Respiratory Flashcards

0
Q

What is the kinetic theory of gases?

A

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.

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1
Q

Explain the broad functions of the respiratory system in health?

A

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.

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2
Q

What is Boyles law?

A

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

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3
Q

What is Charles law?

A

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)

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4
Q

What is the universal gas law?

A

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)

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5
Q

What is partial pressure?

A

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.

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6
Q

What is vapour pressure?

A

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.

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7
Q

What is saturated vapour pressure?

A

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.

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8
Q

What is tension?

A
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.
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9
Q

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

A

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

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10
Q

What is tidal volume?

A

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

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11
Q

What is respiratory rate/ pulmonary ventilation rate?

A

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

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12
Q

What is the difference between the bronchial and pulmonary circulation?

A

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.

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13
Q

What is ventilation perfusion matching?

A

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.

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14
Q

Define the upper respiratory tract

A
Upper Respiratory Tract
The parts of the respiratory system lying outside the thorax
o Nasal Cavity
o Pharynx
o Larynx
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15
Q

Define the lower respiratory tract

A
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
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16
Q

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

A

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.

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17
Q

Describe the structure and function of the nose

A

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.

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18
Q

Describe the structure and function of the conchae (turbinates)

A

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

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19
Q

Describe the structure and function of the para nasal sinuses

A

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.

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20
Q

What are the frontal sinuses?

A

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.

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21
Q

What are the ethmoidal cell sinuses?

A

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.

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22
Q

What are the sphenoidal sinuses?

A

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.

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23
Q

What are the maxillary sinuses?

A

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.

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24
Q

Describe generally the structure and location of the pharynx

A

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.

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25
Q

What are the 3 divisions of the pharynx?

A

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.

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26
Q

What is the larynx?

A

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.

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27
Q

What is the middle ear?

A
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
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28
Q

What type of membranes does the respiratory system contain?

A

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

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29
Q

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

A
Nasal Cavity
Pharynx
Larynx
Trachea
Primary / Secondary Bronchi
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30
Q

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

A

Bronchioles and terminal bronchioles

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31
Q

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

A

Respiratory bronchioles

Alveolar ducts

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32
Q

Which areas of the respiratory system have simple squamous epithelia?

A

Alveoli

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33
Q

Histologically describe the non olfactory region of the nasal cavity

A

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.

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34
Q

Histologically describe the olfactory region of the nasal cavity

A

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

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35
Q

Histologically describe the larynx

A

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

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36
Q

Histologically describe the trachea

A
Pseudostratified ciliated epithelium
o Lamina propria
(many elastin fibres)
o Seromucus glands
o C-Shaped Cartilage Ring
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37
Q

Histologically describe primary bronchi

A

o Similar to trachea

o Cartilage rings completely encircle the lumen

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38
Q

Histologically describe lobar and segmental bronchi

A

o Similar to primary bronchi

o Cartilage in crescent shapes, not Ring or Completely encircling lumen

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39
Q

Histologically describe the bronchus

A

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

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40
Q

Histologically describe the bronchiole

A

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

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41
Q

Histologically describe a terminal bronchiole

A

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

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42
Q

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

A

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

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43
Q

Describe the structure of alveoli

A

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).

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44
Q

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

A
Quiet Breathing
o Inhalation
• Diaphragm
• External Intercostals
o Exhalation
• None
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45
Q

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

A
Forced Breathing
o Inhalation
• Diaphragm
• External Intercostals
• Scalene
• Pectoralis Minor
• Sternocleidomastoid
• Serratus Anterior
o Exhalation
• Internal Intercostals
• Innermost Intercostals
• Abdominal Muscles
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46
Q

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

A

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

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47
Q

How does area affect gas exchange in the alveoli?

A

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.

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48
Q

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

A

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)

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49
Q

How does partial pressure affect gas exchange?

A

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.

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50
Q

How is respiration measured?

A

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

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51
Q

Define tidal volume

A

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

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52
Q

Define inspiratory reserve volume

A

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

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53
Q

Define expiratory reserve volume

A

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

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54
Q

Define residual volume

A

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

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55
Q

What’s the difference between lung volumes and capacities?

A

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

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56
Q

Define vital capacity

A

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.

