Revise Notes Resp

Question 1

Smoking Cessation

Answer 1

Smoking Cessation

Pharmacological management options for smoking cessation include:

Nicotine replacement therapy
Licensed only for patients 12 years and older

Varenicline
Mechanism: Nicotine receptor partial agonist
Contraindications: Suicidal ideation, depression, pregnancy or breastfeeding

Bupropion
Mechanism: Nicotinic antagonist, dopamine reuptake inhibitor
Adverse effects: Seizures (1/1000)
Contraindications: Epilepsy, pregnancy or breast feeding

Question 2

Acid-base Abnormality

Normal values:

pH 7.35-7.45
Pao2 11-13 kPa
PaCO2 4.7-6 kPa
HCO3 22-26 mEq/L
Anion gap- 10-20mmol/L

Answer 2

Key points to assess cause:

1) Check pH- acidosis vs alkalosis

2) Check CO2 and HCO3 - metabolic vs respiratory causes

3) Calculate anion gap if metabolic acidosis to narrow down possible cause

4) Check if in respiratory failure (PaO2 < 8)

5) If in respiratory failure assess whether type 1 (PCO2 < 6) or type 2 (PCO2 > 6)

Question 3

5 steps to gas success

1) Is the patient acidotic or alkalotic?

pH < 7.35 = acidosis

7.35-7.45 = normal

pH > 7.45= alkalosis

Answer 3

2) Is the cause of acidosis or alkalosis respiratory or metabolic

?

If pH < 7.35 and:

pCO2 raised = respiratory acidosis
Bicarbonate (HCO3) low = metabolic acidosis
If pH > 7.45 and:

pCO2 low = respiratory alkalosis
Bicarbonate (HCO3) high = metabolic alkalosis

Note that CO2 and HCO3 can compensate for the above abnormalities in an attempt to normalise the pH,

if the pH is still abnormal this is ‘partial compensation’

Question 5

3) What is the cause of the acid base abnormality?

Answer 5

Respiratory acidosis
COPD
Asthma
Guillain-Barre
Drugs- opioids

Metabolic acidosis
Calculate anion gap- see below
Respiratory alkalosis
Hyperventilation i.e. anxiety or pain
PE
Pneumothorax

Metabolic alkalosis
Vomiting
Congestive cardiac failure
Primary hyperaldosteronism (Conn’s syndrome)
Liver cirrhosis
Milk-alkali syndrome
Drugs- diuretics

Question 6

4) If metabolic acidosis, what is the anion gap?

Answer 6

?

Anion gap= Sum of cations (sodium and potassium) - anions (chloride plus bicarbonate)- normal 10-20

High anion gap
Lactic acidosis
Renal failure
DKA
Alcohol
Drugs- aspirin, metformin, ethylene glycol, methanol

Normal anion gap
Renal tubular acidosis
Diarrhoae
Addison’s disease
Drugs- acetazolamide

Question 7

5) Check for respiratory failure:

Answer 7

Is the patient hypoxic?
Low PaO2 (< 8)= hypoxia= respiratory failure

Is respiratory failure type 1 or type 2?
Normal pCO2 with low PaO2 = type 1 respiratory failure

Raised pCO2 (> 6.0) with low PaO2 = type 2 respiratory failure

Question 8

Type 1 respiratory failure
Type 2 respiratory failure

Answer 8

Common causes of type 1 respiratory failure:

Pulmonary oedema
Pulmonary embolism

Common causes of type 2 respiratory failure:

COPD
Neuromuscular disorders- motor neuron disease, Guillain-Barre syndrome
Obesity
Obstructive sleep apnoea

Question 9

Acute Respiratory Distress Syndrome (ARDS)
ARDS is a severe form of acute respiratory failure characterised by rapid onset hypoxaemia and non-cardiogenic pulmonary edema.

Pathophysiology

Injury to the alveolar-capillary membrane leads to increased permeability.

Protein-rich fluid leaks into alveoli, impairing gas exchange and causing diffuse bilateral lung infiltrates.

Answer 9

Causes

Sepsis
Severe pneumonia
Aspiration of gastric contents
Trauma, including chest trauma
Acute pancreatitis
Inhalation injury
Transfusion-related acute lung injury (TRALI)

Clinical Features

Acute dyspnea and tachypnea
Severe hypoxaemia not responsive to supplemental oxygen
Tachycardia and use of accessory muscles
Diffuse crackles on lung auscultation

Question 10

Management

Supportive care in ICU setting
Treat underlying cause (e.g., antibiotics for pneumonia)

Mechanical ventilation with low tidal volumes and plateau pressures
Prone positioning for severe hypoxaemia

Answer 10

Diagnostic Criteria

Acute onset (within 1 week).

Bilateral opacities on chest imaging not explained by other pathology.

Non-cardiogenic pulmonary oedema
Pulmonary capillary wedge pressure (reflects left atrial pressure - 6-12 is normal) - can be used to rule out cardiac cause.

Severe hypoxaemia (e.g. PO2 < 40kPa)

Question 11

Alpha-1 antitrypsin deficiency
Alpha-1 antitrypsin deficiency (AATD) is a genetic disorder characterised by reduced levels or dysfunction of alpha-1 antitrypsin (AAT) protein, resulting in disease of the lungs and liver.

Aetiology

Autosomal codominant inheritance with mutations in SERPINA1 gene (e.g., PiZZ genotype).

Leads to reduced or dysfunctional alpha-1 antitrypsin (AAT) protein

The primary function of alpha-1 antitrypsin is to protect tissues from proteases, particularly neutrophil elastase, which degrades structural proteins like elastin in tissues.

AATD therefore compromises lung and liver protection, resulting in COPD and liver cirrhosis.

