3 - Respiratory · 2021. 3. 6. · RESPIRATORY – ASTHMA DARWIN’S NOTEBOOK 2 • Intrinsic asthma: o Non-immune mechanisms o Occurs in middle-aged individuals, with no causative

CLINICAL PHASE

RESPIRATORY

DARWIN’S NOTEBOOK

TABLE OF CONTENTS

ASTHMA 1

CHRONIC OBSTRUCTIVE PULMONARY DISEASE 5

BRONCHIECTASIS 10

CYSTIC FIBROSIS 12

TUBERCULOSIS 18

PNEUMOTHORAX 22

LUNG CANCER 24

PLEURAL EFFUSION 27

INTERSTITIAL LUNG DISEASE 29

EXTRINSIC ALLERGIC ALVEOLITIS 31

OCCUPATIONAL LUNG DISEASE 32

OBSTRUCTIVE SLEEP APNOEA 34

RESPIRATORY FAILURE 36

MISCELLANEOUS RESPIRATORY MEDICINE 39

RESPIRATORY – ASTHMA

DARWIN’S NOTEBOOK 1

Be able to understand and interpret the basic metrics of pulmonary function testing

• Spirometry measures the volume & speed flow of air during exhalation and inhalation

• Key metrics include:

o FEV1 ® forced expiratory volume ® volume that has been exhaled at the end of the first

second of forced expiration

o FVC ® forced vital capacity ® volume that has been exhaled after a maximal expiration

following a full inspiration

o KCO ® diffusion capacity of the lung per unit area for CO

o TLCO ® diffusion capacity of the total lung capacity for CO

• Obstructive pattern ® normal (or increased) FVC, reduced FEV1:FVC

• Restrictive pattern ® reduced FVC, normal (or increased) FEV1:FVC

• Decreased TLCO / KCO ® indicate an issue with gas exchange, which can be due to either alveolar

disease or vascular disease ® this rules out chest wall / diaphragm pathology

Define classical features of asthma including episodic wheeze, cough and reversibility

• Asthma is a chronic inflammatory condition of the airways ® characterised by airway hypersensitivity to

a number of factors

• It affects ~10% of children, and 5% of adults

• Symptoms are variable but recurring: o Reversible bronchospasm resulting in airway obstruction:

§ Wheezing & shortness of breath § Classically worse during the night or upon exercise

§ Peak flow worst in the morning ® ‘morning dipping’

§ Subjective feeling of chest ‘tightness’

o Cough ® again classically nocturnal

• On examination ® there will be a widespread expiratory wheeze

• Pulmonary function testing reveals a decreased FEV1 relieved by b2 agonists

• Many children will ‘grow out’ of their asthma

Outline common precipitants of an asthma attack

• Common precipitants:

o Environmental allergens ® pet, grass pollen, dust mites

o Viral infections

o Cold air

o Emotion

o Drugs ® NSAIDs (particularly aspirin), b-blockers

o Atmospheric pollution

o Occupational pollutants ® e.g. flour or chemicals

§ Makes up 10–15% of adult asthma

§ Diagnosed using peak flows before / after work, and at the weekends

Classify asthma into early and late onset and discuss the likely presenting characteristics of

each

• Late onset asthma is much more likely to be intrinsic ® occurring in non-atopic individuals



• Intrinsic asthma: o Non-immune mechanisms

o Occurs in middle-aged individuals, with no causative agent identified

o Generally more severe ® associated with quicker deteriorations in lung function

• Extrinsic asthma: o Type I hypersensitivity reaction o Most frequently occurs in atopic individuals who show positive skin prick tests to common

allergens ® implying a definite extrinsic cause

Describe the morphology and pathological consequences of asthma

• Asthma is an inflammatory condition with both acute & chronic elements

• Acute asthma: o Acute episodes of bronchospasm that are triggered by recognised triggers

o These triggers activate mast cells, which lead to two phases:

§ An early phase of bronchospasm ® due to spasmogen production (histamine,

prostaglandin D2, and leukotrienes)

• Smooth muscle contraction narrows the airway

§ A late phase ® due to chemotaxins attracting eosinophils and mononuclear cells

• Cellular infiltrates & mucosal oedema narrow the airway

• There will also be airway hyper-reactivity in the late phase ® this can lead to

further acute deteriorations

• Chronic asthma: o Many asthmatics will have normal respiratory function between attacks ® but some will

develop persistent airway obstruction that can become indistinguishable from COPD

§ NB: This is more common in intrinsic asthma

o There is bronchoconstriction due to increased responsiveness of bronchial smooth muscle, and hypersecretion of mucus that plugs the airways

o Mucosal oedema further narrows the airways

o The sputum will contain Charcot-Leyden crystals (from eosinophil granules) and Curschman spirals (mucus plugs from small airways)

o In long-standing disease ® this can lead to pulmonary hypertension

Describe the clinical features of an acute asthma attack, including blood gas abnormalities

associated with severe asthma and other clinical indices of severity

• Features of acute severe asthma: o RR >25

o HR >110 o PF 33–50% of best (or predicted best)

o Can’t complete sentences in one breath

• They may halve pulsus paradoxus (abnormally large decrease in SBP during inspiration), and there

will be a bilateral widespread expiratory wheeze in a hyperinflated chest ® accessory muscles of

respiration are often used



• Features of life-threatening asthma: o PEF <33% of best

o SpO2 <92%

o Silent chest, cyanosis or feeble respiratory effort o Bradycardia, hypotension or dysrhythmia

o Exhaustion or confusion

• If a patient has ANY life-threatening feature ® an arterial blood gas is the only immediate investigation

required

• Certain ABG features are markers of a life-threatening attack:

o Normal PaCO2 ® should normally be low due to hyperventilation

o Severe hypoxia ® <8

o Low pH

§ NB: Raised PaCO2 indicates near fatal asthma

Outline the management of acute asthma attack • Initial management:

o Oxygen 15L/min ® via a non-rebreather

o Salbutamol 5mg (or terbutaline 10mg) ® via an oxygen-driven nebuliser

o Ipratropium bromide 0.5mg ® via an oxygen driven nebuliser

o Oral prednisolone 50mg or IV hydrocortisone 100mg

o No sedatives of any kind

o CXR only if suspecting pneumothorax / consolidation ® or if the patient is likely to require

IPPV o If any life-threatening features are present:

§ Discuss with ICU team

§ Add IV magnesium sulphate 2g IVI over 20 minutes ® bronchodilator

§ Give nebulised salbutamol 5mg every 15–30 minutes § Senior clinicians may then consider use of IV aminophylline or IPPV

• If the patient is stable and improving ® continue prednisolone dose for at least 5 days, and the

nebulised salbutamol / ipratropium 4-hourly until discharge

• Chart PEF before and after salbutamol nebulisers ® and at least 4 times daily whilst in hospital

• Prior to discharge ® check inhaler technique, agree on a written asthma action plan, and ensure GP

follow-up within 2 working days

Outline a stepped management approach of asthma

• Aims: o No daytime symptoms

o No night-time waking

o No need for rescue medication o No limitations on activity

• The BTS 2016 guideline moves away from the pure ‘stepwise’ approach:

1) Short-acting b2 agonist ® e.g. salbutamol or terbutaline

a. For all in whom asthma is suspected



2) Add inhaled low-dose corticosteroids ® e.g. beclametasone, budenoside or fluticasone (200–

800 mcg)

a. For all patients with confirmed asthma

3) Add long-acting b2 agonist (e.g. salmeterol) ® often combined with an inhaled steroid, e.g.

simbacort, seretide, fostair a. If no response from LABA ® stop it, and increase inhaled corticosteroid to a medium dose

b. If some benefit, but more control required ® continue LABA and increase inhaled

corticosteroid to a medium dose c. Consider also adding leukotriene receptor antagonist (e.g. montelukast),

theophylline, or long-acting muscarinic antagonist for extra control

4) Increase inhaled corticosteroid to the highest dose, ensure a fourth drug has been added, and refer to specialist

5) Specialist management may include oral b2 agonists, oral corticosteroids, or anti-IgE drugs

(e.g. omalizumab)

o NB: Consider increasing level of treatment if the SABA is required three times per week or

more ® or if symptoms are persistent

Describe the mechanisms of action of the main drugs used to treat asthma

• b2 agonists:

o Relax bronchial smooth muscle ® leading to bronchodilation

o Side effects are due to action on other b adrenoceptors:

§ b1 in the heart ® tachycardia

§ b2 in skeletal muscle ® tremors, cramps, hypokalaemia (K+ uptake)

o SABAs work for 4–6 hours ® whereas LABAs work for >12 hours

• Inhaled corticosteroids:

o Reduce exacerbations due to anti-inflammatory effects

o Side-effects are oral candidiasis & pneumonia ® plus systemic effects of corticosteroids (more

frequent as beclometasone >800 mcg)

o Advisee to rinse mouth after use

• Leukotriene receptor antagonists:

o Block the effects of leukotrienes in the airways ® benefitting the actions of inhaled

corticosteroids o Side effects are thirst, GI disturbances, and very rarely Churg-Strauss syndrome (systemic

vasculitis)

