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Year 2 Medicine @ Lancaster Uni > 2.02 - Respiratory diseases, COPD and Asthma 🫁 > Flashcards

2.02 - Respiratory diseases, COPD and Asthma 🫁 Flashcards

1
Q

What components make up the upper airway?

A
  • Nose
  • Mouth
  • Pharynx (Oro, naso, lary)
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2
Q

What are the components of the lower airway?

A
  • Trachea
  • Right/Left Lung
  • Associated structures
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3
Q

What is the conducting zone of the lungs?

A
  • Larynx -> Trachea -> 1/2/3 bronchi -> Bronchioles -> Terminal Bronchioles
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4
Q

What is the respiratory zone of the lungs?

A
  • From respiratory bronchioles -> Alveolar sacs
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5
Q

What are type 1 alveolar cells?

A
  • Involved in gas exchange
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6
Q

What are type II alveolar cells?

A
  • Secrete surfactant to reduce surface tension
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7
Q

What immune cells are present in the lungs?

A
  • Macrophages
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8
Q

What is the pleura of the lungs?

A
  • It is the lining that protects and attaches the lungs to external structures
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9
Q

What are the two parts of the pleura?

A
  • Visceral = Innermost
  • Parietal = Outermost
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10
Q

What is the function of the pleura?

A
  • Provides lubrication as the lung moves during inspiration/expiration
  • 5ml-15ml in total which is mainly produced by parietal pleura
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11
Q

How many lobes does each lung have?

A
  • Right = 3 lobes
  • Left = 2 lobes
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12
Q

What are the three lobes of the right lung?

A
  • Upper
  • Middle
  • Lower
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13
Q

What are the segments of the right upper lobe?

3

A
  • Apical
  • Anterior
  • Posterior
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14
Q

What are the segments of the middle lobe of the right lung?

2

A
  • Lateral
  • Medial
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15
Q

What are the segments of the lower lobe of the right lung?

5

A
  • Medial basal
  • Anterior basal
  • Posterior basal
  • Lateral basal
  • Superior
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16
Q

What are the two lobes of the left lung?

A
  • Upper
  • Lower
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17
Q

What are the segments of the upper lobe of the left lung?

4

A
  • Inferior lingular
  • Anterior
  • Apicoposterior
  • Superior lingular
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18
Q

What are the segements of the lower lobe of the left lung?

A

Superior
Lateral basal
Anteriomedial basal
Posterior basal

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19
Q

What is the pneumonic for right lung segments?

A

AAPLMMAPLS

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20
Q

What is the pneumonic for left lung segments?

A

IAASSLAP

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21
Q

What are the two types on inspiration?

A
  • Quiet inspiration
  • Forced inspiration
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22
Q

What occurs in quiet inspiration?

A
  • Passive process
  • Diaphragm flattens to increase thoracic volume which causes pressure differential
  • Air flows into lungs
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23
Q

What occurs in forced inspiration?

A
  • Active process
  • Diaphragm flattens = Increased volume
  • Ex. intercostals = Elevate ribcage
  • Acc. muscles = Expand thoracic cavity
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24
Q

What are the two types of expiration?

A
  • Quiet expiration
  • Forced expiration
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25
Q

What occurs during quiet expiration?

A
  • Passive process
  • Elastic recoil of muscles reduce thoracic volume therefore causing pressure differential
  • This forces air out of the lungs
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26
Q

What occurs during forced expiration?

A
  • Active process
  • Int. intercostals = Depression of ribcage
  • Innermost intercostals = Further ribcage depression
  • Abdominal muscles = Increase abdominal pressure under diaphragm
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27
Q

What are the anterior lung surface markings?

A
  • Lower border = 6th rib
  • Oblique fissure = Mid-clav, 6th rib
  • Horizontal fissure = 4th costal cartilage
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28
Q

What are the lateral lung surface markings?

A
  • Oblique fissure = Curves upwards towards the T3
  • Horizontal fissure = Extends to oblique fissure in mid-axillary
  • Lower border = 8th rib, mid axillary line
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29
Q

What are the posterior lung surface markings?

A
  • Oblique fissure = T3
  • Lower border = T10/T11
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30
Q

What are the borders of the superior mediastinum?

A

Superior = Thoracic inlet
Inferior = Inferior mediastinum
Anterior = Manubrium
Posterior = T1-T4 vertebrae
Lateral = Pleura

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31
Q

What is the contents of the superior mediastinum?

A
  • Aortic arch
  • SVC
  • Vagus nerve
  • Phrenic nerve
  • Thymus
  • Trachea/Oesophagus
  • Thoracic duct
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32
Q

What are the borders of the anterior mediastinum?

A

Lateral = mediastinal pleura
Anterior = Body of sternum
Posterior = Pericardium
Roof = Superior mediastinum
Floor = Diaphragm

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33
Q

What is the contents of the anterior mediastinum?

