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Summary Respiratory medicine
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A detailed overview of key conditions in respiratory medicine that you need to know for Medical School final exams.
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Table of ContentsEnvironmental lung disease......................................................................................................................1
Asbestos-related disease.......................................................................................................................................1
Silicosis..................................................................................................................................................................2
Coal worker’s pneumoconiosis..............................................................................................................................2
COPD........................................................................................................................................................3
Pulmonary aspergillus infections...............................................................................................................5
Asthma.....................................................................................................................................................6
Cystic Fibrosis............................................................................................................................................9
Acute respiratory distress syndrome.......................................................................................................10
Respiratory failure..................................................................................................................................11
Pneumonia..............................................................................................................................................12
Lung cancer.............................................................................................................................................15
Bronchiectasis.........................................................................................................................................17
Lung abscess...........................................................................................................................................18
Pulmonary thromboembolism.................................................................................................................19
Interstitial lung disease...........................................................................................................................20
Cor pulmonale.........................................................................................................................................22
Pleural and mediastinal diseases.............................................................................................................22
Pleural effusion....................................................................................................................................................23
Empyema.............................................................................................................................................................24
Pneumothorax.....................................................................................................................................................24
Disorders of ventilation...........................................................................................................................26
Obstructive sleep apnoea....................................................................................................................................26
Hypoventilation...................................................................................................................................................27
Hyperventilation..................................................................................................................................................27
Pulmonary hypertension.........................................................................................................................28
Sarcoidosis..............................................................................................................................................29
Pulmonary oedema.................................................................................................................................31
Smoking cessation...................................................................................................................................31
Environmental lung disease
Asbestos-related disease
Asbestos = long, thin fibrous silicate crystals inflammation and scarring of tissue.
Common occupational exposure = mining, manufacturing, pipefitting, boiler making,
manufacturing safety garments and friction materials (e.g. for cars).
,Pleural plaques indicate asbestos exposure has occurred – typically asymptomatic. Cause mild restrictive ventilatory
defect, parietal pleural thickening and calcification may show on x-ray. Exposure only needs to be light, can occur after 10+
years but most after 20-30 years of long-term light exposure.
Interstitial lung disease (asbestosis) – typically accompanied by severe restrictive ventilative defect, with diffusing
capacity of the lung for carbon monoxide (DLCO – extent to which oxygen passed from air sacs to blood) on pulmonary
function testing. Usually develops 10 years after exposure, no specific Tx available.
Occurs when exposure was heavy. X-ray shows small irregular opaque areas,
usually in lower lobes of lungs, or if severe may have honeycomb appearance.
Benign pleural effusions can also occur from asbestos exposure, in first two
decades following exposure.
risk of lung cancer following exposure, does not typically present for 15 years
after initial exposure. If patient Is a smoker too, risk further. Mesotheliomas
(both pleural and peritoneal) are strongly associated with asbestos exposure, and
not related to smoking. Pleural tissue biopsy (thoracoscopic) is required for
diagnosis. Exposure only needs to be light. Most common presentation is a pleural
effusion, typically with persistent chest wall pain.
Silicosis
Results from exposure to free silica (crystalline quartz) which occurs in mining, stone cutting, abrasive industries (stone,
clay, glass manufacturing), quarrying. Heavy exposures over relatively brief time periods (as little as 10 months) can cause
acute silicosis – shows on CT as “crazy paving”. Acute silicosis can be severe and progressive.
Longer-term exposures simple silicosis, with small rounded opacities in upper lobes of lungs. Calcification of hilar
lymph nodes can give characteristic “eggshell” appearance. Progressive nodular fibrosis masses >1cm in diameter in
complicated silicosis. When masses become very large, the term “progressive massive fibrosis” describes the condition.
Patients at risk of TB, atypical mycobacterial infections and fungal infections due to impaired cell-mediated immunity.
Silica may be a lung carcinogen.
Coal worker’s pneumoconiosis
Occupational exposure to coal dust predisposes to coal worker’s pneumoconiosis
(CWP). Diagnosis is 15-20 years after initial exposure.
Pathophysiology = dust is inhaled and reaches the terminal bronchioles. There it is
engulfed by alveolar and interstitial macrophages. The dust particles are then moved
by the macrophages via the mucociliary elevator and removed from the body as
mucus. In time, the system is overwhelmed and macrophaged begin to accumulate in
the alveoli immune response which damages lung tissue.
,Radiologically – small nodular opacities commonly in upper lobes, not typically symptomatic. risk of COPD.
Development of larger nodules (>1cm), usually in upper lobes (progressive massive fibrosis) = complicated CWP.
Complicated CWP is often symptomatic, associated with pulmonary function and mortality. Complicated sx =
exertional dyspnoea, cough, may be black sputum.
Spirometry = restrictive defect (FVC, FEV1 is reduced a bit – as FVC more than FEV1, the FEV1/FVC ration = >80%)
COPD
Chronic obstructive pulmonary disease is characterised by non-reversible airway obstruction and persistent respiratory
symptoms. It is an umbrella term encompassing both chronic bronchitis and emphysema.
RFs = smoking, age, alpha-1 antitrypsin deficiency, prematurity/ low birth weight, occupational exposure (dust, fumes,
chemicals, cadmium used in smelting), recurrent childhood resp infections, air pollution.
