lung volumes.
Forced vital capacity - total amount of air exhaled.
Forced expiratory volume in 1 second - expired air in one second.
230
How can spirometry be used to diagnose COPD?
The forced expiratory volume in 1 second, divided by the forced vital capacity, is less than 0.7.
FEV1 / FVC = <0.7
No improvement with bronchodilators.
231
Describe the airflow obstruction classification.
232
What is a COPD exacerbation?
Acute worsening of respiratory symptoms that result in additional therapy.
233
What are some symptom-improving therapies for COPD?
Pulmonary rehabilitation.
Bronchodilators - Beta-2 agonists or anti-muscarinics.
Mucolytics - decrease viscosity of mucous.
Lung volume reduction surgery or lung transplant.
Refractory dyspnoea management - low dose opiates, airflow therapy.
234
What are some COPD therapies to improve risk?
235
How can one help to stop smoking, and how can it help COPD patients?
Nicotine replacement therapy, behavioural support and vaping.
Reduces mortality and improves symptoms.
Slows down loss of lung function.
Reduces exacerbations.
Improvement of drug function.
236
How do anti-muscarinics work as bronchodilators, an where are they most effective?
237
How do beta-2 agonists work as bronchodilators, an where are they most effective?
238
What is bronchiectasis?
Irreversible dilatation of bronchi due to destructions of the smooth muscle and elastic fibres in the walls, leading to inflammation and thickening of them.
239
Why is there obstruction of the bronchi in bronchiectasis, and what is the problem with this?
Due to the loss of the elastic recoil of the bronchi, sputum and mucous build up.
This leads to inflammation and microbial infiltration, which can lead to infections.
There is also impaired cilia function.
240
What are symptoms of bronchiectasis?
Cough with mucopurulent sputum, often leading to foul smelling breath.
Breathlessness.
Recurrent sinus and lung infections.
Haemoptysis in 50% of patients.
Chest pain.
Clubbing of the fingers.
Weight loss, fever and fatigue.
241
What are some causes of bronchiectasis?
242
How is the clinical presentation of chronic bronchitis different to that of bronchiectasis?
Chronic bronchitis are almost always smokers, and they produce white/ clear sputum on cough.
Bronchiectasis are most commonly not smokers, they can produce green sputum and have an inspiratory squeak.
243
What is seen in a decreased lung elastic recoil?
Reduced forced expiratory volume.
Air trapping and hyperinflation of the lungs.
244
What is the treatment of bronchiectasis?
Airway clearance - physiotherapy, hypertonic saline, mucolytics.
Low-dose macrolides.
Inhaled corticosteroids and bronchodilators.
Vaccinations.
Treating immunodeficiencies and other causes.
245
How is pseudomonas aeruginosa treated?
Eradication therapy.
Nebulised colomycin.
IV antibiotics.
246
What is the most common gene defect in cystic fibrosis, and what does this affect?
Phe508del - this causes defective transport of the CFTR, poor functioning and stability within the cell membrane.
247
What drugs improve the stability of the CFTR within the cell membrane?
Potentiators.
248
What drugs improve the movement of the CFTR protein?
Chaperone.
249
How does the drug Orkambi improve CFTR function?
It acts as a potentiator and chaperone.
250
What is the function of the CFTR protein?
Regulates the movement of Cl- ions out of the epithelial membrane, and regulates ENaC channels, thus water movement.
251
Why does a defect in the CFTR protein cause issues?
Excessive reabsorption of Na+ and water leads to an increase in thickness of the mucous.
Increased mucous thickness causes impaired cilia function.
Increases the risk of infection.
252
How does the CFTR affect the pancreas, and what can this lead to?
Lack of movement of the exocrine secretions out of the pancreatic duct, can lead to pancreatitis.
Also causes malabsorption.
Inflammation of the pancreas will eventually lead to diabetes mellitus.
253
What is meconium ileus?
Thick newborn stools (meconium), which can lead to intestinal obstruction.
This can predispose to bilious vomiting, abdominal distension and delays in defecation.
254
How can cystic fibrosis affect different systems of the body?
ABPA - allergic bronchopulmonary aspergillosis.
Heat stroke due to excess sweating and loss of NaCl.
255
How is cystic fibrosis treated?
Vaccinations and aggressively treat infections.
Saline clear out of the lungs 2-3x a day.
Nutritional support:
- Pancreatic enzymes given in pill form.
- Increased calorific intake due to the increased energy expenditure.
NaCl supplements due to excess loss in sweat.
Lung transplant, followed by heart transplant due to Cor pulmonale.
256
What is the effect of no CFTR being synthesised?
Incompatible with life.
257
In which countries is TB still prevalent?
South Africa.
Nigeria.
India.
China.
Bangladesh.
Philippines.
Indonesia.
258
What 3 strains of mycobacterium can infect humans?
Mycobacterium tuberculosis.
Mycobacterium bovis.
Mycobacterium africanum.
259
What is the structure of mycobacterium tuberculosis?
Non-motile bacillus, that are obligate aerobes.
They have a long-chain fatty acid, complex wax and glycolipid cell wall, giving rigidity.
260
What is the generation time for MTB?
15-20 hours so are slow-growing.
261
What inhibits macrophages from destroying the MTB?
Long-chain fatty acids in the cell wall.
262
What is the exposure requirements for acquisition of MTB?
At least 8 hours per day for up to 6 months.
But only 1-10 bacilli are required for infection.
263
What immune cell is responsible for the MTB containment?
T-lymphocytes.
264
What is the Gohn focus and Gohn complex?
Gohn focus - primary MTB lesion of the lung.
Gohn complex - Gohn focus and draining hilar lymph node.
265
What is miliary TB?
What predisposes to this?
Where the MTB enters the blood stream and disseminates throughout the body.
Patients often have to be severely immunocompromised for this to occur.
266
What are some investigation of pulmonary TB?
Chest X-ray.
3 early morning sputum samples.
Histology - biopsy of the lymph nodes, usually.
267
What are some second line medications for TB?
Quinolones - moxifloxacin.
PAS.
Cycloserine.
Ethionamide.
268
Other than drug therapy, how else is TB treated?
Vitamin D supplements.
Surgery.
269
What are some symptoms of extra-pulmonary TB, involving:
- Lymph nodes.
- GI tract.
- GU tract.
- Bones.
- CNS.
Lymph nodes - lymphadenitis, abscesses and sinuses.
GI - ascites.
GU - renal disease.
Bones - spinal TB.
CNS - TB meningitis.
270
How is TB spread controlled?
PPE.
Negative pressure isolation of patient.
BCG vaccination.
271
What is the BCG vaccine?
A live-attenuated from the bovis strain.