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57
Q

Define functional residual capacity

A

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

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58
Q

Define inspiratory capacity

A

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

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59
Q

What is serial (anatomical) dead space?

A

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.

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60
Q

What is alveolar (distributive) dead space?

A

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.

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61
Q

What is physiological dead space?

A

Anatomical Dead Space + Alveolar Dead Space = Physiological Dead Space

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62
Q

How is physiological dead space measured?

A

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.

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63
Q

How is serial dead space determined?

A

Nitrogen washout test

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64
Q

Describe the nitrogen washout test

A

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.

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65
Q

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

A

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

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66
Q

How do the lungs and thorax contribute mechanically to respiration?

A

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.

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67
Q

What is pneumothorax?

A

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.

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68
Q

What is lung compliance?

A

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.

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69
Q

How is compliance measured and calculated?

A

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

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70
Q

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

A

Surfactant
Surface tension
Bubbles

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71
Q

Where do the elastic properties of the lungs arise from?

A

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.

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72
Q

What is surface tension and how does it affect compliance?

A

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).

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73
Q

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

A

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.

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74
Q

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

A

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.

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75
Q

Describe resistance in airways and Poisseulles law

A

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.

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76
Q

How does resistance change in the breathing cycle?

A

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.

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77
Q

Describe spirometry

A

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.

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78
Q

Why may vital capacity be less than normal?

A

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
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79
Q

In what conditions is compliance increased?

A

Emphysema

Break down of elastic makes walls more stretchy

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80
Q

In what conditions is compliance decreased?

A

Lung fibrosis

Thickening and fibrosis of elastic makes wall stiff

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81
Q

What is Forced Vital Capacity?

A

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

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82
Q

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

A

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)

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83
Q

What is a vitalograph?

A

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

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84
Q

How is a vitalograph obtained?

A

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

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85
Q

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

A

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

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86
Q

How does a restrictive deficit affect FVC and FEV1?

A

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

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87
Q

Give an example of a condition where a restrictive deficit occurs

A

Muscle weakness

Lung fibrosis

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88
Q

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

A

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

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89
Q

How does an obstructive deficit affect FVC and FEV1?

A

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

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90
Q

Give an example of a condition where an obstructive deficit occurs

A

Asthma

COPD

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91
Q

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

A

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

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92
Q

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

A

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

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93
Q

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

A

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

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94
Q

What is PEFR and how is it determined?

A

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

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95
Q

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

A

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

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96
Q

What does the helium dilution test measure?

A

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

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97
Q

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

A

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

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98
Q

How is the helium dilution test carried out?

A

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)

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99
Q

What is Transfer factor?

A

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

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100
Q

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

A

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

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101
Q

What is the process for measuring transfer factor?

A

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

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102
Q

What measurements are usually shown in a lung function report?

A
Vital capacity
FEV1 (before and after bronchodilator)
Ratio FEV1/FVC
Peak EXPIRATORY Flow rate 
(FRC, RV, TLC, RV/TLC)
Transfer factor
CO conductance
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103
Q

How soluble is oxygen?

A

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

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104
Q

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

A

0.01mmol/L/kPa

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105
Q

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

A

= 0.01 (Oxygen solubility coefficient) x 13.3

= 0.13 mmol/L of dissolved oxygen

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106
Q

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

A

Haemaglobin

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107
Q

What’s the concentration of Hb in the blood?

A

2.2mmol/L

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108
Q

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

A

8.8mmol/L

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109
Q

What is Hb like at the lungs?

A

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

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110
Q

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

A

No as most Hb is usually saturated already

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111
Q

What maintains the composition of alveolar gas?

A

Ventilation and perfusion

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112
Q

What is the alveolar pO2?

A

13.3kPa

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113
Q

What is the mixed venous blood pO2?

A

5.3kPa

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114
Q

What is the alveolar pCO2?

A

5.2kPa

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115
Q

What is the mixed venous blood pCO2?

A

6.6kPa

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116
Q

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

A

O2

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117
Q

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

A

CO2

21 times more that O2

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118
Q

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

A

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

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119
Q

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

A

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

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120
Q

What is Hb like at the tissues?

A

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

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121
Q

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

A

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

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122
Q

What is the Bohr shift? And what causes it?

A

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

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123
Q

Why is CO2 in the blood important?

