Respiratory

Question 0

What is the kinetic theory of gases?

Answer 0

Gases are a collection of molecules moving around a space, generating pressure by colliding with the walls of the space.
As collisions become more frequent, and harder, pressure goes up.

Question 1

Explain the broad functions of the respiratory system in health?

Answer 1

The respiratory system works to ensure that all tissues receive the oxygen that they need and can dispose of the CO2 they produce.
Blood carries gases to and from tissues, where the lungs exchange them with the atmosphere.

Question 2

What is Boyles law?

Answer 2

If a given amount of gas is compressed into a smaller volume, the molecules will hit the wall more often. Therefore pressure will rise.
If temperature is constant, Pressure is Inversely Proportional to Volume

Question 3

What is Charles law?

Answer 3

The kinetic energy of molecules Increases with Temperature.
As temperature increases, the molecules hit the walls more often, so pressure increases.
Pressure is Proportional to Absolute Temperature (scale starts at absolute zero)

Question 4

What is the universal gas law?

Answer 4

The universal gas law allows the calculation of how volume will change as pressure and temperature changes.
Pressure x Volume = Gas Constant x Temperature (0K)

Question 5

What is partial pressure?

Answer 5

In a mixture of gases molecules of each type behave independently. So each gas exerts its own pressure, which is a portion of the total pressure (a partial pressure).
It is calculated as the same fraction of the total pressure as the volume fraction of the gas in the mixture.

Question 6

What is vapour pressure?

Answer 6

In biological systems gas mixtures are always in contact with water.
So gas molecules dissolve, and water molecules evaporate, and then exert their own partial pressure. This partial pressure is known as vapour pressure.

Question 7

What is saturated vapour pressure?

Answer 7

When the rate of molecules entering and leaving water at the same time is equal, this is the Saturated Vapour Pressure.
When gases enter our body, they are completely saturated with water vapour, so they don’t dry out our lungs.

Question 8

What is tension?

Answer 8

Gas tension in liquids indicates how readily gas will leave the liquid, not (at least directly) how much gas is in the liquid.
At equilibrium (achieved very quickly in the body), Tension = Partial Pressure.

Question 9

How is the content of a gas in a liquid determined?

Answer 9

The amount of Gas that enters a liquid to establish a particular tension is determined by Solubility.
Content = Solubility x Tension
(How easily gas will dissolve x How readily it will leave)
If the gas reacts with a component of the liquid however, this reaction must be complete before tension, and therefore content can be established.
Total Content = Reacted Gas + Dissolved Gas
E.g.
Plasma just dissolves O2
A pO2 of 13.3kPa (ppO2 in the lungs), gives a blood content of 0.13 mmol/L of O2
Whole blood contains Haemoglobin, which reacts chemically with Oxygen.
At pO2 of 13.3kPa, Haemoglobin binds 8.8mmol/L of O2
Total Content = O2 Bound to Haemoglobin + O2 dissolved in Plasma
= 8.8 + 0.13
= 8.93 mmol/L

Question 10

What is tidal volume?

Answer 10

The lung volume that represents the amount of air that is displaced between normal inspiration and expiration, when extra effort is not applied

Question 11

What is respiratory rate/ pulmonary ventilation rate?

Answer 11

The number of breaths taken in a set time, usually 60 seconds

Question 12

What is the difference between the bronchial and pulmonary circulation?

Answer 12

The lungs have two circulations – pulmonary and bronchial.
The bronchial circulation is part of the systemic circulation, and meets the metabolic requirements of the lungs. The pulmonary circulation is the blood supply to the alveoli, required for gas exchange.

Question 13

What is ventilation perfusion matching?

Answer 13

For efficient oxygenation, ventilation of the alveoli needs to be matched with perfusion. The optimal Ventilation/Perfusion ratio is 0.8. Maintaining this means diverting blood from alveoli that are not well ventilated.
This is achieved by hypoxic pulmonary vasoconstriction. Alveolar hypoxia results in vasoconstriction of pulmonary vessels, and the increased resistance means less flow to the poorly ventilated areas and greater flow to well ventilated areas.
Chronic hypoxic vasoconstriction can lead to right ventricular failure. The chronic increase in vascular resistance puts a high afterload on the right ventricle, leading to its failure.

Question 14

Define the upper respiratory tract

Answer 14

Upper Respiratory Tract
The parts of the respiratory system lying outside the thorax
o Nasal Cavity
o Pharynx
o Larynx

Question 15

Define the lower respiratory tract

Answer 15

The parts of the respiratory system lying inside the thorax
o Trachea
o Main/Primary bronchi
o Lobar Bronchi
• Three on right
• Two on left
• Bronchi have cartilage in their walls
o Segmental Bronchi
o Sub-segmental Bronchi
o Bronchioles
• No Cartilage in the walls
• More smooth muscle than Bronchi
o Terminal Bronchioles
• ~200,000
o Respiratory Bronchioles
o Alveolar Ducts
o Alveoli
• ~300,000,000

Question 16

What are the broad functions of different parts of the respiratory tract?

Answer 16

The lungs are a means of getting air to one side, and blood to the other of a very thin membrane, with a large surface area.

The trachea and bronchi have cartilaginous rings in order to hold them open and provide a path for air to travel to the alveoli.
Bronchioles draw air into the lungs by increasing their volume, using the smooth muscle in their walls.
Alveoli provide the single cell thickness membrane for diffusion (Type I cells, Simple Squamous epithelia). They also produce surfactant (Type II cells) to reduce the surface tension of the alveoli.

Question 17

Describe the structure and function of the nose

Answer 17

The nose is part of the respiratory tract, superior to the hard palate. It is comprised of the external nose and nasal cavity, which is divided into the right and left cavities by the nasal septum.
The functions of the nose include smelling, respiration, filtration of dust, humidification of inspired air, and reception and elimination of secretions from the paranasal sinuses and nasolacrimal ducts.

Air passing over the respiratory area of the nose is warmed and moistened before it passes through the rest of the upper respiratory tract to the lungs.
The olfactory area contains the peripheral organ of smell.

Question 18

Describe the structure and function of the conchae (turbinates)

Answer 18

The superior, middle and inferior Nasal Conchae (or turbinates) curve inferiormedially, hanging like short curtains from the lateral wall of the nasal cavity.
The conchae are scroll-like structures that offer a vast surface area for heat exchange.
The inferior concha is the longest and broadest and is formed by an independent bone (the Inferior Concha).
The middle and superior conchae are the medial processes of the Ethmoid Bone.
A recess or nasal meatus underlies each of the turbinates, dividing the nasal cavity into four passages.
The Sphenoethmoidal Recess, lying superoposterior to the superior conca, receives the opening of the sphenoidal sinus

Question 19

Describe the structure and function of the para nasal sinuses

Answer 19

The paranasal sinuses are air-filled extensions of the respiratory part of the nasal cavity into cranial bones (Frontal, Ethmoid, Sphenoid and Maxilla).
The sinuses are named according to the bones in which they are located.

Question 20

What are the frontal sinuses?

Answer 20

The Right and Left Frontal Sinuses are between the outer and inner tables of the frontal bone, posterior to the superciliary arches and the root of the nose. They are usually detectable in children by 7 years of age.
They each drain through a Frontonasal Duct into the ethmoidal infundibulum, which opens into the semilunar hiatus of the Middle Nasal Recess.

Question 21

What are the ethmoidal cell sinuses?

Answer 21

The Ethmoidal cells (Sinuses) are small invaginations of the mucous membrane of the middle and superior nasal recesses into the Ethmoid bone.
The Ethmoidal cells usually are not visible in plain radiographs before 2 years of age.
The Anterior Ethmoidal Cells drain directly or indirectly into the middle nasal recess through the ethmoidal infundibulum.
The Middle Ethmoidal Cells open directly into the middle nasal recess.
The Posterior Ethmoidal Cells open directly into the superior nasal recess.

Question 22

What are the sphenoidal sinuses?

Answer 22

The Sphenoidal Sinuses are located in the body of the sphenoid and may extend into the wings of the bone.
The body of the sphenoid is fragile, and only thin plates of bone separate the sinuses from several important structures (Optic nerves and chiasm, the pituitary gland, internal carotid arteries).
They drain directly into the Sphenoethmoidal Recess.

Question 23

What are the maxillary sinuses?

Answer 23

The Maxillary Sinuses are the largest of the paranasal sinuses. They occupy the bodies of the Maxillae.

They drain by one or more openings, the Maxillary Ostium (ostia), into the middle nasal recess by way of the semilunar hiatus.

Question 24

Describe generally the structure and location of the pharynx

Answer 24

The Pharynx is the superior, expanded part of the Alimentary System, posterior to the nasal and oral cavities and extending inferiorly past the larynx. The Pharynx extends from the Cranial Base to the Inferior Border of the Cricoid Cartilage Anteriorly and the Inferior Border of C6 Vertebra Posteriorly. It is widest (Approximately 5cm) opposite the hyoid and narrowest (approximately 1.5cm) at its inferior end, where it is continuous with the oesophagus.

Question 25

What are the 3 divisions of the pharynx?

Answer 25

The Pharynx is divided into Three Parts: o Nasopharynx • Posterior to the nose and superior to the soft palate • Respiratory Function as it is the posterior extension of the nasal cavities • Lymphoid tissue forms a tonsillar ring around the superior part of the pharynx, which aggregates to form Tonsils o Oropharynx • Posterior to the mouth • Extends from the soft palate to the superior border of the epiglottis • Digestive Function • Involved in swallowing (GI LO 2.7) o Laryngopharynx • Posterior to the Larynx • Ends from the superior border of the epiglottis to the inferior border of the cricoid cartilage, where it becomes continuous with the oesophagus.

Question 26

What is the larynx?

Answer 26

The Larynx connects the inferior Oropharynx to the Trachea. It also contains the complex organ of voice production (The ‘voice box’). It extends from the Laryngeal Inlet, through which it communicates with the Laryngopharynx to the level of the inferior border of the cricoid cartilage. Here the laryngeal cavity is continuous with the Trachea. The Larynx’s most vital function is to guard the air passages, especially during swallowing when it serves as the sphincter/valve of the lower respiratory tract, thus maintaining the airway. The voice box controls sound production. It is composed of nine cartilages, connected by membranes and ligaments containing the vocal folds.

Question 27

What is the middle ear?

Answer 27

``` The cavity of the middle ear, or tympanic cavity is the narrow air-filled chamber in the petrous part of the temporal bone. The Tympanic cavity is connected with: o Nasopharynx • Anteromedially • Pharyngotympanic (Eustachian)Tube o Mastoid cells • Posterosuperiorly • Mastoid Antrum ```

Question 28

What type of membranes does the respiratory system contain?

Answer 28

The respiratory system contains: Mucous Membranes, which line the conducting portion of the respiratory tract, bearing mucus-secreting cells to varying degrees Serous Membranes, which line the pleural sacs that envelop each lung

Question 29

What areas of the respiratory tract have Pseudostratified, ciliated epithelia with Goblet Cells?

Answer 29

``` Nasal Cavity Pharynx Larynx Trachea Primary / Secondary Bronchi ```

Question 30

Which areas of the respiratory system have simple columnar ciliated epithelia with Clara cells (dome shaped with microvilli- some secretions)?

Answer 30

Bronchioles and terminal bronchioles

Question 31

Which areas of the respiratory system have simple cuboidal sparsely ciliated epithelia with Clara cells?

Answer 31

Respiratory bronchioles | Alveolar ducts

Question 32

Which areas of the respiratory system have simple squamous epithelia?

Answer 32

Alveoli

Question 33

Histologically describe the non olfactory region of the nasal cavity

Answer 33

Non-Olfactory regions o Pseudostratified ciliated epithelium. o Mucous glands and venous sinuses in lamina propria. o Venous plexuses swell every 20-30 minutes, alternating air flow from side to side to prevent over-drying. o Arterial blood flow warms inspired air o Held open by surrounding cartilage or bone.

