1
Q
How would you classify obstructive lung disease using spirometry?
A
FEV1/FVC ratio < 70%
2
Q
Describe how the severity of COPD is measured.
A
By % predicted FEV1 post bronchodilator
- Mild > 80%
- Moderate 50-80%
- Severe 30-50%
- Very severe <30%
3
Q
How would you distinguish between COPD and asthma using spirometry?
A
- Give salbutamol inhaler and spirometry readings taken before and after
- 15% and 400ml FEV1 reversibility suggests asthma
4
Q
Aside from reversibility seen in spirometry, how else would you investigate asthma?
A
- PEFR – look for diurnal variation, response to inhaled corticosteroid,
- Spirometry – before and after a trial of inhaled local corticosteroid
5
Q
How would restrictive lung disease present in spirometry?
A
- FEV1 and FVC reduced
- FEV1/FVC ratio > 70%
6
Q
List some causes of restrictive lung disease.
A
- Interstitial lung disease
- Kyphoscoliosis/chest wall deformity
- Previous pneumoectomy
- Neuromuscular disease
- Obesity
- Low effort/technique
7
Q
What methods are used to measure lung volume?
A
- helium dilation
- body plethysmography
8
Q
Describe the changes in lung volume seen in obstructive and restrictive disease.
A
obstructive: increased RV and RV/TLC ratio
restrictive: lung volume decreased
9
Q
Discuss the usage of transfer factor and what it is affected by.
A
- single breath of very small conc. of CO
- measure conc. in expired gas to derive uptake in lungs
- affected by: alveolar surface area, pulmonary capillary volume, Hb conc, V/Q mismatch
10
Q
In which conditions is transfer factor reduced?
A
- emphysema
- interstitial lung disease
- pulmonary vascular disease
- anaemia
11
Q
What must you be aware of when giving oxygen to patients with acute asthma, COPD or hypoventilation?
A
their O2 stats will now appear normal
12
Q
Name causes of hypoxaemia.
A
- hypoventilation e.g. drugs, neuromuscular disease
- ventilation/perfusion mismatch e.g. COPD, pneumonia
- shunt e.g. CHD
- low inspired oxygen e.g. altitude, flight
13
Q
What is a ‘shunt’?
A
extreme form of V/Q mismatch where blood bypasses the lungs altogether
14
Q
Describe how you would identify a V/Q mismatch.
A
- alveolar oxygen equation: PaO2 = FiO2 - (1.25 x PaCO2)
- measure pO2 of blood
- difference between calculated alveolar and arterial pO2
- > 4kPa suggests V/Q mismatch
15
Q
Describe the acid-base differences between acute respiratory acidosis and compensated acidosis.
A
- acute: increased pCO2, normal HCO3-, increased H+
- compensated: increased pCO2, increased HCO3-(renal compensation), normal H+
16
Q
Define COPD.
A
- characterised by airflow obstruction
- usually progressive, not fully reversible
17
Q
What are some causes of COPD?
A
smoking, environmental pollution, occupational dusts, alpha 1 anti-trypsin deficiency
18
Q
Describe the effects of cigarette smoking on the airways.
A
- cilia motility reduced
- airway inflammation
- mucus and goblet cell hypertrophy
- increased protease action and decreased anti-protease inhibition
- squamous hyperplasia -> risk increased of lung Ca
19
Q
Define emphysema.
A
abnormal permanent enlargement of airspaces distal to terminal bronchioles
20
Q
Define chronic bronchitis.
A
the production of sputum on most days for at least 3 months in at least 2 years - other causes of cough must be excluded
21
Q
Discuss the pathology of bronchitis.
A
- increased epithelial mucous cells
- squamous metaplasia
- mucus gland hyperplasia
- neutrophil and CD8+ lymphocyte infiltration
- loss of interstitial support
22
Q
Differentiate between bronchitis and bronchiolitis.
