Respiratory Flashcards
1
Q
What are the primary functions of the respiratory system?
A
- Provide area for gas exchange
- Protect respiratory surfaces (against pathogens)
- Sound production
- Control blood pressure, volume and pH
2
Q
What is the anatomical classification of the respiratory system?
A
Upper respiratory system: frontal and sphenoidal sinuses, nasal conchae and cavity, external and internal nares, hyoid bone, nasopharynx, larynx
Lower respiratory system: trachea, bronchi (main, lobar, segmental) bronchioles, terminal bronchioles, respiratory bronchioles, alveolar ducts, alveoli.
3
Q
What is the functional classification of the respiratory system?
A
Conducting zone: no gas exchange, function is to conduct air to respiratory zone and condition it (warm, wet and clean) Involves nares through to terminal bronchioles
Respiratory zone: Site of gas exchange. Involves respiratory bronchioles through to alveoli.
4
Q
What are pseudostratified columnar epithelial cells, where are they and what are their functions?
A
Found in conducting zone. Form a protective barrier, move mucus. Damaged by smoking
5
Q
What are goblet cells, where are they and what are their functions?
A
Found in conducting zone, in the bronchi. Secrete mucus. Damaged in asthma and smokers
6
Q
What are basal cells, where are they and what are their functions?
A
Found in upper bronchi. They are stem cells
7
Q
What are brush cells, where are they and what are their functions?
A
Found in the bronchi. Sensory cells
8
Q
What are small granule cells, where are they and what are their functions?
A
Found in bronchi. Endocrine cells involved in secretion of histamine
9
Q
What are club cells, where are they and what are their functions?
A
Found in bronchioles. Secrete watery mucus and antimicrobials. Marker of COPD
10
Q
What are type I pneumocytes, where are they and what are their functions?
A
Found in alveoli. Very thin squamous cells making up 97% of alveolar surface area
11
Q
What are type II pneumocytes, where are they and what are their functions?
A
They are found in the alveoli. They are cuboidal, highly metabolic cells responsible for secreting surfactant to reduce surface tension in the lungs
12
Q
What are alveolar macrophages, where are they and what are their functions?
A
Found in the alveoli and in alveolar walls, function is defense.
13
Q
Where is cartilage found in the resp. system and what is its function?
A
Found as C rings in trachea
Found as plates in bronchi
Keeps airways patent
14
Q
Where are elastic fibres found in the resp. system and what is its function?
A
Found all the way through.
Responsible for compliance and recoil of lungs. Affected in COPD and emphysema
15
Q
Where is collagen found in the resp. system and what is its function?
A
Found all the way through
Responsible for creating lung tension
Important in fibrosis
16
Q
Where is smooth muscle found in the resp. system and what is its function?
A
Found all the way through up to the alveolar ducts
Controls diameter of bronchi and bronchioles to control airway tone.
Affected in asthma
17
Q
How is mucus transported in the respiratory system?
A
Mucus is biphasic with a serous sol layer in which the cilia beat, and a viscous gel layer on top. The tips of the cilia catch in this layer (which is specialised to trap unwanted particles)
18
Q
What are the functions of the trachea, bronchus and bronchioles?
A
T: Open for large volume of air
B: Open for large volume of air and increased branching to increase surface area
Bl: Control and tone of airflow
19
Q
What are the bones surrounding the chest cavity? How are the ribs attached?
A
Sternum: Made up of manubrium (with jugularnotch)
This transitions to Sternum proper at the attachment of rib 2. These form a convex angle called the angle of Louis. Final part is xiphi process.
There are 12 ribs: 1-7 are true ribs, attaching directly to the sternum. 8-12 are false ribs, attaching via costal cartilage, or in the case of 11/12, floating freely. These have two facets inf. and sup. on their heads to articulate with the vertebral column. The inf. facet attaches to the matching numbered vertebra, the sup. head with the one above. On the inf. inner surface of the rib is the costal groove, where the neurovascular bundle runs.
20
Q
Where are the boundaries of the thoracic cavity?
A
Upper: around rib I, over the jugular notch of the manubrium- forms the superior thoracic aperture. However, some of the pleural extends upwards in the suprapleural membrane
Lower: Costal cartilates of ribes and bottoms of ribs 11/12/ Forms the inferior thoracic aperture
21
Q
What is contained in the costal neurovascular bundle?
A
Contain intercostal vein (superior), intercostal artery (middle) and intercostal nerve (inferior). The nerve may dip below the rib, putting it at risk.
22
Q
What is the arterial supply of the thorax?
A
Aorta gives off:
- Brachiocephalic trunk: gives off right common carotid and right subclavian. Right subclavian gives off right internal thoracic, which then gives off anterior intercostal arteries
- Left carotid artery
- Left subclavian artery. Branches into left internal thoracic, and then gives off posterior intercostal arteries.
23
Q
What are the divisions of the thorax?
A
- Superior mediastinum- above angle of Louis
- Inferior mediastinum- below angle of Louis (includes heart)
24
Q
What are the arteries supplying the breast?
A
Anterior intercostals
Axillary artery
Posterior intercostals
25
How can tumors present in the breast and why?
The breast is a mix of glandular and fatty tissue sitting on pec major. Normally there is a fascial plane between the breast and the muscle which allows sliding. In breast cancer, some tumors can grow through this fascia, and so when the arms are raised the breast will stay in the same place.
26
Where does the lymph of the breast tissue drain?
- 75% to axillary nodes
- Rest to parasternal nodes- this means tumors can cross the midline to metastatise further
- Some to abdominal nodes
27
What are some chest wall deformities?
- Pectus Excavatum: sternum very concave, impacts hung and heart development. Many comorbidities
- Pectus carinatum: Sternum very convex, assoc. with lung and heart issues
Kymphosis and lordosis- assoc. with severe neuromuscular disorder and affects lung function. Predisposes to chest infection
Scoliosis- lateral and rotational deviation of the spinal cord.
28
What is lung volume, and what are the assumptions made in its measurement?
Lung volume has the symbol V and is measured in ml/L. Its measurement is assumed to be at 0 degrees celsius, 101.3kPa/760mmHg of pressure, and dry.
29
How do you convert ambient lung temperature, pressure and humidity to standard conditions?
V(STPD) = (VATPS) x (273/273+T) x (P-PH2O)/760.
30
What is flow and what can it give us?
Flow has the symbolV*. Its units are L/min-1. It gives minute volume- the volume breathed in and out over a minute.
31
What is anatomic dead-space volume and what is its consequence?
It is the volume of the conducting airways- about 1/3 of Vt or approx. 150mL. This means that only 2/3 of each breath is fresh air, and 1/3 breathed out is also fresh air.
It can be used to calculate alveolar flow: V*A = frequency x (Vt-Vd)
VD is responsible for diluting the partial pressure of CO2 exhaled. The volume of the atomic dead space over the tidal volume is equal to the PaCO2-PECO2 / PaCO2. This shows that an absence of CO2 in the exhaled air is the result of a non-gas-exchanging lung, while if arterial/alveolar PCO2 is the same as expired PCO2, then the dead space has not contributed to the volume of expired air.