272
Who is the BCG vaccine given to?
People who have migrated from high risk countries.
Health care workers.
Those in close contact with people with active TB.
NOTE: do not give to those with HIV.
273
Why does air trapping cause a decrease in gas-exchange?
The volume of old air in the lung is increased so new air cannot come in, meaning there is a lower partial pressure of oxygen within the alveoli.
It also flattens the diaphragm, reducing the force of diaphragmatic contraction, decreasing the volume of air inspired.
274
What is the appearance and components of purulent sputum?
Yellow or green.
It is pus, composed of white blood cells, dead tissue, serous fluid and mucous.
275
What is an acute infectious COPD exacerbation?
Acute, severe shortness of breath, fever, chest pain and purulent sputum.
276
What is yellow nail syndrome?
Yellow discolouration of the nail with pulmonary manifestations - chronic cough, bronchiectasis, pleural effusion; and lower limb lymphoedema.
277
What auscultation noises are associated with bronchiectasis?
Crackles, high-pitched inspiratory squeaks and rhonchi - low-pitched rattling sound.
278
What can be seen on CT of an asthmatic patient?
Thickened airway walls but no enlarged or widened airways.
279
What is distal intestinal obstruction syndrome?
Faecal obstruction in the ileo-caecum, due to thick, dehydrated faeces.
Often due to insufficient pancreatic enzymes and salt deficiency.
Palpable mass in the right iliac fossa, which can be seen on chest X-ray.
280
What media is most commonly used for culturing of tuberculosis?
Löwenstein-Jensen medium.
281
What are the nodules at the primary site of TB infection like?
Fibrocalcific.
282
Why is post-primary TB often worse than primary TB?
Marked local immune response, due to previous exposure.
This hypersensitivity-induced host immune response can lead to further damage of the lung.
283
What is seen on a chest X-ray of somebody with miliary pulmonary TB?
Small foci, involving the entire lung.
284
What is given to patients taking INAH (isoniazid), and why?
Pyridoxine - vitamin B6.
Prevents peripheral nerve damage.
285
Why may somebody who was infected with TB test negative on a tuberculin skin test?
They cleared the infection with the innate immune system, and so the T-cells were never exposed to them to form an immune response.
286
What is tram tract sign?
Sign seen on X-ray or CT of a patient with bronchiectasis.
287
What is an inspiratory wheeze called, and why does it occur?
Stridor.
Air vibrations as it passes through large respiratory conduction pathways, such as the trachea.
288
Why can exercise make an asthmatic person cough?
Breathing through the mouth occurs, where the air entering the lungs is colder and drier.
The hypersensitivity of the inflamed bronchi triggers an autonomic response to cough.
289
How does FVC differ from TLC?
Total lung capacity = forced vital capacity + residual volume.
290
What is the difference between a restrictive and obstructive pattern of breathing on spirometry?
Restrictive - both FEV1 and FVC decrease and so the ratio remains normal.
Obstructive - FEV1 decreases more than FVC and so the ratio decreases.
291
How is asthma differentiated from COPD using spirometry?
Both have a FEV1/FVC ratio of less than 0.7.
Asthma will improve by 0.12 or more after bronchodilation therapy, but COPD will not.
292
What is asthma?
Chronic airway inflammation with reversible airway obstruction and bronchospasm, seen in susceptible (genetically-driven) individuals that have increased airway responsiveness to stimuli.
293
What is the difference between the airway in a non-exacerbated and exacerbated asthmatic patient?
Non-exacerbated - thickening but relaxed smooth muscle.
Exacerbated - spasming of the thickened smooth muscle.
294
Why does gas trapping occur in asthma?
The bronchospasms of the hypertrophied bronchi wall and increased mucous secretions into the lumen significantly narrows the airway.
295
What is the pathophysiology of type I hypersensitivity asthma?
Antigen presenting cells present the allergens to CD4+ cells, which form Th2 cells.
These then activate the B-cells, stimulating them to mature into plasma cells and release IgE.
IgE then activates the mast cells.
On re-exposure to the allergen, the mast cells degranulate, releasing histamines, leucotrienes, prostaglandins and tryptase.
This causes the airway smooth muscle to contract - bronchoconstriction - within 15-20 minutes.
296
What are the different types of type IV hypersensitivity asthma?
Eosinophilic and non-eosinophilic.
Neutrophilc inflammation - T1/T17.
Pauci-granulocytic asthma.
297
Explain the pathophysiology of type IV hypersensitivity asthma.
Allergens are presented to the CD4+ cells, forming Th2 cells, by dendritic cells.
These release IL-5.
This causes an increased rate of maturation of eosinophils, attraction of them to the airway and an increase in production in the bone marrow.
The eosinophils then release inflammatory mediators, such as leukotriene C4.
These cause epithelium damage, an increase in goblet cell number and mucus production, a thickening of the basement membrane and hypertrophy and proliferation of the smooth muscle in the bronchi.
298
What can activate type IV hypersensitivity non-eosinophilic asthma?
Viruses or pollutants, mainly.
It causes the same reaction as eosinophilic asthma.
299
What causes the the hyper-responsiveness of the airway, and what are some non-allergen triggers?
Inflammation increases the reactivity of the airway.
Cold air, exercise, strong smells.
300
What airway remodelling occurs in severe asthma?
Increase in number and size of the smooth muscle.
Sub-epithelial inflammation and fibrosis.
Loss of cilia reducing mucus clearance.
Increase in goblet cell number and mucus hypersecretion.
Increased eosinophils and/or neutrophils in the airway lumen.
301
State some asthma triggers.
302
What are some atopic features that may point to an asthma diagnosis?
Eczema.
Allergic rhinitis - hay fever.
Nasal polyps.
303
How is asthma diagnosed?
Peak flow test - should have a reduced peak flow to that expected of someone of their sex and age, that is variable by greater than 20%.
Spirometry - FEV1/ FVC = 0.7 or less. This should improve by 0.12 or more after bronchodilation therapy.
6 week trial of corticosteroids should improve their symptoms.
Blood tests - IgE increased, eosinophilia and increased NO.
304
What non-medicinal treatments should be given to asthmatic patients?
Patient education - utilising inhalers, peak flow recordings and exacerbation education.
Trigger avoidance.
Vaccinations - influenza, Covid-19, pneumococcal.
Annual asthma review.
Peak expiratory flow meter.
305
What is an example of a leucotriene receptor antagonist?
Montelukast.
306
Why may a patients chest become silent in an asthma exacerbation?
They are no longer shifting sufficient air in and out of the lungs effectively, seen in a life threatening exacerbation.
307
What are some asthma-mimicking conditions?