A
- bronchitis: larger airways >4mm diameter - inflammation leads to scarring and thickening of airways
- bronchiolitis: 2-3mm, early feature of COPD
23
Q
What are the cells and components that lead to the inflammation seen in bronchitis?
A
- macrophages, CD8 and CD4 T lymphocytes, neutrophils
- TNF, IL8, neutrophil elastase, proteinase 3, elastase, MMP, ROS
- chemoattractant substances in cigarette smoke
24
Q
Describe the mechanisms that lead to airway obstruction.
A
- loss of elasticity and alveolar attachments due to emphysema: airways collapse on expiration, airtrapping and hyperinflation, increased work of breathing, breathlessness
- goblet cell metaplasia with mucus plugging of lumen
- inflammation of airway wall
- thickening of bronchiolar wall: smooth muscle hypertrophy and peribronchial fibrosis
25
How is COPD diagnosed?
```
CLINICAL PRESENTATION
Consider COPD diagnosis for people who are over 35 and smokers/ex-smokers with any of:
- exertional breathlessness
- chronic cough
- regular sputum production
- frequent winter 'bronchitis'
- wheeze
```
SPIROMETRY
- obstructive pattern: FEV1/FVC ratio <70%
26
Briefly describe the treatment of COPD.
1. Inhaled bronchodilators
- SABA: salbutamol - SAMA: ipatropium bromide
- LABA: salmeterol - LAMA: tiotropium
2. Inhaled corticosteroids
- beclomethasone
- oxygen therapy
3. Oral theophyllines
4. Mucolytics - carbocysteine
5. Nebulised therapy
27
What is the mechanism of action of beta-adrenergic bronchodilators?
Relaxes bronchial smooth muscle, inducing bronchodilation. Inhibit pro-inflammatory cytokine release from mast cells and TNF-α release from monocytes, reducing airway inflammation. Increase mucus clearance from the airways by stimulating cilia action.
28
Describe the mechanism of action of beclomethasone.
Anti-inflammatory effect on the airways.
Decrease formation of pro-inflammatory cytokines.
Up-regulates beta-2-adrenoreceptors in airways.
29
Discuss respiratory failure in COPD in regards to pink puffers and blue bloaters.
PINK PUFFERS
- high respiratory drive
- type 1 RF: PaO2 down, PaCO2 down
- pursed lip breathing
- using accessory muscles
- wheeze
- indrawing of intercostals
- tachypnoea
BLUE BLOATERS
- low respiratory drive
- type 2 RF: PaO2 down, PaCO2 up
- cyanosis
- warm peripheries
- bounding pulse
- flapping tremor (CO2 retention)
- confusion, drowsiness
- right heart failure
- oedema, raised JVP
30
Describe the differences between asthma and COPD.
Inflammation agents:
- asthma: CD4+ T lymphocytes, eosinophils, lymphocytes
- COPD: CD8+ T lymphocytes, macrophages, neutrophils
Asthma has a sensitising agents whereas COPD has a noxious agent.
Asthma is reversible whereas COPD is not.
COPD is seen nearly always in smokers/ex-smokers whereas it is less common in asthma.
Asthma symptoms <35 y/o.
Chronic productive cough in COPD.
Persistent and progressive SOB in COPD, whereas variable in asthma.
Diurnal or day-to-day variation of symptoms in asthma, whereas COPD has less variation
31
What is cor pulmonale?
a clinical syndrome of RHF secondary to lung disease and salt and water retention leading to peripheral oedema
32
What are the 4 signs of cor pulmonale?
1. Peripheral oedema
2. Raised JVP
3. Systolic parasternal heave
4. Loud pulmonary second heart sound
33
How is cor pulmonale treated?
diuretics to control oedema
34
What metabolic disturbances are seen in compensated metabolic acidosis?
increased H+, decreased HCO3-, decreased pCO2
35
Which acid/base disorder causes decreased H+, increased HCO3- and increased pCO2?
compensated metabolic alkalosis
36
Describe the metabolic disturbances seen in compensated respiratory alkalosis.
decreased H+, decreased pCO2, decreased HCO3-
37
What are the normal ranges in the blood for:
1. H+
2. pH
3. pCO2
4. pO2
1. 36-43 nmol/L
2. 7.35-7.45
3. 4.6-6.0 kPa
4. 10.5-13.5 kPa
38
How is anion gap measured? What is the normal range?