Question 34

Histologically describe the olfactory region of the nasal cavity

Answer 34

o Particularly thick Pseudostratified epithelium o No goblet cells • No mucus o Located in posterior, superior region of each nasal fossa o Contains olfactory cells (bipolar neurons) o Bowman’s Glands • Serous glands flush odorants from the epithelial surface

Question 35

Histologically describe the larynx

Answer 35

o Ventricular folds are lined by Pseudostratified epithelium • Ventricles and their folds give resonance to the voice o Vocal cords lined by Stratified Squamous Epithelium • Can stop foreign objects from reaching the lungs • Close to build up pressure when coughing is required

Question 36

Histologically describe the trachea

Answer 36

``` Pseudostratified ciliated epithelium o Lamina propria (many elastin fibres) o Seromucus glands o C-Shaped Cartilage Ring ```

Question 37

Histologically describe primary bronchi

Answer 37

o Similar to trachea | o Cartilage rings completely encircle the lumen

Question 38

Histologically describe lobar and segmental bronchi

Answer 38

o Similar to primary bronchi | o Cartilage in crescent shapes, not Ring or Completely encircling lumen

Question 39

Histologically describe the bronchus

Answer 39

o Small diameter o Cartilage reduced to small islands o Glands in Submucosa

Question 40

Histologically describe the bronchiole

Answer 40

o No cartilage or glands o Surrounding alveoli keep the lumen As bronchioles get smaller, goblet cells give way to Clara cells, interspersed between ciliated cuboidal cells. Clara cells secrete a surfactant lipoprotein, which prevents the walls sticking together during expiration. They also secrete Protein CC16. This is a measurable marker in bronchoalveolar damage or leakage across the air-blood barrier. o CC16 Lowered = Lung Damage o CC16 Raised = Leakage across barrier

Question 41

Histologically describe a terminal bronchiole

Answer 41

o Absence of goblet cells in these very narrow airways is important to prevent individuals ‘drowning’ in their own mucus

Question 42

What is the difference between terminal bronchiole, respiratory bronchiole, alveolar duct, alveolus and alveolar sac

Answer 42

The presence of lack of cartilage, glands and differing diameters distinguishes Bronchi from Bronchioles. Terminal Bronchiole o No alveolar openings Respiratory bronchiole o Bronchiole wall opens onto some alveoli Alveolar Duct o Duct wall has openings everywhere onto alveoli Alveolus o A single alveoli Alveolar Sac o Composite air space onto which many alveoli open

Question 43

Describe the structure of alveoli

Answer 43

o Abundant capillaries o Supported by a basketwork of elastic and reticular fibres o Covering composed chiefly of Type I pneumocytes o Simple Squamous o Cover 90% of surface area o Permit gas exchange with capillaries o Scattering of intervening Type II pneumocytes o Simple Cuboidal o Cover 10% of surface area o Produce surfactant o Macrophages line alveolar surface to phagocytose particles. New alveoli continue to develop up to the age of 8 years, when there are approximately 300,000,000. Alveoli can open into a respiratory bronchiole, an alveolar duct or sac or another alveolus (via an alveolar pore).

Question 44

In quiet breathing what muscles are involved in inhalation and exhalation?

Answer 44

``` Quiet Breathing o Inhalation • Diaphragm • External Intercostals o Exhalation • None ```

Question 45

In forced breathing what muscles and structures are involved in inhalation and exhalation?

Answer 45

``` Forced Breathing o Inhalation • Diaphragm • External Intercostals • Scalene • Pectoralis Minor • Sternocleidomastoid • Serratus Anterior o Exhalation • Internal Intercostals • Innermost Intercostals • Abdominal Muscles ```

Question 46

The rate at which gas exchange occurs across the alveoli depends on which 3 factors?

Answer 46

o Area available for the exchange o Resistance to diffusion o Gradient of partial pressure

Question 47

How does area affect gas exchange in the alveoli?

Answer 47

The greater the surface area, the greater the amount of gas exchange occurring. The area of the alveolar surface is large because there are a huge number of alveoli, generating in a normal lung an exchange area of around 80m2. In normal lungs, the area available is not a limiting factor on gas exchange.

Question 48

How does resistance to diffusion affect gas exchange in the alveoli?

Answer 48

The diffusion pathway from alveolar gas to alveolar capillary blood is short, but there are several structures between the two. First gas must diffuse through the gas in the alveoli, then through: o The alveolar epithelial cell o Interstitial fluid o Capillary endothelial cell o Plasma o RBC membrane This means gases have to diffuse through 5 cell membranes, 3 layers of intra cellular fluid and 2 layers of extra cellular fluid. Despite this the overall barrier is less than 1 micron. Two gases have to diffuse, oxygen into the blood and carbon dioxide out of it. The resistance is not the same for the two gases. For most of the barrier (the cells, membranes and fluid) the rate of diffusion is affected by the solubility of the gas in water, and carbon dioxide diffuses much faster, because it is more soluble. Overall, Carbon Dioxide diffuses 21 times as fast as oxygen for a given gradient. This means that anything affecting diffusion will only change oxygen transport, as that is limiting (If there is a problem affecting the exchange of gases, O2 will be affected first)

Question 49

How does partial pressure affect gas exchange?

Answer 49

The partial pressure of oxygen and carbon dioxide in the alveolar gas must be kept very close to their normal values (O2 – 13.3kPa/CO2 – 5.3kPa) if the tissues of the body are to be properly supplied with oxygen and lose their carbon dioxide. This is achieved by exchange of gas between alveolar gas and atmospheric air brought close to it through the airways of the lung by the process of ventilation. Air is driven through the airways of the lungs by the pressure changes produced by increases and decreases in the volume of the air spaces next to the alveoli. The movement of breathing lowers pressure in the terminal and respiratory bronchioles during inspiration, so air flows down the airways to them and then increased pressure during expiration so air flows back out again. Fresh atmospheric air does not enter the alveoli, and exchange of oxygen and carbon dioxide occurs by diffusion between alveolar gas and atmospheric air in the terminal and respiratory bronchioles.

Question 50

How is respiration measured?

Answer 50

The movement of air during breathing can be measured with Spirometry.

Question 51

Define tidal volume

Answer 51

The lung volume that represents the amount of air that is displaced between normal inspiration and expiration, when extra effort is not applied

Question 52

Define inspiratory reserve volume

Answer 52

The extra volume that can be breathed in when extra effort is applied

Question 53

Define expiratory reserve volume

Answer 53

The extra volume that can be breathed out when extra effort is applied

Question 54

Define residual volume

Answer 54

The volume left in the lungs at maximal expiration. This cannot be measured with a spirometer; it must be measured by helium dilution

Question 55

What's the difference between lung volumes and capacities?

Answer 55

Lung volumes change with breathing pattern. Capacities do not, as they are measured from fixed points in the breathing cycle.

Question 56

Define vital capacity

Answer 56

The biggest breath that can be taken in, measured from the max inspiration to max expiration. It often changes in disease, and is about 5L in a typical adult.

Question 57

Define functional residual capacity

Answer 57

The volume of air in the lungs at resting expiratory level (Expiratory reserve volume + residual volume). It is typically about 2L.

Question 58

Define inspiratory capacity

Answer 58

The biggest breath that can be taken from resting expiratory level (lung volume at the end of quiet expiration). It is typically about 3L.

Question 59

What is serial (anatomical) dead space?

Answer 59

Air enters and leaves the lungs by the same airways. So the last air in is the first air out, does not reach the alveoli and is therefore unavailable for gas exchange. The volume of the conducting airways is known as the Anatomical or Serial Dead Space and is normally about 150ml.

Question 60

What is alveolar (distributive) dead space?

Answer 60

The volume of air in alveoli not taking part in gas exchange is known as the Alveolar (or Distributive) Dead Space. i.e. Due to disease etc. The air contained in the conducting airways is not the only air that fails to equilibrate with alveolar capillary blood. Some alveoli receive an insufficient blood supply; others are damaged by accident or disease, so that even in the air that reaches the alveolar boundary, there is a proportion that fails to exchange.

Question 61

What is physiological dead space?

Answer 61

Anatomical Dead Space + Alveolar Dead Space = Physiological Dead Space

Question 62

How is physiological dead space measured?

Answer 62

Physiological Dead space is determined by measuring pCO2 (or pO2) of expired alveolar air. The alveolar air is diluted by dead space air to form the expired air, and the degree of dilution is a measurement of a physiological dead space.

Question 63

How is serial dead space determined?

Answer 63

Nitrogen washout test

Question 64

Describe the nitrogen washout test

Answer 64

Serial (Anatomical) Dead Space is measured by the Nitrogen Washout Test. o The patient takes a maximum inspiration of 100% oxygen. o The oxygen that reaches the alveoli will mix with alveolar air, and the resulting mix will contain Nitrogen (there is 79% Nitrogen in air) o However, the air in the conducting airways (dead space) will still be filled with pure oxygen. o The person exhales through a one way valve that measures the percentage of Nitrogen in it and volume of air expired o Nitrogen concentration is initially zero as the patient exhales the dead space oxygen. o As alveolar air begins to move out and mix with dead space air, nitrogen concentration gradually climbs, until it reaches a plateau where only alveolar gas is being expired o A graph can be drawn to determine the dead space, plotting Nitrogen % against Expired Volume.

Question 65

How do you calculate alveolar ventilation rate? (The amount of air that actually reaches the alveoli)

Answer 65

Alveolar Ventilation Rate = Pulmonary Ventilation Rate – Dead Space Ventilation Rate Alveolar Ventilation Rate =(Tidal Volume x RR) – (Dead Space Volume x RR)

Question 66

How do the lungs and thorax contribute mechanically to respiration?

Answer 66

Air is drawn into the lungs by expanding the volume of the thoracic cavity. Work is done during breathing to move the structures of the lungs and thorax and to overcome the resistance to flow of air through the airways. The space between the lungs and thoracic wall, the pleural space, is normally filled with a few millilitres of fluid, the surface tension of which forms a pleural seal holding the outer surface of the lungs to the inner surface of the thoracic wall. Therefore the volume of the lungs changes with the volume of the thoracic cage.

Question 67

What is pneumothorax?

Answer 67

If the integrity of the pleural seal is broken, the lungs will tend to collapse. E.g. If air gets in between the two layers of the pleura, fluid surface tension is lost and the lungs collapse.

Question 68

What is lung compliance?

Answer 68

The ‘stretchiness’ of the lungs is known as compliance. It is defined as volume change per unit pressure change. High Compliance means that the Lungs are Easy to Stretch.

Question 69

How is compliance measured and calculated?

Answer 69

Compliance is measured by measuring the change in lung volume for a given pressure. The greater the lung volume the greater the compliance and vice versa. However, even with the constant elasticity of lung structures, compliance will also depend on the starting volume from which it is measured, so it is more usual to calculate Specific Compliance, which is: Volume Change Per Unit Pressure Change / Starting Volume of Lungs

Question 70

What are the 3 main factors that affect the compliance of the lungs?

Answer 70

Surfactant Surface tension Bubbles

Question 71

Where do the elastic properties of the lungs arise from?

Answer 71

The elastic properties of the lungs arise from two sources, Elastic Tissues in the lungs and Surface Tension forces of the fluid lining the alveoli.

Question 72

What is surface tension and how does it affect compliance?

Answer 72

Surface tension is interactions between molecules at the surface of a liquid, making the surface resist stretching. The higher the surface tension, the harder the lungs are to stretch (lowers compliance).

Question 73

What is surfactant? What produces surfactant? And how is surfactant related to surface tension and thus compliance?

Answer 73

At low lung volumes, the surface tension of the lungs is much lower than expected. This is due to the disruption of interactions between surface molecules by Surfactant, produced by Type 2 Alveolar Cells. Surfactant is a complex mixture of phospholipids and proteins, with detergent properties. The hydrophilic ends of these molecules lies in the alveolar fluid and the hydrophobic end projects into the alveolar gas. As a result they float on the surface of the lining fluid, disrupting interaction between surface molecules. Surfactant reduces surface tension when the lungs are deflated, but not when fully inflated. So little breaths are easy, and big breaths are hard, and it takes less force to expand small alveoli than it does large ones.

Question 74

How do the 'bubbles' in the lung affect surface tension and compliance?

Answer 74

Alveoli form an interconnecting set of bubbles. If Laplace’s law is applied (Pressure is inversely related to the radius of a bubble), large alveoli would ‘eat’ small ones. As alveoli get bigger, the surface tension in their walls increases, as surfactant is less effective. So pressure stays high and stops them from ‘eating’ the smaller alveoli.

Question 75

Describe resistance in airways and Poisseulles law

Answer 75

In addition to work done against the elastic nature of the lungs, energy must be expended to force air through the airways. The resistance of an airway to flow is determined by Poiseulle’s Law when flow is laminar, which is true of most of the airways of the lungs. Poiseulle’s Law: The resistance of a tube increases sharply with a falling radius. However, the combined resistance of the small airways is normally low, because they are connected in parallel over a branching structure, where the total resistance to flow in the downstream branches is less than the resistance of the upstream branch. Most of the resistance to breathing therefore resides in the upper respiratory tract. Overall, work is done against: o The elastic recoil of the lungs and thorax o Elastic properties of the lungs o Surface tension forces in the alveoli o Resistance to flow through airways o Of little significance in health, but often affected by disease At rest the work of breathing consumes only 0.1% of total oxygen consumption, so it is efficient.

Question 76

How does resistance change in the breathing cycle?

Answer 76

During inspiration, the bronchioles use their smooth muscle to increase their radius. This decreases their resistance (Poiseulle’s Law), allowing air to be drawn easily through them into the alveoli.

Question 77

Describe spirometry

Answer 77

The patient fills their lungs from the atmosphere, and breathes out as far and fast as possible through a Spirometer. Simple Spirometry allows measurement of many lung volumes and capacities. Vital capacity is particularly significant. Tables can be used to predict the vital capacity of an individual of known age, sex and height.

Question 78

Why may vital capacity be less than normal?

Answer 78

Vital Capacity may be less than normal because the lungs are not: 1. Filled normally in inspiration- due to altered compliance of lungs and force of inspiratory muscles 2. Emptied normally in expiration- due to increase in airway resistance or compression of the lungs 3. Or Both

Question 79

In what conditions is compliance increased?

Answer 79

Emphysema Break down of elastic makes walls more stretchy

Question 80

In what conditions is compliance decreased?

Answer 80

Lung fibrosis Thickening and fibrosis of elastic makes wall stiff

Question 81

What is Forced Vital Capacity?

Answer 81

FVC is the maximum volume that can be expired from full lungs.

Question 82

What is the Forced Expiratory Volume in One Second (FEV1)?

Answer 82

FEV1 is the volume expired in the first second of expiration from full lungs. (>70% FVC) It is affected by how quickly air flow slows down, so is low if the airwards are narrowed (obstructive deficit)

Question 83

What is a vitalograph?

Answer 83

Plot of volume expired (y) against time (x) A type of spirometry which records the volume exhaled following a vital capacity breath. Initial rapid rise which tails into a plateau Helps differentiate between restrictive and obstructive deficit

Question 84

How is a vitalograph obtained?

Answer 84

Restrictive and obstructive deficits can be separated by asking the patient to breathe out rapidly from maximal inspiration through a single breath spirometer, which plots volume expired against time

Question 85

What is a restrictive deficit and how does it come about?

Answer 85

Maximal filling of the lungs is determined by balance between maximum inspiratory effort and the force of recoil of the lungs - if the lungs are unusually stiff, or if inspiratory effort is compromised by muscle weakness, injury or deformity, then a RESTRICTIVE DEFICIT is formed Affects air coming in/ INSPIRATION

Question 86

How does a restrictive deficit affect FVC and FEV1?

Answer 86

FVC is reduced FEV1 >70% of FVC (as both FEV1 and FVC decrease proportionally) So ratio of FEV1:FVC is the same

Question 87

Give an example of a condition where a restrictive deficit occurs

Answer 87

Muscle weakness | Lung fibrosis

Question 88

What is an obstructive deficit and how does it come about?

Answer 88

During expiration, particularly when forced, the small airways are compressed - increases flow resistance eventually to a point where no more air can be driven out of the alveoli - if the airways are narrowed, then excitatory flow is compromised much earlier in expiration producing an OBSTRUCTIVE DEFICIT Affects air going out/EXPIRATION

Question 89

How does an obstructive deficit affect FVC and FEV1?

Answer 89

FEV1 reduced FVC relatively normal So FEV1: FVC ratio is decreased

Question 90

Give an example of a condition where an obstructive deficit occurs

Answer 90

Asthma | COPD

Question 91

What is a flow volume curve and how is it produced?

Answer 91

Plot of volume expired (x) against flow rate (y) - derived from a vitalograph trace (tangents) Sharp increase followed by more gradual decrease

Question 92

Why is a flow volume curve more informative than a vitalograph?

Answer 92

A flow volume curve is a much more sensitive indicator of airway narrowing Can also discriminate large and small airway narrowing

Question 93

How is a flow volume curve broken down into 4 categories? Describe each (A-D and A has a special name)

Answer 93

A- when the lungs are full, airways are stretched so resistance is at a minimum, flow is therefore at a maximum (PEAK EXPIRATORY FLOW RATE) B-D- when lungs are compressed, more air is expired and the airways begin to narrow, so resistance increases and flow rate decreases

Question 94

What is PEFR and how is it determined?

Answer 94

Peak EXPIRATORY flow rate From a flow volume curve - peak flow Can be measured with a simple cheap device, so often used as a screening test for airway narrowing but it's very insensitive

Question 95

PEFR is affected most by the resistance of which airways? How does this affect the flow volume curve?

Answer 95

In normal individuals, peak flow is affected most by the resistance of large airways, but will also be affected by the severe obstruction of the smaller airways (e.g. Asthma) Mild obstruction of airways produces a scooped out EXPIRATORY curve- more severe obstruction will also produce PEFR

Question 96

What does the helium dilution test measure?

Answer 96

Measurement of residual volume by measuring functional residual capacity (FRC)- which can't be measured by spirometry

Question 97

Why is helium used to measure residual volume in the helium dilution test?

Answer 97

Helium- inert, colourless, odourless, tasteless, non toxic gas Helium cannot transfer across the alveolar capillary membrane and so is contained within the lungs

Question 98

How is the helium dilution test carried out?

Answer 98

At end of the normal tidal expiration the patient is connected to a circuit which is connected to a circuit, which is connected to a container containing a gas mixture with a known helium concentration (C1) and volume (V1) - end of tidal expiration - lung volume - FRC = ERV + RV Patient continues to rebreathe into container until quilibrium occurs (4-7mins) New concentration of helium (C2) - C1 x V1 = C2 x V2 - V2 = V1 + FRC Since C1, V1 and C2 are all known, (V2 and then) FRC can be calculated Therefore RV = FRC - ERV (measured by spirometry)

Question 99

What is Transfer factor?

Answer 99

CO transfer factor- measures rate of transfer of CO from alveoli to blood in ml per minute per kPa (ml/min/kPa) Way of measuring the DIFFUSION CAPACITY of the lungs because amount transferred will depend on how well gas diffusion takes place

Question 100

Why is CO used to calculate transfer factor and thus diffusion capacity?

Answer 100

Inhaled CO used because of its very high affinity for haemoglobin - since all CO entering the blood binds to H, very little remains in plasma so we can assume free plasma ppCO is zero So concentration gradient between alveolar ppCO and capillary ppCO is maintained As a result the amount of CO transferred from alveoli to blood is limited only by the diffusion capacity of the lungs

Question 101

What is the process for measuring transfer factor?

Answer 101

Patient performs full expiration, followed by maximum inspiration of a gas mixture composed of air, a tiny fraction of CO and fraction of inert gas such as helium (tiny fraction of CO as it's toxic, fraction of inert gas to make an estimate of total lung volume) Breath held for 10 seconds Patient exhales - gas held mid expiration - to gain a an alveolar sample Concentration of CO and inert gas From these measurements CO Transfer factor is calculated

Question 102

What measurements are usually shown in a lung function report?

Answer 102