32
What factors affect resistance to air flow?
- For air to flow, one pressure must be greater than the other. The volume of air exhanged is equal to the pressure difference over the resistance, where resistance is proportional to viscosity, length and radius of the passage.
Turbulence: If flow becomes turbulent, the volume of flow is proportional to the square root of pressure change- a large gradient is needed to achieve flow
- Diameter and generation: although each bifurcation in the airways makes the radius smaler, the cross sectional area increases. This means that resistance initially increases and then falls to near zero.
33
What nerves are the pleurae supplied by?
- Visceral- supplied by same nerves as the lung- puerly autonomic. Therefore, lung tumors are often not felt.
- Parietal- supplied by the intercostal nerves, so it has the same sensation as the chest.
34
How do the lungs develop?
Initially the lung bud pushes in through the medial surface of the pleura, squishing the fluid filling the sacs to the edges and forming the two layers of membrane.
35
What are pleural recesses and where are they located?
They are sections of the lung where the pleura has folded in onto itself. There are cost-diaphragmatic recesses beneath the lungs, deep to the ribs. These are found meeting at rib 2-4, moving laterally on the LHS at rib 4 and RHS at rib 6, in the midclavicular line at rib 8 and at the midaxillary line around rib 10.
The posterior aspect extends below the level of rib 12, making it increasingly at risk of puncture.
The lung also pops up above the clavicle, making it at risk in the neck.
36
What is the anatomy of the main bronchi?
They divide off the trachea at the point called the carina. The right main bronchus gives off two lobar bronchi and is more vertically aligned (foreign material more likely to be stuck here), while the left is more horizontal and shorter, giving off two lobar bronchi.
37
What is contained within the hilum of each lung?
- Primary bronchus (if not already branched)
- Pulmonary artery
- Pulmonary trunk
- Bronchial arteries
- Bronchial veins
- Pulmonary plexus
- Lymphatics (vessels and nodes)
- Pulmonary ligament (pleura folds back and attaches the lung)
38
Where do the lobes sit for each lung?
Upper lobe in anterior and supieror
Middle lobe is anterior and inferior (beneath horizontal fissure
Inferior lobe is posterior (below the oblique fissure
Upper lobe is anterior
Inferior lobe is posterior
39
What is the circulation of the lungs in adulthood, and how is this different from foetal pulmonary circulation?
Adulthood: SVC and IVC --> RA --> Tricuspid valve --> RV --> pulmonary valve --> Pulmonary trunk --> R and L pulmonary arteries --> Lungs --> Right/Left Pulmonary veins, bronchial veins --> LA --> Mitral valve --> LV --> aortic valve --> aorta
In foetuses, the right ventricle goes straight into the aorta via the ductus arteriosus (which shrivels into the ligamentum arteriosus) and from the right atrium into the left atrium via the foramen ovale (which closes off to form the fossa ovale)
40
What is the pulmonary plexus?
Nerve running anterior and posterior to the hilum of the lungs. There is no somatic supply; rather, it contains sympathetic ANS from the sympathetic trunk (opens bronchioles and vasoconstricts BVs) and the vagus nerve as parasympathetic ANS, shutting the bronchioles and vasodilating the BVs.
41
Where is the best place to insert a chest drain and why?
Best place is just above whatever rib is most appropriate- if you have time you should always get an ultrasound to see where the fluid is located, although in emergencies it's best to go for the subcostal recess as it's less likely to puncture the area
In conscious patients, anaesthetize the area as the needle goes through skin, fascia, external, internal, innermost intercostals and the parietal pleura, all of which have somatic nervous supply.
For fluid, it's best to go lower when a patient is prone, and in a pneumothorax, go higher. (air rises, fluid sinks)
42
What forces need to be acting for inspiration to occur?
- The pressure inside the alveoli must be lower than arometric pressure. The speed of inflow is proportional to this change. This is due to expansion of the chest wall and flattening of the diaphragm lowering the lung pressure.
43
What forces are acting at FRC?
This is the point at which each tidal breath ends. At this point, barometric pressure equals alveolar pressure, and the expansive forces of the chest wall equal the contractile forces of the lung.
44
What is compliance, and what factors affect this?
Compliance is refered to at the change in volume per change in pressure. It is measures in L/(cmH2O-1)
It is affected by tissue compliance, surface tension and atelectasis (alveolar collapse).
45
How does the compliance of a lung change at different pressures?
INHALATION: At only slight negative pressures, the gradient of volume is quite flat, but this increases with decreasing pressure this speeds up- a sigmoid graph. On the exhalation graph, it is smoother. This is called a hysteresis loop.
It's much more responsive when saline is used- therefore the loop is determined by air. With just air, it takes a lot greater pressure to increase the lung- as the alveoli collapse and it's hard to reinflate them.
46
What do soap bubbles have to do with lung compliance?
- The tension of a soap bubble wall is inversely proportional to its radius- those with larger radii have lower tension. However, the small alveoili don't collapse into larger ones due to tethering in the lung- the structures of the alveolar walls prevent their collapse.
47
What is the formula for combined lung/chest wall compliance? What does gravity mean for lunch compliance at different points.
1/CT = 1/CL + 1/CCW
Gravity deforms the lung, pulling the bottom part down and narrowing the top part. This means that in the upright position, the base of the lung is more compliant than the apex. This also means the bottom of the lung is more well ventilated.
48
What are some problems that can cause difficult inspiration?
Pulmonary fibrosis makes inspiration difficult
Alveolar oedema puts water in the alveoli, causing an additional load
Increased blood pressure in the pulmonary veins means it's more difficult to push blood through the pulmonary trunk and the lung becomes stiffer
Atelectasis causes is alveolar collapse
A deficiency in pulmonary surfactant
Anything increasing the stiffness of the thorax
49
What forces must the pressure difference overcome in order to ventilate the lungs?
To inhale, the force exerted must be greater than resistance to airflow and lung compliance.
Change in pressure = change in volume x elastance + flow x resistance.
50
How is Change in pressure = change in volume x elastance + flow x resistance represented on a graph?
Lung pressure: When inhaling, the lung has resistance pressure shown as a smaller downward triangle of lines inside the main one- these are the pressures the lung must overcome to inspire at different lung volumes.
Intrapleural pressure: Similar thing. Except, at the opposite ends of these lines is a line for elastic pressure- overcoming the tendency of the lungs to want to recoil inwards.
The resistance volumes are highest at the greatest rate of volume change.
51
How do you interpret pressure-flow diagrams?
X axis is pressure of the airway opening minus the oesophageal pressure (same as the intrapleural). This results in positive X axis values (representing negativity of intrapleural pressure).
At FRC and at max. volume, V* = 0, as there is no air flowing in or out of the lungs. A vertical line can be drawn between these two points to represent elastance. The closer to this line the pressure-volume loop runs, the slower the breath is, as to inhale at a pressure only just overcoming elastance requires a slow, bare intake of breath.