[Na+] - ([Cl-] + [HCO3-])
| Normal = 8-16 nmol/L
39
What is the clinical use of anion gap? Describe the importance of results of raised and normal anion gap.
Clinical use is in DDx of metabolic acidosis.
Raised = renal failure, DKA, lactic acidosis, toxins
Normal = renal tubular acidosis, diarrhoea, carbonic anhydrase inhibitors, ureteric diversion
40
When is non-invasive ventilation used in COPD?
- COPD exacerbation with persistent hypercapnic RF
| - respiratory acidosis or if acidosis persists despite maximal medical therapy
41
Describe the benefits of non-invasive ventilation in COPD.
- reduces resp. rate
- improves dyspnoea and gas exchange
- lowers mortality
- reduces need for ventilation
- reduces length of hospital stay
42
Define allergy.
- immune system mediated intolerance
| - must have a trigger e.g. cats, birds
43
Define asthma. List some triggers.
reversible airflow obstruction involving airway inflammation
| triggers - cold air, exercise, cats, night time
44
What are the clinical features of asthma?
cough, wheeze, hyperreactivity, hypersensitivity, breathlessness, exercise intolerance
45
Describe the pathological and physiological changes that occur in asthmatic patients.
```
pathological = inflammation, scabby epithelium, thickened BM, thickened SM, mast cells releasing histamine in SM
physiological = yellow mucus, repair pathways, non-elastic airways, hyperresponsiveness, hypersensitivity
```
46
Discuss the pathophysiology of asthma.
Airway allergy drives eosinophilic inflammation
- activation of IL-5, TSLP, IL-13 - activate mast cells, lymphocytes, macrophages
Cytokines drive allergic airways inflammation/remodelling:
- TNFa, TGFb, VEGF, IL-13
- angiogenesis, epithelial cell damage, fibrosis, smooth muscle hypertrophy
- becomes less sensitive to asthma treatment over time
47
What drug treatments are available in asthma?
```
bronchodilators
corticosteroids
anti-leukotriene receptor drugs
anti-IgE biologic therapies
anti-IL-5 therapy
```
48
What is the other name for extrinsic allergic alveolitis?
hypersensitivity pneumonitis
49
List some types of EAA.
bird fancier's lung, mushroom worker's lung, farmer's lung, malt worker's lung, cheese washer's lung, humidifier lung
50
Describe the clinical features of acute EAA.
onset within 4-6 hours of exposure, wheeze, cough, fever, chills, headache, myalgia, malaise, fatigue, may last several days
51
What changes are seen in the lungs in acute EAA?
- thickening of septae
- filling of alveolus with fluid (consolidation)
- zonal distribution
- fine reticulation
52
How is EAA identified?
each type of EAA has a specific antibody that can be measured in serum e.g. avian precipitans (bird fancier's lung) which leads to immune complex formation, chronic cell death and inflammation
53
What changes are seen in the lungs with chronic exposure EAA?
FIBROSIS - interstitial scarring from chronic tissue remodelling
EMPHYSEMA - interstitial destruction from neutrophilic enzyme release
- bronchiocentric pattern
- foamy macrophages in alveolar spaces
- NNGI
54
Describe the consequences of chronic exposure EAA.
- reduced O2 transport into blood - measure by CO gas transfer during full PFTs
- dispace shadowing on CXR
55
How would you manage EAA?
- avoid allergy triggers
- corticosteroids
- oxygen supplementation
56
What is obstructive sleep apnoea?
recurrent episodes of partial or complete upper airway obstruction during sleep, intermittent hypoxia and sleep fragmentation
57
Describe the mechanism by which obstructive sleep apnoea manifests and its consequences.