A
  • No major structures
  • Contains loose connective tissue such as sternopericardial ligaments
  • Fat, lymphatics
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34
Q

What are the borders of the middle mediastinum?

A

Anterior = anterior margin of pericardium
Posterior = posterior margin of pericardium
Laterally = Mediastinal pleura
Superior = Line between sternal angle and T4
Inferior = Diaphragm

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35
Q

What is the contents of the middle mediastinum?

A
  • Heart (inc. pericardium)
  • Tracheal bifurcation
  • Ascending aorta
  • Pulmonary trunk
  • Cardiac plexus
  • Phrenic nerves
  • Tracheobrachial lymph nodes
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36
Q

What are the borders of the posterior mediastinum?

A

Lateral = Mediastinal pleura
Anterior = Pericardium
Posterior = T5-T12
Roof = Line between sternal angle and T4
Floor = Diaphragm

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37
Q

What is the contents of the posterior mediastinum?

A
  • Thoracic aorta
  • Oesophagus
  • Thoracic duct
  • Azygous system of veins
  • Sympathetic trunks
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38
Q

What is a pulmonary embolism?

A
  • An obstruction of a pulmonary artery by a substance that has travelled from elsewhere in the body
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39
Q

What are the most common emboli?

A
  • Thrombus - From clot in a distant vein
  • Fat - Following fracture or orthopaedic surgery
  • Air - Following cannulation in the neck
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40
Q

What score is used to assess the probability of a PE?

A
  • Wells’ score
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41
Q

What is spirometry and what is it used for?

A
  • Graphical representation of a patients lung function
  • Measures volume and speed of air that a person can inhale and exhale
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42
Q

What are the different lung volumes?

A
  • Tidal volume
  • Inspiratory reserve volume
  • Expiratory reserve volume
  • Residual volume
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43
Q

What is tidal volume?

A
  • Volume that enters and leaves with each breath
  • Normal breathing
  • Usually 0.5L
  • Changes with breathing pattern/depth
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44
Q

What is inspiratory reserve volume?

A
  • Extra volume that can be inspired above tidal volume
  • Space left in lungs after normal tidal inspiration
  • Usually 2.5L
  • Relies on muscle strength and lung compliance
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45
Q

What is expiratory reserve volume?

A
  • Extra volume that can be expired following a tidal breath
  • What is left in lungs after normal expiration
  • Usually 1.5L
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46
Q

What is residual volume?

A
  • Volume that remains in the lungs after a maximum expiration
  • Usually 1.5L
  • Cannot be measured by spirometry
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47
Q

What are the different lung capacities?

A
  • Vital capacity
  • Inspiratory capacity
  • Functional residual capacity
  • Total lung capacity

Are fixed and are made up of two or more lung volumes

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48
Q

What is vital capacity?

A
  • Volume that can be exhaled after maximum inspiration
  • Inspiratory reserve + tidal volume + expiratory reserve
  • Usually 4.5L
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49
Q

What is inspiratory capacity?

A
  • Maximal volume breathed in following quiet expiration
  • Tidal volume + Inspiratory reserve
  • Usually 3L
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50
Q

What is functional residual capacity?

A
  • Volume remaning in the lungs following quiet expiration
  • Expiratory reserve + residual volume
  • Usually 3L
  • Affected greatly by height
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51
Q

What is total lung capacity?

A
  • Volume of air in the lungs after maximal inspiration takes place
  • Sum of ALL volumes
  • Usually 6L
  • Restriction < 80% predicted
  • Hyperinflation > 120% predicted
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52
Q

What is anatomical dead space in the lungs?

A
  • Volume of air that never reaches the alveoli to undergo respiration
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53
Q

What is alveolar dead space?

A
  • Volume of air that reaches the alveoli but never takes part in respiration
  • Can reflect alveoli that are ventilated but not perfused
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54
Q

What can helium dilution be used to measure?

A
  • Used to measure total lung capacity
  • Mixes helium with air in lungs and then looks at degree of dilutiom that occurs
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55
Q

What can a nitrogen washout be used for?

A
  • Measuring the presence of dead space both anatomical and alveolar
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56
Q

What is peak expiratory flow rate (PEFR)?

A
  • The maximum flow rate achieved during forced expiration starting from full lung inflation
  • Measured in L/min
  • Reduced in obstructive diseases and in muscle weakness
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57
Q

What is forced vital capacity (FVC)?

A
  • Maximal volume of air that a subject can expel in one maximal expiration from a point of maximal inspiration
  • Reduced with obstructed airways etc.
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58
Q

What is forced expiratory volume in 1 second (FEV1)?

A
  • Maximal volume of air that can be exhaled in one second from a point of maximal inspiration
  • Reduced with obstructive airways etc.
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59
Q

What does the FEV1/FVC ratio show?