As the loop grows larger on the X axis, this represents inhalation, and as it returns smaller this is exhalation.
52
What is involved with the work of breathing?
Work must be done to overcome lung and tissue elastance, and resistance to airflow.
Work must be done during inspiration, and is not done during passive expiration, instead producing heat as work is done by the lung rather than on the lung.
Work increases at high breath frequency, whereas elastic work depends only on the tidal volume.
COPD reduces frequency of breath due to lung stiffness, and decreases tidal volume.
At fixed ventilation work, both resistance and elasticity vary with resp. frequency
Elastance increases at slower resp. frequencies, and resistance increases with higher frequency.
53
What are 3 common lung function tests?
- Forced vital capacity and FEV-1. Forced amount of air out in 1 second- normal is 95%
- Flow rates at various volumes during a forced expiration. Normal increases rate very quickly, which then tapers a little and then a lot.
- Maximum volume of ventilation
54
Why does airway collapse and obstruction cause a poor result for flow rates?
Normally, there are intrapulmonary forces acting on the lung which either force it open or closed. Once the expiratory forces make intrapulmonary pressure positive, it will cause the collapse of the air ducts and air trapping in the lungs. Once this happens, the graph shows a flat flow rate despite increased pressures.
55
What are the four components of the chest that can be abnormal on a chest Xray?
- Mediastinum
- Pleura
- Lungs
- Chest wall
56
What are some common radiological mediastinum abnormalities?
Tumor
| Presence of a surgical pack (when intentional)
57
What are some common radiological pleural abnormalities?
```
Pneumothorax (air in chest cavity)
Pleural effusion (fluid in chest cavity- CHF overload, asbestos exposure, pleurisy, cancer or trauma)- presents with meniscoid appearance
Tumors (with calcium plaques?)
Lung cancer
Metastases
Mesothelioma- thickening of pleura
```
58
What are some common radiological lung abnormalities?
Tumors- can be pulmonary (fuzzy borders, acute angle with lung boundaries). Can be extrapulmonary (lung makes obtuse angles, sharp borders)
59
What are some common radiological chest wall abnormalities?
Tumors- of ribs, soft tissues (eg. osteosarcoma)
| Fractures
60
What is partial pressure of a gas, and how is it calculated?
Partial pressure is the pressure required to prevent a gas from diffusing out of a solution. It is the same in the gaseous form and liquid form.
It is the fraction of the gas in the air multiplied by that gas's barometric pressure.
It is determined by solubility- the increase in content for each increase in partial pressure is determined by how soluble the gas is (content = solubility x pressure)
61
What are the factors affecting alveolar O2 diffusion, and how is diffusive capacity expressed?
Diffusion is affected by:
- Partial pressure of oxygen in the alveolus
- Partial pressure of oxygen in the capillary
- Area of the alveolar membrane (75m2)
- Thickness of the alveolar membrane (500nm)
- Diffusivity of oxygen
- Solubility of oxygen
However, d, A, D, and solubility can't be directly measured- they are combined into 'diffusing capacity of the lung': DL.
62
How do we test the diffusing capacity of the lung?
Using carbon monoxide: This has a similar solubility to O2, and has a high affinity for Hb. Therefore, we know that the CO remaining after expiration is that which has not been taken up, rather than being clouded by what's been expired.
DL(CO) = (V*CO / PA(CO) )
63
How do partial pressures of different gasses change over the time course it's in the capillaries?
It begins its journey at about 40% partial pressure, due to what comes back unused from the tissues. Normally, it is 100% by .25 seconds, but in abnormal capillaries it can take more than .75 seconds.
N2O has a very high solubility and so it can reach 100% pressure very quickly
CO only reaches a small percentage of partial pressure due to the fact that it doesn't sit in the blood plasma, but binds directly to Hb.
64
How do you distinguish between airways of the respiratory zone?
- Respiratory bronchioles- have random alveoli along them
- Alveolar ducts- Literally a row of alveolar buds and smooth muscle plugs
- Alveolar acs- bunch of alveoli
- Alveoli
65
Describe the interalveolar septa
These form the structural barriers between alveoli. They contain elastic fibres allowing recoil during tidal breathing. Collagen is important for structure. Fibroblasts produce both these components
Thin part forms the blood-air barrier, thick part supports and contains blood vessels
66
Describe the dual blood supply of the lungs
Circuit 1: Carries low pressure deoxygenated blood to the alveoli and then the the left atrium. Pulmonary arteries run with airways -> pulmonary capillaries -> pulmonary veins -> run within lobules-> heart
Circuit 2: Carries systemic pressure, oxygenated blood that supplies the conducting zone. Systemic vessels -> bronchial arteries
-> capillaries -> bronchial veins.
The bronchial veins empty into the pulmonary veins, meaning the 'oxygenated' blood is actually partially de-oxygenated
67
Compare and contrast the two lung circuits?
Pulmonary: Large volume, lumens. Arteries Thin walled, carries de-oxygenated blood alongside airways at low pressure. Veins are lonely, found in lung substance. carry ox blood at very low pressures
Systemic: supply airway tissues with O2 blood at systemic pressures. Veins are thin walled, low pressure, carry de-O2 blood
68
What is the general pathology of emphysema?
Inflammation destroys elastin, so decreased elastic recoil and connective tissue. Air spaces increases, so there is increased compliance (air gets trapped in the chest) and the gas exchange area decreases.
69
What are the three most important things determined by pulmonary function testing?
- Is the respiratory pump working?
- Is the alveolar membrane functioning properly?
- Is the lung adequately perfused?
70
What is spirometry and what does it indicate?
- It's a measure of dynamic lung volume- mostly using FVC, FEV1 and max volumes during forced inspiration and expiration. Doesn't measure total lung capacity, but can determine airflow.
It can establish/confirm a diagnosis of obstructive ventilatory defect
Assess effects of intervention
Assesses fitness for activities
Preoperative evaluation of airway obstruction
Impact of workplace exposure on resp function
71
What are the measures of static lung volume and what do they do?
- Plethysmography
- H2 dilution
- N2 washout
These are able t establish/confirm a diagnosis of restrictive ventilatory defect. They can also differentiate lung disease processes. They measure TLC and other static volumes, rather than flow
72
What is plethysmography?
Based on the law (P1 x V1 = V2 x V2)
Patient is seated in a box, breathing into a flow sensing defice, wearing nose clip and supporting cheeks. Patient gently pants, and change in flow over change in pressure in the box is measured to approximate airway resistance.
A mouth shutter is closed, and change in pressure of mouth over box is measured, allowing the measurement of thoracic gas volume.
73
What is helium dilution?
Used to measure functional residual capacity and total lung capacity. It uses (C1 x V1 = C2 x V2). Patient is connected to a chamber with a known concentration and volume of He (C/V1) and breathes deeply and rapidly, while He content is analysed at the mouth. Eventually the concentration stops fluctuating, indicating that lung He = chamber He. Therefore, the volume of chamber+lungs and therefore lungs can be determined.