• Theophylline / aminophylline: o Prescribe by brand name as efficacy is variable, and there is a narrow therapeutic window

o They relax smooth muscle ® so dilate airways but also reduce exacerbations

o Side-effects are dose-related (and similar to caffeine) ® so in high doses, people can get

headache, insomnia, nausea, tachycardia, and arrhythmias

RESPIRATORY – CHRONIC OBSTRUCTIVE PULMONARY DISEASE


Define the term chronic obstructive pulmonary disease and describe the underlying pathology

• COPD is a disease of progressive airflow limitation that is not fully reversible, associated with an

abnormal inflammatory response of the lungs to noxious particles or gases ® predominantly inhaled

cigarette smoke

• The airflow limitation is due to decreased outflow pressure (emphysema) plus increased airway resistance (chronic bronchitis / bronchiolitis)

• Emphysema: o Dilation of any part of the respiratory acinus (air spaces distal to the terminal bronchioles) with

destructive changes in the alveolar walls

o There is an absence of any scarring (fibrosis)

o Tissue destruction is caused by increased secretion and activation of extracellular proteases by inflammatory cells

o The inflammatory cells are stimulated by noxious particles

o Centrilobular emphysema ® these changes are limited to the central part of the lobule

directly around the terminal bronchiole, with normal alveoli elsewhere

§ This is the most common form ® associated with smoking

o Panacinar emphysema ® leads to destruction and distension of the whole lobule

§ This can happen in smokers ® but is more common in a1-antitrypsin deficiency

• NB: a1-antitrypsin normally inactivates neutrophil elastase

o Dilated air spaces >1cm are termed bullae

o Loss of connective tissue in the alveolar walls leads to a loss of elastic recoil of the lungs ®

leading to air entrapment in the lungs and inadequate ventilation o The reduction in the area available for gas exchange means there is reduced oxygen uptake

• Chronic bronchitis: o Daily cough with sputum for at least 3 months per year for two years

o The primary abnormality seen is abnormal amounts of mucus ® which causes plugging of the

airway lumen

o The hypersecretion is associated with hypertrophy and hyperplasia of bronchial mucus-secreting glands

o This can be shown by the Reid index ® the ratio of gland:wall thickness in the bronchus,

which is increased inn chronic bronchitis

o Inflammation is not typically present ® although frequent LRTIs develop, with secondary

inflammation & squamous metaplasia

• Bronchiolitis: o Cigarette smokers also develop inflammation of the airways <2mm in diameter (i.e. the

bronchioles) ® with macrophage and lymphoid cell infiltration

o This is actually the first pathological change in COPD

o It may lead to scarring, and narrowing of the airways

Describe the typical history of a patient with COPD, physical signs including complications,

and clinical features of acute presentations

• Clinical presentation: o Productive morning cough, following many years of ‘smoker’s cough’

o Increased frequency of LRTIs



o Slowly progressive dyspnoea with wheezing ® symptoms exacerbated in the acute infective

episodes

o Respiratory failure

o Chronic right heart failure (cor pulmonale) ® occurs late

• Signs:

o Mild disease ® widespread wheeze

o Severe disease:

§ Observations ® tachypnoea, cyanosis, and flapping tremor of outstretched hand (if

CO2 retainer, >10kPa)

§ Inspection ® hyperinflation, intercostal recession in inspiration, lip pursing on

expiration, signs of respiratory distress

• Signs of respiratory distress include tracheal tug, paradoxical breathing, and accessory muscle use

• May be raised JVP if there is cor pulmonale

• Clubbing is never present in pure COPD

§ Palpation ® poor chest expansion

§ Percussion ® hyper-resonant throughout, loss of cardiac / hepatic dullness

§ Auscultation ® decreased breath sounds, prolonged expiratory phase, polyphonic

wheeze

• Complications: o Acute exacerbations

o Polycythaemia o Respiratory failure

o Cor pulmonale

o Pneumothorax ® due to ruptured bullae

o Lung carcinoma

• Blue bloaters: o Patients with severe chronic bronchitis / COPD become insensitive to CO2, and thus rely on

their hypoxic drive to stimulate respiratory effort

o These patients are not particularly breathless, but are cyanosed and oedematous ®

suggestive of cor pulmonale

o A blood gas will typically show type 2 respiratory failure ® low O2, high CO2

o Oxygen should be given with care in these patients

• Pink puffers: o These patients remain sensitive to CO2 ® thus keep a low CO2 and near normal O2

o These patients are tachypnoeic and tachycardic, using accessory muscles to increase their

ventilation, and are breathless but not cyanosed

o The patients are very thin ® as large amounts of calories are used to breathe

o This can progress to type 1 respiratory failure ® low O2, low CO2

o It is more of an emphysematous process

List recognised risk factors for COPD

• Cigarette smoke exposure: o Stimulates neutrophils to produce elastase



o Can inactivate a1-antitrypsin

o Directly causes mucous gland hypertrophy

• Occupational exposure to dusts

• a1-antitrypsin deficiency:

o Hereditary deficiency ® 1 in 10 are carriers

o Account for 2% of emphysema cases o A small minority will also develop liver disease

• Recurrent chest infections in childhood

• Low socioeconomic status

• Asthma / atopy

Describe relevant investigations in a patient with suspected COPD • There is no single diagnostic test for COPD

• Diagnosis can be clinical if there are typical symptoms inn a patient over 35 in the presence of a risk

factor ® e.g. smoking or an occupational exposure

• Everyone suspected of COPD should then undergo:

o Post-bronchodilator spirometry ® confirm diagnosis & assess severity:

§ Stage 1 (mild) ® FEV1 ≥80% of predicted value (with these values, a diagnosis of

COPD can only be made clinically)

§ Stage 2 (moderate) ® FEV1 50–79% of predicted value

§ Stage 3 (severe) ® FEV1 30–49% of predicted value

§ Stage 4 (very severe) ® FEV1 <30% of predicted value

o CXR ® to rule out other pathology:

§ Classical features will be:

• Hyperinflation ® >6 anterior, >10 posterior ribs

• Flattened hemidiaphragm

• Large central pulmonary arteries

• Reduced peripheral vascular markings

• Bullae

o FBC ® to identify anaemia or secondary polycythaemia

• Further tests may include:

o Sputum culture ® abnormal organisms may suggest an alternate diagnosis of bronchiectasis

o ECG ® signs of RA / RV hypertrophy if cor pulmonale

o ABG ® normal in mild disease, developing to type 1 / type 2 respiratory failure, chronic

compensated respiratory acidosis

o DLCO (diffusion capacity of the lung for CO) ® reduced in emphysema

Describe the management for stable COPD

• Refer to a respiratory specialist if there is diagnostic uncertainty or deteriorating COPD

• Patient education: o How to recognise an exacerbation early

o Action plan / rescue medication for frequent exacerbators:

§ Steroids for increased breathlessness, antibiotics for increased / changing sputum



• Lifestyle advice: o Diet, exercise (to their own level), and most importantly smoking cessation

• Medication: o Level of inhaled medication depends on FEV1:

• Specialist treatments:

o Pulmonary rehabilitation: § Consider if a person is functional disabled by COPD

§ This has been shown to increase exercise capacity, decrease breathlessness, and

increase QoL

§ Involves 3 sessions per week for 6 weeks ® with elements of physical, education &

behavioural training

o Oral aminophylline / theophylline ® consider if a person with stable COPD is still

symptomatic after a trial of triple therapy (or cannot use inhalers)

o Mucolytics ® consider in those with stable COPD and a chronic productive cough

o Nutritional supplementation ® consider for those with a low BMI

o Long-term oxygen therapy (LTOT): § Assess for LTOT if patients have SpO2 <92% on air, FEV1 <30% predicted, cyanosis,

secondary polycythaemia, or cor pulmonale

§ They must be assessed whilst at their best ® i.e. the assessment cannot be done

whilst in hospital for an exacerbation

§ LTOT is introduced by specialists, can be ambulatory, and patients must be warned

not to smoke

§ This increases survival if used for >15h/day ® 3y survival increased by over 50%

o Surgery: § Pleurectomy for recurrent pneumothoraces



§ Bullectomy for isolated bullous disease

§ Lung volume reduction surgery ® removal of diseased tissue allows functioning lung

to expand

Describe management of an acute exacerbation in COPD

• Acute exacerbations are frequently caused by bacterial / viral infections, or exposure to pollutants

• The dyspnoea and wheeze become worse ® with production of purulent sputum

• If the patient has frequent exacerbations they should have rescue medications ® but they should still be

advised to see a health professional when they start their medication

• Hospital admission should be considered if there is: o Severe breathlessness

o Rapid symptom onset o Acute confusion

o Cyanosis

o Low O2 saturations ® <90%

o Worsening peripheral oedema

• Outpatient management:

o Increase the dose / frequency of SABA ® using a spacer If they do not already use one

o Prescribe 30mg prednisolone for 7–14 days for breathlessness interfering with regular activities

