Respiratory Flashcards
What does the respiratory system develop from?
The diverticulum of the pharynx - outgrowth of the embryonic pharynx, which bifurcates multiple times.
What is the conducting part of the airways?
Trachea, primary (main) bronchi, secondary (lobar) bronchi, tertiary (segmental) bronchi, bronchioles and terminal bronchioles.
What is the respiratory part of the airway?
The alveolar bronchioles and alveoli.
What are the borders of the thorax?
Anteriorly - the costal cartilages and sternum.
Laterally - ribs.
Posteriorly - vertebral column.
Inferiorly - diaphragm.
How are the ribs shaped and articulate with the vertebral column, and how does this correlate to the movement formed?
They are wedge-shaped, with their superior and inferior facts articulating with two vertebra to facilitate rotational movements.
What two specific movements can the thoracic wall perform?
Lateral movement - bucket handle movement.
Anterior, elevation movement - pump-handle movement.
How far can the diaphragm move during expiration, from flat?
It can elevate 2 intercostal spaces in distance.
What is the origin of the diaphragm and what does it converge to form?
Originates from the rib cage and costal cartilages to form a central tendon.
What are the 3 layers of the intercostal muscles, and what movements do each of them cause? State the direction of their fibres.
External intercostal - passive inspiration, inferomedial direction.
Internal intercostal - forced expiration, superomedial direction.
Innermost intercostal - forced expiration, superomedial direction.
What are the 3 perforations of the diaphragm and at what level do they pass through?
Vena cava - T8.
Oesophagus - T10.
Aortic hiatus - T12.
What are the accessory muscles of inspiration?
Pectoralis major, sternocleidomastoid, scalenes, and serratus anterior.
What are the intercostal neurovascular bundle, and what happens to them?
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.
What is the azygous system supported by, what does it drain into, and what is its importance in a critical situation?
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.
What is the diaphragms innervation, and why can it have referred pain?
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.
What are the lobes and fissures of the lungs?
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.
What is the relevance of the fissures?
Pleural fluid accumulation can occur in them.
What is the difference between the two main bronchi, relating to potential pathology?
The right main bronchi is more vertical, meaning that foreign bodies entering the lungs will be more likely to enter this.
What is the hilum of the lung and what are the contents locations?
The bronchus is posterior.
The branches of the pulmonary arteries are supero-medial.
The branches of the pulmonary veins are inferior.
What is the difference between the left and right bronchus?
The right bronchus has a branch that supplies the superior lobe and one that supplies the middle and inferior lobes.
What is the costodiaphragmatic/ costophrenic recess, and what is it called when fluid enters this?
It is the space inferior to the lungs that the lungs expand into.
When fluid enters it, it is called pleural effusion.
What is the difference between the sizes of the left and right lungs, and what effect does this have on the diaphragms position?
The right lung bigger and heavier, and is shorter and wider, meaning that the right dome of the diaphragm sits higher.
Where does the parietal and visceral pleura meet, and what does this form?
They meet at the hilum, forming the pulmonary ligament to the mediastinum.
Explain the tracheobrachial tree.
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.
Explain the pulmonary supply to the lungs.
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.
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.
What are the 3 nervous supplies to the lungs?
Sympathetic - post-synaptic neurons.
Parasympathetic - from the vagus nerve.
Visceral afferent fibres.
What is the function of the sympathetic innervation of the lungs?
Bronchodilation, vasoconstriction and decreased glandular secretion.
What is the function of the parasympathetic innervation to the lungs?
Bronchoconstriction, vasodilation and increased glandular secretions.
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.
What two different nervous supplies does the parietal pleura have?
Phrenic nerves.
Intercostal nerves (pain).
What is the neural control of ventilation?
Neurons in the respiratory centres of the brain, specifically the medulla.
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.
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.
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.
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.
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.
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.
What is ventilation?
The volume of air that enters and leaves the lungs.
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.
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.
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.
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.
What is the trans pulmonary pressure?
The intrapulmonary pressure - pleural pressure.
What is compliance?
The distensibility of the lungs - the change in volume / the change in pressure.
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.
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.
When is surfactant synthesised?
It begins to be synthesised from week 24-26.
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.
What are interstitial lung diseases?
Thickening of the alveolar septa, fibroblast proliferation and collagen deposition.
What is the end result of interstitial lung disease?
Pulmonary fibrosis.
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.
Outline the different types of interstitial lung diseases.
How does interstitial lung diseases effect gas exchange?
The thickening of the alveolar walls means that it is harder for gases to diffuse across.
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.
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.
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.
What is emphysema?
This is where elastases break down the elastin in the lungs, increasing compliance and decreasing elastic recoil, leading to narrow airways.
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.
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.
What are two causes of emphysema?
Alpha-1 antitrypsin deficiency.
Smoking - emphysematous COPD.
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.
What are the symptoms of emphysema patients?
Shortness of breath, reduced exercise tolerance and cough.