Pathophysiology =
Emphysema – destruction of terminal bronchioles and distal air spaces enlargement of air spaces distal to
terminal bronchioles loss of alveolar SA and gas exchange
o Lung hyperinflation as elastin destruction compliance
o Small airway narrowing due to loss of elastic fibres exerting radial traction (outward pull)
o Irreversible enlargement of air sacs bullae - SA for gas exchange
Chronic bronchitis – chronic inflammation of large airways chronic mucus hypersecretion due to goblet cell
proliferation. Defined clinically by a cough (productive of sputum) on most days for 3 months in each of 2
successive years
o goblet cell number
o Enlargement of mucus secreting glands
o Ciliary dysfunction
Presentation = Cough (productive of sputum), dyspnoea (exertional), wheeze. In severe cases, right-sided HF may develop
peripheral oedema. May present with an acute exacerbation - SOB, cough, sputum. Weight in severe COPD.
Pursed lip breathing ( pressure in airways, breathing this way stops/ delays airway closure), barrel chest
(increased anteroposterior diameter)/ hyperinflation of lungs (cricosternal distance), RR, use of accessory
muscles (SCM, pec major + minor, serratus anterior, lat dorsi), cyanosis
hyper-resonant percussion note (air trapping), air entry, wheeze, may hear coarse crackles (mucus and sputum
in airways)
Pink puffers in emphysema - alveolar ventilation breathless but not cyanosed. Normal PaO2. Normal or low
PaCO2. Can type 1 respiratory failure.
Blue bloaters in chronic bronchitis - alveolar ventilation cyanosed but not breathless. PaO2 and PaCO2. Can
type 2 respiratory failure.
Classing disease severity:
MRC (medical research council) dyspnoea score:
, By FEV1
Investigations: (diagnosis on clinical presentation + spirometry)
Consider diagnosis in patients >35 yrs who are smokers/ ex-smokers, and have Sx e.g. exertional breathlessness,
chronic cough or regular sputum production.
Bloods – may show polycythaemia, WCC in infective exacerbation
o Polycythaemia as in EPO due to not enough O2 reaching tissues (chronic hypoxia). EPO increases blood
cells production.
Spirometry – obstructive picture. FEV1:FVC = <70%. Also do post-bronchodilator spirometry - limited reversibility
following treatment with bronchodilators.
o FEV1 is the forced expiratory volume in 1 second. Forced vital capacity is the
overall lung capacity
CXR – hyperinflation (>6 ribs anteriorly), prominent pulmonary arteries, bullae.
o Also important to exclude lung cancer
Sputum culture in infective exacerbation
BMI – baseline so can later assess weight loss (due to severe COPD) or gain (due to
steroid use)
ABG if sats <92%. May show pO2 and hypercapnia (type 2 resp failure)
Transfer factor for CO (TLCO) – this is in COPD. It can give an indication about the
severity of the disease.
Management:
General Mx
o Smoking cessation – may need to offer nicotine replacement
therapy
o Annual flu vaccine
o One off pneumococcal vaccine
o Pulmonary rehabilitation – break the cycle of deconditioning
(feeling SOB stopping activities that make you feel SOB
muscles weaken get even more SOB so avoid activities even
more), encourages exercise. 6-12-week program. MRC grade 3+.
o Review 1-2 yearly
MDT management – GPs, specialist nurses, physiotherapists, pharmacists, OH, dieticians
Bronchodilator therapy (can be given via nebuliser if severe)
o 1st line = short-acting beta 2 agonist (SABA) e.g. salbutamol or short-acting muscarinic antagonist (SAMA
– prevent SM contraction) e.g. ipratropium bromide for symptom relief PRN
SABA SEs = tachycardia, palpitations, tremor, K+
SAMA SEs = dry mouth, urinary retention, glaucoma, cough, constipation, sore throat
o 2nd line if no asthmatic features/steroid responsiveness = long-acting beta 2 agonist (LABA) + long-acting
muscarinic antagonist (LAMA) (can be given in combination inhalers e.g. Anoro Ellipta
o 2nd line if asthmatic or steroid responsive features = LABA + ICS (given in combination e.g. Fostair,
Symbicort).
3rd line if asthmatic or steroid responsive features = LABA + LAMA + ICS (trimbo)
Mucolytics – carbocysteine (breaks up mucus). Consider if chronic productive cough
Oral theophylline (methylxanthine – causes bronchodilatation, resp drive + anti-inflammatory) – only after trials
of SABAs and LABAs, or in people who can’t use inhaled therapy.
Oral prophylactic Abx with azithromycin. Given in patients who don’t smoke, who have optimised standard
treatments but still have exacerbations.
Long term O2 therapy
o Assess patients for LTOT if any of the following:
FEV1 <30%.
Cyanosis
Polycythaemia
Peripheral oedema (sign of right-sided HF secondary to pulmonary HTN), JVP
O2 sats <92% RA/ pO2 consistently <7.3 kPa (<8 if cor pulmonale)
o Do not offer LTOT who continue to smoke, or to patients that retain high CO2 levels.
o Aim for PaO2 >8 for >15 hours/day (survival 50%)
**Smoking cessation and LTOT increase survival**
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