A
  • Indicates the proportion of lung capacity that can be exhaled in the first second of a forced breath
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60
Q

What lung function results are seen in obstructive lung diseases?

A
  • FEV1 = < 80% of predicted
  • Reduced due to increased resistance
  • FVC = Slight reduction
  • FEV1/FVC < 0.7
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61
Q

What are examples of obstructive lung diseases?

A
  • Asthma (Reversible)
  • COPD
  • Tracheal stenosis
  • Large airway tumours
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62
Q

What lung function results are seen in restrictive lung diseases?

A
  • FEV1 = < 80% of predicted
  • Reduced due to poor lung expansion
  • FVC = < 80% of predicted
  • FEV1/FVC ≥ 0.7
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63
Q

What are examples of restrictive lung diseases?

A
  • Intersitial pulmonary fibrosis
  • Muscle weakness
  • Obesity
  • Tense ascites
  • Kyphoscoliosis
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64
Q

When would carbon monoxide transfer be reduced?

A
  • A reduction is seen in pulmonary fibrosis, emphysema, oedema, embolism and anaemia
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65
Q

When would ‘spooning’ be seen in a flow-volume curve?

A
  • Seen in obstructive diseases
  • As small airways begin to collapse
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66
Q

Why are arterial blood gases (ABG’s) useful in diagnosing respiratory conditions?

A
  • Blood straight from lungs before it reaches target tissues
  • Contain max volumes of gases
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67
Q

What is the normal expected pH range of blood seen in an ABG?

A

7.35 - 7.45

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68
Q

How is the pH of blood controlled?

A
  • Tight control is provided by the buffer system comprising of bicarbonate and carbon dioxide
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69
Q

What is PaCO2 and what does it indicate?

A
  • The amount of CO2 dissolved in the blood
  • Dependant on ventilation, respiratory drive and CO2 production
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70
Q

What is PaO2 and what does it indicate?

A
  • The amount of dissolved O2 in the blood (Not the oxygen saturation)
  • Dependant on volume of O2 inspired and the surface area of the lungs
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71
Q

What are the two types of respiratory failure?

A
  • Type I - Hypoxemic resp. failure
  • Type II - Hypercapnic respiratory failure
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72
Q

What is type I respiratory failure and what can cause it?

A
  • Hypoxemic
  • When there is low PaO2 in blood with normal/low PaCO2
  • Involves inadequate oxygen exchange, alveoli problems and perfusion issues
  • Causes include: ARDS, Pneumonia, PE, Interstitial lung disease, PnTx
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73
Q

What are the clinical features of type I respiratory failure?

A
  • SOB
  • Tachypnoea
  • Cyanosis
  • Confusion or altered mental state
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74
Q

What is the initial management of type I respiratory failure?

A
  • Oxygen therapy usually high flow oxygen via a nasal cannula
  • Mechanical ventilation in severe cases
  • Treatment of underlying causes ie. Infection etc.
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75
Q

What is type II respiratory failure and what can cause it?

A
  • Hypercapnic
  • When there elevated PaCO2 and often a low PaO2
  • Involves the inadequate removal of carbon dioxide usually due to reduced ventilation
  • Causes include: COPD, Asthma, Neuromuscular issues, Chest wall disorders, CNS disorders
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76
Q

What are the clinical features of type II respiratory failure?

A
  • SOB
  • Rapid, shallow or laboured breathing
  • Headache
  • Flushed skin
  • Confusion or drowsiness
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77
Q

What is the initial management of type II respiratory failure?

A
  • Non-invasive ventilation (NIV)
  • Mechanical ventilation
  • Medications such as bronchodilators, corticosteroids etc.
  • Treatment of underlying cause
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78
Q

What is the definition of COPD?

A
  • A common progressive condition that is characterised by airway obstruction
  • FEV < 80% of predicted
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79
Q

What is the epidemiology around COPD?

A
  • 4th leading cause of death and disability worldwide
  • Prevalence of 10%-20% in over 40’s
  • Onset ususally occurs >35 years old
  • Being white and male increase likelihood
  • Smokers with greater the 10PY history are highly likely
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80
Q

Which two conditions can result in the development of COPD?

A
  • Emphysema
  • Chronic bronchitis
81
Q

What is chronic bronchitis?

A
  • When there is a productive cough on most days for at least 3 months during the last two years
82
Q

What are the features associated with chronic bronchitis?

A
  • BLUE BLOATERS
  • Decreased alveolar ventilation
  • Low PaO2/ High PaCO2
  • Cyanosed but not breathless
  • Progress to cor pulmonale often
  • Rely on hypoxic drive to retain oxygen and breath
  • Care to be taken with supplemental oxygen
83
Q

What are the clinical features of chronic bronchitis?