Psychosocial factors - anxiety, depression, panic disorder; can affect adherence to asthma therapy.
Inducibile laryngeal obstruction - abnormal closing of vocal cords.
Breathing pattern disorder - brain altering the breathing pattern as a response to carbon dioxide.
308
What is asthma characterised by?
A triad of bronchial smooth muscle contraction, airway inflammation and increased secretions.
309
What is atopy?
A genetic disposition to develop an allergic reaction, producing elevated levels of IgE.
310
Which prostaglandins are released from mast cells in the immediate response?
Prostaglandin D2.
311
What causes the shedding of the epithelial cells?
Leukotriene C4, released from eosinophils.
312
What factors reduce the airway calibre?
Mucosal swelling due to vascular leak.
Thickening of the bronchial wall due to infiltration of inflammatory cells.
Mucous overproduction that is thick, which can form mucous plugs.
Smooth muscle hypertrophy and contraction.
Shedding of the epithelium.
313
What drugs can cause asthma exacerbations?
NSAIDs and beta-blockers.
314
How do we check for image quality of an X-ray?
RIPE.
Rotation - spinous processes are in the midline. Equidistance of the clavicles from the spinous processes.
Inspiration - 8-10 posterior ribs or 5-6 anterior ribs should be visible. Apices of the lungs and costophrenic angles should be seen.
Projection - PA chest X-rays are more suitable.
Exposure - vertebrae should be visible behind the heart and the hemi-diaphragms should be visible all the way across.
315
Why is a PA X-ray more reliable?
The heart is not artefactually enlarged and so cardiomegaly can be assessed.
The scapulae do not obstruct the view of the chest.
316
How do we asses an X-ray?
ABCDE.
Airway - centrally located trachea, carnia and the left and right bronchi. Any paratracheal masses or lymphadenopathy.
Breathing - lung fields; upper, middle and lower zones; pleura, ensuring the lungs follow the contour of the chest.
Cardiac contour - cardio-thoracic ratio; right and left hilar points; pulmonary arteries.
Diaphragm - costophrenic angles; higher right hemidiaphragm due to liver; stomach bubble seen.
Everything else - soft tissues; bones - fractures or masses within; pacemakers, wires or NG tubes. Central lines.
317
What is a normal and abnormal cardio-thoracic ratio?
0.35-0.5.
>0.5 is cardiomegaly.
318
For a patient with pneumonia, when should the follow-up X-ray be, and why?
After 6 weeks.
To exclude lung cancer.
319
What is erythema multiforme, and what lung condition can it be seen in?
Circular, red lesions of the skin. It is seen in mycoplasm infections.
320
What is X-ray exposure?
Having an adequate amount of radiation applied in the X-ray to pass through, enabling us to see the vertebra behind the heart.
It is dependent on the size of the patient.
321
What are the appearance of the anterior and posterior ribs on an X-ray?
Posterior ribs are horizontal.
Anterior ribs are angled.
322
What are the hilar angles of the chest X-ray and what forms the hilar points?
The hilar points are concave - the left should always be higher than the right.
They are formed on X-ray by the superior and inferior pulmonary arteries.
323
What is the paratracheal stripe?
A thin-watery stripe between the air column of the trachea and the right lung.
It should always be clear.
324
What is seen in a left lower lobe collapse, and what is it due to?
The loss of the left hemi-diaphragm, leading to a decrease in size of perfused lung tissue.
It is due to a blockage of the left lower bronchi.
325
What is seen in a left upper lobe collapse on X-ray, and what is it due to?
A loss of the left heart border. There is a decrease in size of perfused lung, and is due to an obstruction in the left upper bronchi.
Trachea pulled to the left.
326
What is seen in a right upper lobe collapse on X-ray, and what is it due to?
Opacity in the right upper zone, with the trachea pulled to the right.
It is due to a blockage in the right upper bronchi.
327
What is seen on an X-ray with a right middle lobe consolidation?
Opacity within the right middle zone region.
The loss of the right heart margin.
328
What can be seen in this X-ray?
Miliary foci.
Paraspinal mass - suggests spinal TB due to miliary TB.
329
What is seen in this X-ray?
Bilateral hilar lymphadenopathy.
The hilar angle has been obliterated and is no longer concave.
330
What is seen on this X-ray?
Left pleural effusion.
Costophrenic angle loss with complete hazing of the left lung.
331
What is seen in this X-ray and what is it typical of? Explain why.
Peri-hilar air space opacification. Bat wing appearance.
It is typical of heart failure.
This is because there is fluid around the hilar spaces due to pulmonary oedema, causing a bilateral fluffy appearance.
332
What is seen in this X-ray?
Right pleural effusion with mediastinal widening, usually due to a mass.
Loss of the costophrenic angle.
333
What is seen in this X-ray?
Pneumothorax.
There is shrinkage of the lung away from the chest wall and loss of the costophrenic angle.
334
What causes pushing of the trachea?
A large pleural effusion or a tension pneumothorax.
335
What causes pulling of the trachea?
Consolidation with lobar collapse.
Pulmonary fibrosis.
336
What is the cause of air under the right diaphragm?
Pneumoperitoneum - rupture of an air-containing organ.
337
What can cause a raise in the hemidiaphragm?
A phrenic nerve injury.
338
What is this and what is it due to?
Ginkgo-leaf sign.
Subcutaneous emphysema, where fluid shift into the subcutaneous space, due to placing a tube inside the body, usually due to mechanical ventilation.
339
What is the typical course of infection in the lung?
Alveolar macrophages fail to stop the pathogen.
Cytokines released from the macrophages to recruit more macrophages.
An increase in capillary permeability causes inflammation.
Influx of neutrophils, lymphocytes, antibodies occurs.
340
What causes the formation of the alveolar microbiotia?
Influx of bacteria due to:
- Aspiration.
- Spread from the blood stream.
- Direct spread, e.g. lower respiratory tract infections.
341
What are the virulence factors of:
- Chlamydia pneumoniae.
- Mycoplasm pneumoniae.
- Influenza.
- Steptococcus pneumoniae/ neisseria meningitidis.
- Pneumococcus.
- Mycobacterium/ legionella.
Chlamydia pneumoniae - inhibit the function of the cilia.
Mycoplasm pneumoniae - shear off cilia.
Influenza - thickens mucus.
Steptococcus pneumoniae/ neisseria meningitidis - splits IgA.
Pneumococcus - capsule inhibits phagocytosis.
Mycobacterium/ legionella - resistant to phagocytosis (intracellular survival).
342
What are most upper respiratory tract infections caused by?
Viruses - rhinovirus, coronavirus, influenza, respiratory syncytial virus, COVID-19.