``` Vital capacity FEV1 (before and after bronchodilator) Ratio FEV1/FVC Peak EXPIRATORY Flow rate (FRC, RV, TLC, RV/TLC) Transfer factor CO conductance ```

Question 103

How soluble is oxygen?

Answer 103

Oxygen is not sufficiently soluble in body fluids for adequate gas transport in simple solution- 21 times less soluble than CO2

Question 104

What is the solubility coefficient of oxygen at a partial pressure of 13.3kPa and temp of 37C?

Answer 104

0.01mmol/L/kPa

Question 105

How much oxygen does plasma contain at partial pressure of 13.3 kPa and temp of 37C?

Answer 105

= 0.01 (Oxygen solubility coefficient) x 13.3 | = 0.13 mmol/L of dissolved oxygen

Question 106

What protein in the blood helps with the transport of oxygen around the body, despite its low solubility?

Answer 106

Haemaglobin

Question 107

What's the concentration of Hb in the blood?

Answer 107

2.2mmol/L

Question 108

How much Oxygen is carried in the blood, when it's fully saturated?

Answer 108

8.8mmol/L

Question 109

What is Hb like at the lungs?

Answer 109

Blood leaves the lungs with the Hb almost saturated with oxygen R state

Question 110

Will an increase in oxygen in all parts of the lungs increase the content of oxygen in the blood?

Answer 110

No as most Hb is usually saturated already

Question 111

What maintains the composition of alveolar gas?

Answer 111

Ventilation and perfusion

Question 112

What is the alveolar pO2?

Answer 112

13.3kPa

Question 113

What is the mixed venous blood pO2?

Answer 113

5.3kPa

Question 114

What is the alveolar pCO2?

Answer 114

5.2kPa

Question 115

What is the mixed venous blood pCO2?

Answer 115

6.6kPa

Question 116

Does CO2 or O2 diffuse more rapidly in a gas phase?

Answer 116

O2

Question 117

Does CO2 or O2 diffuse more rapidly in a liquid phase?

Answer 117

CO2 | 21 times more that O2

Question 118

How long does it usually take for sufficient gas exchange to occur at the alveolar capillary membrane?

Answer 118

500ms (half the time blood spends in the capillaries=1000ms/1s)

Question 119

Under normal conditions, what's the difference between the composition of alveolar air and alveolar capillaries?

Answer 119

Alveolar capillaries have the same gaseous composition as alveolar air - therefore arterial gas tensions are determined by alveolar gas composition - and so respiration has to be controlled to keep alveolar pCO2 at 5.3kPa and alveolar pO2 at 13.3kPa

Question 120

What is Hb like at the tissues?

Answer 120

Unloading of oxygen depends on fall of pO2 in capillaries Changes in Hb brought about by different conditions in the tissues T state

Question 121

The extent that capillary pO2 can fall without compromising diffusion of O2 into cells depends on what?

Answer 121

Capillary density - Higher capillary density means that O2 is spread more sparsely So pO2 can fall a lot before it affects the diffusion of O2 into the tissues E.g. Myocardium -capillary pO2 can fall further due to their being lots of capillaries and so there will be large amounts of oxygen about

Question 122

What is the Bohr shift? And what causes it?

Answer 122

Shift of O2 Hb curve to the right due to Low pH in tissues High temp in tissues Increased 2,3 DOG Low O2 tension Conditions favour the T low affinity state for oxygen

Question 123

Why is CO2 in the blood important?

Answer 123

Essential part of BUFFER systems - controls pH of ECF

Question 124

Why is a large amount of CO2 found in the arterial blood? (Even though it's til now been known as 'waste' and thus has been transported from tissues to lungs to be expired)

Answer 124

Lots of CO2 is found in arterial blood too (as well as that found in the venous blood as 'waste' because it is required for ACID BASE BALANCE

Question 125

How does CO2 react with H2O?

Answer 125

CO2 dissolves in H2O H+ + HCO3-

Question 126

What enzyme catalyses (CO2 dissolves in H2O H+ + HCO3-) reaction?

Answer 126

Carbonic anhydrase

Question 127

How much carbonic anhydrase is found in the plasma and how does affect the reactions of CO2 in plasma?

Answer 127

Little found | Makes reactions slower

Question 128

How much carbonic anhydrase is found in the red blood cells and how does affect the reactions of CO2 in RBCs?

Answer 128

Lots found | Faster reactions

Question 129

What pushes this reaction forward? | CO2 dissolves in H2O H+ + HCO3-

Answer 129

An increase in dissolved CO2 which is proportional to pCO2 | ventilation related

Question 130

What opposes the forward direction of this reaction? | CO2 dissolves in H2O H+ + HCO3-

Answer 130

An increase in HCO3- | Metabolism related

Question 131

What ratio does plasma pH depend on?

Answer 131

pCO2 : [HCO3-] | 1:20

Question 132

If pCO2 of plasma is high (ie. pCO2 : [HCO3-] is high), is pH high or low?

Answer 132

Low

Question 133

If [HCO3-] of plasma is high (ie. pCO2 : [HCO3-] is low), is pH high or low?

Answer 133

High

Question 134

Why does the pCO2: [HCO3-] buffer work far from its pK (dissociation constant)?

Answer 134

Because of excess HCO3-

Question 135

What is the Henderson Hasselbach equation?

Answer 135

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

Question 136

Where does most HCO3- come from in the plasma?

Answer 136

NaHCO3 Negligible HCO3- is formed from the dissolution of CO2 In body fluids with few or no other buffer systems (plasma CSF) concentration of HCO3- is not significantly affected by changes in pCO2 and remains effectively constant over all physiological values of pCO2 unless changed by other mechanisms

Question 137

In this reaction CO2 dissolves in H2O H+ + HCO3 in RBCs where does the H+ produced bind to?

Answer 137

Haemoglobin which has a large buffering capacity | This is enhanced further when haemoglobin is deoxygenated at the tissues and H+ is high

Question 138

The binding of H+ to Hb in this reaction (CO2 dissolves in H2O H+ + HCO3) in RBCs has what affect on the equilibrium of the reaction?

Answer 138

Reaction is pushed to the right More HCO3- is produced The amount produced depends primarily on the buffering effects if haemoglobin with only minor effects of changes in pCO2

Question 139

How is HCO3- exported from the red blood cell during this reaction? (CO2 dissolves in H2O H+ + HCO3)

Answer 139

HCO3- which is being produced in large quantities in the red blood cell due to the constant removal of H+ by Hb, is exported from the red cell in exchange for the inward movement of Cl- Used elsewhere in body- liver (check with LMSRS)

Question 140

The pH of overall body fluids is dependent on the relationship between what 2 molecules in the plasma and Red cell?

Answer 140

Amount of CO2 dissolved in the PLASMA AND | Amount of HCO3- formed from CO2 in the RED CELL by reaction involving Hb

Question 141

What are carbonamino compounds?

Answer 141

Protein part of Hb to which CO2 binds to | Contributes to CO2 transport but not acid base balance

Question 142

Describe the overall contents of arterial blood

Answer 142

Plasma dissolves 0.7mmol CO2/litre of blood (plasma only 60% of total volume) Plasma contains 15.2mmol HCO3-/litre of blood Cells dissolve 0.3mmol HCO3-/litre Cells contain 4.3mmol HCO3-/litre Blood has 1mmol carbaminos/litre Contains 21.5mmol CO2/litre

Question 143

Describe the overall contents of venous blood

Answer 143

Plasma dissolves 0.8mmol CO2/litre of blood (plasma only 60% of total volume) Plasma contains 16.3mmol HCO3-/litre of blood Cells dissolve 0.4mmol HCO3-/litre Cells contain 4.8mmol HCO3-/litre Blood has 1.2mmol carbaminos/litre Contains 23.5mmol CO2/litre

Question 144

How much CO2 is transported? Given that arterial blood contains 21.5mmol CO2/litre and venous blood contains 23.5mmol CO2/litre.