- pharyngeal narrowing - airway collapses, stopping air from traveling to and from the lungs
- negative thoracic pressure
- arousal
- sleep disruption = sleepiness, decreased quality of life, RTAs
- blood pressure surge = MI, stroke
58
What are the symptoms of OSA?
- snoring
- witnessed apnoeas
- disrupted sleep: nocturia/choking/dry mouth/sweating
- unrefreshed sleep
- daytime somnolence
- fatigue/low mood/poor concentration
59
What investigations are carried out in OSA?
- limited polysomnography
- full polysomnography
- TOSCA (transcutaneous oxygen saturations and carbon dioxide assessment)
60
Describe the differences between
1. apnoea
2. hypopnoea
3. respiratory effort related arousals.
1. cessation or near-cessation of airflow, 4% oxygen desaturation lasting >10s
2. reduction in airflow to a degree insufficient to meet criteria for an apnoea
3. arousals associated with a change in airflow that does not meet above criteria
61
What is AHI? And how is it used to diagnose OSA?
number of apnoea's + hypopnoea's, divided by total sleep time (in hours)
normal < 5
OSA > 15
62
What are the consequences if OSA is left untreated?
- hypertension
- right heart strain
- poor concentration
- 4x more likely to have RTA
63
How is OSA treated?
treat the symptomatic i.e. OSAS (manifests in daytime sleepiness)
- weight loss, avoid triggers, treat underlying conditions
- continuous positive airways pressure
- mandibular advancement device
- sleep position trainers
64
What is a pneumothorax?
air within the pleural cavity - any breach of pleural space leads to collapse of the elastic lung
65
What are the symptoms and signs of a pneumothorax?
- pleuritic chest pain
- breathlessness
- respiratory distress
- reduced air entry on affected side
- decreased vocal resonance
- tracheal deviation if tension
66
List the DDx of pneumothorax.
pneumonia, PTE, MSK pain
67
How does a tension pneumothorax develop?
- 'one way valve' leads to increased intrapleural pressure
- venous return impaired and so CO and BP fall
- PEA arrest without intervention
68
What is the immediate management of a tension pneumothorax?
insert venflon 2nd IC space midclavicular line to relieve pressure
69
What are the different types of pneumothorax?
1. traumatic e.g. stabbing, fractured rib
2. iatrogenic e.g. CT guided lung biopsy
3. spontaneous
- primary - no underlying disease
- secondary - underlying lung disease
70
Describe the pathophysiology of primary pneumothorax.
- development of subpleural bullae at lung apex
- microscopic emphysema below surface of visceral pleura
- spontaneous rupture leads to tear in visceral pleura
- air flows from airways into pleural space
- elastic lung collapses
71
By what mechanisms can secondary pneumothorax develop?
- inherent weakness in lung tissue e.g. emphysema
- increased airway pressure e.g. asthma
- increased lung elasticity e.g PF
72
Aside from venflon insertion what other methods of management for pneumothorax are there?
- intercostal drain with underwater seal
- video assisted thoracic surgery if not resolved in 5 days
- talc pleurodesis
- pleural abrasion
- surgical pleurodesis
73
Discuss the aetiology of lung cancer.
SMOKING, passive smoking, ionising radiation, pollution, asbestos, fibrosis, HPV, genetics
74
What are the signs and symptoms of lung cancer?
cough, haemoptysis, SOB, chest pain, weight loss, malaise
75
Where might a lung cancer spread and how would it manifest?
LOCAL
- pleura = haemorrhagic effusion
- hilar lymph nodes
- adjacent lung tissue = large blood vessel, haemoptysis
- pericardium = effusion
- mediastinum = SVC obstruction (oedema of face and arms, raised JVP, dilated veins on chest wall), recurrent laryngeal n, phrenic n
- pancoast tumour = brachial plexus, Horner's syndrome
DISTANT
- haematogenous = liver, bone, brain, adrenal
- lymphatic = cervical
76
Discuss some of the non-metastatic effects of lung cancer.