343
What is acute bronchitis, who is it mainly seen in, and what are the symptoms?
It is inflammation of the medium sized airways and increased mucous production, narrowing the lumen.
It mainly seen in smokers.
They present with a cough, fever, increased sputum production and increasing shortness of breath.
344
What causes acute bronchitis and what is the treatment of it?
Most commonly viruses.
It can also be caused by streptococcus pneumoniae, haemophilus influenza and moraxella catarrhalis.
It is treated with bronchodilation, physiotherapy to remove the mucous, anti-pyretics and antibiotics if bacterial cause.
345
What is ventilated acquired pneumonia?
Development of pneumonia after 48 hours of intubation.
346
What are typical and atypical pneumonia organisms?
Don’t name them.
Typical pneumonia organisms are those that cause the classical pathogenesis - acute inflammatory response with fibrin-rich exudate and infiltration of neutrophils & macophages into the alveoli.
Atypical pneumonia organisms are less common and usually cause a different pathophysiology. They are not grown on normal agar plates, and are often more diffuse, causing extra-pulmonary manifestations.
347
What are some typical pneumonia organisms, and what percentage of pneumonia infections do these account for?
85%.
348
What are some atypical pneumonia organisms, and what percentage of pneumonia infections do these account for?
15%.
349
What is the diagnosis of community acquired pneumonia?
Clinical picture and imaging:
- Cough (with or without sputum), dyspnoea, fever, tachycardia, crackles and bronchial breathing, dull percussion, and pleuritic chest pain.
- Consolidations, infiltrates or cavitations.
350
What non-microbiology investigations can be used to guide a pneumonia diagnosis?
FBC.
U&E.
CRP.
ABG.
Chest X-ray.
351
What are some microbiological investigations to diagnose pneumonia?
Blood cultures.
Sputum staining.
Nose and throat swabs for viral causes - epithelial cells with virus within.
Urine - antigen testing for legionella or pneumococcus.
352
What is the treatment of mild-moderate pneumonia, and why?
Amoxicillin, or doxycyline/ erythromycin/ clarithromycin if penicillin allergic.
This is because it is usually caused by streptococcus pneumoniae.
353
What is the treatment of moderate-severe, requiring hospital admission pneumonia, and why?
Amoxicillin/ co-amoxiclav AND clarithyromycin/ doxycycline.
This is because a macrolide is required to cover atypical causes of pneumonia.
354
What are the most common causes of hospital acquired pneumonia?
355
What is given for hospital-acquired pneumonia patients, why?
Co-amoxiclav to cover staphylococcus aureus, gram negative bacteria and atypical pathogens.
Second line is piperacillin/ tazobactam or meropenem.
356
Who is aspiration pneumonia most commonly seen in, why?
Patients who have epilepsy, have had strokes, or alcoholics due to aspiration of endogenous secretions.
Patients who have nearly drowned, due to aspiration of exogenous material.
357
What kinds of infectious organisms can be seen in aspiration pneumonia and how is it treated?
Viridans streptococci and anaerobes.
Only if it is relatively severe is it treated, as if it is mild then it is most frequently chemical pneumonitis.
It is treated with co-amoxiclav.
358
What are the most common organisms that cause LRTI with the following conditions:
- HIV.
- Neutropenia.
- Bone marrow transplant immunosuppression.
- Splenctomy.
359
How can the following border help to localise consolidations?
Right heart border.
Right hemidiaphragm.
Left heart border.
Left hemidiaphragm.
360
What can be some causes for cavities on chest X-rays?
361
What is the MacFarlane approach to acute bronchitis?
<21 days.
Cough with another 1 of; sputum production, wheeze, chest pain.
362
What is bronchiolitis?
Viral infection of the bronchioles, caused by respiratory syncytial virus, in children younger than 12 months.
363
What is empyema?
Collection of pus in the pleural cavity, associated with pneumonia, or post-thoracic surgery or trauma.
364
What is a lung abscess?
Why do they occur?
Collection of pus in the lung that leads to cavity formation, a thickened wall and air-fluid levels within the cavity on X-ray.
They commonly occur due to microbial infection causes necrosis of the lung parenchyma. They can lead to a purulent cough.
365
What is the infection prevention within the alveoli?
Surfactant has anti-microbial activity.
Alveolar macrophages.
Alveolar flora.
366
What are some technique issues with spirometry?
Breathing through the nose.
Coughing or laughing.
Submaximal effort.
Premature termination of exhalation.
Incomplete seal around the mouthpiece.
367
What kind of spirometry error is shown in the graph, what is the test implication and how is this corrected?
Premature termination.
Falsely reduced FVC, which can be interpreted as a restrictive impairment.
Coach the subject to keep blowing out until told to stop.
368
What kind of spirometry error is shown in the graph, what is the test implication and how is this corrected?
Cough.
Falsely reduced or elevated FEV1, depending on the strength of the cough. Significant coughing could also falsely reduce FVC.
Offering a drink of water prior to the test initiation.
369
What kind of spirometry error is shown in the graph, what is the test implication and how is this corrected?
Sub-maximal inhalation.
Falsely reduced FVC, indicating a restrictive breathing impairment.
Coach the subject to fill their lungs, taking in as much air as they can.
370
Why perform pulmonary function tests?
Diagnose patients with respiratory symptoms.
Establish severity and progression of the lung disease.
Assess treatment response.
Monitor patients on medication that are potentially lung toxic.
371
What respiratory problem can develop as a result of chemotherapy?
Pneumonitis - non-infectious inflammation of the lung parenchyma.
372
What is the ‘normal’ result of a peak expiratory flow test, and what is it used for?
Greater than or equal to 80% of the predicated average value based on the patient’s height, gender at birth, age and ethnicity.
It is useful for monitoring asthma as their peak flow may be reduced before they experience symptoms, and for a baseline when asymptomatic to be able to determine if an exacerbation is occurring.
373
What device measures peak expiratory flow?
Peak flow rate meter.
374
What is tidal volume?
The amount of air moving in and out of our lungs at rest.
375
What is inspiratory reserve volume?
The additional amount of air that can be inhaled after normal inspiration - volume of air breathed in above tidal volume.
376
What is expiratory reserve volume?
The additional amount of air that can be exhaled after normal expiration - the volume of air breathed out beyond tidal volume.
377
What is inspiratory capacity, and how do we calculate it?
The total volume of air that can be inspired following a normal expiration.
IC = tidal volume + inspiratory reverse volume.
378
What is functional residual capacity, and how do we calculate it?
The volume of air present in the lungs at the end of passive expiration.
FRC = expiratory reserve volume + residual volume.
379
What is vital capacity and how do we calculate it?
The volume of air that can be exhaled after maximal inspiration.