Answer 144

``` 23.5-21.5= 2mmol/litre of blood (Only 10% of total) 80% travels as H2CO3 11% carbaminos 8% as dissolved CO2 ```

Question 145

What is hypoxia?

Answer 145

Fall in alveolar and thus arterial pO2 (because pO2 is usually the same in both)

Question 146

What is hypercapnia?

Answer 146

Rise in alveolar and thus arterial pCO2

Question 147

What is hypocapnia?

Answer 147

Fall in alveolar and thus arterial pCO2

Question 148

What is hyperventilation?

Answer 148

Ventilation increases with no change in metabolism | Breathing more than you actually have to - decrease in pCO2 and increase in pO2

Question 149

What is hypoventilation?

Answer 149

Ventilation decreases with no change in metabolism | Breathing less than you actually have to - increase in pCO2 and decrease in pO2

Question 150

What's a large problem when pO2 decreases but pCO2 stays the same? (Ie. On a high mountain)

Answer 150

If pO2 is low and pCO2 is high as a result of hypoventilation It would be corrected by breathing more (increase in ventilation rate) BUT if pO2 is low and pCO2 is normal (inspiratory defects like fibrosis of the lung or at at height)- correcting the hypoxia by increasing the ventilation rate will result in hypocapnia and an alteration of acid base balance of the blood- So system has to choose which one to control, pO2 or pCO2

Question 151

What is the lowest value of pO2 before hypoxia is diagnosed?

Answer 151

pO2 can fall to 8kPa before saturation of Hb is significantly reduced Any further falls leads to to a large reduction in O2 transport (oxygen saturation of about 89%- hence it is critical when ox sat falls below this)

Question 152

What is arterial pO2 monitored by?

Answer 152

Peripheral chemoreceptors

Question 153

Where are peripheral chemoreceptors found?

Answer 153

In carotid and aortic bodies

Question 154

When a large fall in pO2 is detected by peripheral chemoreceptors what changes occur to correct this?

Answer 154

Increased breathing - hyperventilation HR changes Diversion of blood flow to brain

Question 155

Why is the chemical control of pCO2 important?

Answer 155

pCO2 affects plasma CO2 At constant HCO3- if pCO2 rises, pH falls and vice versa Small changes in pCO2 leads to large changes in pH

Question 156

What detects changes in pCO2?

Answer 156

Peripheral chemoreceptors will detect changes- but are rather insensitive Central chemoreceptors are the main detectors and are much more sensitive

Question 157

Where are central chemoreceptors found?

Answer 157

Medulla oblongata found in brain

Question 158

How do central chemoreceptors detect changes in pCO2?

Answer 158

Actually respond to changes in CSF CSF separated from blood by BBB CSF [HCO3-] controlled by choroid plexus cells CSF pCO2 determined by arterial pCO2 CSF pH determined by [HCO3-] [HCO3-] fixed in short term Decrease in pCO2 causes an increase in CSF pH --> increase in pCO2 causes a decrease in CSF pH But persisting changes in pH are detected by choroid plexus cells which change [HCO3-]

Question 159

What are the effects of having acidic blood pH<7?

Answer 159

Plasma k+ increases to dangerous levels and enzymes are lethally denatured

Question 160

What are the effects of having alkaline blood pH>7.6?

Answer 160

Free calcium concentration falls enough to produce fatal tetany

Question 161

What is respiratory alkalosis? How is it compensated?

Answer 161

Hyperventilation (respiratory) causes pCO2 to fall and pH to rise (alkolosis) (Can cause lethal tetany) Compensated by kidneys decreasing [HCO3-] in the blood Takes 2-3 days

Question 162

What is respiratory acidosis? How is it compensated?

Answer 162

Hypoventilation (respiratory) leads to a rise in pCO2 and so a fall in pH (acidosis) (Causes massive increase in plasma K+ and enzyme denaturation) Compensated by kidneys increasing [HCO3-] Takes 2-3 days

Question 163

What is metabolic alkalosis? How is it compensated?

Answer 163

If plasma [HCO3-] rises e.g. After vomiting (metabolic) this causes plasma pH to rise (Alkalosis) Can be compensated to a degree by decreasing ventilation

Question 164

What is metabolic acidosis? How is it compensated?

Answer 164

If tissues produce acid (metabolic) this reacts with HCO3- Therefore if there is a decrease in HCO3- this causes a decrease in pH (acidosis) Can be compensated by increasing ventilation (decreases pCO2)

Question 165

What is the role of choroid plexus cells?

Answer 165

CSF [HCO3-] determines which pCO2 is associated with normal CSF pH Therefore CSF [HCO3-] therefore sets the control system to a particular pCO2 It can be reset by changing CSF [HCO3-]

Question 166

How does choroid plexus cells determine what pCO2 is associated with a 'normal' CSF pH?

Answer 166

Elevated pCO2 drives CO2 into CSF across BBB CSF [HCO3-] is initially constant, so CSF pH falls Fall in CSF pH is detected by central chemoreceptors Drives increased ventilation, lowers pCO2 and restores pH of CSF

Question 167

Describe what happens in metabolic acidosis to CSF

Answer 167

Decrease in pH and decrease in [HCO3-] in blood Can't cross BBB [HCO3-] in CSF does not change Blood= acid detected by peripheral chemoreceptors Central chemoreceptors can't work because their pH does not change Breathe more to get pH back to normal Decrease in pCO2 in brain as [HCO3-] has not changes Brain becomes alkali (central chemoreceptors) Eventually get to breathe more!!! ******

Question 168

Describe what happens with persisting hypoxia

Answer 168

Diseases affect diffusion of O2 across the membrane - ventilation perfusion matching Peripheral chemoreceptors - need to breathe more to get more O2 in But pCO2 falls- CSF and blood (central chemoreceptors) - alkali makes you want to breathe less - overtime balances as pCO2 regulated via HCO3 ****

Question 169

Describes what happens with persisting hypercapnia

Answer 169

When pH is low this can lead to persisting hypercapnia (High pCO2) Choroid plexus cells increase [HCO3-] - takes up acid in CSF - keeps central chemoreceptors happy Long term- kidneys alter the amount of HCO3- in blood so that it becomes normal CO2 is controlled short term very precisely but not in the long term *****

Question 170

Describe some features of acute hypoxia

Answer 170

``` pO2<8kPa Peripheral chemoreceptors Increased ventilation Effects on pCO2 Central chemoreceptors ```

Question 171

Describe some features of chronic hypoxia

Answer 171

Renal correction of acid base balance | Increased ventilation

Question 172

What is respiratory failure?

Answer 172

Respiratory failure - not enough O2 enters blood, not enough CO2 leaves the blood (don't necessarily occur together) Arterial pO2 falls below 8kPa when breathing air at sea level (as above sea level tends to decrease pO2)

Question 173

What are the 5 broad factors necessary to maintain arterial pO2 in normal range?

Answer 173

``` pO2 in inspired air Ventilation rate Effective diffusion Ventilation perfusion matching Normal right to left cardiac shunts ```

Question 174

How may a problem with pO2 in inspired air result in hypoxia and respiratory failure?

Answer 174

Low pO2 in inspired air (ie. Living at a high altitude) Everything is normal - air breathed in just has low pO2 So arterial pO2 is thus low

Question 175

How does a problem with ventilation result in hypoxia and respiratory failure?

Answer 175

Hypoventilation is always associated with an increase in pCO2 --> Type 2 respiratory failure and decrease in pO2

Question 176

What neuromuscular problems cause Hypoventilation and thus type 2 respiratory failure (due to increase in pCO2 and well as decrease in pO2)?

Answer 176

``` Respiratory depression due to opiate overdose Head injury Muscle weakness (NMJ/ nerve/ muscle diseases) ```

Question 177

What chest wall problems cause Hypoventilation and thus type 2 respiratory failure (due to increase in pCO2 and well as decrease in pO2)?

Answer 177

Scoliosis/ kyphosis Morbid obesity Trauma Pneumothorax

Question 178

What problems making it hard to ventilate the lungs cause Hypoventilation and thus type 2 respiratory failure (due to increase in pCO2 and well as decrease in pO2)?

Answer 178

Airway obstructions- asthma and COPD when airway narrowing is severe and widespread Sever fibrosis

Question 179

How does an impairment of diffusion result in hypoxia and respiratory failure?

Answer 179

O2 diffuses much less readily than CO2, so always affected first pCO2 is therefore low / normal = always type 1 Respiratory failure Structural changes - lung fibrosis causing thickening of alveolar capillary membrane Increased path length- pulmonary oedema (fibrosis- fibro sing alveoli this, extrinsic allergic alveolitis, pneumoconiosis, asbestosis) Total area for diffusion reduced - emphysema

Question 180

How does a ventilation perfusion mismatch result in hypoxia and respiratory failure?

Answer 180

O2 diffuses much less readily than CO2 so is always affected first pCO2 is therefore low/ normal - always type 1 respiratory failure Reduced ventilation of some alveoli- lobar pneumonia Reduced perfusion of some alveoli- pulmonary embolism

Question 181

How does abnormal right to left cardiac shunts result in hypoxia and respiratory failure?

Answer 181

E.g. Cyanotic heart disease such says tetrology of fallot Pulmonary stenosis RV hypertrophy Ventricular septal defect Overriding aorta

Question 182

What is type 1 respiratory failure?

Answer 182

Arterial hypoxia accompanied by a normal or low pCO2 Increase in RR Decrease in pO2 Decrease in pCO2 Symptoms: Breathlessness, exercise intolerance, central cyanosis Caused by: pneumonia, vasoconstriction

Question 183

What is type 2 respiratory failure?

Answer 183

Arterial hypoxia accompanied by an elevated pCO2 Increase in RR Decrease in pO2 Increase in pCO2 Symptoms: ACUTE- breathlessness (some compensation, poor ventilation prevents full compensation); CHRONIC- CO2 retention (CSF acidity corrected by choroid plexus, central chemoreceptors reset to higher CO2 levels, persisting hypoxia, reduction of respiratory drive which is now driven by hypoxia (via peripheral chemoreceptors)) Caused by: Poor respiratory effort (narcotics), muscle weakness, chest wall problems

Question 184

What is asthma?

Answer 184

Chronic disorder characterised by airway wall inflammation and remodelling - reversible airflow obstruction

Question 185

What is the general pathophysiology of asthma?

Answer 185

Thickened smooth muscle, and basement membranes | Triggers cause airways smooth muscle to contract- reducing airway radius, increasing resistance, reducing airflow

Question 186

What are some examples of some air borne allergies that cause asthma?

Answer 186

House dust mites Pollens Air pollution Tobacco smoke (post/pre natal)

Question 187

What are specific allergens?

Answer 187

Specific allergens that trigger asthma attacks

Question 188

What are non specific allergens?

Answer 188

Due to hyper responsiveness of the airways- cold air and fumes which are non specific can trigger asthma attacks

Question 189

Describe the history of someone with asthma

Answer 189

More than one of the following symptoms - wheeze- high pitched, polyphonic (variable intensity and tone), expiratory, originates in airways which have been narrowed by compression or obstruction - cough- often worse at night - lack of sleep, poor performance at work; exercise induced - decreased participation in activities; dry - breathlessness- with exercise - chest tightness - variable airflow obstruction

Question 190

Describe the examination of someone with asthma

Answer 190

Inspection - chest- scars, deformities, hyper expansion (Barrel chest) - general health- eczema, hay fever, lethargy, can they speak? - room- meds, charts - percussion- hyper resonant - auscultation- polyphonic wheeze

Question 191

Describe the investigation of someone with asthma

Answer 191

Spirometry - flow volume loop - low PEFR - low FEV1/FVC ratio - 12% increase in FEV1 following salbutamol Allergy testing - skin prick to aero allergens - cat, dog, ADMs - blood IgE levels to specific aero allergens Chest x rays - performed to exclude other diseases / inhalation of foreign bodies/ pneumothorax

Question 192

Describe the detailed pathophysiology of asthma - inflammation and remodelling

Answer 192

Inflammation o Mast Cells • Increased in asthma • Release prostaglandins, histamine etc o Eosinophils • Large numbers in the bronchial wall and secretions of asthmatics o Dendritc Cells and Lymphocytes • Dedritic cells have a role in the initial uptake and presentation of allergens to lymphocytes • T-Helper lymphocytes (CD4) release cytokines that play a key part in the activation of mast cells • Th2 phenotype favour the production of antibody production by B lymphocytes to IgE. Remodelling o Epithelium • Stressed and damaged with a loss of ciliated columnar cells o Basement membrane • Deposition of collagens, causing it to thicken o Smooth Muscle • Hyperplasia causing thickening of the muscle

Question 193

Other than spontaneity, what are the 3 main precipitating factors of asthmatic attacks?

Answer 193

Although they may occur spontaneously, asthma exacerbations are most commonly caused by: o Lack of treatment adherence o Respiratory Virus Infections associated with the common cold o Exposure to allergen or triggering drug (e.g. NSAID)

Question 194

How is asthma treated and managed?