74
What is N2 washout?
Uses (C1 x V1 = C2 x V2).
Patient breathes 100% O2 until there is no more N2 being exhaled- the total volume of N2 expired is therefore known and can be used to calculate total thoracic volume
75
What is the problem with H2 dilution and N2 washout methods?
Both are prone to error as lung pathology can change these concentrations
76
How do you measure airway resistance? What does this indicate?
1. Panting with shutter open- measures volume and flow
2. Panting with shutter closed- measures pressure and plethysmograph lung volume
Airway resistance = pressure/flow
Indicates restrictive ventilatory defect. Differentiates lung disease process. Aids in diagnosis of obstructive lung diseases
77
What is a bronchodilator response and what does it indicate?
The performance of a test (mostly FEV1) before and after use of a bronchodilator.
Percentage change = (highest pre FEV1 - Highest Post FEV1) / Highest pre FEV1 x100
To be considered successful it has to have an increased FEV1 of 12-15% and at least 200mL
Indicates reversibility of airway obstruction
Evaluaton of drug regimens
Reversal of bronchospasm
Postoperative evaluation
78
What is bronchoprovocation testing and what does it indicate?
Drying out of airways with various drugs, inducing narrowing of airways. No drug is 100% sensitive or specific though- some room for error.
% change = highest pre- FEV1 - highest post FEV1 / Highest pre- FEV1 x 100. Response is counted when FEV decreases by either 15 or 20%
Indicates asthma, although can overlap with COPD and other causes of airflow limitations
79
What is exhaled NO testing and what does it indicate?
These levels rise during asthma exacerbation and fall with steroid therapy- indicates level of responsiveness in asthmatics and non.
Indications are similar to bronchoprovication and bronchodilator responses.
80
What is alveolar-capillary diffusion assessment and what does it indicate?
Used to evaluate transfer of gas from distal air spaces to pulmonary capillaries.
Uses CO as Pc(CO) can be considered 0 .
1. Measure rate of CO uptake (analyse CO breathed in and out)
2. Estimate CO driving pressure (known conc. in inhaled air)
While it can't measure individual alveolar uptake, it can measure overall
Indicates diseases involving lung parenchyma
Evaluation of emphysema
Differentiation of bronchitis, emphysema and asthma
Evaluates pulmonary involvement in systemic diseases
Evaluates CV diseases
Predicts arterial desaturation during exercise
Evaluates disability due to interstitial lung disease
81
What is a progressive exercise test and what does it indicate?
Combines ECG, BP and power output measurements with exhaled gas analysis and Hb saturation. Ordered due to SoB, dyspnoea on exertion exercise intolerance or preoperative risk assessment.
Measures VO2 max, and any limitations to it.
Indicates exercise capacity and cause of exercise impairment
Identifies abnormal response to exercise
Results and risk for treatment
Stratification for training
Evaluation of disability and dyspnoea
Selection for transplantation
82
What are MEPS and MIPS?
Max ins/exp pressures, showing diaphragm strength
Measures max pressures against a blocked mouthpiece
Indicate degree of muscular weakness, ubstructive lung disease, chest deformities and dyspnoea
Diagnosis of diaphragm injury
Assessment of progressive disease on resp. system
Effectiveness of muscle strength therapy
83
How does the partial pressure of oxygen change through the body?
It is highest in atmosphere
Saturation causes obligatory dilution to approx 150mmHg
Dead space volume results in dilution to 104mmHg in the alveoli
PaCO2 is regulated to about 40mmHg. therefore there is some CO2 in the alveoli, further diluting PAO2
Not all O2 makes it through the alveolus, so PO2 is reduced to 100mmHg
Degree of partial pressure in plasma depends on the amount of time it spends in the capillary
Atriovenous shunting- de-ox blood combined with ox blood, further reducing partial pressure, or some venous blood doesn't reach the capillary but bypasses it. This drop in oxygen content can have a profound effect in a partial pressure drop
Ventilation/Perfusion mismatch- alveolus may be well ventilated but poorly supplied. Alveolus may be well supplied but poorly ventilated.
PO2 also declines in systemic capillaries- O2 is used up by tissues
PO2 also declines through interstitial fluid, cell membranes and cytoplasm
84
What is the difference between anatomical and physiological shunting?
Anatomical can be due to:
- Combination with bronchial circulation
- Component of coronary circulation
- AV fistula
- Patent ductus arteriosus with pulmonary hypertension
- Patent foramen ovale
Physiological are:
- Any admixture of venous blood with pulmonary capillary blood. The shunt will put some de-o2 blood into the O2 blood, which is able to be calculated. In healthy individuals, this is about 1-1.5% of cardiac output
The small change in content can have a large effect on partial pressure due to the sigmoidal shape of the oxyhaemoglobin equilibrium
85
What is the difference in ventilation around the lung?
The lung's weight makes intrapleural pressure more negative at the base, so airways there are relatively compressed- this means ventilation is greater here as there is more opportunity for compliance.
Ventilation is enhanced in areas of: increased lung compliance, low airflow resistance. However, this is lost at very small volumes- the relationship between pressure and volume is sigmoidal, so when pressure is too low, the higher lung is on the more vertical part of the curve.
86
How does blood supply differ around the lung? How is it measured?
It is best perfused at its base, due to higher pressures leaving the lung further down, as more post-capillary vessels are added coming down from the top, requiring greater pressures to keep pushing past it
- Measured by flow of O2 / (CaO2 - CvO2)
87
What is the ventilation perfusion ratio and what are the consequences of change to this?
It is the ratio of partial pressures in the alveoli to capillaries.
If airway blocked, alveolar part. pressures equilibrate to capillary ones.
It blood vessel blocked, blood equilibrates to alveolar pressures.
Blocked blood vessel leads to decreased PCO2.
Blocked airway leads to decreased PO2
88
How does ventilation perfusion ratio change across the lung?
Higher up, there is a higher ratio, whereas this becomes lower the further down the lung you get. This is because while both V and Q increase towards the lung base, Q changes more dramatically and V changes more slowly.
89
What mechanism can remedy VQ inequalities?
- Hypoxic vasoconstriction: the blood gets diverted to a better-ventilated alveolus. This increases pulmonary arterial resistance, increasing pulmonary arterial pressure, causing increased pressure-volume work by the right heart
90
Where does the diaphragm sit?
It peaks around T8, and has 2 crurae (the right one is higher due to heart not being present.
Has 2 openings- canal opening allows IVC through the tendon to prevent compression (ant, TVIII)
Oesophageal hiatus allows oesophagus through (mid,TX)
Behind the diaphragm the aorta passes down, and enters the abdominal cavity through the aortic hiatus (post, TXII)
91
What is the action of the diaphragm and how is it innervated?
It flattens, pulled down as you inspire. It relaxes to a superior position during expiration.
Innervated by phrenic nerve from C3,4,5.
92
What are the ligaments of the diaphragm and where do they run?