VC = inspiratory reserve volume + tidal volume + expiratory reserve volume.
380
What is total lung capacity and how do we calculate it?
The volume of air within the lungs at the end of a maximal inspiration.
TLC = inspiratory reserve volume + tidal volume + expiratory reserve volume + residual volume.
381
What is FEV1?
Forced expiratory volume in 1 second - the maximum volume of air that can be forcefully expired within 1 second after maximal inspiration.
382
What is FVC?
Forced vital capacity - the total amount of air forcefully exhaled after maximal inspiration, that occurs over 6 seconds.
383
What is the initial gradient of a volume-time plot?
The peak expiratory flow rate - the maximal speed of expiration.
384
What can be calculated using a flow-volume loop?
Tidal volume.
Expiratory reserve volume.
Inspiratory reserve volume.
Inspiratory capacity.
385
What are the changes in lung volumes seen in an obstructive lung disease pattern, and why?
Total lung capacity, functional residual capacity and residual volume all increased due to air trapping from collapse of the small airways on expiration.
Reduced FVC and FEV1 but FEV1 more - FEV1:FVC < 0.7.
386
What is the pattern of the flow-volume graph seen in an obstructive lung disease patient and why?
Scalloping - obstruction on expiration due to narrowing or collapse of the small airways.
387
What are the changes in lung volumes seen in a restrictive lung disease pattern, and why?
All lung volumes are decreased.
FEV1 and FVC are reduced, but roughly proportionately.
There is a decreased ability for air to be taken in, and so less air can be removed.
388
What are the appearances of a patients volume-time and flow-volume loop graphs, with a patient with a restrictive lung disease?
Volume-time plot will show low volumes but with a normal shape - FVC and FEV1 are proportionately reduced as there is less air to breathe out.
Flow-volume plot is a similar shape to normal but smaller volumes at all points, showing a wizards hat appearance.
389
What is a DLCO test, what does it measure and what conditions can a decrease be seen in?
A diffuse capacity carbon monoxide - testing the diffusion capacity of the lungs, providing information about the alveolar-capillary membrane.
It can be decrease in:
- Emphysema due to a decreased surface area.
- Pulmonary fibrosis due to an increased diffusion distance.
390
What would an abnormal DLCO with a normal chest X-ray and spirometry suggest?
An issue with the capillary membrane, such as idiopathic pulmonary arterial hypertensions, chronic thrombo-embolic disease of the lung.
391
What is bird-fanciers lung?
A hypersensitive pneumonitis, which can progress to interstitial lung disease and pulmonary fibrosis.
392
How can restrictive lung diseases be differentiated between?
A parenchymal lung disease will show a spirometry restrictive pattern and an abnormal DLCO.
A chest wall abnormality or neuromuscular disease will show a spirometry restrictive pattern but normal DLCO.
393
What does the helium dilution test test for, and how is it performed?
Functional residual volume, and therefore residual volume:
- At the end of normal tidal expiration, a person is connected to a container with a known concentration of helium.
- The container is a closed circuit and the volume is known.
- The person continues to rebreathe into the container until equilibrium is reached at 4-7 minutes.
- A new concentration of helium is established within the container, as it mixes with the air that was already within the lungs.
394
Why does the helium dilution test work, and how are functional residual capacity and residual volume calculated?
Helium cannot cross the alveolar-capillary membrane.
C1xV1 = C2xV2.
C1 is known as the initial helium concentration.
V1 is known as the volume in the contained.
C2 is known as the end concentration of helium.
V2 = volume in the container + functional residual capacity.
Residual volume = functional residual capacity - expiratory reserve volume (spirometry).
395
What does a nitrogen washout measure and how is it performed?
Anatomical dead space - volume in the conducting airways that does not undergo gas exchange:
- Subject takes a maximum inspiration of 100% oxygen.
- This O2 mixes with the alveolar air, which contains nitrogen.
- Person exhales through a one-way valve measuring the percentage of nitrogen in the exhaled air and the volume exhaled.
396
How does the nitrogen washout calculate the anatomical dead space?
Nitrogen concentration of exhaled air gradually increases until a plateau is reached where only alveolar gas is being exhaled.
At this plateau, a line is drawn onto a plotted curve at the percentage of nitrogen exhaled, where the X-axis shows the anatomical dead space.
397
How is the carbon monoxide transfer factor performed?
Subject first fully exhales, and then takes a maximal inspiratory breath of air, containing a tiny fraction of carbon monoxide.
The breath is held for 10 seconds.
The patient then exhales and gas is collected mid-exhale, as an alveolar sample.
The concentration of CO measured shows how well it diffused across.
398
Why can the carbon monoxide transfer factor be used reliably?
CO bind with a very high affinity for Hb.
The concentration gradient is maintained for the entire time the gas is in contact with the blood, meaning the limiting factor is the diffusion capacity.
399
How is spirometry performed?
400
Why does bronchiectasis cause an obstructive lung disease?
Inflammatory infiltrate in the walls of the small airways, narrowing the lumen.
Increased and thickened mucous secretions within the lumen of the small and medium airways.
401
How long can the expiration during spirometry be, with a COPD patient?
Up to 15 seconds.
402
When are pulmonary functions tests classed as abnormal?
When the result falls outside of the 95% confidence range for height, sex and age.
403
What is body plethysmography?
A breathing assessment to determine volumes within the lungs when breathing in and out, and can show total lung capacity.
404
Identify the aorta pulmonary window.
Describe what it is and what can be found within it.
A space between the aortic arch and pulmonary artery - recurrent laryngeal nerve and lymph nodes.
405
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
Hyperinflation of the lungs leading to a flattened diaphragm and blunting of the costophrenic angle.
It is most commonly seen in COPD patients.
406
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
State some differentials.
Left middle-upper zone opacity, near the hilum.
Most likely lung cancer due to the well-defined border, but could also be:
- Lymphoma/ lymphadenopathy.
- TB.
- Solitary metastasis.
407
What cancers commonly metastasise to the lungs?
Breast.
Bladder.
Colon.
Prostate.
Germ cell.
Head and neck squamous cell carcinomas.
408
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
State two differentials.
Diffuse, bilateral pulmonary round opacities.
Multiple lung metastases, but could be:
- Diffuse pulmonary pneumonia.
- ARDS.
409
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
Right upper zone opacity.
Slight tracheal deviation to the right.
Pancoast tumour.
410
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
Opacity in the upper zone of the left lung.
Elevated left hemidiaphragm.
Pancoast tumour that has invaded the phrenic nerve.
411
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
C-shaped curve (meniscus) of the lung with lower zone opacities suggesting pleural effusion.
412
What should be done with a pleural aspiration to aid diagnosis?