A

Essential part of BUFFER systems - controls pH of ECF

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124
Q

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)

A

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

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125
Q

How does CO2 react with H2O?

A

CO2 dissolves in H2O H+ + HCO3-

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126
Q

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

A

Carbonic anhydrase

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127
Q

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

A

Little found

Makes reactions slower

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128
Q

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

A

Lots found

Faster reactions

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129
Q

What pushes this reaction forward?

CO2 dissolves in H2O H+ + HCO3-

A

An increase in dissolved CO2 which is proportional to pCO2

ventilation related

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130
Q

What opposes the forward direction of this reaction?

CO2 dissolves in H2O H+ + HCO3-

A

An increase in HCO3-

Metabolism related

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131
Q

What ratio does plasma pH depend on?

A

pCO2 : [HCO3-]

1:20

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132
Q

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

A

Low

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133
Q

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

A

High

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134
Q

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

A

Because of excess HCO3-

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135
Q

What is the Henderson Hasselbach equation?

A

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

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136
Q

Where does most HCO3- come from in the plasma?

A

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

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137
Q

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

A

Haemoglobin which has a large buffering capacity

This is enhanced further when haemoglobin is deoxygenated at the tissues and H+ is high

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138
Q

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?

A

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

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139
Q

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

A

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)

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140
Q

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

A

Amount of CO2 dissolved in the PLASMA AND

Amount of HCO3- formed from CO2 in the RED CELL by reaction involving Hb

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141
Q

What are carbonamino compounds?

A

Protein part of Hb to which CO2 binds to

Contributes to CO2 transport but not acid base balance

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142
Q

Describe the overall contents of arterial blood

A

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

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143
Q

Describe the overall contents of venous blood

A

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

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144
Q

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

A
23.5-21.5= 2mmol/litre of blood
(Only 10% of total)
80% travels as H2CO3
11% carbaminos 
8% as dissolved CO2
145
Q

What is hypoxia?

A

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

146
Q

What is hypercapnia?

A

Rise in alveolar and thus arterial pCO2

147
Q

What is hypocapnia?

A

Fall in alveolar and thus arterial pCO2

148
Q

What is hyperventilation?

A

Ventilation increases with no change in metabolism

Breathing more than you actually have to - decrease in pCO2 and increase in pO2

149
Q

What is hypoventilation?

A

Ventilation decreases with no change in metabolism

Breathing less than you actually have to - increase in pCO2 and decrease in pO2

150
Q

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

A

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

151
Q

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

A

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)

152
Q

What is arterial pO2 monitored by?

A

Peripheral chemoreceptors

153
Q

Where are peripheral chemoreceptors found?

A

In carotid and aortic bodies

154
Q

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

A

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

155
Q

Why is the chemical control of pCO2 important?

A

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

156
Q

What detects changes in pCO2?

A

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

157
Q

Where are central chemoreceptors found?

A

Medulla oblongata found in brain

158
Q

How do central chemoreceptors detect changes in pCO2?

A

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-]

159
Q

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

A

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

160
Q

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

A

Free calcium concentration falls enough to produce fatal tetany

161
Q

What is respiratory alkalosis? How is it compensated?

A

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

162
Q

What is respiratory acidosis? How is it compensated?

A

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

163
Q

What is metabolic alkalosis? How is it compensated?

A

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

164
Q

What is metabolic acidosis? How is it compensated?

A

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)

165
Q

What is the role of choroid plexus cells?

A

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-]

166
Q

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

A

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

167
Q

Describe what happens in metabolic acidosis to CSF

A

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!!!
****

168
Q

Describe what happens with persisting hypoxia

A

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
**

169
Q

Describes what happens with persisting hypercapnia

A

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
*****

170
Q

Describe some features of acute hypoxia

A
pO2<8kPa
Peripheral chemoreceptors 
Increased ventilation
Effects on pCO2
Central chemoreceptors
171
Q

Describe some features of chronic hypoxia

A

Renal correction of acid base balance

Increased ventilation

172
Q

What is respiratory failure?

A

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)

173
Q

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

A
pO2 in inspired air
Ventilation rate
Effective diffusion
Ventilation perfusion matching
Normal right to left cardiac shunts
174
Q

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

A

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

175
Q

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

A

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

176
Q

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

A
Respiratory depression due to opiate overdose
Head injury
Muscle weakness (NMJ/ nerve/ muscle diseases)
177
Q

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

A

Scoliosis/ kyphosis
Morbid obesity
Trauma
Pneumothorax

178
Q

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)?