A
  • Persistent productive cough
  • SOB
  • Wheeze
  • Chest discomfort
  • Frequent URTI/LRTI
84
Q

What are the features associated with emphysema?

A
  • PINK PUFFERS
  • Increased alveolar ventilation
  • Low PaO2/ High PaCO2
  • Breathless but not cyanosed
  • Progress to T1RF often
  • Usually older and thinner
  • Caused by enlarged airspaces casued by alveolar wall destruction
85
Q

What are the clinical features of emphysema?

A
  • Often older and thinner
  • SOB
  • CXR shows hyperinflation
  • Quiet chest on auscultation
  • CXR shows flattened diaphragm
86
Q

What are the symptoms associated with COPD?

A
  • Productive cough
  • Wheeze
  • Dyspnoea
87
Q

What clinical signs are seen in COPD?

A
  • Tachypnoea
  • Accessory muscle use
  • Bullae
  • Cyanosis
  • Tripod pose
  • Hyperinflation
  • Decreased cricosternal distance
  • Hyperresonant sounds
  • Wheeze
  • Cor pulmonale
88
Q

What are the main aetiological features of COPD?

A
  • Long term exposure to irritants/toxic particles (Cigarette smoke = 90%)
  • Other occupational hazards
  • Can be caused by a-1 antitrypsin deficiency which increases likelihood of emphysema
  • Low socio-economic status
  • Low birth weight related to reduced lung capacity
89
Q

What can form part of the lifestyle management of COPD?

A
  • Smoking cessation
  • Pulmonary rehab
  • Exercise training
  • High calorie supplements for those with low BMI’s
90
Q

What is the first line management of COPD?

A
  • SABA or SAMA as needed
  • SABA = Salbutamol
  • SAMA = Ipratropium
91
Q

What is the second line management of COPD?

A
  • LABA or LAMA
  • LABA + ICS
  • LABA = Salmeterol
  • LAMA = Tiotropium
  • ICS = Beclamethasone
92
Q

What is the third line management of COPD?

A
  • Dependant on exacerbations
  • LABA + LAMA + ICS
  • LABA = Salmeterol
  • LAMA = Tiotropium
  • ICS = Beclamethasone
93
Q

What are SABA’s and how do they work?

A
  • Short acting beta agonist
  • Example = Salbutamol
  • Stimulate G-Protein coupling binding to B2 receptors
  • Inhibits parasympathetic innervation which leads to smooth muscle relaxation
  • Stimulates Na+/K+ pump
94
Q

What are SAMA’s and how do they work?

A
  • Short acting muscarinic agent
  • Example = Ipratropium
  • Inhibit acetylcholine binding to muscarinic receptors
  • Lead to increased HR and a decrease in smooth muscle tone
  • Leads to bronchodilation
95
Q

What are LABA’s and how do they work?

A
  • Long acting beta agonist
  • Example = Salmeterol
  • Salmeterol acts on B2 receptors in the smooth muscle cells
  • Activation of these receptors leads increased cAMP levels.
  • Elevated cAMP levels = relaxation of bronchial smooth muscle, leading to bronchodilation and improved airflow.
96
Q

What are LAMA’s and how do they work?

A
  • Long acting muscaranic agents
  • Example = Tiotropium
  • Tiotropium is a antagonist at muscarinic receptors, specifically the M3 receptors, which are found in smooth muscle cells
  • By blocking, tiotropium inhibits the action of acetylcholine
  • The net effect is bronchodilation and reduced mucus production
97
Q

What are ICS’s and how do they work?

A
  • Inhaled corticosteroids
  • Example = Beclamethasone
  • Beclometasone binds to glucocorticoid receptors within the cells of the respiratory tract.
  • Upon binding it leads to decreased production of inflammatory mediators
  • This reduces airway inflammation, mucus production, and bronchial hyperreactivity.
98
Q

What is the pathological process behind the development of emphysema?

A
  • Pollutants enter the lungs and are attacked by macrophages
  • Neurtrophils are attracted and begin to produce elastase
  • Elastase breaks down elastin in the alveolar walls
  • Usually balanced by a-1 antitrypsin
  • Elastin breakdown = Loss of elasticity -> Airway collapse
99
Q

What is the pathogical process behind chronic bronchitis?

A
  • Pollutants are trapped by mucus in the lungs
  • Goblet cells begin to produce more mucus in response
  • This excess of mucus causes cilliary dysfunction which leads to build up of mucus in lungs
  • This build up causes air obstruction and subsequent air trapping
100
Q

What investigations are undertaken in the diagnosis of COPD?

A
  • Lung function tests
  • CXR
  • ECG
  • ABG
  • FBC
101
Q

What could be seen on an CXR of someone with COPD?

A
  • Possible hyperinflation
  • Flat hemi-diaphragms
  • Large,central pulmonary arteries
  • Decreased peripheral vascular markings
  • Bullae (Blistering of lungs, cystic structure)
  • Cylindrical heart
  • Denser hilar markings
102
Q

What could be seen on an ECG of someone with COPD?