Send a sample to microscopy, culture and sensitivities for infection potential.
Send to histology for suspicion of neoplasms.
Check for protein within the fluid:
- If it has protein it is exudate and more likely to be an infective/ cancerous cause.
- If it does not have protein then it is transudate and is more likely to be congestive heart failure.
413
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
Cardiomegaly.
Loss of the left costophrenic angle.
Bat-wing sign.
Pulmonary oedema due to heart failure.
414
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
‘Air space shadowing’
Bulging or thickening of the fissures.
Right upper lobe opacity.
Pneumonia.
415
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
State some things that can also be seen due to this.
Rounded opacity in the right upper zone.
Not seen in this but can be seen:
- Pleural effusion.
- Lymphadenopathy.
Lung cancer.
416
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
State some things that can also be seen due to this.
‘Bat wing’ perihilar shadowing.
Lots of peripheral lines due to interstitial fluid.
Bilateral, diffuse patchy shadowing.
Things that could also be seen:
- Kerley B lines - short, sharp lines at the edge of the lung.
- Pleural effusions.
Pulmonary oedema.
NOTE: frothy pink-white sputum!!
417
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
Dextrocardia - apex of the heart points to the incorrect side.
Aortic arch on the right.
Stomach on the right.
Liver on the left.
Situs inversus totalis.
418
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
Multifocal peripheral opacities.
Ground-glass densities.
COVID-19.
419
What is Kartagener syndrome?
Situs inversus totalis, bronchiectasis and chronic sinusitis.
420
Why are osteophytes not seen on the left side of the vertebral column?
The pulsations of the aorta prevents their formation.
421
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
State some things that can also be seen due to this.
Bronchiectasis - tram-track signs.
Diffuse thickening of the bronchial walls.
Venous catheter.
Could also see:
- Airway plugging - bronchi with mucous occluding it, making them look opaque.
422
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
State some things that can also be seen due to this.
Wedge-shaped opacity due to infarction.
May also be able to see:
- Straightening of interventricular septum on CT due to the increased pressure in the right ventricle.
Often a normal chest X-ray.
Pulmonary embolism.
423
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
State some things that can also be seen due to this.
Streaky linear lucencies parallel to the mediastinum, due to air running between the fascial layers.
Gas in the neck.
May also see gas in the axillae.
Pneumomediastinum.
424
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
Pleural plaques (calcifications) on the diaphragm and peripheral lung pleural, due to asbestos exposure.
Holly-leaf sign.
425
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
Reduced volume of the lung.
Lung encased by rind of tissue.
Thickening of the pleura.
Mesothelioma.
426
What percentage of people survive lung cancer for 10 years or more?
10%.
427
What percentage of lung cancers are preventable?
79%.
428
Why is the median survival for lung cancer so poor?
Because they present late, where the presentation of the patient is often either stage 3 or 4.
They are also more common in the elderly population, who have a poorer tolerance to treatments and more co-morbidities.
The most common cause is smoking, which often causes coronary heart disease and other complications first.
429
What percentage of lung cancer deaths are caused by smoking?
70-80%.
430
What are some non-smoking causes of lung cancer?
Asbestos.
Radon.
Other occupational carcinogens, such as chromium, nickel and arsenic.
Genetic/ familial causes.
431
How is lung cancer screened for?
Low-dose CT scans.
432
What do each of the 3 factors in the TNM staging for lung cancer consist of?
T - tumour size, location and number of nodules.
N:
- N1 = ipsihilar lymph nodes.
- N2 = ipsilateral mediastinal lymph nodes.
- N3 = contralateral mediastinal or hilar lymph nodes. Scalene or supraclavicular lymph nodes.
M - metastases inside the lung, outside the lung in one organ or outside the lung in several organs.
433
What is the difference between a chest CT and a staging CT?
Staging CT scan further down, to the bottom of the kidneys to look for metastatic spread to distant organs.
434
What stages of lung cancer is surgery available for?
Stages 1 and 2.
435
What are some imaging tests for staging?
CT scan.
PET scan.
Chest X-ray.
Ultrasound.
ECHO.
MRI.
Bone scan.
436
Why use a PET scan?
Help differentiate between benign and malignant tumours, and between localised and metastatic tumours.
Can look for metastases in the bone and bowel that a CT scan does not.
437
What are some tissue sampling techniques for lung cancer?
Bronchoscopy - endobronchial.
Ultrasound.
CT biopsy.
Thorscopy.
Surgical.
438
What are some symptoms due to primary tumour lung cancer?
439
What are some symptoms due to lung cancers regional metastases?
440
What are some symptoms due to lung cancers distant metastases?
441
What are some symptoms due to lung cancers effect on metabolism?
442
What are some endocrine paraneoplastic syndromes?
443
What are some neurological paraneoplastic syndromes?
444
What are some haematological, cutaneous and skeletal paraneoplastic syndromes?
Haematological - anaemia and thrombocytosis.
Cutaneous - dermatomyositis.
Skeletal - finger clubbing.
445
Why would a biopsy not be performed?
If the cancer is too advanced so treatment would not be beneficial.
If the patient has too many health problems to withstand effective treatment.
If the patient does not want treatment.
446
What are the different types of lung cancers?
Non-small cell lung cancer:
- Squamous cell carcinoma.
- Adenocarcinoma.
- Large cell carcinoma.
Small cell carcinoma.
Rare tumours, such as carcinoid.
447
What is the performance status of a patient?
448
What are the different uses for radiotherapy?
Radical - with curative intent.
Palliative - symptom control.
449
What are the different uses for combination chemotherapy?
For small cell, it is potentially curative.
Non-small cell, predominantly for symptoms control.
Neoadjuvant - to shrink the tumour before surgery.
Adjuvant - to remove remaining cancer cells after surgery.
450
What are non-small cell lung cancers and what are their treatments, generally?
They are a group of cancers consisting of squamous cell carcinoma, adenocarcinoma, and large cell carcinoma.
They metastasise slower and so surgery is usually more successful.
451
What percentage do squamous cell carcinomas make up in lung cancer and what are they often associated with?
40%.
They are often associated with PTHrP paraneoplastic syndrome - humoural hypercalcaemia of malignancy.
452
What type of lung cancer is most commonly associated with non-smokers?
Adenocarcinoma.
453
What is mesothelioma and what is the most common risk factor?
Cancer of the pleura.
Asbestos exposure.
454
What are small cell lung cancers and what are their treatments, generally?
Cancer of the lung that is most commonly associated with paraneoplastic syndromes and metastasise rapidly.
Chemo-responsive.
455
What are paraneoplastic syndromes due to?
An abnormal immune response to cancer.