A

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

179
Q

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

A

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

180
Q

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

A

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

181
Q

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

A

E.g. Cyanotic heart disease such says tetrology of fallot

Pulmonary stenosis
RV hypertrophy
Ventricular septal defect
Overriding aorta

182
Q

What is type 1 respiratory failure?

A

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

183
Q

What is type 2 respiratory failure?

A

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

184
Q

What is asthma?

A

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

185
Q

What is the general pathophysiology of asthma?

A

Thickened smooth muscle, and basement membranes

Triggers cause airways smooth muscle to contract- reducing airway radius, increasing resistance, reducing airflow

186
Q

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

A

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

187
Q

What are specific allergens?

A

Specific allergens that trigger asthma attacks

188
Q

What are non specific allergens?

A

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

189
Q

Describe the history of someone with asthma

A

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
190
Q

Describe the examination of someone with asthma

A

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
191
Q

Describe the investigation of someone with asthma

A

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

192
Q

Describe the detailed pathophysiology of asthma - inflammation and remodelling

A

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

193
Q

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

A

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)

194
Q

How is asthma treated and managed?

A
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
195
Q

How is severe acute asthma treated?

A

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.

196
Q

How must life threatening asthma be treated?

A

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

197
Q

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

A

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

198
Q

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

A

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.

199
Q

What drugs are eosinophils very sensitive to?

A

Steroid therapy

200
Q

What causes airway narrowing in asthma?

A

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

201
Q

What 3 things does airway inflammation in asthma cause?

A

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

202
Q

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

A

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

203
Q

What are some observable effects of airway narrowing in asthma?

A

 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;

204
Q

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

A

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)

205
Q

What are some triggers of an asthma attack?

A

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.

206
Q

What is the treatment/ management of asthma?

A

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.

207
Q

Why are bronchodilators used to treat asthma?

A

Q

208
Q

Why are steroids used to treat asthma?

A

Q

209
Q

Define COPD

A

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.

210
Q

What are the main causes of COPD?

A

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

211
Q

What do the noxious substances trigger in COPD?

A

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.

212
Q

What are the 6 pathological changes that occur in COPD?

A

 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.

213
Q

What are the two conditions which fall under COPD?

A

Emphysema and chronic bronchitis

214
Q

What’s the difference between emphysema and chronic bronchitis?

A

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.

215
Q

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

A

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).

216
Q

Describe the history of someone with COPD

A

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.

217
Q

Describe what could be found on examination of someone with COPD

A

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.

218
Q

Describe the investigations involved in the diagnosis of COPD

A

 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.

219
Q

What would the treatment for COPD be?

A

 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.

220
Q

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

A

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.

221
Q

How is acute exacerbation of COPD managed?

A

 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

222
Q

What are some potential complications of COPD?

A

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

223
Q

What is TB? And what causes it?

A

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

224
Q

Describe mycobacterium tuberculosis bacteria

A

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.

225
Q

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

A

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.

226
Q

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?

A

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.

227
Q

Describe the pathophysiology of TB

A

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.

228
Q

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

A

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.

229
Q

Describe primary infection of TB

A

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.

230
Q

Describe latent infection of TB

A

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)

231
Q

What is the importance of the tuberculin skin test?

A

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.

232
Q

What are the statistics and risks associated with TB?

A

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

233
Q

What is primary TB?

A

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.

234
Q

What is post primary TB?

A

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

235
Q

What is post primary pulmonary TB?

A

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.

236
Q

What are the general symptoms associated with TB?

A

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

237
Q

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

A

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

238
Q

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

A

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

239
Q

How is TB diagnosed?

A

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.

240
Q

What is the general treatment given for TB infections?

A

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.

241
Q

What are the common normal flora of the respiratory tract?

A

o Viridans streptococci
o Neisseria spp
o Anaerobes
o Candida spp

242
Q

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

A

o Streptococcus pneumonia
o Streptococcus pyogenes
o Haemophillus influenza

243
Q

What are some other normal flora of the respiratory tract?

A

o Pseudomonas

o E. coli

244
Q

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

A
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
245
Q

What are some common infections of the upper respiratory tract?