A
  • Right atrial and ventricular hypertrophy which is suggestive of cor pulmonale
  • Large P waves
103
Q

What could be seen in a FBC of someone with COPD?

A
  • Polycythaemia (High RBC count) -> Measure haematocrit
  • Normocytic normochromic anaemia of chronic disease which is seen in around 20% of cases
  • HB and PCV may be raised
104
Q

What could be seen in the lung function test of someone with COPD?

A
  • FVC < 80% of predicted value
  • FEV1/FVC < 0.7
  • Increased residual volume
105
Q

Which tool can help with predicting the prognosis of someone with COPD?

A
  • BODE Tool
  • BMI
  • Obstruction of airflow
  • Dyspnoea
  • Exercise capacity
  • 0-2 = 4yr mortality of 10%
106
Q

What are the different stages of COPD?

A
  1. Mild
  2. Moderate
  3. Severe
107
Q

What are the features of mild COPD?

A
  • FEV% = 60%-80%
  • Symptoms often variable and few
  • SOB on moderate exertion (Ie. walking on an incline)
108
Q

What are the features of moderate COPD?

A
  • FEV% = 40%-60%
  • Acute exacerbations occur
  • Some limitations on daily activity
109
Q

What are the features of severe COPD?

A
  • FEV% = < 40%
  • Frequent and severe exacerbations
  • Severe limits on activity that can be undertaken
110
Q

Is there a genetic component in the development of COPD?

A
  • COPD mainly develops due to environmental and lifesyle factors which lead to the destruction of airways
  • Only know component is the a-1 antitrypsin gene which regulates lung protection from pollutants
111
Q

In acidemia (Decrease in arterial pH) what can be the two outcomes?

A
  • Respiratory acidosis = Increase in PaCO2
  • Metabolic Acidosis = Decrease in HCO3- concentration
112
Q

In Alkalemia (Increase in arterial pH) what can be the two outcomes?

A
  • Respiratory alkalosis = Decrease in PaCO2
  • Respiratory acidosis = Increase in HCO3- concentration
113
Q

When can respiratory acidosis occur and what are its features?

A
  • Can occur in asthma and emphysema
  • A reduced rate of respiration
  • Increased CO2 -> Increased H+ ions -> Reduced pH
114
Q

When can respiratory alkalosis occur and what are its features?

A
  • Can occur in trauma, anxiety and low altitudes
  • An increased rate of respiration
  • Decreased CO2 -> Decreased H+ ions -> Increased pH
115
Q

What is the definition of asthma and what are its key features?

A
  • A chronic lung condition where the there is inflammation and hypersensitivity of the airways
    1. Airflow limitation - Usually reversible
    1. Airway hyper-responsiveness - Over stimulation
    1. Bronchi inflammation
116
Q

Which cells can cause brochi inflammation?

A
  • Eosinophils
  • CD4+ T Lymphocytes
  • Mast cells
117
Q

In which two ways can asthma be divided depending on aetiology?

A
  • Extrinsic (Atopic)
  • Instrinic (Non-Atopic)
118
Q

What is extrinsic (Atopic) asthma?

A
  • Seen by a positive skin prick test
  • Very common and makes up 90% of childhood cases
  • Accompanied by eczema
  • Type I hypersensitivity to inhaled allergens
119
Q

What is intrinsic (Non-Atopic) asthma?

A
  • Less common
  • Often starts in middle age with a late onset
  • No identifiable trigger
  • Inflammation by local IgE production
120
Q

What is the epidemiology surrounding asthma?

A
  • Increasing incidence in western countries
  • Affects 5%-8% of population
  • 50% of those who grow out of asthma will have some form of a relapse
121
Q

What are the symptoms associated with asthma?

A
  • Intermittent dyspnoea
  • Wheeze
  • Nocturnal cough
  • White sputum
  • Breathlessness
122
Q

What are the clinical signs associated with asthma?

A
  • Tachypnoea
  • Polyphonic wheeze
  • Hyperinflated chest
  • Hyper-resonant percussion (Drum like)
  • Decreased air entry
123
Q

What are some common precipitants of asthma?

A
  • Cold air
  • Exercise
  • Emotion
  • Infection
  • Pollution
  • NSAID’s
  • Beta blockers
  • Allergens
  • Smoking
124
Q

What are the signs of a severe asthma attack or exacerbation?

A
  • Unable to produce full sentences
  • Tachycardic >110 BPM
  • Tachypnoea >25 breaths/min
  • Silent chest sounds
  • Cyanotic
  • Peak expiratory flow = 50%>
125
Q

What are common aetiologies relating to asthma?