456
What paraneoplastic syndromes are most commonly associated with small cell carcinoma?
SIADH.
Cushing’s disease - ACTH release.
Lamberton-Eaton syndrome - body attacks the neuromuscular junctions causing myaesthenia.
457
What paraneoplastic syndrome is most commonly associated with adenocarcinoma of the lung?
Hypertrophic pulmonary osteoarthropathy.
458
What is hypertrophic pulmonary osteoarthropathy.
A triad of:
- Serositis.
- Finger clubbing.
- Arthropathy of the large joints.
459
Why can dyspnoea occur in lung cancer?
Central tumours may occlude the airways.
Malignant pleural effusions may occur.
They are often co-existing with other lung conditions, such as COPD.
460
How may a pancoast tumour present?
C8/T1 dermatome numbness due to invasion of the brachial plexus.
Small muscles of the hand wasting, associated with the ulna nerve.
Horner’s syndrome - miosis, ptosis and anhidrosis - due to invasion of the sympathetic chain.
Hoarseness of the voice due to recurrent laryngeal nerve invasion.
461
Why may haemoptysis present in lung cancer?
Tumour erosion of the airway.
462
What is the CT chest screening age for lung cancer in the UK?
55-74.
463
What is a simple pneumothorax?
A hole within the pleura that allows air to move in and out, leading to pressure equilibration with the atmospheric pressure.
464
What is the pressure difference between the pressure inside the lung and the intrapleural pressure called?
Transpulmonary pressure.
465
What are the borders of the ‘safety triangle’?
Anterior - pectoralis major.
Posterior - latissimus dorsi.
Inferior - 5th intercostal space.
466
If a chest drain was inserted out of the safety triangle, what could be affected?
Liver.
Heart - potentially cause cardiac tamponade.
Pulmonary vessels.
Lung and other pleura.
467
Why should chest drains be inserted with care in COPD patients?
They are more at risk of secondary pneumothoraces due to rupture of bullae.
468
When can chest drains be removed and what is the follow-up for this?
48 hours after the bubbling stops, and chest X-ray confirms there is no longer a pneumothorax.
48 hours after the removal of the chest drain, another chest X-ray is performed to ensure a recurrent pneumothorax has not occurred.
469
What is empyema a risk factor for, and what should be done for this?
Pulmonary embolism.
Give prophylactic anti-coagulants.
470
What is CPAP?
Continuous positive airway pressure - maintains a continuous pressure to constantly stent the airways open, preventing airway collapse.
471
What condition should CPAP never be used for?
State why.
Pneumothorax.
Introducing positive airway pressure can shear the pleura, leading to increased pressure within the pleural space, compressing the mediastinum, which can cause cardiac arrest and often results in death.
472
What is breathlessness?
A subjective awareness of increased effort of breathing.
473
State some potential causes of chest pain.
474
Why is breathing in more painful when coughing or breathing in, with pleuritic chest pain?
The parietal and visceral pleura slide over each other.
When breathing in, there is an increase in intrapulmonary pressure, leading to the pleura rubbing against each other.
When coughing, there is an increased intrathoracic pressure, which leads to increased friction between the parietal and visceral pleura.
475
What is the commonest cause of an acute cough?
Why?
Upper respiratory tract infection.
Post-nasal drip irritates the vocal cords (cough receptors), causing an acute cough to develop.
476
What conditions see the following sputum types:
- Clear.
- Yellow/ green.
- Large volumes of yellow or green.
- Bloody.
- Pink-frothy.
Clear - chronic bronchitis or COPD.
Yellow/ green - infection (neutrophils present).
Large volumes of yellow or green - bronchiectasis.
Bloody - lung cancer, TB, PE.
Pink-frothy - left ventricular heart failure.
477
What are some extra-thoracic airway structures that, when narrowed, can cause stridor?
Supraglottis.
Glottis.
Infraglottis.
Trachea.
478
What oxygen saturation and partial pressure of oxygen can central cyanosis occur in?
<85%.
<8kPa.
479
What does a stony-dull percussion suggest?
There is fluid accumulation in the lung/ pleural space.
480
What are crackles in auscultation caused by, and what are some types and examples of them?
Snapping open or shut of the alveoli and/or small bronchi. Excess fluid in the airway.
Fine - pulmonary fibrosis.
Course - COPD and bronchiectasis.
481
What is the mechanism behind course crackles?
Consolidation, such as air bubbling through mucous secretions.
482
Why does a pneumothorax cause dyspnoea?
There is an increase in air within the pleural space, increasing the pressure here.
This means that there is loss of the pleural seal, and so the lung moves away from the thoracic wall.
The air within the pleura and the elastic recoil of the lungs limits the expansion of the lungs.
There are higher pressures within the lungs and smaller volumes so less air moves into the lungs, impairing inspiration and gas exchange.
483
What is a spontaneous pneumothorax, and what are the two types?
Accumulation of air within the pleural space without obvious trauma or iatrogenic causes.
Primary - no underlying lung disease.
Secondary - has an underlying lung disease.
484
What are the different types of traumatic pneumothoraces?
Iatrogenic - caused by an invasive medical procedure, such as a pleural tap, biopsy, fine needle aspiration or central vein cannulation.
Accidental - direct injury to the thorax, such as a penetrating injury or a fractured rib.
485
What is a tension pneumothorax?
Where air goes into the pleural space but cannot be removed, increasing the pressure within the pleural space, increasing the pressure on the mediastinum, leading to cardiovascular collapse.
486
How is a simple pneumothorax treated?
Needle aspiration.
Intercostal chest drain - slowly lets the air out, is more likely to work but is more invasive and uncomfortable.
487
Where should a chest drain be placed?
Within the triangle of safety, above the rib.
488
How is air prevented from entering the pleura with a chest drain?
Describe.
Water seal - water moves up into the drain, but doesn’t enter the lung on inspiration, and then is pumped out on expiration.
Hickman valve.
489
How is a transudate or exudate pleural effusion distinguished between?
Light’s criteria for exudate:
- Ratio of serum protein to pleural fluid > 0.5
- Ratio of serum LDH to pleural fluid > 0.6
- Pleural fluid LDH > 2/3rds of the upper limit of the normal serum value.
490
How are pleural effusions treated?
Depends on the cause.
Removal of the fluid:
- Drain.
- Diuresis if transudate.
Antibiotics to remove pathogen.
491
Describe the cough reflex.
Irritation of cough receptors via chemical or mechanical stimuli.
Vagus nerve sends impulses to the cough centre within the medulla.
Efferent impulses are then sent down the vagus, phrenic and spinal motor nerves:
- Phrenic nerve stimulates the contraction of the diaphragm for a large inspiration.