Median arcuate ligament- runs in front of aorta
Median crurate ligaments-attach vertebrae to diaphragm- Psoas runs behind it, as well as the sympathetic chain
Lateral arcuate ligaments- run between vertebral processes and ribs- quadratus lumborum runs behind.
93
What nerves are sympathetic vs. parasympathetic?
P: All Cranial nerves, S2,3,4.
S: CIII, VII, Ix, X. T1-5
94
What is horner's syndrome?
Sympathetic chain disruption to head and neck- presents as ptosis (eyelid drooping), miosis (constricted pupil) and anhydrosis (lack of sweating) on affected side. Due to compression of sympathetic chain
95
What is phrenic nerve irritation?
Presents as shouldertip pain. Can be due to a low lung tumor, or liver/gallbladder pathology.
96
What is the epidemiology of asthma?
- It's one of the most common in NZ- 1/6 adults and 1/4 children.
- Hospitalisations increasing, most common children's cause of hospitalisation
- Highest YLD disease in males, 3rd for females.
- Mortality related to smoking, age, lung function, FEV1 etc.
97
What can asthma present as? (categories)
Episodic- acute exacerbations between symptom-free periods
Chronic- daily airway obstruction that is mild/moderate/severe, with additional acute exacerbations
Life threatening- slow or fast onset, fatal within 2 hours
98
What are the main symptoms of asthma?
```
Wheezing
SOB
Chest tightness
Coughing
Sputum production
Airflow obstruction
Worse at night- diurnal variation
```
99
What are the 3 main changes associated with asthma?
- Inflamed, swollen airways
- Increased mucus production
- Contracted smooth muscle in airways
100
What main tests can be performed for diagnosis of asthma, and what is a positive result?
- Lab studies- eosinophilia greater than 4% suports. IgE greater than 100IU are indicative of allergic reactions, but non specific. (normal doesn't exclude asthma)
- Imaging studies- may rule out other pulmonary diseases. Sinus CT can excude chronic sinusitis
- Pulmonary function tests- reduced ratio of FEV1 to FVC demonstrates obstruction. In asthma, both are reduced but FEV will decrease more proportionally.
101
What are some alternative tests that can be performed for asthma?
Fraction of NO in exhalate is increased in inflammation
Allergy skin testing guides allergic rhinitis diagnosis
Reflux and asthma can diagnose a connection between the two symptoms
Bronchoprovocation helps to determine asthma even when FEV/FVC are normal.
102
What is the pathophysiology of athsma?
Airway inflammation: Increased mast cells (acute), t cells (control), macrophages (pro-inflammatory release), neutrophils (corticosteroids) basophils (release inflam proteins) and eosinophils. Goblet cells produce more mucus.
Airway hyperresponsiveness: Direct or indirect stimulation of smooth muscle by mediator-secreting cells
Airflow obstruction: caused by bronchoconstriction, emema, mucus plug formation, airway remodelling.
103
What are the risk factors for asthma?
```
Infections
Family history- genetic component assoc. with TH2 response
Atopic disease
Environmental exposures
Lifestyle
Comorbidity
Occupational exposures
Genetic factors
Pharmacological stimuli
Psychological factors
```
104
What do eosinophils do in asthma?
Produce leukotrines which synthesize mast cells and eosinophils, prolong bronchoconstriction, and increase mucus secretion and edema.
Produce IgE, good for fighting parasite infections as well as allergen antigens. Trigger mast cells in airway walls
105
What do mast cells do in asthma?
Produce and secrete mediators like histamine and leukotrines. Cause smooth muscle contraction, mucus production and edema.
Activated by allergin binding and cross liking of 2 IgE molecules. Live in submucosa, smooth muscle and adventitia.
Involved in: exercise induced asthma, immediate allergen response and cooling.drying of airways
106
What do T lymphocytes do in asthma?
Produce IL3,4,5
Respond in allergy- mediated asthma attacks.
TH1 cells involved in cell-mediated immune response
TH2 cells involved in antibody-mediated immune response
107
What other changes occur due to asthma?
Subepithelial fibrosis
Increased smooth muscle
Increased bronchial vascularity
108
What other syndromes can be causing asthma-like symptoms?
Upper airway obstruction
Endobronchial disease
Chronic bronchitis
Eosonophilic pneumonias
109
What is the difference between atopic and non-atopic asthma?
Atopic is most common, early onset and triggered by the environment. It is preceded by other allergic symptoms and involves a family history
Non-atopic asthma is less common, late onset and involved with respiratory tract infection. It can be induced by medicine
110
What is atypical asthma presentation?
Dyspnoea without wheeze
| Chronic cough
111
How does FEV1 change at different asthma stages?
Acute phase lasts 5-10 minutes, and shows much decreased FEV1
Late phase lasts 4-6 hours, causes longer term decreased FEV1
When both occur, they are both worsened.
112
What are the potential classes of asthma drugs?
Relievers: Bronchodilators (act in bursts, taken when needed)
Preventers: Anti-inflammatory agents and mast cell stabilizers (long term control, taken daily)
Others
113
What are the different classes of bronchodilators?
Inhaled- B-Adrenergic agonists
Inhaled cholinergic agents
Theophylline
114
What are the features of short-acting beta agonists?
```
Used for acute bronchospasm
Have a rapid onset
Prevent exercise-induced bronchospasm
Regularly scheduled use not recommended
Can mark disease control
```
115
What are the different types of short-acting beta agonists? How do they work?
```
Adrenaline: Promotes B2 receptors, which stimulate cAMP and smooth muscle reaction due to sympathetic response. However, it also constricts blood vessels and inhibits mediator release
Isoprenaline: B1 and B2 agonists- although B1 activation increases HR
Fast acting (salbutamol and terbutaline): resistant to breakdown, so last a few hours
```
116
How are short-acting beta agonists administered?
Inhalers for fewer side effects and fast action. However, can cause tachycardia and tremor in skeletal muscles due to contractility.
Can be metered dose (aerosol) or dry powder device (can deliver more)
117
What are some issues with inhalers?
Tachyphylaxis- developing resistance- although even a down-regulated response can cause dilation
Mucus plugging can block drug action
Hypokalaemia- decreased K+ in cells due to action of agonists
118
What are some features of long acting beta agonists?
Act for 12 hours or more
Used for maintenance control for moderate or severe persistent asthma
Uses corticosteroids with long hydrocarbon tails to make them more lipid soluble and add a functional group at the tail to bind the drug glose to the receptor
119
What are some adverse effects of long acting beta agonists?
Can activate B2 receptors in non-target tissue. More frequent with oral and systemic administration
Commonly tachycardia, increased O2 demand, and arrhythmia, as well as tremor and hypokalemia.
120
What are the targets of ACh agent drugs?
M3 receptors- their binding causes relaxation of smooth muscle
121
What are the different types of Anticholinergic agents and their issues?
Ipratropium (atropine): blocks ACh binding and dilating airways. Has a slower and lower peak, but good for when beta agonists aren't tolerable. Problem: reduced mucociliary clearance, so can cause blockages
Tiotropium: acts over 24h and is used for COPD. Problems with dry mouth in 10-15% Can also cause constipation, blurred vision and urinary retention
122
What does theophylline do, what are its side effects and what impacts its clearance?