§ NB: Ensure osteoporosis prophylaxis for patients on >3 courses per year

o Prescribe oral antibiotics for people with purulent sputum or clinical signs of pneumonia ®

depending on local antibiotic prescribing guidelines

o ‘Safety net’ ® then follow up patient 6 weeks later to optimise their medical treatment once

stable

• Inpatient management: o Oxygen should be titrated according to the patient’s alert card

o If unknown patient, titrate saturations to 88–92% using a venturi system ® start on a 28%

mask at 4L/min

o Management as per outpatient regime ® with targeted oxygen therapy and regular monitoring

Discuss smoking cessation methods

• Population level ® national campaigns, advertisement bans, and high taxes

• Any smoker who wants to stop should have access to specialised stop smoking clinics ® to provide

behavioural and pharmacological support

• Nicotine replacement therapy (NRT) and bupropion are effective in those that smoke >10/day o NB: These should only be used in those who commit to an initial stop date

RESPIRATORY – BRONCHIECTASIS


Describe the typical history of a patient with bronchiectasis and differentiate it from COPD

• Bronchiectasis ® chronic dilatation of the airways, leading to chronic infection / inflammation

• Symptoms:

o Recurrent cough ® producing copious quantities of infected sputum

o Intermittent haemoptysis ® this can be the only symptom

o Persistent halitosis o Dyspnoea

o Recurrent febrile episodes, and episodes of pneumonia

• Signs: o Finger clubbing

o Coarse inspiratory crackles over infected areas ® typically bibasal

o Wheeze o Often low body habitus due to high energy demands

List recognised risk factors and outline the morphology and pathological consequences of

bronchiectasis

• Most commonly, no cause is found ® i.e. idiopathic bronchiectasis

• However, anything that interferes with drainage of bronchial secretions, or causes recurrent / persistent infection, can lead to bronchiectasis:

o Post-infective ® TB, measles, pertussis, pneumonia

o Cystic fibrosis o Bronchial obstruction ® tumour / foreign body

o Allergic bronchopulmonary aspergillosis o Ciliary dyskinetic syndromes ® Kartagener’s syndrome, Young’s syndrome

o Immune deficiency ® specific IgA, hypogammaglobulinaemia

o Connective tissue diseases ® ~1/3 of RA patients develop bronchiectasis

• Pathology:

o Any bronchi may be involved ® but most commonly at the lung bases

o Airways are dilated, with purulent secretions & chronic inflammation in the wall, with

inflammatory granulation tissues ® granulation tissue can bleed, leading to haemoptysis

o With repeated exacerbations, there can be fibrous scarring ® leading to respiratory failure

• Complications: o Pneumonia

o Pneumothorax

o Empyema o Lung abscess

o Haematogenous spread of infection

o Severe life-threatening haemoptysis ® more common in CF

Outline the investigations of a patient with suspected bronchiectasis

• Sputum culture ® atypical organisms

o The most common organism isolated from these patients is Haemophilus ® however,

Pseudomonas, Klebsiella & Strep. pneumoniae are also common

• CXR ® cystic / ring shadowing

RESPIRATORY – BRONCHIECTASIS


• CT ® to assess distribution of disease, and can see dilated airways with ‘signet ring’ sign

• Spirometry ® obstructive pattern, reversibility should be assessed

• Other tests can be used to look for a specific cause ® e.g. serum immunoglobulins, CF sweat tests,

aspergillus precipitins

Discuss treatment of bronchiectasis

• Assess for rare but treatable causes ® e.g. immune deficiencies

• Stop smoking

• Physiotherapy ® inspiratory muscle training:

o Good evidence of effectiveness for non-CF related diseases

• Postural drainage: o The patient’s body is positioned so that the trachea is inclined downwards and below the

affected chest area

o It is done 2–3 times daily for up to 30 minutes

o It can be done at night to reduce coughing at night ® but should be avoided after meals

o Can be done in the morning to clear secretions accumulated during the night

o Bronchodilators can be used 15 minutes before postural drainage is done to maximise its

benefits

• Antibiotics for exacerbations ® given according to known sensitivities, or constant rotating antibiotics

in severe disease

• Immunisations

• Bronchodilators can be useful in some cases

• Surgery is rarely indicated, as the disease is rarely confined to one lobe o Lobectomy used to be common

RESPIRATORY – CYSTIC FIBROSIS


Describe the clinical presentation of a patient with cystic fibrosis with respect to disease of

the lung and pancreas, and describe its inheritance

• Cystic fibrosis: o Autosomal recessive condition ® affecting 1 in 2500 live births

o Caucasians have a carrier frequency of 1 in 25

o It is caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene on chromosome 7, position 508

o Genetic screening is available for the four most common mutations ® this identifies ~90% of

cases o The most common abnormality is a point deletion

o CFTR codes for a cAMP-regulated chloride channel present on multiple epithelial surfaces ®

predominantly in the pancreas and respiratory tract

o Malfunctioning CFTR genes lead to abnormally thick secretions ® thus leading to pancreatic insufficiency and recurrent chest infections

o Life expectancy now exceeds 30 years

Describe pathological changes in the lungs and the natural history of disease in a typical

patient

• Recurrent childhood chest infections with failure to thrive

• Breathlessness & haemoptysis develop in later years ® as progressive bronchiectasis develops

• Spontaneous pneumothorax is common ® due to hyperinflation, as air is trapped behind mucin plugs

• Most will have chronic sinusitis, and many will have nasal polyps

• Respiratory failure & cor pulmonale can eventually develop ® due to scarring of the pulmonary

vasculature

Outline the non-respiratory manifestations of cystic fibrosis • GI effects:

o Meconium ileus is common at birth

o Steatorrhoea due to pancreatic dysfunction ® associated with malabsorption

o Increased frequency of gallstones & peptic ulceration

o Cirrhosis develops in 10% of older patients

• Other effects: o Finger clubbing

o Infertility in most males ® due to congenital absence of the vas deferens

o Subfertility in females

o Diabetes mellitus ® ~10%

o Rickets / osteomalacia ® due to vitamin D deficiency

List the usual organisms causing lung infection

• The pulmonary infections are initially mainly caused by S. aureus, Haemophilus influenzae, and gram-

negative bacilli ® but later Pseudomonas predominates, and this is associated with a poor prognosis

• Allergic bronchopulmonary aspergillosis is also more common in CF ® this is where the body’s

response to the common fungus Aspergillus fumigatus causes worsening of breathing difficulties

RESPIRATORY – CYSTIC FIBROSIS


Describe the main principles of treatment including physiotherapy, antibiotics, pancreatic

enzymes, DNAse, and lung transplantation

• Investigations:

o Bloods ® FBC, LFTs, U&Es, clotting

o Sodium sweat test ® levels >70 mmol/L are characteristic

o Annual diabetes screening o Sputum cultures

o CXR ® hyperinflation, evidence of bronchiectasis

o Abdominal USS ® fatty liver / cirrhosis, chronic pancreatitis

o Spirometry ® obstructive defects

• Management is MDT based, with specific attention to psychosocial and physical health

• Chest management:

o As per bronchiectasis ® with physiotherapy, antibiotics, and bronchodilators

o Two parenteral antibiotics are used for exacerbations ® to decrease resistance, often one with

pseudomonal cover

§ Experts may decide to employ regular prophylaxis ® e.g. azithromycin

o Mucolytics ® DNAse daily nebulisers

o Airway clearance devices ® e.g. acapella

o Lung transplant ® if respiratory failure develops

• GI management:

o Pancreatic enzyme replacement ® creon

o Fat-soluble vitamin supplementation ® ADEK

o Liver transplantation ® for advanced cirrhosis

• Other management:

o Treatment of diabetes o Fertility treatment

o Genetic counselling

RESPIRATORY – PNEUMONIA


Describe the typical presentation of a patient with community-acquired pneumonia and the

features that identify severe pneumonia

• Pneumonia can be defined as signs of infection of the pulmonary parenchyma plus new shadowing on

CXR ® separating it from bronchitis

• It is more common in males, the elderly, smokers, alcoholics, and those with chronic disease

• It can also develop secondary to bronchial obstruction ® e.g. lung cancer

• Clinical features:

o Acute systemic illness ® fever, rigors & vomiting

o Cough ® initially short, dry & painful, progressing to productive with mucopurulent sputum

o Dyspnoea

o Pleuritic chest pain ® may be referred to shoulder or anterior abdominal wall

o Elderly populations may report very few symptoms but be very unwell ® often present with

acute confusion

• On examination: o Tachypnoea

o Decreased chest expansion on the affected side

o Dullness to percussion over the affected area

o Coarse crackles & a pleural rub over the affected area ® with bronchial breathing

o Increased vocal resonance and tactile vocal fremitus

o Upper abdominal tenderness ® in lower lobe pneumonia

• The CURB65 score is used to determine the severity of CAP:

o Confusion ® mini-mental test score <8

o Urea ® >7 mmol/L

o Respiratory rate ® >30

o Blood pressure ® SBP <90 mmHg or DBP <60 mmHg

o 65 years or older

• One point is given for each new finding:

o CURB65 0/1 ® non-severe CAP (<3% mortality)

o CURB65 2 ® moderately severe CAP (9% mortality)

o CURB65 ≥3 ® severe CAP (15–40% mortality)