Answer 194

``` Education Educate patients to correctly recognise their symptoms, to use their medication timely, use services appropriately and to develop their own Personal Asthma Action Plan. Primary Prevention o Stop smoking o Fresh air o Reduce exposure to allergens/triggers o Weight Loss Pharmacological Management o b2-adrenoagonists o Muscarinic antagonists o Short term relief o E.g. Salbutamol o Anti-inflammatory agents o Corticosteroids o Preventer therapies ```

Question 195

How is severe acute asthma treated?

Answer 195

It is vital to assess patients for features of acute severe asthma which requires immediate treatment and hospitalisation. Treatment of acute severe asthma includes nebulised B2 agonists and ipratropium delivered in oxygen and intravenous steroids followed by a short course of high dose oral prednisolone. Other drugs such as magnesium sulphate and aminophylline may also be required.

Question 196

How must life threatening asthma be treated?

Answer 196

Patients with features of life threatening asthma need ITU management and may require ventilation.

Question 197

What cells drive the chronic inflammatory reaction of asthma and how?

Answer 197

Asthma is a chronic inflammatory process driven by Th2 cells Macrophages process and present antigens to T lymphocytes. This ‘activates’ T cells, with TH2 cells being preferentially activated. TH2 cells release cytokines, which attract and activate inflammatory cells, including mast cells and eosinophils. TH2 cells also activate B cells, which produce IgE

Question 198

Typically what is the 2 phase response to allergens/ antigens in asthma?

Answer 198

Typically, in a sensitized atopic asthmatic, exposure to antigen results in a 2 phase response consisting of an immediate response (reaching maximum in about 20 minutes) followed by a late phase response ( 3 – 12 hours later). 1. The immediate response is an example of type 1 hypersensitivity. It is caused by interaction of the allergen & specific IgE antibodies, leading to mast cells degranulation and release of mediators (histamine, tryptase, prostaglandin D2 and leukotriene) which cause bronchial smooth muscle contraction → bronchoconstriction . 2. The Late phase response is an example of type IV hypersensitivity. It is complex, involving the full spectrum of inflammatory cells, including eosinophils (eosinophils release Leukotriene C4 and other mediators, some of which are toxic to epithelial cells, and causes shedding of epithelial cells), mast cells, lymphocytes, & neutrophils, which release an array of mediator and cytokines, which cause airway inflammation.

Question 199

What drugs are eosinophils very sensitive to?

Answer 199

Steroid therapy

Question 200

What causes airway narrowing in asthma?

Answer 200

The air way inflammation causes reduced airway calibre (airway narrowing) due to:  Mucosal swelling (oedema) due to vascular leak,  Thickening of bronchial walls due to infiltration of by inflammatory cells  Mucous over production; the mucus is also abnormal- it is thick, tenacious & slow moving. The cough is therefore usually dry or only productive of scanty, white sputum. In severe cases many airways are occluded by mucus plugs.  Smooth muscle contraction  The epithelium is shed and is incorporated into the thick mucus

Question 201

What 3 things does airway inflammation in asthma cause?

Answer 201

Airway narrowing Hyper responsive of airways to non specific stimuli Airway remodelling (some of which may not be reversible)

Question 202

What pathological remodelling occurs in an airway in asthma over a long term?

Answer 202

 hypertrophy & hyperplasia of smooth muscle,  hypertrophy of mucus glands  thickening of the basement membrane

Question 203

What are some observable effects of airway narrowing in asthma?

Answer 203

 causes wheezing & other clinical features of asthma  results in an obstructive pattern on Spirometry (↓ FEV/FVC ratio < 70% ) & typical flow volume loops; which shows reversibility with bronchodilators, or over a period of time  air trapping with increased residual volume;

Question 204

What are the effects of pathological changes in asthma on gas exchange?

Answer 204

Airway narrowing leads to reduced ventilation of the affected alveoli → this causes a ventilation / perfusion mismatch in the affected area. Hyperventilation of better ventilated areas of the lung cannot compensate for the hypoxia, but can compensate for CO2 retention by increased breathing out of CO2. Hence, In mild to moderate asthma – the picture is one of ↓pCO2 and ↓pO2 = type 1 respiratory failure In severe attacks = extensive involvement of airways (fewer unaffected areas where hyperventilation wash out CO2), and exhaustion (which limits respiratory effort), limits the amount of CO2 which can be breathed out, leading to a rise in CO2 Thus the blood gas analysis reveals ↑pCO2 and ↓pO2 = type 2 respiratory failure Therefore increasing pCO2 is a sign of life threatening Asthma. (Disease is severe & extensive and patient is exhausted--- these patients often require assisted ventilation)

Question 205

What are some triggers of an asthma attack?

Answer 205

cold air; allergens - pollen, animals (animal hair/dander), house dust mite faeces; exercise; emotional distress; fumes - Car exhaust, cigarette smoke, perfumes; chemicals - Isocyanates and acid anhydrides (varnish/paint); drugs - NSAIDS and beta blockers Because of airway hyper-responsiveness, non-allergic stimuli like cold air & fumes can also trigger attacks.

Question 206

What is the treatment/ management of asthma?

Answer 206

Patient education Drug treatment using the BTS stepwise approach. Bronchodilators and steroids are 2 important classes of drugs used in treatment, and inhalers are used to deliver the drugs in an aerosol form.

Question 207

Why are bronchodilators used to treat asthma?

Answer 207

Q

Question 208

Why are steroids used to treat asthma?

Answer 208

Q

Question 209

Define COPD

Answer 209

COPD is a disease state characterised by airflow limitation that is not fully reversible. It encompasses both emphysema and chronic bronchitis. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases. It is primarily caused by cigarette smoking.

Question 210

What are the main causes of COPD?

Answer 210

Tobacco smoking is responsible for 90% of COPD cases. Air pollution and occupational exposure are other causes. Alpha-1 antitrypsin deficiency which is an inherited condition is less common. Alpha-1 antitrypsin is an antiproteinase; the imbalance in proteinases and antiproteinase leads to destruction of alveolar walls and to emphysema that usually presents at an early age

Question 211

What do the noxious substances trigger in COPD?

Answer 211

The host response to inhaled cigarette smoke and other noxious substances causes a chronic inflammatory process and oxidative injury, which affects central and peripheral airways, lung parenchyma, alveoli, and pulmonary vasculature.

Question 212

What are the 6 pathological changes that occur in COPD?

Answer 212

 enlargement of mucus-secreting glands of the central airways,  increased number of goblet cells ( which replace ciliated respiratory epithelium)  ciliary dysfunction  breakdown of elastin leading to destruction of alveolar walls and structure, and loss of elastic recoil.  formation of larger air spaces with reduction in total surface area available for gas exchange  vascular bed changes leading to pulmonary hypertension.

Question 213

What are the two conditions which fall under COPD?

Answer 213

Emphysema and chronic bronchitis

Question 214

What's the difference between emphysema and chronic bronchitis?

Answer 214

In emphysema, which is a subtype of COPD, the final outcome is elastin breakdown and subsequent loss of alveolar integrity leading to permanent destructive enlargement of the airspaces distal to the terminal bronchioles. In chronic bronchitis, another phenotype of COPD, the final outcome is excessive mucus secretion and impaired removal of the sections (due to ciliary dysfunction). Usually features both emphysema and chronic bronchitis co-exist in patients with COPD. In both conditions, changes are progressive and usually not reversible.

Question 215

How do the pathological changes in COPD lead to increased airway resistance and thus eventually right sided heart failure?

Answer 215

These changes lead to increased airway resistance due to (a) luminal obstruction of airways by secretions, (b) narrowing of small bronchioles which are usually kept open by the outward pull (radial traction) exerted on their walls by elastin in the surrounding alveoli. (c) Decreased elastic recoil leads to reduced expiratory force, hence air trapping. Expiratory flow limitation promotes hyperinflation. Airway narrowing and destruction of lung parenchyma, predisposes COPD patients to hypoxia, particularly during activity. Progressive hypoxia causes pulmonary vaso constriction and vascular smooth muscle thickening with subsequent pulmonary hypertension and right heart failure (Cor pulmonale).

Question 216

Describe the history of someone with COPD

Answer 216

COPD has a gradual onset and usually presents in older people with a long history of smoking. Cough  Usually the initial symptom of COPD.  Frequently a morning cough, but becomes constant as disease progresses.  Usually productive, and sputum quality may change with exacerbations or superimposed infection. Shortness of breath occurs initially on exertion but may progress to shortness of breath even at rest.

Question 217

Describe what could be found on examination of someone with COPD

Answer 217

Tachypnoea: increased respiratory rate to compensate for hypoxia and hypoventilation.  Use of accessory muscles of respiration (recall these muscles) due to difficulty in moving air in and out of lungs.  Barrel chest (increased antero-posterior diameter of the chest) is due to hyperinflation and air trapping secondary to incomplete expiration  Hyper- resonance on percussion due to hyperinflation and air trapping  Reduced intensity (distant) breath sounds caused by barrel chest, hyperinflation, and air trapping.  Reduced air entry (poor air movement) secondary to loss of lung elasticity and lung tissue breakdown.  Wheezing may be present  Late features include  Central cyanosis – hypoxia due to respiratory failure  Flapping tremors due to CO2 retention (hypercapnia)  Signs of right-sided heart failure (distended neck veins, hepatomegaly, and ankle oedema) secondary to pulmonary hypertension.

Question 218

Describe the investigations involved in the diagnosis of COPD

Answer 218

 Lung Function Tests: Spirometry shows an obstructive pattern with FEV1/FVC ratio <70% and limited reversibility following treatment with bronchodilators. Time volume plots (vitalograph) and Flow volume loops show the typical obstructive pattern. Decreased diffusing capacity of the lung for carbon monoxide (DLCO) is a feature of emphysema  CXR: Hyper inflated lungs may result in (a) a flattened diaphragm, (b) hyperlucent lungs and (c) an increased antero-posterior diameter of the chest. It may also show complications of COPD, such as pneumonia and pneumothorax, and is also useful to rule out other pathologies (e.g. lung CA in a patient presenting with chronic cough).  Pulse oximetry and/or ABG analysis: is carried out in acutely unwell patients to assess for hypoxia and hypercapnia. ABG is also done to screen for those requiring treatment with home oxygen therapy.  Alpha-1 antitrypsin level: Checked if there is high suspicion such as a positive family history and atypical COPD (young patients and non-smokers). The levels are low in patients with alpha-1 antitrypsin deficiency.

Question 219

What would the treatment for COPD be?

Answer 219

 Smoking cessation  Patient education;  Pneumococcal vaccination is strongly recommended in COPD patients  Patient weight, nutrition status, and physical activity should be monitored.  Bronchodilators  Inhaled corticosteroid  Pulmonary rehabilitation: many COPD patients avoid exercise because of breathlessness. This leads to muscle weakness and leads to a vicious cycle of worsening symptoms, social isolation and depression. Pulmonary rehabilitation aims to break this cycle with a MDT (multi-disciplinary team) programme of exercise, disease education and nutritional advice.  Long term oxygen treatment – extended periods of hypoxia cause pulmonary hypertension. Continuous low dose oxygen therapy at home for at least 16 hours a day has been shown to improve survival.  Surgical interventions: such as removal of large bullae, lung volume reduction, and lung transplant) are the last step in the management of COPD. They are used to improve lung dynamics, exercise adherence, and quality of life.

Question 220

What is an acute exacerbation of COPD? How does it present?

Answer 220

Acute exacerbation of COPD is defined as an event characterised by a change in the patient's baseline dyspnoea, cough, and/or sputum that is beyond normal day- to-day variations and is acute in onset. Acute infectious exacerbations present with acute, severe shortness of breath, fever, and chest pain.

Question 221

How is acute exacerbation of COPD managed?

Answer 221

 Monitoring for hypoxia and hypercapnia, using Pulse oximetry and ABG analysis  Appropriate antibiotics particularly to cover Haemophillus influenzae and Streptococcus pneumoniae is very important,  Nebulised bronchodilators  Oral steroids ( a short course of high dose oral prednisolone)  24% or 28% Oxygen therapy while keeping under review for CO2 retention (Recall the physiology behind this possible complication)  Consider non-invasive ventilation for worsening type 2 respiratory failure

Question 222

What are some potential complications of COPD?

Answer 222

 Recurrent pneumonia  Pneumothorax: Occurs because of lung parenchyma damage with sub-pleural bulla formation and rupture  respiratory failure  Cor pulmonale (Right heart failure

Question 223

What is TB? And what causes it?

Answer 223

TB is a chronic communicable disease caused by Mycobacterium tuberculosis (MTB).

Question 224

Describe mycobacterium tuberculosis bacteria

Answer 224

TB bacilli are aerobic, acid & alcohol fast bacilli. They can be demonstrated on smears (e.g. sputum smears) stained by the Ziehl-Nielsen method and grow slowly on culture (on media such as the Lowenstein-Jensen Medium) taking 2-6 weeks to form colonies.

Question 225

How does TB spread from person to person (replete nuclei? And how does this vary being inside and outside?

Answer 225

TB is transmitted from person to person by aerosolized droplets. The unit of infection is a small particle called a droplet nucleus. Coughing, sneezing, talking and other respiratory manoeuvres by infective individuals will produce small respiratory droplets which undergo evaporation to form droplet nuclei. These disperse in the air without settling, and the organisms they contain remain viable for extended periods of time. Outdoors, the organisms in droplet nuclei are eventually eliminated by infinite dilution and by radiation from the sun.

Question 226

For someone on treatment for TB, how long does it take for infectivity to become minimal? But for how long shall treatment still be taken?

Answer 226

The infectivity of sputum becomes minimal after 2 weeks of commencing treatment with effective anti-TB chemotherapy. However, treatment must continue for the full duration (e.g.six months for pulmonary TB) to eradicate disease in the infected person.

Question 227

Describe the pathophysiology of TB

Answer 227

Alveolar macrophages phagocytose MTB deposited in alveoli but are unable to kill them (the cell wall lipids of MTB apparently block fusion of the phagosomes & lysosomes ). These macrophages initiate the development of cell mediated immunity which eventually leads to the emergence of activated macrophages with enhanced ability to kill MTB. This takes about 6 weeks to develop.

Question 228

How does a tubercle form and what does it consist of?

Answer 228

Ingestion of MTB by macrophages causes a granulomatous reaction. The characteristic lesion of tuberculosis is a spherical granuloma with central caseation (also known as tubercles) Microscopically a TB granuloma consists of a necrotic cheese like core (caseous necrosis) surrounded by epithelioid macrophages, Langerhans giant cells, and lymphocytes.

Question 229

Describe primary infection of TB

Answer 229

The Primary Infection occurs on first exposure. The deposition of TB bacilli in the alveoli is followed usually by development of sub-pleural focus of tubercles called the primary focus or Ghon’s focus. This may be in any lung zone. TB bacilli drain from the primary focus into the hilar lymph nodes. The primary (Ghon’s) focus+ the draining lymph (hilar) nodes together are called the primary complex. Most primary infections will heal with or without calcification of the primary complex. However, in the majority of subjects, before healing occurs, some TB bacilli enter the blood stream (probably via lymph drainage to the venous system) and haematogenous spread occurs resulting in the seeding of tubercle bacilli to other parts of the lung as well as other organs (extra pulmonary sites). With the development of cell mediated immunity the infection is contained. The primary complex heals, but a small number of organisms remain viable in the lungs/other organs.

Question 230

Describe latent infection of TB

Answer 230

This state, where TB bacilli can persist within the human host, without causing disease, for years or until death due to other causes, is known as latent tuberculosis. The person remains well but the potential for reactivation at any site is always present. Reactivation usually occurs when the patient’s immune mechanisms wane or fail (eg old age, malnutrition, HIV, immunosuppression)

Question 231

What is the importance of the tuberculin skin test?

Answer 231

Latent TB is characterised by a positive tuberculin skin test (or positive ‘Quantiferon’ test). The skin test is based on demonstrating a type IV hypersensitivity reaction to proteins derived from Mycobacteria. In the naturally infected host, immunity and hypersensitivity usually develop simultaneously.

Question 232

What are the statistics and risks associated with TB?

Answer 232

Those infected with TB have about a 10% life time risk of developing active disease: 5% develop primary TB at the time of the initial infection, while another 5% develop post primary TB due to reactivation of latent TB after a variable period of time (up to 60 years) following the primary infection

Question 233

What is primary TB?

Answer 233

The primary complex does not heal but continues to progress, and causes disease which is known as Primary Tuberculosis. The pathological changes in primary TB are similar to those seen in reactivation TB.

Question 234

What is post primary TB?

Answer 234

The vast majority of clinical cases of TB are due to reactivation of latent TB and occurs most often in the lungs. Post primary TB can also be due to reinfection

Question 235

What is post primary pulmonary TB?

Answer 235

Is most often seen in the upper lung zones. The high ventilation/perfusion ratio with higher alveolar pO2 in upper zones of the lungs relative to the other parts of the lung is believed to predispose to reactivation of TB bacilli at these sites. This can result in the following sequelae: Proliferation of TB bacilli in the caseous centres is followed by softening and liquefaction of the caseous material which may discharge into a bronchus resulting in cavity formation. Fibrous tissue forms around the periphery of such tuberculous lesions but is usually incapable of limiting extension of the tuberculous process. Haemorrhage resulting from extension of the of the caseous process into vessels in the cavity walls-causes haemoptysis. Spread of caseous and liquefied material through the bronchial tree may disseminate the infection to other lung zones with or without the development of a vigorous inflammatory exudate. A marked inflammatory exudate filling the alveoli causes consolidation and is known as tuberculous pneumonia. (i.e. clinically and radiologically it may appear similar to a bacterial pneumonia, but the causative organism is mycobacterium tuberculosis). Seeding of TB bacilli in the pleura, or hypersensitivity can result in a pleural effusion. Rupture of a caseous pulmonary focus into a blood vessel may result in miliary tuberculosis with the formation of multiple ‘miliary’ (millet seed like) 0.5 – 2mm tuberculous foci in the lung and in other organs of the body.

Question 236

What are the general symptoms associated with TB?

Answer 236

The diagnosis is usually suggested by findings of compatible x-ray changes during investigation of patients with:-  persistent cough  haemoptysis  unresolved pneumonia  nonspecific symptoms – e.g. fever, weight loss

Question 237

What is the classical triad of symptoms that a TB patient presents with?

Answer 237

The classical presentation is with:  Cough - not always productive,  Often with fevers towards the end of the day, &  Weight loss and general debility

Question 238

What does a chest x ray of a patient with TB show?

Answer 238

The chest x-ray reveals pulmonary shadowing, which may be patchy solid lesions,cavitated solid lesions, streaky fibrosis, or flecks of calcification.

Question 239

How is TB diagnosed?

Answer 239

TB is diagnosed by clinical and radiological features plus the identification of the tubercle bacillus in the appropriate body fluid by direct smear and subsequently culture. It is very important to isolate the organism and determine its susceptibility to drugs.

Question 240

What is the general treatment given for TB infections?

Answer 240

TB is treatable by a combination of antibiotics. The drugs used include rifampicin, isoniazid, pyrazinamide, ethambutal and streptomycin. A prolonged follow up is needed. TB is a notifiable disease, and its diagnosis has public health implications.

Question 241

What are the common normal flora of the respiratory tract?

Answer 241

o Viridans streptococci o Neisseria spp o Anaerobes o Candida spp

Question 242

What are the less common normal flora of the respiratory tract?

Answer 242

o Streptococcus pneumonia o Streptococcus pyogenes o Haemophillus influenza

Question 243

What are some other normal flora of the respiratory tract?

Answer 243

o Pseudomonas | o E. coli

Question 244

What are the natural defences of the respiratory system tract against infection?

Answer 244