Theophylline blocks all phosphodiesterases, of which type 4 is the most relevant. This causes increased bronchodilation, diaphragm strength, mucociliary clearance, and decreased fatigue and dyspnoea.
Minor side effects: Nausea, headache, tremor, insomnia
Major side effects: Tachycardia, atrial fibrillation, seizures
Heart failure, erythromycin, betal blockers, genetics and ciprofloxacin decrease clearance
Smoking and phenytoin increase clearance, so it's easier to overdose
123
What is the main type of anti-inflammatory asthma drug, and what does it do?
Glucocorticoids: bind to glucocorticoid receptor, which up-regulates expression of anti-inflammatory proteins, and represses anti-inflammatory proteins by preventing translocation of transcription factors into the nucleus.
124
How do you tell if a glucocorticoid is systemically introduced or inhaled?
Inhaled start with B, F and T. Anything else is systemic.
125
How do glucocorticoids bind to glucocorticoid receptors?
Receptors are located in the cytoplasm, so glucocorticoids must first diffuse through the cell membrane. All GCs are lipophilic. The higher the binding affinity, the greater the anti-inflammatory activity
126
How do GCs undergo nuclear translocation?
GCs with receptors bind to CS and the complex undergoes nuclear translocation
127
How do GCs perform transactivation?
The CS-GCR complex activates specific DNA sites, which then go on to activate coactivator proteins, multiple genes.
128
How do GCs perform transrepression?
They prevent transcription factors from interacting with coactivator proteins. This results in the inhibition of inflammatory cytokine expression.
They also suppress circulating inflammatory cells' recruitment, migration, activation, survival and proliferation.
129
What are the different CGs used to treat asthma?
Cortisone- oral, very effective anti-inflam
Prednisone: acts as an immunosuppressant, metabolised in the liver to activate. Reduced ankle swelling and water/salt retention
Dexamethasone- synthetic, both anti-inflam and immunosuppressant. 25x more potent than cortisone
130
What are the systemic adverse effects of GCs?
- Inhaled- around 20% is inhaled while he rest is swallowed and metabolized- so high doses can cause problems
- May bypass metabolism
- Cushing syndrome- body redistributed to trunk, back of neck and face
- Increased gluconeogenesis- causes diabetes, and muscle breakdown
- Osteoporosis
- Increased BP
- Euphoria
- Verbal psychosis
- Cataract risk
- TB susceptibility
- Salt water retention
131
What are the local adverse effects of GCs?
Hoarseness, cough, thrush due to immunosuppressants and myopathy of vocal cords
Can be prevented by rinsing mouth or using a spacer
132
How are leukotrine receptor antagonists used for asthma?
- Prevents aspirin and exercise induced asthma by decreasing responsiveness. Performs bronchodilation and can be used in addition to a B2 inhibitor
Can cause headaches, GI issues, hepatitis
133
How are mast cell inhibitors used for asthma?
Prevent allergen responses, reduce airway reactivity and have almost no side effects.
134
How is immunotherapy used for asthma?
Increases allergen tolerance, by risk of anyphrylaxis
135
How are anti-IgEs used for asthma?
More rapid onset, but delivered dangerously
136
How is O2 therapy used for asthma?
Delivered with helium in an 80%He, 20%O2 gas. No side effects. Improves PEF and reduces turbulence.
However, can get oxygen toxicity, which results in free radical production
Can also cause seizures, atelectosis and retinal damage
137
What is the typical presentation of a lung cancer patient?
Most 50-80 (but most 60-70), male and smokers
138
What are the types of lung cancer? What are the features of each?
Non-small-cell lung cancer- 70-75% of cancers. Treated with erlotanib and gefitinub.
Includes:
- Squamous cell lung cancer- associated with years smoked, some genetics (SNPs, polymorphism). Due to bronchial epithelium damage, causes dysplasia, then carcinoma in situ, and then malignancy. Mostly involves the major bronchi, in a firm, grey and ulcerated cancer. Can see keratin pearls. They extend into the parenchyma and can cause necrosis .
- Large cell lung cancer
- Adenocarcinoma: common in female, non smokers. Peripheral cancer. Subtype= bronchioalveolar cancer
Small cell lung cancer- 20-25% of cancers, associated with years smoked and genetics. Highly malignant, showing necrosis and haemorrhage. Mostly peri-hilar and can exhibit neuroendocrine features
139
How do different lung cell types differ?
Both in origin- mutations in K-ras, EGFR gene, or alk mutations- and in clinical treatment
140
What can some complications of small cell lung cancer be?
Increased ADH can cause hyponaturaemia
141
What can some complications of NSCLC be?
- Can see hypercalcaemia due to increased PTH
142
What are the clinical features of lung cancer?
Cough, dyspnoea, haemoptysis, chest pain, obstructive pneumonia.
143
What are some complications of lung cancer?
- Local spread: Pleural effusions, nerve entrapment (horner's syndrome)
- Mediastinal spread: SVC obstruction, nerve entrapment (recurrent laryngeal nerve palsy (hoarseness due to impaired vocal cords))
Common spread to lymph, brain, bone, liver and adrenal glands
Paraneoplastic features due to cytokines (finger clubbing)
Pulmonary metastatic disease- more common than primary lung cancer
Malignant mesothelioma- compresses lung, assoc. with asbestos
144
What are the features of horner's syndrome and SVC obstruction?
Horners: Ptosis (eyelid drooping), decreased pupil size and decreased sweating on affected side
SVC obstruction: face turns red during arm raising due to blood trappnig
145
By what factors can the components of oxygen consumption (in alveoli and in capillaries) change during maximal exercise?
```
VO2- 20x
VT- 4x
f- 3.5x
(FIO2 - FEO2)- 1.5x
Vs- 2x
fheart- 3x
(CaO2- CvO2)- 3x
```
146
How do we differentiate between non-maximal VO2 and VO2 max? How efficient are we?
Sub-maximal VO2 is a linear graph where our oxygen uptake increases with the work done to a plateau, called VO2 max, the maximal rate at which O2 can be consumed by the mitochondria. This can be improved by endurance training
The efficiency can be found in the slope- 0.2 This means we are actually only 20% efficient
147
What effect does exercise have on the oxy-haemoglobin curve and why?
- Increase in energy demand is assoc. with local decrease in Po2
- Causes arteriolar vasodilation, increasing capillary bood flow and O2 offloading
- Local increases of temperature and PCO2, while pH falls (inversely proportional to PCO2)
- Increased temp, CO2 and acidity all cause right shifts in the oxy-haemoglobin curve, resulting in less O2 being able to be gained in the lungs at a certain parital pressure- bur more can be offloaded at the tissues at a certain PO2.
148
How does exercise affect the lung processes?
Increased recruitment of 'supernumary' capillaries in the lungs, increasing DL
Increased gradient between alveolar partial pressure and capillary partial pressure, increasing rate of oxygen consumption
Decreased transit time in the capillaries means that pulmonary venous blood is not fully O2.