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).
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.
What is atelectasis?
Incomplete expansion of the lungs, producing areas of airless pulmonary parenchyma.
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.
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.
What is hypoventilation?
Poor expansion of the thoracic cavity or lungs, leading to hypercapnia.
What can inhalation of food molecules lead to?
Airway obstruction.
Infection - aspiration pneumonia.
What is the glottis?
The vocal cords and aperture (hole) between the cords - laryngeal inlet.
How do the vocal cords become adducted, and what nerve innervates this?
Intrinsic laryngeal muscles, innervated by the recurrent laryngeal nerve.
What is the concave aspect of the manubrium called?
Jugular notch.
What do the intercostal neurovascular bundle supply?
Intercostal muscles, parietal pleura and overlying skin.
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.
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.
What abdominal organs are protected by the ribs?
Liver, spleen, stomach and upper kidneys.
What is the hemi-thorax made up of?
Thoracic rib cage, diaphragm and mediastinal surfaces.
What is the angle between the left and right main bronchi called?
Carina - the distal aspect of the trachea.
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.
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.
What nerve fibres are involved in the stimulation of the cough reflex?
The vagal afferent fibres.
What is the surface marking for the horizontal fissure?
The 4th rib, starting at the 4th costochondral junction.
How much further down does the pleural cavity extend from the lungs?
2 ribs lower.
What nerves can be compressed by enlarged hilar lymph nodes?
Phrenic nerve.
Recurrent laryngeal nerve.
What are the terms for blood and lymphatic fluid accumulation within the pleural space?
Blood = haemothroax.
Lymphatic fluid = chlyothorax.
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.
What are type 1 pneumocytes connected to each other by?
Tight junctions.
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.
What are the secretions from the trachea and bronchi?
Mucin and water, forming mucous.
IgA.
Antiproteases.
Lysozyme.
Serum proteins.
How are bronchioles kept open?
They have elastic muscle fibres within the walls.
The alveoli surround the bronchioles, tethering them open - radial traction.
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.
What is the alveolar interstitium formed of?
Predominantly elastin fibres with some collagen fibres.
What is the distance between the alveoli and its capillary?
0.2 um.
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.
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.
Between which layers of the intercostals are is the neurovascular bundle located?
Between the inner and innermost intercostal muscles.
What proportion of the inspired air in tidal volume reached the alveoli?
2/3rds.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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).
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.
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.
State some conditions where V:Q < 1.
Fibrosis of the lungs.
Pneumonia.
Asthma.
COPD.
Cystic fibrosis.
Pulmonary oedema - left sided heart failure.
State some conditions where the V:Q > 1.
Right sided heart failure.
Pulmonary embolism.
Hypovolaemia.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
What is the maximum unloading of oxygen, and what is normal oxygen extraction?
Maximum = 70%.
Normal = 30%.
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.
What are the symptoms of carbon monoxide poisoning?
Headache.
Nausea.
Vomiting.
Slurred speech.
Confusion.
Initially few respiratory symptoms.
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.
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.
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.
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.
In arterial blood gas analysis, what can be used to determine the binding of different gasses to haemoglobin?
Co-oximeter.
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.
What is Farmer’s lung?
An interstitial lung disease.
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.
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.
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.
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.
What are the 3 methods of carbon dioxide transport, and their proportions?
Carbamino compounds - 30%.
Bicarbonate ions - 60%.
Dissolved in plasma - 10%.
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.
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.
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.
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.
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.
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.
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.
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.
What is the neural cause of passive expiration?
The ceasing of action potential firing from the neurons, leading to muscular relaxation.
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.
Where are the dorsal respiratory group of neurons located?
On the dorsal surface of the medulla oblongata of the brainstem.
Where are the pontine respiratory group of neurons located?
On the ventral-lateral surface of the pons of the brainstem.
Where is the ventral respiratory group of neurons located?
In the medulla oblongata of the brainstem.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
What can central chemoreceptors detect changes in, and what is their sensitivity?
PaCO2 - highly sensitive.
Arterial pH - less sensitive.
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.
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.
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.
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.
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.
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.
What two muscles does the dorsal respiratory group send action potentials to?
Diaphragm and external intercostal muscles.
Where is the majority of the bicarbonate ions reabsorbed and synthesised in the nephron?
Reabsorbed - PCT.
Synthesised - collecting duct and PCT.
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.
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.
What drug can be given to mothers to increase surfactant production in pre-term infants?
Corticosteroids.
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.
What ECG changes can be seen on a patient with a pulmonary embolism?
Sinus tachycardia.
Right bundle branch block.
S1, Q3, T3.
What may be seen on X-ray due to an occluding pulmonary embolism?
Wedge-shape infarction.
Hampton hump.
Why may a patient with severe asthma no longer be wheezing?
Asthmatic fatigue.
Define respiratory failure.
Impairment of gas exchange causing hypoxaemia with or without hypercapnia.