List the common pathogens causing community-acquired and hospital-acquired pneumonia

and outline predisposing factors

• The clinical context in which pneumonia develops is highly suggestive of the likely organisms: o Community acquired pneumonia (CAP)

o Hospital acquired pneumonia (HAP) ® pneumonia that develops at least 48h after admission

to hospital, with no signs of incubation on admission, or develops in somebody hospitalised in

the past 10 days o Pneumonia occurring in immunocompromised individuals, or patients with underlying lung

damage

• CAP causes:

o ‘Conventional’ bacteria (60–80%) ® mostly Streptococcus pneumoniae, also Haemophilus influenzae (more common in COPD)



o ‘Atypical’ bacteria (10–20%) ® mycoplasma, chlamydia, or Legionella pneumoniae

o Viruses (10–20%) ® influenza / parainfluenza (often in outbreaks)

• S. pneumoniae: o Most common cause of CAP in those who do not have COPD

o There is a vaccine ® often given to immunosuppressed patients

o Causes a classical lobar pneumonia, and ‘rust-coloured’ sputum

• H. influenzae:

o The capsulated strain was previously a major cause in children prior to the HiB vaccine o The non-capsulated strain is an important cause of disease in COPD

• M. pneumoniae:

o Suspect in young patients ® causes >40% of CAP in 17–44 year olds

o Can occur in epidemics

o Presents with a long history of illness with prominent extra-pulmonary features ® rash,

hepatitis, D&V, pericarditis, meningoencephalitis o There is classical patchy consolidation on CXR across multiple lobes

o Treatment is with erythromycin for at least two weeks

• L. pneumoniae:

o Causes both sporadic CAP and outbreaks ® classically in smokers who have recently

returned from holiday (resides in air conditioning units)

o Often causes severe disease ® with features of hyponatraemia (SIADH) and neurological

involvement (CN palsies)

o There is often proteinuria / haematuria ® classically affects both lung bases on CXR

o Treatment is again with erythromycin

• C. pneumoniae: o Causes URTIs in infancy, and CAP in the elderly

• NB: CAP during an influenza outbreak may be caused by S. aureus ® this is treated with flucloxacillin added to standard regimens

Describe the pathology of acute lobar pneumonia and bronchopneumonia

• Pneumonia can be classified into lobar pneumonia or bronchopneumonia ® based on the main site

of the inflammatory response within the lung parenchyma

• Inflammatory exudate within the alveolar air spaces is what renders thee infected areas of the lung

macroscopically solid in consolidation ® this occurs classically in bacterial pneumonias, with viral

infections generally sparing the air spaces and affecting the interstitium, causing interstitial pneumonia or pneumonitis

• Bronchopneumonia: o Primary infection centres around the bronchi ® spreading to involve adjacent alveoli which

become consolidated

o The initial consolidation is patchy (involves lobules) ® but if untreated can become confluent

(involves whole lobes)

o Most common in infancy & old age, due to immobility and retention of secretions ® thus

bronchopneumonia most commonly affects the lower lobes due to the effect of gravity



• Lobar pneumonia: o Organisms gain entry to distal air spaces rather than colonising bronchi ® thus, three is rapid

spread of infection through alveolar air spaces

o Macroscopically, the whole of the lobe becomes consolidated and airless o These patients are normally adults, and become severely ill with associated bacteraemia

Describe the investigation of a patient presenting with community-acquired pneumonia and

interpret investigations

• Observations & oxygenation assessment

• Bloods ® FBC, CRP, U&Es & LFTs

• Blood cultures

• CXR

• Sputum culture ® plus mycoplasma PCR if suspected

• Urine ® for legionella / pneumococcal antigen if moderate / severe (as empirical treatment will not

cover legionella)

• Serum mycoplasma IgM if suspected

• Throat swab in viral transport medium ® if severe pneumonia or suspected viral pneumonia

Outline the complications of pneumonia

• Parapneumonic effusion / empyema

• Post-infective bronchiectasis

• Lung abscess ® clubbing

• Sepsis

Outline the clinical management of a patient with pneumonia, emphasising the need for

radiological follow-up until the consolidation has cleared

• Management of CAP: o CURB65 0/1:

§ Oral amoxicillin ® managed as outpatients

§ Oral doxycycline if penicillin-allergic

o CURB65 2:

§ Oral amoxicillin and clarithromycin ® usually admitting the patient

§ Oral doxycycline if penicillin-allergic

o CURB65 ≥3:

§ IV clarithromycin plus co-amoxiclav ® admit to high-dependency unit

§ If the patient is penicillin-allergic or MRSA is suspected ® treat with levofloxacin and vancomycin

§ Treatment will be for at least 10 days

o If aspiration is suspected in CAP of any severity ® metronidazole will be added

o Inpatients may have chest physiotherapy to encourage effective coughing

• Management of HAP:

o Assess MRSA risk factors ® known colonisation / previous infection, long-term indwelling line /

catheter, admitted from a nursing home with skin breaks o Mild HAP is treated with oral doxycycline



o Severe HAP is treated with oral co-trimoxazole

o These patients should be discussed with microbiology

• Patients should ALWAYS have a follow-up CXR at 6 weeks to ensure resolution of consolidation and

assess for persistent abnormalities of the lung parenchyma ® non-resolution should raise the possibility

of endobronchial obstruction as a cause of the pneumonia (e.g. lung cancer)

RESPIRATORY – TUBERCULOSIS


Describe the process of infection by the tubercle bacillus together with the route of spread

• Infection with Mycobacterium tuberculosis predominantly affects the lungs, lymph nodes, and gut

• Primary TB ® the syndrome produced by M. tuberculosis infection in those not previously affected

• There is a mild inflammatory response at the site of infection ® followed by spread to regional lymph

nodes

o Common sites of infection are sub-pleural in the mid-zones of the lungs, in the pharynx, or in the terminal ileum

o Infection will then spread to hilar, cervical or mesenteric lymph nodes respectively

• The combination of infective focus and lymph node involvement is known as the primary complex

• In the lung ® the infective focus is known as the Ghon focus

• 1-2 weeks after infection, with the onset of immune sensitivity, the tissue reaction at both sites of the

primary complex changes to form characteristic caseating granulomas ® in the majority of cases,

these heal with fibrosis, and frequently calcify without therapy

• Patients are usually asymptomatic, or have a single enlarged lymph node that may be palpable is cervical

• Viable bacteria may remain walled off within the primary complex ® giving latent TB

• There are several methods by which primary TB can become symptomatic:

o The Ghon focus can erode through the visceral pleura to discharge organisms and cause TB pleurisy / pleural effusions

o Enlarged hilar lymph nodes can cause bronchial obstruction and collapse

o The hilar lymph nodes can also erode into the bronchus and rupture ® causing TB bronchopneumonia

o The enlarging nodes can also erode into vessels ® giving miliary dissemination to the lung

(via pulmonary arteries) or systemic dissemination (via the pulmonary vein)

o Erythema nodosum is also common in primary disease § NB: These are all more common in immunocompromised patients

Discuss the presentation of post-primary tuberculosis from reactivation of infection

• Post-primary (secondary) TB ® M. tuberculosis reinfection in tuberculin-sensitive individuals

• Infection can be from exogenous sources® or more commonly ‘reactivation’ from a healed primary

complex

• There is an immediate granulomatous response to the disease ® thus regional lymph node involvement

is not common

• In the lung, this creates a classical apical lesion termed a Simon (or Assmann’s) focus ® with

destruction of the lung parenchyma leading to cavitation

• Again, the lesion may heal with fibrosis & calcification if the immune system is strong ® or will

progressively enlarge in those with poor immune systems

• This has greater risks of eroding into vessels / airways, and causing the complications described above

• Symptoms:

o Earliest symptoms are non-specific ® malaise, night sweats, anorexia, weight loss

o Specific symptoms may occur late, only in established disease: § Productive mucoid cough

§ Repeated small haemoptysis

§ Pleural pain



o Can present with pneumonia or pleural effusion

o On examination ® there may only be a fever & apical crepitations, with late signs of

consolidation or pleural effusion o Patients may show finger clubbing in advanced disease

• Either in primary or post-primary TB ® release of tubercle bacilli into the main bronchus allows them to

be coughed into the atmosphere in droplets

• Diagnosis is frequently made with pre-symptomatic CXR

Outline common predisposing factors

• High risk patients are those who: o Were born in endemic areas

o Previously treated for TB o Have close contacts with TB

o Have immunosuppressive comorbidities or drug treatments

o Live in overcrowded conditions o Are alcohol / drug abusers

Outline the investigation of a patient with suspected TB

• If a patient has suspected active pulmonary TB:

o Sputum samples ® take at least three, including on morning sample:

§ Microscopy ® for acid-fast bacilli, results within 24h

§ PCR ® if rapid diagnostic results are required or suspected MDR-TB

• NB: This will not differentiate between active and latent TB

§ Culture ® gold standard diagnostic test, but takes 6 weeks, on Lowenstein-Jensen

medium

o If sputum samples are negative ® bronchoscopy with biopsy or bronchoalveolar lavage may be useful

o CXR ® upper lobe cavitation, pleural effusions, lymphadenopathy

o Investigate for extrapulmonary disease as clinically indicated

• To investigate for latent TB (e.g. contact tracing):

o Mantoux test ® TB antigen injected, and size of the wheal reaction monitored

§ >5mm ® considered positive in immunosuppressed individuals, those with prior TB or

recent contacts

§ >10mm ® positive in those with risk factors for TB

§ >15mm ® positive in any individual

o Interferon-gamma release assay ® IGRA blood test is also required to diagnose latent TB in

immunocompromised individuals, as they can have false negatives in the skin tests

o Positive results should lead to assessment for active TB (as these tests cannot differentiate

between latent & active TB) ® and if no evidence then treat for latent TB

• Always do standard bloods (e.g. FBC, U&Es & LFTs) to rule out other causes / as a baseline ®

considering the therapy these patients are likely to receive

• NB: Every patient diagnosed with TB should be offered screening for HIV and Hep B/C before starting treatment



Describe the principles of treatment of confirmed cases ACTIVE TB

• If the patient is severely unwell, admission may be required ® this must be in a negative pressure side

room with droplet precautions

• If admission is not needed, arrange referral to a specialist TB service within 2 weeks ® do not delay

referral & treatment for culture confirmation if results are highly suggestive of active TB

• Assess risk factors for MDR-TB ® assess with PCR if suspected:

o Previous TB treatment o From endemic areas

o Contacts with MDR-TB

o Poor adherence to current treatment o Aged 24–45

o HIV co-infection

• The usual antibiotic regimen is 6 months of isoniazid (with pyridoxine) & rifampicin ®

supplemented in the first 2 months with pyrazinamide & ethambutol • If there is CNS involvement ® the isoniazid & rifampicin are continued for 12 months

• Care should be coordinated through a specialist team ® including a key worker who should monitor the

person’s adherence to treatment, clinical response, and any adverse effects

• People considered to be at high risk of poor adherence to treatment may have ‘directly observed

therapy’ (DOT) ® where drug treatment is given under the observation of a key worker

MDR-TB

• Continue infection control measures until pulmonary / laryngeal disease has been excluded

• Treat with at least 6 drugs to which it is sensitive

LATENT TB

• Treat with 3 months of isoniazid (with pyridoxine) & rifampicin

DRUG SIDE EFFECTS

• Rifampicin ® abnormal LFTs, pink urine

• Isoniazid ® peripheral neuropathy / encephalopathy (very rare with prophylactic pyridoxine)

• Pyrazinamide ® hepatotoxicity (rare but severe)

• Ethambutol ® optic neuritis (assess with colour vision testing)

Outline the principles of contact tracing

• If diagnosis is confirmed ® TB is a notifiable disease

• All household members & close contacts should be traced and assessed for latent TB ® or active TB if

any symptoms

• Casual contacts (such as work colleagues) should be traced only if the person with TB is particularly infectious (≥10% of close contacts develop TB) OR if casual contacts are at increased risk of infection

(e.g. healthcare workers, people with HIV)



List the common sites of non-pulmonary TB infection and outline the pathological features

• When small numbers of tubercle bacilli escape into the blood ® most die if host defence mechanisms

are effective

• For unknown reasons, some bacilli settle in specific organs ® they may remain dormant for many

years, appearing later to cause disease:

o Lymphatic TB ® painless lymphadenopathy

o Joint / spinal TB ® monoarthritis

o Renal TB ® sterile pyuria

o TB meningitis ® meningitic syndrome

o Cutaneous TB ® erythema nodosum (shins) / lupus vulgaris (face & neck)

o TB pericarditis ® chest pain

Describe the global picture of TB, its relation to the AIDS epidemic, and patterns of multidrug

resistant tuberculosis

• TB kills 2 million people per year worldwide ® with 350 deaths/year in the UK

• TB is the most common cause of death in people with HIV ® as HIV progresses they become more

susceptible, and are at risk of drug interactions and poor drug absorption due to enteropathy

• The most common drug resistance in the UK is isolated isoniazid resistance ® with rifampicin being the

marker for multi-drug resistant TB

RESPIRATORY – PNEUMOTHORAX


Describe the typical clinical presentation and recognised risk factors for a pneumothorax,

together with the underlying pathology and investigations

• Pneumothorax may be asymptomatic in young patients with a small pneumothorax ® or present with a

sudden onset of unilateral pleuritic pain with progressive breathlessness

• Similarly, there may be few physical signs, or:

o Reduced expansion o Increased resonance to percussion

o Decreased breath sounds and reduced vocal resonance

• A tension pneumothorax is suggested by tracheal deviation away from the affected side ® there may

also be signs of haemodynamic compromise

• Pneumothorax can be divided into: o Spontaneous pneumothorax:

§ Primary ® lung parenchyma otherwise normal, caused by rupture of the apical bled,

often in tall, thin young men

§ Secondary ® underlying lung disease / abnormality, e.g. COPD, pneumonia, CF,

asthma, malignancy

o Traumatic pneumothorax ® penetrating trauma, rib fractures

o Iatrogenic pneumothorax ® lung biopsy, endoscopy, subclavian cannulation, positive

pressure ventilation

• Investigations:

o Expiratory CXR ® trace the outline for areas devoid of lung markings, and always look for

tracheal deviation

o ABG ® if signs of respiratory distress or chronic lung disease

Distinguish between simple and tension pneumothorax including features that aid in

recognition of critically ill patients presenting with a tension pneumothorax

• Tension pneumothorax ® air in the pleural space leading to cardiac compromise

o Thought to be caused by a valvular mechanism allowing air entry into the pleural space during

inspiration, but no air exit during expiration

o The intrapleural pressure is very high ® deflating the lung and decreasing venous return to the

heart

• A tension pneumothorax is suggested by: o Respiratory distress

o Pallor

o Haemodynamic compromise o Distended neck veins

o Tracheal deviation

• Treatment: o 100% oxygen

o Insert a large-bore cannula into the 2nd intercostal space in the midclavicular line o CXR

o Insert chest drain

RESPIRATORY – PNEUMOTHORAX


Describe treatment options for a pneumothorax and outline the indications for surgical

pleurectomy and pleurodesis

• If the rim of air is <2cm and the patient is not short of breath: o Discharge, advising to avoid strenuous exercise

o Interval CXR every 2 weeks until resolution

o Advise to quit smoking ® as this is a large risk factor for recurrence

• If the rim of air is >2cm or the patient is short of breath: o Attempt aspiration, and admit for at least 24h if secondary cause

o If this fails, or there is recurrence ® insert a chest drain

• Aspiration: o Insert a 16G cannula under local anaesthetic into second intercostal space in the

midclavicular line ® attach to a 3-way tap and a 50ml syringe to aspirate

o Stop when resistance is felt ® or if the patient coughs excessively

o If successful (check with CXR) ® consider discharging in a primary pneumothorax, with a

repeat CXR at 24h and 7 days

• Chest drain:

o CXR to confirm location

o Usually insert in the ‘safe triangle’ ® anterior to the midaxillary line in the 4th to 6th intercostal space

o Infiltrate down to the pleura with 1% lignocaine ® then use the seldinger technique to insert

the drain

o The drain should be attached via tubing to the underwater seal ® which must be below the

level of the patient

o Check the drain is swinging with respiration & bubbling ® check positioning with repeat CXR

• After a pneumothorax, flying should be avoided for 6 weeks ® diving should be permanently avoided

• If there is a recurrent pneumothorax (>2 occasions), or pneumothorax that does not resolve within 5

days with a chest drain ® then surgery may be indicated:

o Pleurectomy ® if the patient is fit

o Talc pleurodesis ® if the patient is not fit, and there is some risk of recurrence

RESPIRATORY – LUNG CANCER


Outline the major pathological classification of lung cancers and their prognosis

• Lung cancers are generally split into small cell disease (20%) and non-small cell disease (80%)

• 70% of tumours arise in relation to the main bronchi or hilum ® 30% arise peripherally

• Non-small cell lung cancer:

o Squamous cell carcinoma ® 50%

o Adenocarcinoma ® 20%

o Large cell anaplastic tumours ® 10%

• Squamous cell carcinoma: o SCCs arise from squamous metaplasia of the normally pseudostratified ciliated columnar

epithelium, in response to cigarette smoke

o They are usually central, and close to the carina ® thus frequently present with collapse /

infection secondary to obstruction

o They may secrete PTH, causing hypercalcaemia ® beware, as this can also be due to

secondary bone metastases

o They are friable tumours ® so can often be diagnosed with sputum cytology

o They are relatively slow growing compared to other tumours, and may be resectable