A
  • Occupational sensitivities
  • LMW = Reactive chemicals
  • HMW = Flour, dust etc.
  • Exercise
  • Strong emotions such as anxiety
126
Q

What are the different pathological processes that can be involved in the development of asthma?

3

A
  • Non-Atopic
  • Aspirin Induced
  • Occupational
127
Q

How can aspirin induce asthma?

A
  • Intake of aspirin can cause increased levles of leukotrienes and decreased levels of prostagladins
  • Aspirin inhibits COX enzymes
  • Other NSAID’c can also cause this reaction
128
Q

What are type I hypersensitivity reactions?

A
  • Occurs in response to allergen exposure which causes the release of IgE antibodies from plasma cells
  • IgE binds to receptors on mast cells
  • Mast cell degranulation and histamine release
  • Causes smooth muscle contraction, mucous production and bronchoconstriction
129
Q

In what ways can asthma be managed extrinsically?

A
  • Control of extrinsic factors:
    1. Reduction of provocating factors
    2. Avoid all Beta blockers
    3. Good hygeine
    4. Various complementary therapies
130
Q

What is the first line treatment for newly diagnosed asthma in adults?

A
  • SABA
131
Q

What is second line treatment for asthma in adults?

A

2nd = SABA + Low dose ICS + LTRA
3rd = SABA + ICS + LABA +/- LTRA

132
Q

What is the third line treatment for asthma in adults?

A

3rd = SABA + ICS + LABA +/- LTRA

133
Q

What occurs in the early phase of pathological development of asthma?

A
  • Allergen inhalation
  • IgE antibodies bind to mast cells which causes mass degranulation and histamine release
  • Causes smooth muscle contraction and bronchoconstriction
134
Q

What occurs in the late phase of pathological development of asthma?

A
  • Recruitment of a variety of inflammatory cells such as T cells occurs
  • More complex as there is additional processes
  • B-agonists do not cause complete reversal in this stage
135
Q

What changes occur in the chronic stage of asthma development?

A
  • Fibrous tissue deposits begin to form
  • These fibrous growths begin to remodel sections of the lungs
  • This remodeling causes obstruction
136
Q

Which investigations should be undertaken when there is a low clinical suspicion of asthma?

A
  • Investigation/treatment of a more likely or alternative diagnosis
137
Q

What investigations should be undertaken when there is a moderate clinical suspicion of asthma?

A
  • Lung function testing
  • Assess variability
  • Assess eosinophilic inflammation
138
Q

What investigations should be undertaken when there is a high clinical suspicion of asthma?

A
  • Trial of treatment (SABA inhaler)
  • Reassess lung function
139
Q

Is there a genetic component to the development of asthma?

A
  • More likely to develop asthma if a family member also has asthma
  • Partly due to genetics
  • Partly due to environmental
140
Q

What is dyspnoea?

A
  • Difficult or laboured breathing
141
Q

What tool can be used to assess the severity of a patient’s dyspnoea?

A
  • The MMRC scale
  1. With strenous activity
  2. With slight incline
  3. Stop when walking
  4. Stop after 100m
  5. When getting dressed
142
Q

What are the red flag symptoms that can accompany dyspnoea?

A
  • Chest pain
  • Haemoptysis
  • Weight loss
  • Fever
  • Lethargy
  • Asbestos exposure
  • Limb oedema
  • Smoking
143
Q

What are some acute differentials for asthma?

A
  • Asthma exacerbation
  • Pneumonia
  • Acute pulmonary oedema
  • ACS
  • PE
  • Tension pneumothorax
144
Q

What are some chronic differentials for asthma?

A
  • Lung malignancy
  • COPD
  • Interstital lung disease
  • CHF
145
Q

What is haemoptysis?

A
  • Coughing up of blood from respiratory tract
146
Q

What accompanying feature alongside haemoptysis is a red flag?

A
  • Weight loss
147
Q

What should be considered when investigating haemoptysis?

4

A
  1. Time frame
  2. Blood features
  3. CVS/Respiratory symptoms
  4. General symptoms
148
Q

What are some differentials for haemoptysis?

A
  • Acute bronchitis (Most common)
  • Lung malignancy (Most serious)
  • PE
  • Pneumonia
  • TB
  • Bronchiectasis
  • Lung abcess
  • Bullae
149
Q

What is the definition of pneumonia?

A
  • Inflammation of lung parenchyma
  • Alveoli become filled with bacteria and inflammatory cells
150
Q

What is the most common micro-organsism that causes pneumonia?

A
  • Strep. pneumonia
  • Gram positive
151
Q

What are the five different types of pneumonia?

A
  1. CAP
  2. HAP
  3. Aspiration
  4. Immunocompromised
  5. VAP
152
Q

What are the two types of community acquired pneumonia?

A
  • Typical CAP
  • Atypical CAP
153
Q

What are the features of typical CAP?