It can be an acute or chronic condition.
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.
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.
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.
What is the broad cause of type I respiratory failure?
Issue with gas exchange, causing oxygenation of the haemoglobin to decrease.
What is an intrapulmonary shunt?
Pulmonary arterial blood that does not participate in gas exchange as it passes through the lung.
What common condition increases the alveolar dead space?
Pulmonary embolism.
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.
How do you initially treat a loss of surfactant, in an acute setting?
Give positive pressure ventilation to keep the alveoli open.
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.
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.
What is the Henderson-hasselbach equation for CO2?
What are some causes of motor disorders?
Tetanus.
ALS.
Motor neurone disease.
Spinal cord lesions at C3.
What are some issues at the neuromuscular junction?
Myasthenia gravis.
Organophosphate toxicity.
Botulism.
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.
Why can oxygen treatment of type II respiratory failure have negative impacts on the patient?
What 3 pathophysiology factors increase the risk of a pulmonary embolism?
Virchow’s triad:
- Hypercoagulability.
- Vessel wall damage.
- Stasis/ turbulence.
State some causes of stasis, vessel wall damage and hypercoagulability.
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.
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.
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.
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.
Why can pulmonary emboli cause respiratory failure?
Low right ventricle output.
V/Q mismatch, as some alveoli not perfused.
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.
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.
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.
How can a PE be interpreted on a CTPA?
What are some thrombolysis used for treatment of PE’s?
Fibronolytics - streptokinase or tPA.
What is percutaneous catheter thrombectomy?
The mechanical removal of a thrombus using a wire.
What are the treatments of severe pulmonary emboli?
Haemodynamic support.
Respiratory support.
Thrombolysis/ surgical intervention.
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.
What are some prophylactic mechanisms regarding virchows triad?
What is the oxygen supply chain?
Describe the airflow obstruction classification.
What are some COPD therapies to improve risk?
How do anti-muscarinics work as bronchodilators, an where are they most effective?
How do beta-2 agonists work as bronchodilators, an where are they most effective?
What are some causes of bronchiectasis?
How can cystic fibrosis affect different systems of the body?
ABPA - allergic bronchopulmonary aspergillosis.
Heat stroke due to excess sweating and loss of NaCl.
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.
What is seen on a chest X-ray of somebody with miliary pulmonary TB?
Small foci, involving the entire lung.
What is tram tract sign?
Sign seen on X-ray or CT of a patient with bronchiectasis.
State some asthma triggers.
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.
What are the appearance of the anterior and posterior ribs on an X-ray?
Posterior ribs are horizontal.
Anterior ribs are angled.
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.
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.
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.
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.
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.
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.
What can be seen in this X-ray?
Miliary foci.
Paraspinal mass - suggests spinal TB due to miliary TB.
What is seen in this X-ray?
Bilateral hilar lymphadenopathy.
The hilar angle has been obliterated and is no longer concave.
What is seen on this X-ray?
Left pleural effusion.
Costophrenic angle loss with complete hazing of the left lung.
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.
What is seen in this X-ray?
Right pleural effusion with mediastinal widening, usually due to a mass.
Loss of the costophrenic angle.
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.
What is the cause of air under the right diaphragm?
Pneumoperitoneum - rupture of an air-containing organ.
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.
What are some typical pneumonia organisms, and what percentage of pneumonia infections do these account for?
85%.
What are some atypical pneumonia organisms, and what percentage of pneumonia infections do these account for?
15%.
What are the most common causes of hospital acquired pneumonia?
What are the most common organisms that cause LRTI with the following conditions:
- HIV.
- Neutropenia.
- Bone marrow transplant immunosuppression.
- Splenctomy.
How can the following border help to localise consolidations?
Right heart border.
Right hemidiaphragm.
Left heart border.
Left hemidiaphragm.
What can be some causes for cavities on chest X-rays?
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.
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.
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.
What is the initial gradient of a volume-time plot?
The peak expiratory flow rate - the maximal speed of expiration.
What can be calculated using a flow-volume loop?
Tidal volume.
Expiratory reserve volume.
Inspiratory reserve volume.
Inspiratory capacity.
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.
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.
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.
How is spirometry performed?
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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!!
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.
What are the abnormalities seen on this X-ray and what is the most likely diagnosis?
Multifocal peripheral opacities.
Ground-glass densities.
COVID-19.
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.
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.
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.
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.
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.
What are some symptoms due to primary tumour lung cancer?
What are some symptoms due to lung cancers regional metastases?
What are some symptoms due to lung cancers distant metastases?
What are some symptoms due to lung cancers effect on metabolism?
What are some endocrine paraneoplastic syndromes?
What are some neurological paraneoplastic syndromes?
What is the performance status of a patient?
State some potential causes of chest pain.
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.
What are the two indexes which are asked to determine someone’s addiction to smoking?
What are the 6 steps for treating tobacco dependency?
Provide both short acting and long acting nicotine products.