``` o Cough and sneezing reflex o Muco-ciliary clearance mechanisms --> Ciliated columnar epithelium --> Nasal hairs o Respiratory mucosal immune system --> Lymphoid follicles of the pharynx and tonsils --> Alveolar macrophages --> Secretary IgA and IgG ```

Question 245

What are some common infections of the upper respiratory tract?

Answer 245

``` o Rhinitis (common cold) o Pharyngitis o Epiglottitis o Laryngitis o Tracheitis o Sinusitis o Otitis media (Inflammation of middle/inner ear) ```

Question 246

What e the viruses that most commonly cause upper respiratory tract infections?

Answer 246

o Rhinovirus o Coronavirus o Influenza/parainfluenza o Respiratory Syncytial Virus (RSV)

Question 247

How can an upper respiratory tract infection form from an URTI?

Answer 247

Bacterial super infection - second infection superimposed on by an earlier one ``` May also be caused by Bacterial Super-Infection: o Common with sinusitis and otitis media o Can lead to • Mastoiditis • Meningitis • Brain abscess ```

Question 248

What is a pneumonia?

Answer 248

Pneumonia is a general term denoting inflammation of the gas-exchanging region of the lung, usually due to infection (bacterial or viral). Pneumonia is therefore an infection of the lung parenchyma. Inflammation due to other causes, such as physical or chemical damage is often called pneumonitis.

Question 249

What is a lobar pneumonia?

Answer 249

Pneumonia localised to a particular lobe/s of the lung. | Most often due to Streptococcus pneumoniae

Question 250

What is bronchopneumonia?

Answer 250

Pneumonia that is diffuse and patchy. Infection starts in the airways and spreads to adjacent alveoli and lung tissue. Streptococcus pneumoniae, Haemophilus influenza, Staphylococcus aureus, anaerobes, coliforms

Question 251

What is aspiration pneumonia?

Answer 251

Aspiration of food, drink, saliva or vomit can lead to pneumonia. This is more likely in individuals with an altered level of consciousness, e.g. due to anaesthesia, alcohol or drug abuse, or if there are problems swallowing due to nerve or oesophageal damage. Organisms include oral flora and anaerobes.

Question 252

What is interstitial pneumonia?

Answer 252

Inflammation of the Intersticium of the lung | Alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues

Question 253

What is chronic pneumonia?

Answer 253

Inflammation of the lungs that persists for an extended period of time

Question 254

What bacteria commonly cause community acquired pneumonia?

Answer 254

``` Common Bacteria o Streptococcus pneumoniae ​– 30% o Haemophilus influenza ​– 13% o Klebsiella pneumoniae Atypical Bacteria o Chlamydia pneumophilia​- 10% o Mycoplasma pneumoniae o Legionella pneumophila ```

Question 255

What bacteria commonly cause hospital acquired pneumonia?

Answer 255

o Gram –‘ve enteric bacteria​- 10% o Pseudomonas o Staphylococcus aureus o MRSA

Question 256

What type of bacteria are commonly involved in the formation of aspiration pneumonia?

Answer 256

o Anaerobes | o Oral flora

Question 257

What pathogens most commonly cause pneumonia in an immunocompromised patient?

Answer 257

Pneumocystitis jiroveci, aspergillus spp, cytomegalovirus Pathogens infecting immunosuppressed hosts may be: o Virulent infection with common organism o Infection with opportunistic pathogen • Viruses – Cytomegalovirus (CMV) • Bacteria – Mycobacterium avium intracellulare • Fungi – Aspergillus, candida, pneumocystis jiroveci • Protozoa – Cryptosporidia, toxoplasma

Question 258

What are some clues of a pneumonia infection by S. Pneumoniae?

Answer 258

S. pneumoniae | Elderly, co-morbidities, acute onset, high fever, Pleuritic chest pain

Question 259

What are some clues of a pneumonia infection by H. influenza?

Answer 259

H. influenza | COPD

Question 260

What are some clues of a pneumonia infection by legionella?

Answer 260

Legionella | Recent travel, younger patient, smokers, illness, multi-system involvement

Question 261

What are some clues of a pneumonia infection by Mycoplasma?

Answer 261

Mycoplasma | Young, prior antibiotics, extra-pulmonary involvement (haemolysis, skin and joint)

Question 262

What are some clues of a pneumonia infection by S. Aureus?

Answer 262

S. aureus | Post-viral, Intra-Venous Drug User

Question 263

What are some clues of a pneumonia infection by Chlamydia?

Answer 263

Chlamydia | Contact with birds

Question 264

What are some clues of a pneumonia infection by Coxiella?

Answer 264

``` Coxiella Animal contact (sheep) ```

Question 265

What are some clues of pneumonia infection by Klebsiella?

Answer 265

Klebsiella | Thrombocytopenia, leucopenia

Question 266

What are some clues of pneumonia infection by S. milleri?

Answer 266

S. Milleri | Dental infections, abdominal source, aspiration

Question 267

What are some general symptoms of pneumonia?

Answer 267

``` o Fever, chills, sweats, rigors o Cough o Sputum • Clear / purulent / ‘rust coloured / haemoptysis o Dyspnoea o Pleuritic chest pain o Malaise o Anorexia and vomiting o Headache o Myalgia o Diarrhoea o Chest Signs • Bronchial breath sounds • Crackles • Wheeze • Dullness to percussion • Reduced vocal resonance ```

Question 268

What are some common features of hospital acquired pneumonia?

Answer 268

Hospital Acquired Pneumonia o Pneumonia occurring 48hrs after hospital admission o Makes up ~15% of all hospital acquired infections o Common in ventilated/post surgical patients

Question 269

How may the severity of pneumonia be assessed?

Answer 269

CURB 65 Score The severity of pneumonia can be assessed using the CURB 65 score, where the presence of two or more of the following features is an indication for hospital treatment, and patients with high scores may required ICU treatment. C – New mental Confusion U – Urea > 7mmol/L R – Respiratory rate > 30 per minute B – Blood pressure (Systolic < 90 or Diastolic < 60 mmHg)

Question 270

What samples are collected in the investigation of pneumonia?

Answer 270

``` Samples Collected to Investigate Pneumonia o Sputum o Nose and Throat swabs o Endotracheal aspirates o Broncho Alveolar Lavage fluid (BAL) o Open Lung Biopsy o Blood culture • Preferably before antibiotics o Urine • Detect the antigens of legionella/pneumococcus o Serum • Antibody detection ```

Question 271

What are the microbiological investigations of pneumonia?

Answer 271

``` Microbiological Investigations of Pneumonia o Macroscopic • Sputum, purulent, blood stained o Microscopy • Gram staining, Acid fast o Culture • Bacteria and viruses o PCR • Respiratory viruses o Antigen detection • Legionella o Antibody detection • Serology ```

Question 272

What is the common management pathway of a patient with pneumonia?