• Adenocarcinoma: o Equal gender incidence ® less related to smoking

o Characteristically originate in peripheral locations ® potentially in areas of previous lung

scarring

o Bronchoalveolar carcinoma is a special type of adenocarcinoma ® account for <5% but

associated with a better prognosis

• Large cell anaplastic carcinoma: o Features showing SCC or adenocarcinomatous origins may be seen ® but they are not

differentiated enough to be classified o They have a poor prognosis, and are often widely disseminated at diagnosis

• Small cell anaplastic carcinoma: o Aka oat cell carcinoma ® as the cell nuclei resemble oat grains

o Usually centrally located, and rapidly growing

o The most highly malignant of lung cancers ® often metastasised at diagnosis

o Originate from the bronchial epithelium ® but differentiate into neuroendocrine cells to

secrete active products:

§ ADH ® symptoms of SIADH, i.e. dilutional hyponatraemia due to retention of water

but not solute, leading to muscle weakness, Cheyne-Stokes respiration, and

neurological signs

§ ACTH ® Cushing’s syndrome

o They can also rarely cause myasthenia gravis-like symptoms in Lambert-Eaton syndrome:

§ Manifests as proximal arm and leg weakness, and reduced tendon reflexes ®

typically affects the legs more than the arms (in contrast to MG)

§ Can be accompanied by dry eyes, sexual impotence, and neuropathy

§ Symptoms get better with usage ® unlike MG



Outline the epidemiology of lung cancer in developed countries and risk factors

• Lung cancer is the most common cause of death from neoplasia in the UK in both sexes ® and the 3rd

most common cause of death overall

• The peak incidence is at 65 years of age ® with a 3:1 male predominance

• Smoking is the most common risk factor ® with 10% not due to smoking

• Stopping smoking decreases the risk by half in 5 years

• Other risk factors are passive smoking, urban living, and occupational exposure (e.g. asbestos)

Describe the common clinical presentation of lung cancer

• Clinical features:

o Persistent cough (80%) ® due to distal infection

o Haemoptysis (70%) ® due to ulceration of the tumour

o Dyspnoea (60%) ® due to local extension of the tumour

o Chest pain (40%) ® due to pleural / chest wall involvement

o B symptoms • On examination:

o Clubbing o Cachexia o Signs of anaemia o Hypertrophic pulmonary osteoarthropathy:

§ Paraneoplastic syndrome ® clubbing and painful periostitis of small joints of the

hand, especially the distal IP and MCP joints o Chest signs of collapse / consolidation / effusion o Signs of metastases

List relevant investigations for lung cancer and interpret results

• FBCs ® anaemia / secondary polycythaemia

• LFTs ® signs of liver metastases

• U&Es ® hypercalcaemia / hyponatraemia

• CXR ® ANY patient with haemoptysis should have a CXR

o Symptomatic tumours are almost always visible o A normal CXR in a symptomatic patient should warrant further investigation for central tumours

• Sputum / pleural fluid cytology • Staging CT ® head to pelvis

• Biopsy ® CT guided if peripheral (risk of pneumothorax), via bronchoscopy if central

• Pulmonary function tests ® useful if planning surgery

• PET scan / radionucleotide bone scan ® if suspected metastatic disease

Outline local metastatic manifestations of lung cancer and describe systemic non-metastatic

manifestations • Paraneoplastic syndromes include:

o Hypertrophic pulmonary osteoarthropathy

o Lambert-Eaton syndrome ® small cell tumours

o SIADH ® small cell tumours



o Secondary Cushing’s ® small cell tumours

o Hyperparathyroidism ® squamous cell carcinoma

• Other complications are due to local invasion or distant metastases

• Local invasion:

o Recurrent laryngeal nerve palsy ® change in voice, left vocal cord paresis

§ If present, indicates inoperability

o Phrenic nerve palsy ® asymptomatic if unilateral

o SVC obstruction ® raised JVP, raised arm BP, arm swelling, facial swelling

§ Common presenting feature of lung cancer § Often due to local nodes rather than the tumour itself

o Pancoast syndrome ® malignant neoplasm of the lung apex, leading to destructive lesions of

the thoracic inlet, often involving the brachial plexus

§ Horner’s syndrome ® miosis, ptosis, anhidrosis

§ Shoulder pain ® radiating along the ulnar forearm & hand

§ Atrophy of hand / arm muscles

§ Oedema ® due to blood vessel compression

o Pericarditis

o Atrial fibrillation

• Distant metastases often go to the brain, bone, liver or adrenal gland

o Adrenal metastases can present as per Addison’s disease

• Acanthosis nigricans or dermatomyositis can indicate underlying malignancy

Outline the treatment options for a patient with confirmed lung cancer

• Non-small cell:

o Surgical excision if peripheral enough with no lymph nodes / metastatic spread ® with

adjuvant chemotherapy

§ Must be >2cm from the carina

o Curative radiotherapy can be an alternative if poor respiratory reserve ® with adjuvant chemotherapy

o Chemo-radiotherapy for more advanced disease

• Small cell:

o Nearly always disseminated at presentation ® but may respond to chemotherapy ± radiotherapy

o They may have prophylactic cranial radiotherapy

• Palliation: o Radiotherapy for obstruction symptoms (SVC / bronchial) or bone pain

o SVC stenting o Pleural drainage / pleurodesis for symptomatic effusions

RESPIRATORY – PLEURAL EFFUSION


Classify causes of a pleural effusion

• There are several types of collections which may accumulate in the pleural space:

o Empyema / pyothorax ® accumulation of pus, due to infection

o Chylothorax ® accumulation of lymph, due to thoracic duct leakage

o Haemothorax ® accumulation of blood, due to trauma

o Fluid effusion ® transudative or exudative

§ Transudates ® occur due to increased hydrostatic pressure or decreased oncotic

pressure

§ Exudates ® occur due to increased capillary permeability

• Transudative effusion causes:

o Cardiac failure ® LHF leading to increased hydrostatic pressure

o Liver failure ® decreased protein production decreasing oncotic pressure

o Renal failure ® nephrotic syndrome decreasing oncotic pressure

o Peritoneal dialysis o Rarer causes can be hypothyroidism, or ovarian tumours (Meig’s syndrome)

• Exudative effusion causes:

o Infections ® bacterial pneumonia, TB

o Neoplasm ® lung primary or secondary, mesothelioma

o Pulmonary embolism o Autoimmune disease ® RA, SLE

o Abdominal disease ® pancreatitis, subphrenic abscess

Describe the clinical features and typical examination findings of a pleural effusion

• The patient may be asymptomatic ® or present with dyspnoea and pleuritic pain

• On examination:

o Decreased chest expansion ® tracheal deviation away if large

o Stony dull to percussion

o Decreased breath sounds § Can be bronchial breathing above effusion due to compressed lung

o Reduced vocal resonance

o Mediastinal deviation ® in massive effusion

• Examination should also focus of features of possible aetiology ® e.g. signs of malignancy, chronic liver

/ kidney disease, cardiac failure, RA / SLE, etc.

• An empyema is caused by bacterial invasion of the pleural space ® either spreading into an exudative

effusion from adjacent pneumonia, or from direct inoculation (e.g. poor aseptic technique in a chest

drain) o Clinically present as fever plus signs of pleural effusion

o Aspirated fluid is yellow & turbid, with pH <7.2, low glucose, high LDH

o These will require IV antibiotics, and often a chest drain

Discuss the investigation of a pleural effusion • Unilateral effusions are more likely to be exudative ® bilateral effusions are more likely to be

transudative

RESPIRATORY – PLEURAL EFFUSION


• Investigations:

o CXR ® can be detected when >300ml fluid is present ® a flat upper border implies there is

also a pneumothorax

o USS ® recommended by BTS to guide aspiration

§ If unavailable, percuss upper body & go 2 intercostal spaces below

o Aspiration ® fluid sent to microbiology (for MC&S), clinical chemistry (protein, LDH, glucose),

and cytology, as well as run through a blood gas machine to determine pH

§ Exudates have a protein level >30 g/L, transudates have a protein level of <30 g/L

§ If the protein level is between 25–35 g/L ® one positive element of Light’s criteria

will suggest an exudate:

• Pleural fluid protein divided by serum protein is >0.5

• Pleural fluid LDH divided by serum LDH is >0.6

• Pleural fluid LDH more than two-thirds the upper limits of normal serum LDH

Discuss the management of a pleural effusion

• If aspirated fluid is purulent / turbid ® place a chest drain and consider IV antibiotics

o NB: If pH <7.2 ® this also suggests empyema

• Drainage should also take place if symptomatic ® either with aspiration as per the diagnostic tap, or

using an intercostal drain

• Manage the underlying cause of the effusion

RESPIRATORY – INTERSTITIAL LUNG DISEASE


Describe the clinical and pathological features of interstitial lung disease, outline the common

causes, and list the differential diagnosis in patients who present with established pulmonary

interstitial fibrosis

• The interstitium is the tissue that lies between the alveoli and pulmonary capillaries