A
  • Classical symptoms
  • Commonly caused by strep. pneumoniae, haemophilius influenzae, Moraxella catarrhalis
  • Hallmark sign is a productive cough
154
Q

What are the features of atypical CAP?

A
  • Insidious onset
  • Pulmonary and extrapulmonary symptoms
  • Non-zoonotic: Mycoplasma pneumoniae, Legionella pneumophilia
  • Zoonotic: Chlamydia psittaci, Francisella tularensis
155
Q

What is HAP and why is it so dangerous?

A
  • Hospital acquired pneumonia
  • Prognosis is generally poor due to significant co-morbidities
  • Drug-resistant bacteria such as staphylococcus aureus pose a serious threat (Gram negative bacilli)
  • Also caused by legionella pneumophilia
156
Q

What is aspiration pneumonia?

A
  • Inhalation of oropharyngeal/gastric contents
  • This brings unwanted contents into the lungs
  • Can be seen as a result of anaesthesia
  • Related to Mendelson’s syndrome
157
Q

What is Mendelson’s syndrome?

A
  • Chemical injury caused by the inhaltion of sterile gastric contents
158
Q

Why is immunocompromised pneumonia so dangerous?

A
  • Patients are less able to fight infection
  • More susceptible to further infections
  • Such as those from: Bacteria, Viruses, Fungi, Parasites
159
Q

What are the most common bacteria that can cause pneumonia to develop?

A
  • Strep. pneumoniae - Gram +ve
  • Mycoplasma pneumoniae
  • Legionella pneumophilia - Gram -ve
  • Klebsiella pneumophilia - Gram -ve
160
Q

What are symptoms associated with pneumonia?

A
  • Fever
  • Malaise
  • Cough
  • Dyspnoea
  • Pleuritic chest pain
161
Q

What are the clinical signs associated with pneumonia?

A
  • Dull percussion due to consolidation
  • Reduced sounds
  • Coarse crackles
  • Tachycardic
  • Hypotensive
  • Confusion
  • Cyanotic
  • Bronchial breathing
162
Q

What investigations should be undertaken when pneumonia is suspected?

A
  • Sputum sample
  • ECG
  • FBC, U&E, Culture and sensitivity
  • CXR -> Visible consolidation
163
Q

What tool can be used to help assess symptoms on pneumonia?

A

CURB-65
- Confusion
- Urea > 7
- Resp. rate > 30
- BP < 90 sys. / < 60 dia.
- 65 or older

164
Q

What are the different levels of care suggested by the CURB-65 tool?

A

0-1 = Outpatient
2 = Inpatient
3 = ICU

165
Q

What are examples of viruses that can cause pneumonia?

A
  • Influenza A or B
  • Parainfluenza
  • Measles
  • Respiratory syncitial virus
  • Adenovirus
  • Cytomegalovirus
  • Herpes-simplex virus
  • Varicella-zoster virus
166
Q

What are examples of fungi that can cause pneumonia?

A
  • Aspergillus fumigates/flavus
  • Pneumocystis jirovecii
167
Q

What could be seen on a CXR of someone with a pneumonia?

A
  • Evidence of infiltration shown by white-out consolidation
168
Q

What results would be seen on a FBC of someone with pneumonia?

A
  • Increased WCC, CRP and ESR
  • Possible anaemia
  • Blood cultures
169
Q

What may been seen in a urine sample of someone with a pneumonia caused by legionella pneumophilia?

A
  • Legionella is a water-borne pneumonia
  • Therefore a urine sample may show legionella antigens
170
Q

Why may a pleural fluid aspiration be conducted when a pneumonia is suspected?

A
  • To assess for organisms
  • A transthoracic aspiration may be performed under CT guidance
  • Help to identify lesions, empyema and abscesses
171
Q

What is the typical first line treatment of a typical CAP in adults?

A
  • Local guidelines should be followed
  • Usually a broad-spectrum antibiotic with a macrolide
  • Examples include: Azithromycin, Clarithromycin, Co-amoxiclav, Flucloxicllin, Penicllin
172
Q

What are the different lung sounds that can be heard in a patient with a pneumonia?

A
  • Wheeze
  • Stridor
  • Coarse crackles
  • Fine crackles
  • Pleural rub
173
Q

What is the cause of a wheeze and what does it sound like?

A
  • A sign of localised narrowing in the bronchial tree
  • Prolonged musical sounds heard on expiration
  • Single wheeze suggests tumour
  • Multiphonic suggests multiple sites of consolidation
174
Q

What is the cause of stridor and what does it sound like?

A
  • A sign of a narrowing or obstruction in a large airway
  • A harsh, high-pitched sound
  • Occurs in both inspiration and expiration
  • More marked in inspiration
175
Q

What is the cause of coarse crackles and what do they sound like?