Answer 272

``` Management of Pneumonias o Oral fluid/IV fluids if severe • Avoid dehydration o Anti-pyretic drugs • Reduce fever and malaise • E.g. Paracetamol o Stronger analgesics • Deal with the pain (Pleuritic) o Oxygen • If there is cyanosis o Antibiotics • The infection is treated with antibiotics, which vary with the type of pneumonia. ```

Question 273

What antibiotic is used most of the time in community acquired pneumonia?

Answer 273

Community Acquired Pneumonia | The target organism is normally Pneumococcus, which is usually sensitive to Penicillin or related antibiotics.

Question 274

What antibiotic is commonly used in hospital acquired pneumonia?

Answer 274

Hospital Acquired pneumonia The target organism is more likely to be Gram –‘ve, making it necessary to use antibiotics that cover these organisms, e.g. IV Co-Amoxiclav.

Question 275

What are the common outcomes of pneumonia?

Answer 275

``` o Resolution • Organisation (Fibrous scarring) o Complications • Lung abscess • Bronchiectasis • Empyema (pus in pleural cavity) • Pleural effusion ```

Question 276

How is pneumonia prevented?

Answer 276

o Immunization • Flu vaccine – Given annually to high risk patients • Pneumococcal vaccine – Two vaccines o Chemoprophylaxis • Oral penicillin / erythromycin to patients with higher risk of lower respiratory tract infections • E.g. asplenia, dysfunctional spleen, immunodeficiency

Question 277

What does a chest x ray of a patient with pneumonia usually show?

Answer 277

Reveals shadowing in at least one section of lung fluid

Question 278

What's the incidence distribution of lung cancer?

Answer 278

o Males • Commonest male cancer • Mortality rate is around 100 per 100,000 • Incidence slowly falling due to reduction in smoking o Females • Exceeds breast cancer as a cause of death in women • Mortality rate is around 40 per 100,000 • Incidence is steadily rising o Socio-economic groups • Wide variation • Rate three times higher in lowest compared with highest

Question 279

What are some common causes of lung cancer?

Answer 279

Smoking Lung cancer is overwhelmingly related to smoking, with the risk being proportional to the duration of the habit and the number of cigarettes smoked. Around 90% of lung cancer in men and 80% in women are caused by smoking. ``` Other Aetiological Factors include: o Asbestos exposure o Radon exposure o Genetic factors o Dietary factors ```

Question 280

What are the common symptoms indicative of a primary lung cancer tumour?

Answer 280

``` Cough Dyspnoea Wheezing Haemoptysis Chest pain Post-obstructive pneumonia Weight loss Lethargy / Malaise ```

Question 281

What are the common symptoms indicative of regional metastases of lung cancer?

Answer 281

Superior vena cava obstruction Hoarseness (Left recurrent Laryngeal nerve palsy) Dyspnoea (Phrenic nerve palsy) Dysphagia

Question 282

What are common symptoms indicative of distant metastases to lung cancer?

Answer 282

``` Bone pain / Fractures CNS symptoms (Headache, double vision, confusion etc.) ```

Question 283

What is the paraneoplastic syndrome of lung cancer? (Common clinical guns associated with the disease)

Answer 283

``` Paraneoplastic syndrome is the presence of a symptom or disease due to the presence of cancer in the body, but not due to the local presence of cancer cells. They are mediated by humoral factors (cytokines and hormones) secreted by tumour cells, or the immune response against tumour cells. o Endocrine • Hypercalcaemia • Cushing’s syndrome o Neurological • Encephalopathy • Peripheral neuropathy o Skeletal • Finger clubbing o Haematological • Anaemia • Thrombocytopenia • Disseminated Intravascular Coagulation (DIC) o Other • Nephrotic syndrome • Anorexia or cachexia ```

Question 284

What imaging techniques are used in diagnosis of lung cancer?

Answer 284

``` Imaging investigations of various types are central to both the diagnosis and assessment of the disease (staging). o First clinical suspicion • Plain Chest X-Ray o Diagnosis and staging • CT scan • PET scan • Isotope bone scan ```

Question 285

What are the two staging systems for lung cancer?

Answer 285

TNM and number | Staging is one of the most important determinants of treatment and prognosis

Question 286

What is the number staging system of lung cancer?

Answer 286

Number Staging System Stage 1 – Small cancer, localised to one area of the lung Stage 2 and 3 – Larger Cancer, may have grown into surrounding tissues (lymph nodes) Stage 4 – Cancer has metastasised

Question 287

What is the TNM staging of lung cancer?

Answer 287

T – Size and position of tumour o T1 – Cancer contained within lung ( 7cm diameter) • Invading chest wall, mediastinal pleura, diaphragm, pericardium • Complete lung collapse • > 1 cancer nodule in the same lobe of lung o T4 • Cancer invading mediastinum, heart, major blood vessel, trachea, carina, oesophagus, spine, recurrent laryngeal nerve • Cancer nodules in more than one lobe of the same lung N – Lymph node involvement o N0 – No cancer in lymph nodes o N1 – Cancer in lymph nodes nearest the affected lung o N2 – Cancer in lymph nodes in mediastinum, on the same side o N3 – Cancer in lymph nodes on the opposite side of the mediastinum / supraclavicular lymph nodes M – Metastases o M0 – No evidence of distal cancer spread o M1 – Lung cancer cells in distant parts of the body, such as pleura, opposite lung, liver or bones etc

Question 288

What are the three most common methods of obtaining material for histological diagnosis?

Answer 288

Tissue for diagnostic purposes is usually obtained either by bronchoscopy, needle biopsy of the lung or Surgical biopsy. Making a histological diagnosis is important not only to confirm that the patient has lung cancer, but also to decided the cell type, which important both in terms of the prognosis and treatment.

Question 289

What are the two types of lung cancer and how are they differentiated?

Answer 289

o Non-Small Cell Lung Cancer More than 2/3rds have inoperable disease at presentation o Small Cell Lung Cancer ¾ have metastatic disease at presentation ``` Prognosis of either depends on: o Cell type • Small Cell worse than Non-Small Cell o Stage of disease o Performance status o Biochemical markers o Co-morbidities • E.g. Cardiac or chronic respiratory disease ```

Question 290

What are the different treatments available for lung cancer?

Answer 290

``` o Surgery • Mostly Non-Small Cell (<20% operable) o Radiotherapy • Radical – Curative • Palliative – Symptom control o Chemotherapy • Small cell – Potentially curative (Minority) • Non small cell – Modest survival increase, symptom control o Combination therapy • Combination of chemo and radiotherapy o Biological targeted therapies • E.g. EGFR and VEGF o Palliative care ```

Question 291

How is non small cell lung cancer usually managed?

Answer 291

Management of Non-Small Cell Lung Cancer Usually involves multiple modality therapy: o Palliative Radiotherapy for local symptoms o Chemotherapy – 50 – 60% response rates. o Combination Therapy – Important in locally advanced disease o Targeted Agents – EGFR and VEGF

Question 292

How is small cell lung cancer usually managed?

Answer 292

``` Management of Small Cell Cancer o Rarely operable o Combination Therapy – Responds well, adding ~1 year o Palliative Chemotherapy for symptoms o Death from cerebral metastases common ```

Question 293

What are some general nuclear features of malignancy (lung cancer)?

Answer 293

Nuclei of irregular shape (pleomorphic) and size (anisonucleosis) Nuclei are dark staining (hypochromatic) Increased nuclei size compared to cytoplasm (increased nuclear: cytoplasmic ratio) Frequent / abnormal mitoses (hyper proliferative) Prominent / multiple nucleoli

Question 294

What are some architectural features of malignancy (lung cancer)?

Answer 294

``` Ulceration Necrosis Infiltrative margins Vascular invasion Reaction in surrounding tissue (=stroma) Little resemblance to parent tissue ```

Question 295

What are three types of non small cell carcinoma?

Answer 295

Squamous cell carcinoma Adenocarcinoma Large cell carcinoma

Question 296

What are some histological features of squamous cell carcinoma?

Answer 296

``` Often central tumours Angula the cells Eosinophilic (pink) cytoplasm Intercellular bridges- prickles = desmosomes Keratinisation Keratin pearls Immunochemsitry - CK5/6 and P63 + TTF-1 ```

Question 297

What are some histological features of adenocarcinoma?

Answer 297

``` Often peripheral tumours Columnar/cuboidal cells Form glands (acini) Papillary structure May line alveoli (in situ) Some produce mucin Immunochemistry- most TTF-1 + CK5/6, P63- ```

Question 298

What are some histological features of small cell carcinoma?

Answer 298

``` Oat cell carcinoma Very cellular tumour Small nuclei - c.f. Size of lymphocyte Little cytoplasm Nuclear moulding Often necrosis and lots of mitoses Immunochemistry: CD5/6, synaptophysin+ and chromogranin + ```

Question 299

What are the main features usually seen on a chest x ray?

Answer 299

1. Trachea 2. Hila 3. Lungs 4. Diaphragm 5. Heart 6. Aortic knuckle 7. Ribs 8. Scapulae 9. Breasts 10. Stomach Costophrenic recess/angle o (PA film) Right main bronchus, left main bronchus, joining at the Carina.

Question 300

What would a lobar collapse look like on a CXR?

Answer 300

Displacement of the horizontal fissure is an indicator of lobar collapse. If there is volume loss of the right upper lobe (e.g. collapse), the horizontal fissure is displaced upwards. If there is volume loss of the right lower lobe (e.g. collapse), the horizontal fissure is displaced downwards.

Question 301

What is consolidation and what does it look like on a CXR?

Answer 301

If alveoli and small airways fill with dense material, the lung is said to be consolidated. This may be due to infection (pneumonia, pus), fluid (pulmonary oedema), blood (haemorrhage) or cells (cancer). If an area of the lung is consolidated it becomes dense and white. If the larger airways are spared, they are of relatively low density (blacker). This phenomenon is known as air bronchogram and it is a characteristic sign of consolidation.

Question 302

What is a pleural effusion and what does it look like in a CXR?

Answer 302

A Pleural effusion is a collection of fluid in the pleural space. Fluid gathers in the lowest part of the chest, according to the patient’s position. If the patient is upright when the X-ray is taken, a pleural effusion will obscure the Costophrenic angle/Hemidiaphragm. If a patient is supine, a pleural effusion layers along the posterior aspect of the chest cavity, and is difficult to see on a chest X-Ray. Pleural effusions appear on X-rays as uniformly white, with a concave area at the top. This is called the Meniscus sign.

Question 303

What is a pneumothorax and what does it look like on a CXR?

Answer 303

A pneumothorax forms when there is air trapped in the pleural space. This may occur spontaneously, or as a result of underlying lung disease. The most common cause is trauma, with laceration of the visceral pleura by a fractured rib

Question 304

What is a tension pneumothorax and what does it look like on a CXR?

Answer 304

One side of the pleural cavity completely filled with air due to lung collapse. Hemi thorax will look black due to lung collapse. One lung will be completely compressed. If there is tracheal or mediastinal shift away from the pneumothorax, the pneumothorax is said to be under tension. This is a medical emergency. Trachea is pushed away by air in the pleural Hemi diaphragm on side of lung collapse will be collapsed.

Question 305

What is tracheal displacement in a CXR indicative of?

Answer 305

If the trachea is genuinely displaced to one side (the patient is not rotated) try to establish if it has been pushed or pulled by a disease process.

Question 306

What will push the trachea and mediastinum away from the affected side?

Answer 306

Anything that increases pressure or volume in one hemithorax will push the trachea and mediastinum away from that side. (E.g. Tension pneumothorax, pleural effusion, tumour)

Question 307

What will pull the trachea and mediastinum towards the affected side?

Answer 307

Any disease that causes volume loss in one hemithorax will pull the trachea over towards that side. (E.g. collapsed lung, fibrosis)

Question 308

What are asbestos plaques and what do they look like on a CXR?

Answer 308

Calcified asbestos related pleural plaques have a characteristic appearance, and are generally considered to be benign. They are irregular, well defined and classically said to look like holly leaves.

Question 309

How can you identify lung hyper expansion on a CXR? And what causes this?

Answer 309

COPD can lead to hyperinflation of the lungs. This leads to blunting of both costophrenic angles, and flattened hemidiaphragms

Question 310

What is a pneumoperitoneum and how does it look on a CXR?

Answer 310

Lungs are normal, but air is seen under the diaphragm. This is a sign of bowel perforation.

Question 311

How do you work out the cardiac thoracic ratio?

Answer 311

The widest part of the heart and ribcage are measured laterally. If the heart is over 50% of the width of the thorax, it is enlarged.

Question 312

What is the lung interstitial space?

Answer 312

The Interstitial space is a potential space between alveolar cells and the capillary basement membrane, which is only apparent in disease states, when it may contain fibrous tissue, cells or fluid.

Question 313

What are lung interstitial diseases?

Answer 313

This is a group of diseases affecting the interstitial space of the lungs with a variety of causes that have similar pathophysiological effects and clinical features.

Question 314

What is the general pathophysiology of interstitial lung disease?

Answer 314

o The development of fibrous tissue in the Intersticium, making lungs less compliant, producing a restrictive ventilatory defect. o Airway resistance is NOT increased. In fact, the FEV1/FVC ratio can be > 70%, due to the increased radial traction on the airway, which keeps the airway open. o Lengthening of the diffusion path between alveolar air and blood impairs gas exchange, with oxygen uptake being affected selectively, as CO2 diffuses much more readily.