A
o Rhinitis (common cold)
o Pharyngitis
o Epiglottitis
o Laryngitis
o Tracheitis
o Sinusitis
o Otitis media (Inflammation of middle/inner ear)
246
Q

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

A

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

247
Q

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

A

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
248
Q

What is a pneumonia?

A

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.

249
Q

What is a lobar pneumonia?

A

Pneumonia localised to a particular lobe/s of the lung.

Most often due to Streptococcus pneumoniae

250
Q

What is bronchopneumonia?

A

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

251
Q

What is aspiration pneumonia?

A

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.

252
Q

What is interstitial pneumonia?

A

Inflammation of the Intersticium of the lung

Alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues

253
Q

What is chronic pneumonia?

A

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

254
Q

What bacteria commonly cause community acquired pneumonia?

A
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
255
Q

What bacteria commonly cause hospital acquired pneumonia?

A

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

256
Q

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

A

o Anaerobes

o Oral flora

257
Q

What pathogens most commonly cause pneumonia in an immunocompromised patient?

A

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

258
Q

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

A

S. pneumoniae

Elderly, co-morbidities, acute onset, high fever, Pleuritic chest pain

259
Q

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

A

H. influenza

COPD

260
Q

What are some clues of a pneumonia infection by legionella?

A

Legionella

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

261
Q

What are some clues of a pneumonia infection by Mycoplasma?

A

Mycoplasma

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

262
Q

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

A

S. aureus

Post-viral, Intra-Venous Drug User

263
Q

What are some clues of a pneumonia infection by Chlamydia?

A

Chlamydia

Contact with birds

264
Q

What are some clues of a pneumonia infection by Coxiella?

A
Coxiella
Animal contact (sheep)
265
Q

What are some clues of pneumonia infection by Klebsiella?

A

Klebsiella

Thrombocytopenia, leucopenia

266
Q

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

A

S. Milleri

Dental infections, abdominal source, aspiration

267
Q

What are some general symptoms of pneumonia?

A
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
268
Q

What are some common features of hospital acquired pneumonia?

A

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

269
Q

How may the severity of pneumonia be assessed?

A

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)

270
Q

What samples are collected in the investigation of pneumonia?

A
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
271
Q

What are the microbiological investigations of pneumonia?

A
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
272
Q

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

A
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.
273
Q

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

A

Community Acquired Pneumonia

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

274
Q

What antibiotic is commonly used in hospital acquired pneumonia?

A

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.

275
Q

What are the common outcomes of pneumonia?

A
o Resolution
• Organisation (Fibrous scarring)
o Complications
• Lung abscess
• Bronchiectasis
• Empyema (pus in pleural cavity)
• Pleural effusion
276
Q

How is pneumonia prevented?

A

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

277
Q

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

A

Reveals shadowing in at least one section of lung fluid

278
Q

What’s the incidence distribution of lung cancer?

A

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

279
Q

What are some common causes of lung cancer?

A

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
280
Q

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

A
Cough
Dyspnoea
Wheezing
Haemoptysis
Chest pain
Post-obstructive pneumonia
Weight loss
Lethargy / Malaise
281
Q

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

A

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

282
Q

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

A
Bone pain / Fractures
CNS symptoms (Headache, double vision, confusion etc.)
283
Q

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

A
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
284
Q

What imaging techniques are used in diagnosis of lung cancer?

A
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
285
Q

What are the two staging systems for lung cancer?

A

TNM and number

Staging is one of the most important determinants of treatment and prognosis

286
Q

What is the number staging system of lung cancer?

A

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

287
Q

What is the TNM staging of lung cancer?

A

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

288
Q

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

A

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.

289
Q

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

A

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
290
Q

What are the different treatments available for lung cancer?

A
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
291
Q

How is non small cell lung cancer usually managed?

A

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

292
Q

How is small cell lung cancer usually managed?

A
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
293
Q

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

A

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

294
Q

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

A
Ulceration
Necrosis
Infiltrative margins
Vascular invasion
Reaction in surrounding tissue (=stroma)
Little resemblance to parent tissue
295
Q

What are three types of non small cell carcinoma?

A

Squamous cell carcinoma
Adenocarcinoma
Large cell carcinoma

296
Q

What are some histological features of squamous cell carcinoma?