- ACTH secretion - adrenal hyperplasia, increased cortisol, Cushing's
- ADH secretion - water retention, dilutional hyponatraemia (SIADH)
77
Describe the histological appearance of a small cell carcinoma.
- oval to spindle shaped cells
- inconspicuous nucleoli
- scant cytoplasm
- nuclear moulding
- apoptotic bodies
78
Which is the most aggressive form of lung cancer?
small cell carcinoma - metastasises early and widely
79
Describe the appearance of non-small cell squamous carcinoma.
- malignant epithelial tumour showing keratinisation and/or intracellular bodies
- tend to arise centrally from major bronchi
80
Which type of NSCLC produces mucin and appears glandular, solid, papillary or lepidic?
adenocarcinoma
81
What is a carcinoid tumour?
tumour of neuroendocrine cells
82
Describe a large cell lung carcinoma.
undifferentiated malignant epithelial tumour that lacks cytological features of SCLC and glandular or squamous differentiation
83
What is a mesothelioma and what is its most common cause?
primary pleural tumour due to asbestos exposure
84
Where do metastases to the lungs commonly arise?
breast, colorectal, kidneys, head and neck, testicular, bones, sarcoma, melanoma, thyroid
85
Discuss the target therapies for lung cancer.
1. Epidermal growth factor receptor e.g. cetuximab and erlotinib
2. ALK-EML4 fusion gene e.g. crizotinib
3. PDL1 e.g. nivolumab
86
What is sarcoidosis?
multisystem inflammatory disease of unknown aetiology that predominantly affects lungs and intrathoracic lymph nodes - NON-NECROTISING GRANULOMATOUS INFLAMMATION
87
Describe the clinical presentation of sarcoidosis.
5%: asymptomatic
45%: systemic e.g. fever, anorexia, fatigue, night sweats
50%: dyspnoea on exertion, cough, chest pain, haemoptysis, wheeze
88
What are the 4 classes of sarcoidosis seen in CXR?
1. bilateral hilar lymphadenopathy without infiltration
2. bilateral hilar lymphadenopathy with infiltration
3. infiltration alone
4. fibrotic bands, bullae, hilar retraction, bronchietasis, diaphragmatic tenting
89
What is idiopathic pulmonary fibrosis?
the clinical manifestation of the pathological diagnosis of usual interstitial pneumonia
90
What are the signs and symptoms of IPF?
- progressive breathlessness
- bibasilar crackles and clubbing
- hacking dry cough
- appetite and weight loss
- fatigue and weakness
- subpleural honeycombing
91
List 6 causes of PF with an example of each.
1. occupation/environmental e.g. asbestos, HSP
2. drug induced e.g. amiodarone
3. connective tissue disease e.g. lupus
4. primary diseases e.g. sarcoidosis
5. idiopathic (25%)
6. genetics
92
How is pulmonary fibrosis diagnosed?
high resolution CT
93
Discuss the pathophysiology of pulmonary fibrosis.
- cause e.g. genetics, idiopathic, environment
- repetitive alveolar epithelial injury
- altered alveolar microenvironment
- dysregulated repair
- loss of epithelial cells
- accumulation of mesenchymal cells
- fibrosis
94
Miconazole, ketaconazole and clotrimazole are examples of what type of drug? And how do they work?
- azoles - antifungals
- inhibitors of 14-methylsterol a-demethylase which produces ergosterol which is an essential part of the fungal plasma membrane
95
Describe the mechanism of action of amphotericin B.
- exploits presence of ergosterol
| - forms a pore in fungal membranes -> leakage of intracellular cations
96
Which fungal pathogen is commonly associated with meningitis and secondary infection with HIV?
cryptococcus neoformans
97
Aspergillus fumigatus is a type of fungus. Which disease does it cause associated with asthma and CF? And how is it treated?
allergic bronchopulmonary aspergillosis
| prednisolone
98
What 3 diseases does aspergillus fumigatus cause?
allergic bronchopulmonary aspergillosis
invasive pulmonary aspergillosis
aspergilloma
99
Define aspergilloma. How is it managed?
a fungal ball that develops in an area of past lung disease or lung scarring e.g. TB
no treatment unless bleeding occurs then surgery
100
Describe the management of asthma exacerbation.