• Interstitial lung disease ® a generic term used to describe a number of conditions that diffusely affect

the lung parenchyma, sharing certain common features: o Repeated exogenous / endogenous stimuli

o Chronic inflammation

o Fibrosis of the interstitium o Restrictive lung disease

• Aetiology: o Secondary to exogenous stimuli:

§ Occupational / environmental ® asbestosis, silicosis, coal dust inhalation

§ Drugs ® nitrofurantoin, amiodarone, sulfasalazine, methotrexate

§ Hypersensitivity reactions ® extrinsic allergic alveolitis

§ Infections ® TB, fungal / viral infections

o Secondary to endogenous stimuli / systemic disorders: § Sarcoidosis § Rheumatoid arthritis § Connective tissue disorders ® SLE, systemic sclerosis, Sjögren’s

o Idiopathic pulmonary fibrosis ® most common cause of interstitial lung disease

• Clinical presentation: o Classical features are dyspnoea on exertion and a non-productive ‘dry’ cough

• On examination:

o Inspection ® may be signs of respiratory distress, can be clubbing

o Palpation ® reduced expansion

o Percussion ® normal unless secondary pathology

o Auscultation ® ‘fine end-inspiratory crackles’, sometimes expiratory wheeze

o There may also be signs of decompensation ® i.e. signs of pulmonary hypertension and right

heart failure

o Restrictive spirometry (normal FEV1, reduced FVC) with reduced DLCO

• Idiopathic pulmonary fibrosis: o Aka cryptogenic fibrosing alveolitis o The most common cause of interstitial lung disease

o Classically onsets in the late 60s ® more common in males

o Aetiology unknown ® with smoking, chronic aspiration, antidepressants, and infections

stipulated to play a part

o Along with dry cough and exertional dyspnoea ® patients will report malaise and weight loss,

with arthralgia

o On examination ® there will be fine end-inspiratory crackles, and also can be cyanosis with

finger clubbing

o Complications are type 2 respiratory failure, pulmonary hypertension, and increased risk of

lung cancer

RESPIRATORY – INTERSTITIAL LUNG DISEASE


Outline the investigations and treatment options for a patient with suspected interstitial lung

disease

• General investigations for interstitial lung disease of unknown origin:

o Bloods ® FBC, ANA / RF (if suspecting CTDs)

o CXR ® reduced lung volume, bilateral reticulo-nodular shadowing

o High-resolution CT ® more sensitive, essential for diagnosis

§ ‘Honeycombing’ is seen on CT

o Spirometry ® restrictive deficit, reduced gas exchange

• Further investigations:

o Bronchoalveolar lavage ® may indicate disease activity in IPF / EAA

o Lung biopsy ® via bronchoscopy or surgical, only if diagnosis is uncertain

• General management of interstitial lung disease:

o Many cases will be unresponsive to treatment o 20% respond to long course of prednisolone, tapered down

o Some patients will be suitable for lung transplantation

RESPIRATORY – EXTRINSIC ALLERGIC ALVEOLITIS


Outline the nature of the allergic reaction underlying EAA and how this is used to establish the

diagnosis

• Aka hypersensitivity pneumonitis ® caused by immune reactivity in the lungs to inhaled antigens

• This can cause an acute type III hypersensitivity response with immune complex formation ® or with

repeated exposure, there is a type IV cell-mediated hypersensitivity reaction & granuloma formation

• The chronic inflammation eventually results in interstitial fibrosis

• Investigation:

o FBC ® there will be a neutrophilia

o Serum precipitant levels ® only indicate exposure

o CXR / CT / lung function tests ® confirm interstitial disease

o Bronchoalveolar lavage ® confirms diagnosis

§ Shows increased T lymphocytes and mast cells

Describe the typical clinical presentation and list common causes

• Clinical features of acute exposure come on 4–6 hours post-exposure: o Fever, rigors, and myalgia

o Dry cough & dyspnoea ® with possible wheeze

• Chronic features are as per idiopathic pulmonary fibrosis ® dry cough, exertional dyspnoea, malaise,

weight loss, and arthralgia

• Aetiology:

o Farmer’s lung ® caused by micropolyspora

o Bird fancier’s lung ® caused by proteins in bird droppings

o Malt worker’s lung ® caused by aspergillus

Outline the treatment options for EAA

• Treatment of the acute attack is with oxygen and oral prednisolone (with tapered reduction in dose)

• Long-term treatment:

o Aim for prevention ® with no exposure

o Long-term prednisolone may give physiological improvement

o Established fibrosis is not amenable to treatment

o NB: Farmer’s lung is compensable in the UK

RESPIRATORY – OCCUPATIONAL LUNG DISEASE


Describe the clinical features of the main conditions associated with asbestos inhalation, and

describe the natural history of pleural plaques, mesothelioma, and asbestosis

• Patients will generally be over the age of 50, and suffered exposure before legislation became effective in the late 1960s

• Those at risk will have worked in the building industry or in shipyards

• There can be a latent period of up to 50 years between exposure and clinical onset of disease

• The risk of disease is proportional to the intensity of exposure

• Asbestos bodies: o Not pathological in themselves ® merely act as a marker of asbestos exposure

o They can only be seen histologically ® following lung biopsy

• Pleural plaques, effusion & thickening: o Pleural plaques occur after light exposure, and are normally asymptomatic

o There may be a mild restrictive disease on spirometry ® with pleural thickening & calcification on CXR

o They are non-progressive

o In the first two decades following exposure ® they may be associated with recurrent pleural

effusions

o More heavy exposure can cause diffuse pleural thickening (affecting >1/4 of the pleural

surface) ® which will produce restrictive deficits, exertional dyspnoea, and can be

progressive

• Mesothelioma: o Caused by light exposure ® with an interval of 20–40 years between exposure to disease

onset

o There will be pleuritic chest pain, increasing dyspnoea ® with a unilateral pleural effusion on CXR

o Survival is poor ® with a median survival of 2 years from diagnosis

• Asbestosis: o Caused by heavy exposure ® with an interval of 5–10 years from exposure to disease

o There will be progressive dyspnoea ® with diffuse bilateral streaky strikes with honeycombing on CXR

o The outcome is poor ® and can progress after exposure ceases

• There can also be asbestos-related carcinoma of the bronchus ® with features as above, plus those

of bronchial carcinoma

• NB: Patients can obtain occupational compensation for bilateral diffuse pleural thickening, asbestosis, mesothelioma, and asbestos-related bronchial carcinoma

Discuss the effect of inhalation of coal dust on lung function and its relation to

pneumoconiosis • Pneumoconiosis is a disease of the lungs caused by the inhalation of dusts ® generally used to refer

to pathology caused by coal dust

• The dust is toxic to macrophages (the normal defence for inhaled dusts) ® thus, there will be a local

inflammatory response similar to that seen in COPD

RESPIRATORY – OCCUPATIONAL LUNG DISEASE


• If this becomes chronic ® there will also be fibrosis leading to restrictive lung disease

• Silicates are the main dusts causing industrial pulmonary fibrosis ® often mixed with coal

• The risk of developing coal worker’s pneumoconiosis is related to the degree of exposure to dust

Describe the pathology of simple and complicated coal worker’s pneumoconiosis

• Simple coal worker’s pneumoconiosis: o Presence of small nodule (2–5mm) on CXR ® not associated with any clinically significant

impairment of respiratory function

o May progress to PMF

• Progressive massive fibrosis (PMF): o Presence of large nodules (>10mm) on CXR ® and the disease progresses relentlessly,

leading to a mixed obstructive & restrictive pattern o It may present long after active exposure

o Culminates in COPD ® dyspnoea & cough productive of sputum, sometimes black

o This can progress to respiratory failure o NB: Occupational compensation is available to patients with PMF

RESPIRATORY – OBSTRUCTIVE SLEEP APNOEA


Outline the clinical presentation of a patients with obstructive sleep apnoea, describe the use

of sleep studies in its investigation, and outline the principles of treatment

• Aka obstructive sleep apnoea hypopnea syndrome (OSAHS) • Interrupted & repeated collapse of the upper airway during REM sleep ® associated with hypopnea /

apnoea & desaturations

• Hypoxia leads to increasing respiratory effort until the patient overcomes the resistance

• The combination of central hypoxia & respiratory effort briefly wakes the patient ® leading to excess

daytime sleepiness

• The patient is unaware of the awakenings from sleep

• Correctable factors include:

o Respiratory depressants ® opioids, alcohol, sedatives

o Nasal obstruction ® adenoids, rhinitis, polyps

o Encroachment on the pharynx ® obesity, acromegaly

• Presenting complaints:

o Loud snoring during sleep o Daytime somnolence

o Morning headaches

o Decreased libido o Nocturnal choking

o Witnessed apnoeic episodes

• Complications: o Pulmonary hypertension & cor pulmonale

o Type II respiratory failure o Hypertension & increased cardiac risk

• Investigations:

o Epsworth sleepiness scale ® to distinguish from simple snoring

o Endoscopic examination of the upper airway ® by ENT

o Home pulse oximetry ® high false negatives (30%), and also false positives in patients with