A
Often central tumours
Angula the cells
Eosinophilic (pink) cytoplasm
Intercellular bridges- prickles = desmosomes
Keratinisation
Keratin pearls
Immunochemsitry - CK5/6  and P63 + TTF-1
297
Q

What are some histological features of adenocarcinoma?

A
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-
298
Q

What are some histological features of small cell carcinoma?

A
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 +
299
Q

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

A
  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.

300
Q

What would a lobar collapse look like on a CXR?

A

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.

301
Q

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

A

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.

302
Q

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

A

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.

303
Q

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

A

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

304
Q

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

A

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.

305
Q

What is tracheal displacement in a CXR indicative of?

A

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.

306
Q

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

A

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)

307
Q

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

A

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

308
Q

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

A

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.

309
Q

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

A

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

310
Q

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

A

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

311
Q

How do you work out the cardiac thoracic ratio?

A

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.

312
Q

What is the lung interstitial space?

A

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.

313
Q

What are lung interstitial diseases?

A

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.

314
Q

What is the general pathophysiology of interstitial lung disease?

A

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.

315
Q

What are the general clinical features of interstitial lung disease?

A

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.

316
Q

What are the broad causes of interstitial lung disease?

A
Occupational 
Treatment related
Connective tissue disease
Immunological
Idiopathic
317
Q

What is fibrosing alveolitis?

A

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

318
Q

What is extrinsic allergic alveolitis?

A

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.

319
Q

What is asbestosis?

A

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

320
Q

What is sarcoidosis?

A

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.

321
Q

What would a fibrosing alveolitis x ray look like?

A

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

322
Q

What would an acute extrinsic allergic alveolitis look like?

A

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

323
Q

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

A

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

324
Q

What would an asbestosis x ray look like?

A

Sarcoidosis
Miliary and Nodular shadowing
Diffuse fibrosis

325
Q

What would a sarcoidosis x ray look like?

A

Asbestosis
Plaques – Holly leaf
Fibrosis
Mesothelioma

326
Q

Briefly describe the pleura

A

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.

327
Q

Briefly describe the pleural cavity

A

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.

328
Q

Describe pleural fluid

A

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

329
Q

What is a pleural effusion? And the different types?

A

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

330
Q

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

A

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

331
Q

What are transudates?

A

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
332
Q

What are exudates?

A

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
333
Q

What is pleurisy / pleuritis?

A

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

334
Q

What are the common causes of pleurisy / pleuritis?

A
o Infection is the most common cause
• TB
• Pneumonia
o Autoimmune
• SLE
• RA
o Lung Cancer
o Pneumothorax
o Pulmonary Embolism
335
Q

What is pleural fibrosis?

A

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.

336
Q

What are pleural tumours?

A

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

337
Q

What are some chest wall abnormalities which may affect breathing?

A

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

338
Q

What are some neuromuscular diseases which may affect breathing?

A

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.

339
Q

Type 1 resp failure

A

X

340
Q

Type 2 resp failure

A

X

341
Q

What 5 cartilages make up the larynx?

A

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

342
Q

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

A

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

343
Q

What is the glottis?

A

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

344
Q

What is a rima glottides?

A

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

345
Q

Describe the vocal cords in respiration

A

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

346
Q

Describe the vocal cords in speech

A

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

347
Q

Describe the vocal cords while swallowing

A

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

348
Q

Describe the vocal cords in coughing

A

Vocal cords adducted in initial part if cough reflex - involuntary

349
Q

Describe the vocal cords in straining

A

Voluntarily adducted

350
Q

What muscles control vocal cord movements?

A

The intrinsic laryngeal muscles (not the extrinsic laryngeal muscles)

351
Q

What are the extrinsic laryngeal muscles involved in?

A

Moving the entire larynx but not the vocal cords

352
Q

What nerve supplies the intrinsic laryngeal muscles

A

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

353
Q

How can laryngeal disease present as?

A

Airway obstruction and difficulty in breathing

354
Q

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

A

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

355
Q

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

A

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

356
Q

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

A

The largest airways- nose

357
Q

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

A

The smallest airways

358
Q

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

A

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.

359
Q

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

A

To reduce resistance and anatomical dead space

360
Q

How do we cough?

A

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.