- high flow oxygen
- nebulised bronchodilators
- oral prednisolone
- oral doxycycline
- IV magnesium
- discussion with ITU
- consider IV aminophylline infusion
101
What are the side effects associated with B2 agonists?
tremor, low K+, high glucose, flushing, increased HR, arrhythmias
102
Describe the mechanism of action of antimuscarinics.
inhibits cholinergic M1 and M3 receptors
| inhibits parasympathetic mediated bronchoconstriction
103
List the side effects of antimuscarinics.
blurry vision, dry mouth, urinary retention, nausea, constipation
104
How does aminophylline work?
- non-selective inhibition of phosphodiesterase
- increased intracellular cAMP
- bronchial SM relaxation
- increased mucus clearance
- anti-inflammatory effect
105
Describe how corticosteroids work in lung disease.
bind to activated glucocorticoid receptors to suppress multiple pro-inflammatory genes at are activated in asthmatic airways by reversing histone acetylation
106
Which drug is useful for prophylaxis of exercise-induced asthma? How does it work?
leukotriene receptor antagonists
- bind to CysLT1 inhibiting action of LTD4 in SM cells of airway macrophages
- decreased airway oedema and smooth muscle contraction
107
What are the two biologic therapies currently available in asthma?
1. Omalizumab: anti-IgE antibody for severe persistent allergic asthma
2. Mepolizumab: anti-IL5 antibody for severe refractory eosinophilic asthma
108
Which drug is used additionally in COPD to decrease viscosity of mucus and therefore decreased exacerbations?
carbocysteine
109
What is a pleural effusion?
accumulation of abnormal volume of fluid in the pleural space > 15ml
110
How is a pleural effusion seen on CXR?
blunting of costophrenic margin
111
List the clinical signs of pleural effusion.
- decreased chest expansion
- decreased tactile vocal fremitus
- stony dull percussion
- quiet breath sounds
112
Discuss the mechanisms by which pleural effusions develop.
- imbalance between pleural fluid production and absorption
- increased hydrostatic pressure (CCF)
- decreased osmotic pressure (hypoalbuminaemia)
- increased vascular permeability (pneumonia)
113
What is the immediate management if the effusion is seen to be bilateral?
treat the cause (usually obvious), no need to sample initially
114
Heart failure causes right or left pleural effusions?
right
115
How would you investigate a unilateral pleural effusion?
- always consider pleural infections: sepsis? empyema? needs sampling and drainage
- if not sepsis: contrast CT chest/abdo/pelvis, consider breast/gynae malignancy, asbestos, TB?
116
Differentiate between transudate and exudate pleural effusions.
- protein > 30g/l in exudate (transudate normal)
- pleural/serum lactate dehydrogenase ratio >0.6 in exudate = Light's criteria (transudate normal)
- transudate bilateral, exudate unilateral
- transudate clear, exudate clear, cloudy or bloodstained
117
What are the common causes of transudate and exudate pleural effusions?
- transudate: cardiac failure, cirrhosis, nephrotic syndrome, hypoalbuminaemia
- exudate: bacterial pneumonia, malignancy, mesothelioma, TB
118
Describe the management of pleural malignancy effusions.
drain to dryness once and discharge
medical pleurodesis
thoracoscopic pleurodesis
indwelling pleural catheter
119
What test results would show the presence of a complex parapneunomic effusion?
pH < 7.2, LDH > 1000, glucose < 2.2, located on US
120
What is the management plan of an empyema?
small bore chest drain, sterile saline flushes, IV antibiotics, DVT prophylaxis, fibrinolytics
Phase 3
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