- Glottis closes, increases the intra-thoracic pressure.
- Accessory muscles of expiration contract for the glottis to open and rapid excursion of air to occur.
492
What are the parameters for acute, sub-acute and chronic cough?
Acute - < 3 weeks.
Sub-acute - 3-8 weeks.
Chronic - > 8 weeks.
493
What are some causes of an acute cough?
URTI
COVID-19.
Acute bronchitis.
Pneumonia.
Pneumothorax.
Pulmonary embolism.
Acute exacerbations of asthma, COPD, bronchiectasis.
494
Where are cough receptors found?
Trachea, main carina, branching points of the large airways and more distal smaller airways, as well as the pharynx.
495
What are some causes for sub-acute cough?
Post-infectious cough - mycoplasm pneumoniae, bordetella pertussis. Often dry, persistent cough after obvious respiratory tract infection.
496
What are some causes for chronic cough?
Upper airway cough syndrome - post-nasal drip.
COPD.
Bronchiectasis.
497
What is the examination appearance of a post-nasal drip?
Visible mucous.
Cobblestone appearance of the posterior oropharyngeal wall and local upper airway structures.
498
What suggests whooping cough?
Cough lasting more than 14 days.
Possible vomiting after coughing.
Inspiratory whoop.
499
What MI are GI upset, nausea and vomiting associated with?
Inferior wall.
500
What are the symptoms of a pleural effusion?
Pleuritic chest pain and a dull ache.
Shortness of breath.
501
What are the examination findings of a pleural effusion?
Asymmetrical chest expansions.
Stony dullness to percussion.
Decreased tactile fremitus (vibration of chest wall).
Decreased vocal resonance.
Absent breath sounds.
502
What are some investigations of pleural effusions?
Chest X-ray - blunting of costophrenic angle, opacification of lower lung field. Pleural thickening can be seen in pleural tumours.
Pleural tap.
503
What is the pathophysiology of a primary spontaneous pneumothorax?
A rupture of an underlying sub-pleural bleb (<1cm) or bulla (>1cm), creating an opening in the visceral pleura.
504
What is the greatest risk factor for a primary spontaneous pneumothorax?
Smoking - increasing the risk 10-20 fold.
505
What are the haematological and pneumatological signs of a tension pneumothorax, why?
Elevated JVP and dilation of the veins in the upper limbs and head.
Tachycardia due to decreased pre-load and therefore stroke volume.
Tachypnoea due to impaired gas exchange.
Tracheal shift.
Hypotension.
506
What are the presenting complains of a pneumothorax?
Pleuritic chest pain.
Breathlessness.
507
What is the mechanism of a pleural effusion?
Disruption of the balance between hydrostatic and oncotic pressures, or disrupted lymphatic drainage.
508
What protein content is classed as an exudative pleural effusion?
>30g/L.
509
What are the common causes of transudative pleural effusion?
Congestive heart failure - increased capillary hydrostatic pressure.
Nephrotic syndrome and cirrhosis - decreased capillary oncotic pressure.
510
What are the common causes of exudative pleural effusion?
Increased capillary permeability due to;
- Bronchial carcinoma.
- Pneumonia.
- Tuberculosis.
- Pulmonary infection from a PE.
- Metastases.
511
What is the most common cause of an exudative pleural effusion?
Malignancy - primary or secondary.
512
What 3 types of pleural effusion may pneumonia be associated with?
Simple parapneumonic effusion.
Complex parapneumonic effusion.
Empyema.
513
How do you calculate smoking pack years?
Multiply the number of packs of cigarettes smoked per day by the number of years the person has smoked for.
514
What is occupational asthma and who may it be seen in?
Asthma that comes on when exposed to certain substances which are the breathed in, such as dust, chemicals, fumes and animal fur.
This may be seen in cleaners and hairdressers, amongst others.
515
What lung condition can working in a textile mill predispose you to?
Pulmonary fibrosis.
516
What is allergic alveolitis?
State some conditions which this is categorised as.
A hypersensitivity interstitial lung disease, which occurs due to immune-related reactions to substances which affect the lung parenchyma.
Bird fanciers lung and farmers lung are two types.
517
What is the pathophysiology of bronchial breathing?
Where there is accumulation of material within the lungs, leading to turbulent airflow in the large airways.
It can suggest the presence of consolidation or fibrosis.
518
What volumes of pleural fluid are required for blunting of the costophrenic angles, and for meniscus formation?
Blunting of the costophrenic angles = 50ml.
Meniscus formation = 200ml.
519
What test is performed for diagnosis of extra-pulmonary TB?
Urine sample for acid-fast bacilli culture.
520
What test is done for diagnosis of active TB?
Obtaining 3 sputum samples for acid-fast bacilli smear microscopy and culture.
521
If a patient contracts TB, what proportion of patients will not clear it, and then will go on to develop symptoms?
70% of patients that contract TB will clear the TB before colonisation, through the immune system.
30% will then develop primary TB:
- 90% of these are latent infections.
- 10% will form active TB, which can spread via the haematological route to become disseminated.
522
What is seen in this chest X-ray and what condition is it most frequently seen in?
Bilateral hilar lymphadenopathy, most commonly seen in sarcoidosis.
523
What is the biggest cause of preventable disease-related morbidity?
Tobacco use.
524
What proportion of people in the UK smoke, and who is it seen more in?
1 in 8 people.
It is seen in 80% of homeless people, 40% of people with mental health diseases and 25% of manual workers.
It is far more common in more deprived households.
525
Name some conditions that smoking can cause.
Lung cancer - kidney, bladder, prostate are all increased.
COPD.
Asthma.
Stroke.
Myocardial infarctions.
Sexual dysfunction.
Rheumatoid arthritis.
Infections.
Hearing loss.
Sudden infant death.
Macular degeneration.
526
What are the two indexes which are asked to determine someone’s addiction to smoking?
527
What is the cycle of smoking addiction?
The nicotine released from cigarettes acts on nAChRs within the brain.
This causes dopamine to be released.
This causes satiety and positive feelings.
As the amount of nicotine reduces, there is a reduction in dopamine released, causing withdrawal symptoms.
528
What drug is champix and what is its mechanism?
State the other drug which has the same action.
Varenicline.
It is a partial agonist for nAChR, which causes dopamine release.
Cytisine.
529
What is the action of buproprion for smoking treatment?
It inhibits the re-uptake of dopamine, increasing the positive feelings that are felt.
530
What is done to test for smoking in pregnancy?
Measuring the carbon monoxide levels - 10-20ppm suggests that they are still smoking.
531
What are the 6 steps for treating tobacco dependency?
Provide both short acting and long acting nicotine products.