Question 315

What are the general clinical features of interstitial lung disease?

Answer 315

Symptoms: o Shortness of breath, reduced exercise tolerance, dry cough Signs: o Tachypnoea, tachycardia, reduced chest movement (bilaterally) and coarse crackles. Cyanosis and signs of right heart failure may be present. Clubbing is seen in cryptogenic fibrosing alveolitis.

Question 316

What are the broad causes of interstitial lung disease?

Answer 316

``` Occupational Treatment related Connective tissue disease Immunological Idiopathic ```

Question 317

What is fibrosing alveolitis?

Answer 317

o Progressive inflammatory condition, unknown cause o Relatively rare, 3-5 cases per 100,000. Two times more common in males o Histologically there are increased activated Alveolar Macrophages • Attract Neutrophils and Eosinophils • Local lung damage due to ROS and proteases • Tissue destruction and fibrosis o Patients report progressive shortness of breath on exercise, often with non-productive cough. o Most patients have finger clubbing o Chest X-Ray shows small lungs with micro-nodular shadowing predominating in the lower loves, with ragged heart borders o Can be restrained by treatment with high dose oral steroids in the early stages, less effective once fibrosis has developed • Effectiveness of treatment is monitored by repeated lung function tests

Question 318

What is extrinsic allergic alveolitis?

Answer 318

o Inhalation of organic material triggers an allergic reaction in alveoli and bronchioles. o Condition may be Acute or Chronic: Acute o Sudden onset, rapidly progressing o Farmer’s Lung • Antigen = Thermophillic actinomycetes found in mouldy hay • Influenza like illness 4-9 hours later with a dry cough and breathlessness on exertion • Fine mid and late inspiratory crackles • May be a wheeze Chronic o Bird Fancier’s Lung • Long Term Antigen Exposure = Pigeons / budgerigars • Insidious malaise (feeling particularly unwell) • Dry cough and breathlessness over months and years • Inspiratory crackles o Finger clubbing does not occur in either Acute or Chronic. o Acute disease chest x-ray shows diffuse micro-nodular infiltrate denser towards the hila. o Chronic disease chest x-ray may be almost normal, progressing to fibrosis in late disease. o Lung function tests will show reduced compliance and reduced gas transfer.

Question 319

What is asbestosis?

Answer 319

o Inhalation of asbestos fibres, disease often develops long after the exposure. o Asbestosis inhalation is associated with three forms of disease (along with a marked increase in lung cancer): • Benign pleural plaques • Asbestosis (pulmonary fibrosis) • Mesothelioma o Asbestos fibres that penetrate to the alveoli produce alveolitis • Influx of macrophages produces characteristic asbestosis bodies • Alveolitis progresses to fibrosis o History of asbestos exposure o Patient breathless on exertion and a dry cough. o Inspiratory crackles at the lung bases, which rise as the disease advances. o No treatment o Lung function tests show small lungs, reduced compliance and impaired gas transfer

Question 320

What is sarcoidosis?

Answer 320

o Disease of unknown cause, characterise by Non-Caseating Granulomas (Non-necrotising) in multiple organs and body sites o Most commonly in the lungs o Fluid is collected by lavage of the airways, and alveoli contain lots of cells, including macrophages and lymphocytes o Commoner in Afro-Caribbean and Asians than in Caucasians • Genetic predisposition o Highest incidence in 30’s and 40’s with more female cases o Often asymptomatic, but may have Cough, breathlessness o Grading system 0 – 4 o X-ray shows miliary and nodular shadowing and diffuse fibrosis o Stages 1 – 3 steroids are usually effective in suppressing the disease o Lung function tests show small lungs, reduced compliance and impaired gas transfer. May be evidence of air flow obstruction.

Question 321

What would a fibrosing alveolitis x ray look like?

Answer 321

Fibrosing Alveolitis Small lungs Micro-nodular shadowing (Lower lobes) Ragged heart borders

Question 322

What would an acute extrinsic allergic alveolitis look like?

Answer 322

Extrinsic Allergic Alveolitis (Acute) Micro-nodular infiltrate, denser towards the hila.

Question 323

What would a chronic extrinsic allergic alveolitis x ray look like?

Answer 323

Extrinsic Allergic Alveolitis (Chronic) Almost normal, progressing to fibrosis in late disease

Question 324

What would an asbestosis x ray look like?

Answer 324

Sarcoidosis Miliary and Nodular shadowing Diffuse fibrosis

Question 325

What would a sarcoidosis x ray look like?

Answer 325

Asbestosis Plaques – Holly leaf Fibrosis Mesothelioma

Question 326

Briefly describe the pleura

Answer 326

The pleura is a serous membrane consisting of a single layer of mesothelial cells with a thin layer of underlying connective tissue. The Parietal Pleura lines the inside of each hemi thorax (the bony thoracic cage, diaphragm and mediastinal surface) and becomes continuous at the hilum of the lung with the Visceral Pleura, which lines the outside of the lung. The visceral pleura extend between lobes of the lung into the depths of the oblique and horizontal fissures.

Question 327

Briefly describe the pleural cavity

Answer 327

The pleural cavity, or space, is a potential space between the two layers of pleura that are continuous at the hilum. Both layers of pleura are covered with a common film of fluid produced from the parietal surface and absorbed by the parietal lymphatic vessels. The pleural fluid allows the two layers to slide on one another, thus in health the pleura allows movement of the lung against the chest wall while breathing. The surface tension of the pleural fluid provides the cohesion that keeps the lung surface in contact with the thoracic wall. As a result, when the thorax expands in inspiration, the lung expands along with it and fills with air.

Question 328

Describe pleural fluid

Answer 328

o 15ml turnover per day (Can increase to 300ml) o Produced by Capillary Filtration at the Parietal Pleura (Starling Forces) • ⬆️ Lung interstitial fluid increase • ⬆️ Hydrostatic Pressure (E.g. heart failure) • ⬆️ Permeability (E.g. inflammation, spesis or malignancy) • ⬇️ Oncotic Pressure (E.g. liver failure) o Absorbed via lymphatic drainage • ⬇️ Lymphatic blockage • ⬆️ Systemic venous pressure

Question 329

What is a pleural effusion? And the different types?

Answer 329

Any collection of extra fluid in the pleural space is known as a ‘Pleural Effusion’. Blood – Haemothorax Chyle (Lymph with fats in it) – Chylothorax Pus – Empyema Serous Fluid – Simple Effusion

Question 330

How are simple pleural effusions (pleural fluid) further characterised?

Answer 330

Simple pleural effusions (Serous Fluid) is further characterised by protein content: Transudates have low protein content – < 30g/Litre Exudates have high protein content – > 30g/Litre

Question 331

What are transudates?

Answer 331

Transudates have low protein content – < 30g/Litre ``` o Increased Hydrostatic Pressure • Cardiac Failure o Decreased capillary Oncotic Pressure • Hypoalbuminaemia • Nephrotic Syndrome o Increased capillary Permeability • Sepsis ```

Question 332

What are exudates?

Answer 332

Exudates have high protein content – > 30g/Litre ``` o Neoplasms • Cancer involving pleural surface • Secondary’s from breast, lung, ovarian, GI, lymphoma • Primary tumour of pleura o Infection • Pneumonia, TB o Immune Disease • Connective tissue diseases (RA, SLE) o Abdominal Disease • Pancreatitis (Diaphragmatic inflammation) • Ascites (Transverse the diaphragm) • Subphrenic abscess ```

Question 333

What is pleurisy / pleuritis?

Answer 333

Pleurisy, or pleuritis, is an inflammation of the pleura. o Sharp Pain on inspiration o Pain worse with coughing, sneezing, laughing etc. o Patients take small breaths, and hold affected side of chest o Involvement of diaphragmatic pleura causes pain in the shoulder on the same side (Referred pain) o Characteristic physical sign is Pleural Rub, a creaking noise heard through a stethoscope with respiratory movements

Question 334

What are the common causes of pleurisy / pleuritis?

Answer 334

``` o Infection is the most common cause • TB • Pneumonia o Autoimmune • SLE • RA o Lung Cancer o Pneumothorax o Pulmonary Embolism ```

Question 335

What is pleural fibrosis?

Answer 335

Unabsorbed pleural effusion may lead to fibrosis of the pleura. A small degree of thickening has no effects, but wide spread fibrosis restricts expansion, with a measurable reduction in lung volumes and compliance.

Question 336

What are pleural tumours?

Answer 336

o Secondary deposits of tumours are not uncommon in the pleura. o The commonest primary tumour is a malignant mesothelioma. o Almost all victims exposed to asbestos 20 – 40 years before o Early symptoms are lose of pleural effusion, but with a duller pain o Signs are that or a large pleural effusion

Question 337

What are some chest wall abnormalities which may affect breathing?

Answer 337

Deformation of the ribs, sternum and thoracic spine o Sternal abnormalities (E.g. Pectus Carcinatum/excavatum) rarely produce functional impairment, just cosmetic o Scoliosis and kyphosis may produce significant function impairment of the thoracic cage Acquired abnormalities: o Trauma producing broken ribs, possible pneumothorax o Some old patients may have had surgery for TB, designed to collapse their lung

Question 338

What are some neuromuscular diseases which may affect breathing?

Answer 338

The muscles involved in breathing may be affected by generalised muscular diseases, such as muscular dystrophy or by neurological disease such as motor neurone disease or polio. Muscle weakness produces respiratory failure with lower resistance to respiratory tract infections because of poor clearance of secretions.

Question 339

Type 1 resp failure

Answer 339

X

Question 340

Type 2 resp failure

Answer 340

X

Question 341

What 5 cartilages make up the larynx?

Answer 341

3 unpaired cartilages- epiglottis, thyroid and cricoid cartilage 1 paired cartilage- arytenoid cartilage

Question 342

How is the middle ear cavity connected to the nasopharynx? And what is the importance and clinical relevance of this?

Answer 342

Eustachian tube Importance: allows air pressure in middle ear cavity to be equalised to atmospheric air pressure Clinical relevance: pathway through which URTI's can pass to middle ear cavity - pseudomonas aeruginosa

Question 343

What is the glottis?

Answer 343

Vocal cords and the aperture (rima glottides) found between them in the larynx

Question 344

What is a rima glottides?

Answer 344

The aperture found between the two vocal cords in the glottis in the larynx

Question 345

Describe the vocal cords in respiration

Answer 345

They are fully abducted allowing the free movement of air through the open aperture

Question 346

Describe the vocal cords in speech

Answer 346

They are partially abducted- to produce sound as air flows through the narrowed aperture making the vocal cords vibrate and produce sound

Question 347

Describe the vocal cords while swallowing

Answer 347

Vocal cords are fully adducted during eating to prevent aspiration of food- this is entirely involuntary

Question 348

Describe the vocal cords in coughing

Answer 348

Vocal cords adducted in initial part if cough reflex - involuntary

Question 349

Describe the vocal cords in straining

Answer 349

Voluntarily adducted

Question 350

What muscles control vocal cord movements?

Answer 350

The intrinsic laryngeal muscles (not the extrinsic laryngeal muscles)

Question 351

What are the extrinsic laryngeal muscles involved in?

Answer 351

Moving the entire larynx but not the vocal cords

Question 352

What nerve supplies the intrinsic laryngeal muscles

Answer 352

Recurrent laryngeal nerve- but it does not supply the cricothyroid muscle

Question 353

How can laryngeal disease present as?

Answer 353

Airway obstruction and difficulty in breathing

Question 354

What may be some causes in difficulty of breathing in the upper respiratory tract?

Answer 354

Narrowing of the glottis due to - laryngeal tumour or vocal cord tumours - laryngeal oedema due to allergic reactions or severe infections such as a croup or acute epiglottitis - bilateral vocal cord paralysis which causes a loss of vocal cord abduction Pharyngeal obstruction - airway of an unconscious person may be obstructed by tongue rolling back to obstruct pharynx- so must be kept in recovery position - sleep apnoea syndrome- loss of tone in pharyngeal muscles during sleep causes them to become floppy and obstruct the airways in sleep

Question 355

What are the three main effects of surfactant in the lungs?

Answer 355

Increases compliance by reducing surface tension when. Lung volume is low Stabilises the lung by preventing small alveoli from collapsing into larger alveoli Prevents the surface tension in alveoli from creating a suction force tending to cause transudation fluid from pulmonary capillaries

Question 356

Which part of the airways have the greatest resistance in peak inspiration?

Answer 356

The largest airways- nose

Question 357

Which part of the airways have the greatest resistance in force expiration?

Answer 357

The smallest airways

Question 358

In forced expiration how does the fact that the smallest airways have the greatest resistance result in a residual volume?

Answer 358

During forced expiration small airways get compressed by the increased pressure within the pleural cavity. This is why all the air in the lungs can’t be expelled even by forced expiration; there is always a residual volume left.

Question 359

Why do we tend to breathe through our mouths when extensively exercising?

Answer 359

To reduce resistance and anatomical dead space

Question 360

How do we cough?

Answer 360

Cough is coordinated by the medulla oblongata. Cough is initiated by irritation of Cough receptors in upper airway. The glottis closes, and strong contraction of the expiratory muscles (abdominal muscles and internal intercostals) builds up intrapulmonary pressure, whereupon the glottis suddenly opens causing an explosive discharge of air.