In combination with the right shift of the oxy-haemoglobin curve, the Oxygen content drops markedly.
149
How do Q and the oxy-haemoglobin curve relate during exercise and at rest?
Cardiac output is maintained, as the vasculature must be protected. The difference in PO2 between onloading and offloading of oxygen therefore remains the same, even as the curve shifts.
As the curve shifts right and downward, the same delivery rate of O2 to the tissues can be acheived at a reduced cardiac output. Dt also increases with exercise, due to capillary recruitment.
150
What are the advantages of protecting the cardiovascular system by decreasing HR and right-shifting the Hb curve while exercising? What mechanisms acheive this?
Maintain the PO2 going into tissues without loss of driving pressure due to increased cardiac output.
After being used up by the tissues, the PvO2 remains constant (at approx. 40mmHg) due to the skin allowing heat to escape through non-O2 absorbing vessels, shifting the curve to the left.
151
How does the work of breathing required change at different levels of exercise? How does the VO2 of the respiratory muscles change?
The work of breathing goes up steadily, showing that muscle efficiency is constant regardless of demand. This means that exhaustion is caused by the cardiovascular system rather than respiratory.
The demand by respiratory muscles is not linear- it increases disproportionately, beginning at approx. 500kg/m/min-1 of power. It can represent 3-10% of total VO2. This demonstrates that the accessory respiratory muscles are not as efficient as the skeletal muscles.
152
What are the 5 stages of pre/peri-natal lung development and what are their features?
Embryonic: 26d-7w: lung bud arises ventrally from foregut endoderm, with primary to tertiary bronchi formation
Pseudoglandular: 5-17w: More branching, formation of bronchi, bronchioles and terminal bronchioles. Resembles gland. Conducting zone ONLY at this stage
Canalicular: 16-25w: Rise of respiratory bronchioles with alveolar ducts (although lined by cuboidal cells). Limited blood supply. Gas exchange possible but very limited
Saccular: 24w to neonatal: Formation of primitive alveoli, close assoc. with blood and lymph. Beginning of surfactant (although not significant until 30w)
Alveolar: increased sacs, mature alveoli, more intimate capillary contact.
Note timing crossovers occur as the base of the lung matures later than cranial lung
153
What is secondary septation?
The building of additional parenchyma between alveoli
154
What 2 main respiratory changes occur at birth?
- Lung circulation turns from high pressure (due to fluid in lungs) to low pressure
- Foramen ovale and ductus arteriosus close
155
What are tracheooesophageal fistulae and how are they diagnosed/treated?
Oesophagus ends in a blind pouch while trachea is also connected to stomach- noticed as baby will regurgitate food shortly after birth. 1/2000 births require surgical intervention.
156
What is the general purpose of surfactant?
It reduces surface tension, and therefore stiffness, of the lungs. With no surfactant, the surface tension would rise from 5-28cmH20, resulting in higher stress and work for cells, and thicker membranes, need for increased ventilation etc.
157
What makes up surfactant?
Surfactant is 95% phosopholipid and 5% protein.
The phospholipids form a monolayer, a laminar structure that is secreted, broken into tubular myelin and arranged. The surfactant heads are hydrophilic, sitting on the H20 surface between molecules. The tails stick up and prevent adhesion between surfaces.
The proteins can be A & D (large, hydrophilic, regulatory) or B/C (small, lipophilic, forming and stabilizing). Surfactant is turned over every 3-11h. It can be taken up by type II cells/macrophages or sent up the mucociliary escalator.
Surfactant molecules beneath the top monolayer are able to insert into the membrane when SA increases and vice versa. However, the work to inflate the membrane is less than the work to deflate it.
158
What is laplace's law?
Pressure= surface tension/r1 + surface tension/r2. As a sphere has the same radii, it simplifies to P=2t/r. A larger radius results in less pressure.
159
What are the secondary functions of surfactant?
- Reduces chance of fluid being sucked into airspace, as fluid being pushed towards the alveoli by collapsing lungs is 'caught' by surfactant
- Helps to move particles, as things move from an area of low to high surface tension
- Surfactant proteins A&D bind pathogens to aid macrophages
- Reduces formation and maintenance of liquid plugs
160
What is neonatal RDS and how is it treated?
- Presents as intercostal retractions as the chest is being sucked in by the diaphragm as it attempts to inhale. Due to a lack of surfactant at birth
- Can give antenatal steroids to kickstart surfactant
- Once born, can give exogenous surfactant.
161
Why is lung defence particularly important?
The lung is in direct communication with the environment, allowing for many occurences and different types of insults. The high ventilation rate (especially during exercise) means we bypass our upper respiratory conditioning.
162
Where do bacteria sit in the respiratory tract?
There are always bacteria in our URT, although they increase in number, as well as alter when there is illness
It is unknown whether the LRT is colonised permanently or transiently, but some very different bacteria live there.
There is also cross-talk between the lung and gut bacteria.
When disease is present, diversity decreases
163
What are the defence mechanisms of the upper respiratory tract?
- The nose- large surface area for pathogens to get stuck to mucus
- Coordinated swallowing prevents foreign objects from lodging in the airways
The glottis and hypopharynx prevent food passing into the respiratory tract
Cough and sneeze
164
Where do particles tend to get stuck in the respiratory tract and why?
Distribution depends mainly on size (but also individual bacterial factors)
>10um - nose
5-10um- large airways
<2um- alveolar airways- mostly expelled during expiration
165
What types of particles can get stuck in the respiratory tract?
Micro-organisms
Dust
Allergens
Thereapeutic drugs of some kind- droplets, suspension (inhalers), dry powder, specialized
166
What is important for mucociliary escalator function?
Presence of periciliary fluid in which the cilia perform the recovery stroke- this is critical for cilia function. It's produced by clara and epithelial cells, and regulated by ion transport. This means it can be affected by disease (eg. CF) and treated as such.
Immotility or randomness of cilia (due to bacterial toxins and pro-inflammatory substances)
167
What is mucus and why is it important?
Mucus is made up of H20, glycoprotein mucins (coded for by 14 genes), proteoglycans, lipids, lysozyme and defensins.
Produced by goblet cells and mucus glands
DNA is important in diseases involving mucus- can be treated with gene therapy
It protects epithelium, traps and removes particles, and degrades pathogens itslef
168
What does coughing do?
Removes material from 16th-17th generation of branching. Involves contraction of airway muscles, generation of high thoracic pressure, and very high velocity airflow which picks up excessive (not normal) mucus.
169
What defences are present past the 17th generation of branching?
- Alveolar macrophages- phagocytose, present antigens, regulate response
- PMN neutrophils- recruited by macrophages
- Immunoglobulins
- Lymphoid tissue aggregates
- Surfactant
170
What is the process of pneumonia as a disease?