A
  • A sign of fluid/secretions in the large bronchi
  • Bubbling noise
  • Can usually be cleared/altered by coughing
176
Q

What is the cause of fine crackles and what do they sound like?

A
  • Early inspiratory: Chronic bronchitis, bronchiectasis
  • Late inspiratory: LVF, Fibrosis, Pneumonia
  • A inspiratory, high-pitched, explosive sound
  • Involves forceful popping open of small airways
177
Q

What is the cause of pleural rub and what does it sound like?

A
  • Caused by inflammed surfaces rubbing together
  • Produces a creaking sound
  • Usually heard in both inspiration and expiration
178
Q

What is tuberculosis?

A
  • Chronic, infectious disease caused by Myocbacterium tuberculosis (gram +ve bacillus)
  • One of the worlds most common and deadly infective diseases
179
Q

What are the three types of Mycobacterium that can infect humans?

A
  • M. tuberculosis - Most common
  • M. bovis - Bovine TB
  • M. africanum
180
Q

What are the different phases of TB?

A
  1. Latent TB
  2. Active TB
181
Q

What occurs during latent TB?

A
  • Individuals who were able to suppress initial infection
  • No active disease or infection
  • Approximately 1.7 billion people worldwide
  • Possible to reactivate
182
Q

What occurs during active TB?

A
  • Individuals who have progressive/symptomatic disease
  • Presents with specific symptoms
183
Q

What is the immune response triggered by TB?

A
  • Activates class II of major histocompatibility complex (MHC)
  • This activates CD4+ cell to release interferon gamma
  • These stimulate macrophages to secrete TNF-alpha (Tumour necrosis factor)
  • This necrotises groups of TB and forms small caseating granulomas
184
Q

What are some risk factors that increase the likelihood of contracting TB?

A
  • Having HIV (13% cases are co-morb)
  • Overcrowded living conditions
  • Ethnic minority groups
  • Malnutrition
  • IV drug use
  • Homelessness
  • Chronic lung disease
  • Immunosuppression
185
Q

What are the clinical features of TB?

A
  • Persistent cough (lasting three weeks or longer)
  • Hemoptysis (coughing up blood)
  • Chest pain
  • Fatigue and weakness
  • Weight loss
  • Fever
  • Night sweats
  • Loss of appetite
  • Enlarged lymph nodes
  • Weight loss
186
Q

What may be seen on a CXR of someone with TB?

A
  • Patchy nodual shadows in the upper zones
  • Cavitating lesions
  • Fibrous contractions
  • Air space consolidation
  • It may be difficult to differentiate between active or latent TB on a CXR alone
187
Q

What samples can be taken when there is a clinical suspicion of TB?

A
  • Sputum
  • Pus
  • Tissue biopsy
188
Q

How is tuberculin protein used to determine presence of latent TB?

A
  • Tuberculin protein is injected into dermis
  • Patient re-presents for assessment
  • Level of inflammatory response is measured at injection site
189
Q

What are meanings behind the different results possible in a tuberculin protein test?

A
  • Diameter of infection gives indication of likelihood of TB infection
190
Q

What does a >5mm induration in a tuberculin protein test show?

A
  • Positive result in patients who have HIV, immunosuppression or recent contact with a known TB case
191
Q

What does a >10mm induration in a tuberculin protein test show?

A
  • Positive result for those in high risk areas or moved from a high risk area or moved from a high risk area in the last 5 years
  • Also IV drug users, residential care and hospital patients
192
Q

What does a >15mm induration in a tuberculin protein test show?

A
  • Positive result in those with no underlying risk factors
193
Q

When and why can false postives occur in a tuberculin protein test?

A
  • False positives in the previously immunised
  • Certain conditions such a sarcoidosis and Hodgkin’s lymphoma
194
Q

What is the recommended treatment regimen for latent TB?

A
  • Single antibiotic for 3-6 months
195
Q

What drug regimen is used in active disease TB?

A

RIPE
R - Rifampicin
I - Isoniaizid
P - Pyrazinamide
E - Ethambutol

  • All 4 for two months
196
Q

What is the lymphatic system?

A
  • Network of tissues and organs that help to maintain fluid balance in the cells
  • Made up of lymphatic vessels and nodes, spleen, thymus, tonsils etc.
197
Q

What are the different functions of the lymphatic system?

A
  • Returns fluid from tissues to blood
  • Returns large molecules to the blood
  • Absorption and transport of fats
  • Hemopoiesis
  • Body defense and immunity
198
Q

What is the path of flow of lymph?

A

Intersititial -> Lymph -> Capillary -> Afferent vessels -> Nodes -> Efferent vessels -> Trunks -> Ducts -> Subclavian -> SVC

199
Q

How do lymph vessels ensure flow in only one direction?

A
  • They contain single direction valves
  • So even at low pressures, they are able to maintain a single direction

Year 2 Medicine @ Lancaster Uni (15 decks)

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