COPD

o Polysomnography ® gold standard for diagnosis, with in-patient assessment of variable

parameters (EEG, EMG, electro-oculogram, respiratory airflow, thoraco-abdominal movement, ECG, oximetry, snoring sound & video)

§ This is diagnostic, but rarely used clinically ® limited sleep studies may be used

instead ® these involve pulse oximetry, breathing sensor under the nose, and

sensors on the chest & abdomen to detect breathing movements

• Diagnosis is made with the occurrence of >15 episodes of apnoea / hypopnea during one hour of sleep

• Management:

o Behavioural changes ® allow partner to sleep first, sleep on side

o Weight reduction o Avoidance of alcohol & tobacco

o CPAP via a nasal mask ® positive pressure keeps the pharynx open

o 50% will not tolerate CPAP ® so alternatives include:

§ Intra-oral devices

RESPIRATORY – OBSTRUCTIVE SLEEP APNOEA


§ Daytime stimulants ® e.g. modafinil

§ Upper airways surgery ® if upper airways pressure assessments can localise a level

of obstruction

RESPIRATORY – RESPIRATORY FAILURE


Distinguish type I from type II respiratory failure and describe the implications of having a high

arterial pCO2

• Type I respiratory failure ® PaO2 low (<8kPa), PaCO2 normal or low

• Type II respiratory failure ® PaO2 low (<8kPa), PaCO2 high (>6kPa)

• Clinical features of hypoxia are: o Dyspnoea o Agitation

o Confusion

o Central cyanosis

• Clinical features of hypercapnia are:

o Headache o Tachycardia

o Bounding pulse

o CO2 retention ‘flap’ o Papilloedema

o Features of acidosis:

§ Kussmaul respiration ® air hunger, giving deep & laboured breathing

§ Cardiovascular dysfunction ® acidosis is negatively ionotropic

§ Potassium abnormalities ® acidosis leads to K+ loss from cells, leading to

hypokalaemia if renal function is good, or hyperkalaemia if impaired

§ Cerebral dysfunction ® confusion or coma

§ Peripheral vasodilation & increased permeability ® leading to oedema

Outline the conditions that may cause respiratory failure, including neuromuscular and

musculoskeletal disease

• Type I respiratory failure ® occurs with diseases of the lung parenchyma:

o Pulmonary oedema, pneumonia, PE, COPD, ARDS o Asthma is initially type I, with type II RF indicating a peri-arrest state

• Type II respiratory failure ® occurs when alveolar ventilation is insufficient to excrete the volume of

CO2 being produced by tissue metabolism:

o Severe pulmonary disease ® asthma, COPD, pulmonary fibrosis, OSA

o Reduced respiratory drive ® CNS pathology, sedative drugs

o Thoracic wall disease ® rib fracture (pain), kyphoscoliosis, flail chest

o Neuromuscular disease ® diaphragmatic paralysis, MG, Guillain-Barré, cord lesions,

poliomyelitis

§ NB: Usually causes restrictive pathology

• Other chest wall abnormalities:

o Pectus excavatum ® displaces the heart and causes slight breathlessness, not RF

o Pectus cavinatum ® no clinically significant

Outline the treatment for acute ventilatory failure

• Investigations to determine the underlying cause:

o Bloods ® FBC, U&Es, CRP



o ABG ® done in anyone with unexpected deterioration

o CXR

o Sputum / blood cultures ® if febrile

• T1RF: o Treat underlying cause o Give high flow oxygen (60%) via a face mask

o Consider assisted ventilation if PaO2 remains <8kPa despite 60% O2 ® e.g. CPAP

• T2RF: o Respiratory centre may be reliant on hypoxic drive, so oxygen therapy should be given with

care ® starting at 24% O2, and rechecking the ABG after 20 minutes

o Treat the underlying cause

Be able to understand an ABG

CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3- 1) How is the patient? 2) Assess oxygenation

a. PaO2 should be >10kPa on air OR ~10kPa less than the % inspired concentration

3) Determine the pH a. <7.35 is acidaemic, >7.45 is alkalaemic

4) Determine the respiratory component

a. If acidaemic, is the PaCO2 >6 ® respiratory acidosis

b. If alkalaemic, is the PaCO2 <4.7 ® respiratory alkalosis

5) Determine the metabolic component

a. If acidaemic, is the HCO3- <22 ® metabolic acidosis

b. If alkalaemic, is the HCO3- >26 ® metabolic alkalosis

6) Is there any evidence of compensation?

• Base excess ® used to assess the metabolic component:

o Negative in metabolic acidosis

o Positive in metabolic alkalosis

• Lactate: o Should be <1 ® can go up to 2 in a stressed patient

o High lactate is suggestive of shock

ACIDOSIS

• Respiratory acidosis ® can be caused by any cause of type II respiratory failure

• Metabolic acidosis: o The anion gap is helpful to determine the cause ® (Na+ + K+) – (Cl- + HCO3-)

o The normal range is 11–18 mmol/L

o A normal anion gap in a metabolic acidosis suggests loss of bicarbonate:

§ Renal tubular acidosis § Diarrhoea

§ Drugs ® acetazolamine

§ Pancreatic / intestinal fistula



o A raised anion gap indicates production of organic acids:

§ Lactic acidosis ® shock, hypoxia

§ Ketosis ® DM, alcohol

§ Urate ® renal failure

§ Drugs ® NSAIDs, biguanides, methanol

ALKALOSIS

• Respiratory alkalosis: o Caused by hyperventilation:

§ Anxiety

§ Pain § Altitude

§ Increased metabolic demands ® fever, sepsis, pregnancy, hyperthyroid

§ Drugs ® NSAID OD, stimulants

• Metabolic alkalosis: o Excess base ® ingestion of base (e.g. antacids)

o Loss of acid:

§ Vomiting

§ Hypokalaemia ® e.g. excess diuretics

§ Burns

§ Hyperaldosteronism

RESPIRATORY – MISCELLANOUS RESPIRATORY MEDICINE


LOBECTOMY

• Indications: o Lung cancer

o Bronchiectasis ® less common now

o Chronic lung abscess / TB

o Fungal infections ® life-threatening haemoptysis due to aspergillus

• Inspection ® thoracotomy scar (can be laparoscopic), with chest wall flattening on the side of the

surgery (ribs pulled in over the surgical site)

• Palpation ® tracheal displacement towards the surgical site, and reduced expansion on that side

• Percussion ® hyper-resonant on side of the lobectomy, as the remaining lung expands to fill the cavity

• Auscultation ® reduced air entry over the site

SARCOIDOSIS

• Systemic, non-caseating granulomatous disease ® most commonly affecting the lungs, mediastinal

lymph nodes, and skin

• Typically occurs in females, aged 20–40 ® presenting as a subacute illness with non-specific features

of malaise, arthralgia, etc.

• This acute form is usually self-limiting (2 months to 2 years) ® but it can present as a chronic insidious

disease with progressive dyspnoea

• Pulmonary manifestations lead to fibrosis, and erythema nodosum is common

• Sarcoidosis can also lead to glomerulonephritis, cardiomyopathy, arthritis, and cranial nerve lesions

• Treatment is normally simple analgesia and NSAIDs ® with occasional corticosteroid courses if there

is progressive lung fibrosis

ASPERGILLUS

• Most people breath in this fungus commonly found in mould / soil every day without coming to harm ®

but it can affect the lungs in 5 ways:

o Asthma ® type I hypersensitivity to spores

o Extrinsic allergic alveolitis (EAA) ® malt worker’s lung

o Allergic bronchopulmonary aspergillosis ® more common in asthmatics & CF patients,

with a type I and II reaction giving asthma-like symptoms with a productive cough, needing

steroid treatment

o Aspergilloma ® fungal ball formation within pre-existing lung cavities (e.g. TB):

§ May be asymptomatic, causing general malaise / weight loss, or torrential

haemoptysis

§ Single lesions may be resected

o Invasive aspergillosis ® affects immunocompromised individuals, and needs aggressive

treatment with antifungals ® mortality is high

CAUSES OF CLUBBING

• Intrathoracic neoplasm ® primary / secondary

• Suppurative lung disease ® lung abscess, CF, bronchiectasis, fungal infection

• Fibrotic lung disease ® IPF, asbestosis

• Cardiovascular disease ® congenital lesions, infective endocarditis, aortic aneurysm

RESPIRATORY – MISCELLANOUS RESPIRATORY MEDICINE


• Gastrointestinal disease ® IBD, coeliac

• Liver disease ® chronic active hepatitis, cirrhosis

• Thyroid acropathy

Documents

3 - Respiratory · 2021. 3. 6. · RESPIRATORY – ASTHMA DARWIN’S NOTEBOOK 2 • Intrinsic asthma: o Non-immune mechanisms o Occurs in middle-aged individuals, with no causative