- When neutrophils are recruited, exudation causes fluid to pour into the alveoli (coughing is due to assoc. bronchitis). Reduced ventilation to perfusion matching, causing blood to be redirected to better ventilated portions of the lung. This causes the lung to become red (exudation) then grey (reduced blood flow)- red and grey hepatization
171
What are the risk factors for pneumonia?
- Poor dental hygeine
- Impaired swallowing
- Many bacteria in the throat
- More microaspirations at night
- Smoking causing a reduction in cilia and mucus functioning
- Deconditioned muscles, poor glottic closure, abnormal airways and mucus causing impaired coughing
- Impaired immunity due to age, comorbidities or existing treatment
172
What are the features of breathing in premature babies? Why does this happen?
Accessory muscles are in use
See intercostal retraction
Their lungs are stiff, with low O2 and high CO2 partial pressure, due to thicker tissue in undeveloped alveoli, low surfactant and atelectasis
173
What can be used to treat neonatal RDS?
Artificial surfactant (steroids before birth or a nasal spray)
Oxygen
CPAP (applied over the nose)
Mechanical ventilation and intubation
174
What harm can mechanical ventilation cause?
Hyperoxaemia
Damage to the lung due to high pressures
Can cause CLDP
175
What is CLDP?
Chronic lung disease of prematurity
This is defined as presistent increased work of breathing, associated with abnormal chest radiographs and requiring O2 at 36w gestation when born <32
Early features: Areas of atelectasis and emphysema, epithelial hyperplasia, and interstitial oedema
Late features: Interstitial fibrosis, hypertrophy of airway smooth muscle and pulmonary arteriolar muscle
Premature lungs are more susceptible to O2 damage, barotrauma and volutrauma, as well as surfactant deficiency and free radicals (due to an immature antioxidant defence system)
176
How does GORD present in children?
Episodes of spilling and wheezing after feeds
177
How does paroxysmal cough present in children? What does it indicate?
Inability to stop coughing once it's started, which can last between 90-120 seconds. This, along with an absence of foreign bodies and being well between coughs, indicates whooping cough
178
How does pneumonia present in children?
- Cough and difficulty breathing
- Tachypnoea (>50 breaths per min)
- Indrawing
- No wheezing
179
How does asthma present in children, how is it treated and what else could the symptoms indicate?
Asthma presents as bouts of cough and whoop. However, these could also be indications of bronchiolitis (which appears almost exclusively in babies and young children)
Asthma can be treated with bronchodilators (B agonists) or anti-inflammatories (corticosteroids). In very young children, the best method of giving drugs is with a spacer, although some drug will get caught in the nose
180
What does bronchiectasis present as in children, how is it treated, and what other conditions can the symptoms be mistaken for?
It presents as a wet productive cough, with lung crackles upon auscultation that don't clear
It can also be indicative of TB, a retained foreign body, pneumonia and cystic fibrosis.
Bronchiectasis is often secondary to other lung disease- damaged airways due to repeated and severe pneumonia, which dilates and scars airways.
It lowers FVC and FEV1, suggesting an obstruction
Treated with antibiotics and chest physiotherapy, helping to clear sputum. This is often done by doing Positive expiratory pressure (PEP) exercises. It involves breathing out against a weight to open the airways and lift sputum under the expiratory pressure.
181
What are the different pattern of lung abnormalities?
Can be focal, multifocal or diffuse
182
What are some examples of focal lung abnormalities, and how do they present & show up on X ray?
TB granuloma- shows as a single calcified lump
Focal pneumonia- shows as a shadow on X ray, with fever, SOB, haemoptysis and cough
Tumors- present as focal and well defined, with SOB, haemoptysis and potential chest pain (if abuting chest wall)
183
What is the radiological difference between a tumor and pneumonia?
The history, symptoms, time course, exam and x ray appearance- sometimes the X ray doesn't differentiate and this is called a mass-like opacity. You treat it like an infection and follow it up once the treatment should have worked
184
What are multifocal lung abnormalities, and how do they present?
Abnormality in lots of defined sites, or that involves the lymph nodes. Can be acute, subacute or chronic
- Infection- eg. TB (shown as upper lobe pattern/miliary with lymphadenopathy. Presents with intermittent fever and weight loss).
Can have complete consolidation of a lobe, with cough, chest pain and SOB
Metastases of cancer- see nodules everywhere, along with SOB
185
What are diffuse lung abnormalities? How do they present?
History is critical to determining acute vs. chronic. Nodes, effusions and cardiac size are all clues. Acute tends to be fluid, bus and blood. Chronic tends to be destruction of lung tissue, malignancy or fibrotic lung disease
Symptoms can include increased heart size, involvement of the azygous vein, dyspnoea, chest pain and orthopnoea (increased SOB when lying down)
Silicosis- from working in mines. Involves calcified lympth nodes.
186
What does the lung look like in CT when diseased?
Like a honeycomb- scarring separates out bronchopulmonary segments. It can show fibrosis
187
What are the diseases associated with each lobe of the lung?
Upper: TB, radiation, eosinophilic pneumonia, sarcoidosis, silicosis
Lower: UIP, asbestosis, lymphangitic metastases
Anywhere: Metastases
188
What is the definition of COPD?
Characterised by airflow limitation that is not fully reversible. This is usually progressive and associated with abnormal inflammatory responses.
Lungs lose elasticity, so the flow is lost early from collapsible small airways, and raises lung volumes.
As tidal breathing begins on a higher (and flatter) part of the hysteresis loop, more work is required for adequate breathing
189
What are some common COPD risk factors?
```
Exposure to tobacco smoke, occupational chemicals, air pollution (indoor or ourdoor)
Genes
Lung prematurity
Oxidative stress
Gender and age
Resp infections
SES and nutrition
Co-morbidities
```
190
What is the difference between COPD and asthma?
Asthma early onset, COPD late
Asthma symptoms vary day/night and between days, COPD symtpms constant but slowly progressive
Asthma reversible, COPD irreversible
Asthma family history, COPD not
191
What are the different classes of COPD severity?
Mild- FEV1 60-80% of normal
Moderate- FEV140-59% of normal
Severe- FEV1 <40% of normal
192
How do you treat COPD?
Initially with bronchodilators and glucocorticoids to help prevent exacerbations
Also flu and pneumococcal vaccines
O2 prevents hypoxia, which prevents V/Q mismatch, which prevents pulmonary hypertension and RHS heart failure by increasing FAO2
Can also use Long-acting bronchodilators or muscular agonists (LAMA and LABA)
193
What is pulmonary rehabilitation ad who qualifies for it?
It is a programme for those with chronic diseases functionally limiting their lungs. There is a priority for hospital admission-COPD patients.
It involves exercise, as the factors most correlated with COPD are exercise capacity, dyspnoea and quality of life. By limiting exercise causing SOB, SOB worsens
It's a 6-8 week program with 2 classes per week, in a hospital or community venue working with a multidisciplinary team
194
What are the effects of pulmonary rehabilitation?
```
Increased treatment adherence
Decreased frequency and severity of symptoms, decreased hospital admissions
Improved mood and motivation
Increased quality of life
Decreased dependency
```