Answer 11

Clinical features

Symptoms:

Lung Manifestations: Early-onset emphysema, COPD.
Dyspnea, wheezing, recurrent respiratory infections, chronic cough.
Suspect AATD in young patients with symptoms of COPD, particularly if non smokers.

Liver Manifestations: Deranged LFTs, jaundice, later cirrhosis in severe cases.

Examination Findings:

Reduced breath sounds, wheezing.
Signs of respiratory distress in advanced disease.

Hepatomegaly or signs of chronic liver disease in severe liver involvement.

Question 12

Alpha-1 antitrypsin deficiency

Investigations

Serum Alpha-1 Antitrypsin Level: First line investigations - confirms deficiency

Genetic Testing: Identifies specific AAT genotypes (e.g., PiZZ, PiSZ).

Lung Function Tests: Obstructive pattern - reduced Fev1/FVC (spirometry, lung volumes).

Imaging: Chest X-ray and CT scan - features of emphysema.

Answer 12

Management

Smoking Cessation: Essential for slowing disease progression.

Inhaled Bronchodilators: Improve airflow and symptoms.

Alpha-1 Antitrypsin Augmentation Therapy: Intravenous AAT protein slows lung decline.

Pulmonary Rehabilitation: Enhances exercise capacity and quality of life.

Liver Transplantation: Considered in severe liver disease.

Question 13

Asthma
Asthma is a chronic airway disease characterised by chronic inflammation of the airways, and variable

and recurrent symptoms of reversible airflow obstruction/bronchospasm.

Key Learning Points - Management

Answer 13

Step 1: New Diagnosis
AIR therapy - e.g. Budesonide / Formoterol 100/6, only as-required symptom relief.

Step 2: Poorly Controlled Asthma
Low dose MART - e.g. Budesonide / Formoterol 100/6, regularly for maintenance and PRN.

Step 3: Moderate-Dose MART
E.g., Budesonide / Formoterol 200/6.

Step 4: Additional management
Check FeNO and blood eosinophil count:
If raised → Refer to asthma specialist
If normal → trial LTRA or LAMA

Switching from Older Regimens:
SABA-only users: Switch to as-needed AIR therapy.

For uncontrolled asthma on low-dose ICS/LABA, switch to low-dose MART.

Question 15

Clinical features

Dyspnoea
Chest tightness
Nocturnal cough
Wheeze
Diurnal variability

Triggers: Allergens, exercise, cold air, infections

Atopic conditions: Eczema, allergic rhinitis, food allergies

Answer 15

Investigations & Diagnosis

Key Principles

Asthma should not be diagnosed without a suggestive clinical history and objective testing.
All tests only confirm a diagnosis of asthma with clinical features suggestive of asthma.

Patients 5-16 years

1st line:
Measure Fractional exhaled nitric oxide (FeNO)

FeNO ≥ 35 parts per billion (ppb) → Asthma confirmed.

2nd line:
Spirometry with Bronchodilator Reversibility (if FeNO negative/unavailable)

FEV₁ ≥ 12% increase post-bronchodilator → Asthma confirmed.

3rd line:
PEF Variability (if spirometry unavailable)
Variability > 20% over 2 weeks → Asthma diagnosis confirmed.

Further testing (e.g., skin prick test, IgE, eosinophil count) if diagnosis remains unclear.

Specialist referral if persistent uncertainty or poor response to treatment.

Question 16

Adults (17 years+)

1st line:
FeNO or Blood Eosinophils
FeNO ≥ 50 ppb → Asthma confirmed.
Eosinophils above reference range → Asthma confirmed.

2nd line:
If asthma is not confirmed by FeNO or blood eosinophils: Spirometry with Bronchodilator Reversibility
FEV₁ ≥ 12% AND ≥ 200 mL increase post-bronchodilator → Asthma confirmed.

3rd line:
Peak Expiratory Flow (PEF) Variability (if spirometry unavailable)
Variability > 20% over 2 weeks → Asthma diagnosis confirmed.

Specialist referral if inconclusive (e.g., for bronchial challenge test

Answer 16

Spirometry

Obstructive picture: Fev1/FVC = < 70%

Reversibility:
Adults – an increase of 12% or more AND 200ml of volume following bronchodilator

Children – an increase of 12% or more (any volume)

FeNO

In lung inflammation, FeNO (fraction of exhaled nitric oxide) is elevated

Adult - FeNO > 50 parts per billion (ppb) = positive result
Children - FeNO > 35 ppb = positive result

Question 17

PEFR monitoring

Answer 17

PEFR monitoring

Variability in PEF readings supports a diagnosis of asthma, and should be considered if there is uncertainty regarding diagnosis following FeNO/objective testing of airway obstruction/airflow limitation.

NICE states : “a value of more than 20% variability after monitoring at least twice daily for 2-4 weeks is regarded as a positive result”

Question 18

Management of Chronic Asthma - Updated with 2024 guidelines

Step 1

Answer 18

New diagnosis of asthma

Commence AIR therapy
“AIR therapy” stands for Anti-Inflammatory Reliever therapy which refers to using a combination inhaler containing (ICS/LABA such as budesonide/formoterol) to treat asthma symptoms as needed.

PRN Low-dose inhaled corticosteroid (ICS) / long-acting beta agonists (LABA)

e.g. budesonide / formoterol used only as-needed - i.e. when symptomatic, before exercise or allergen exposure

Note - although formoterol is a LABA, it is useful in AIR/MART therapy, because it has quick-onset bronchodilator effects.

Question 19

Chronic asthma mng

Answer 19

Step 2

If uncontrolled (e.g., frequent symptoms, nocturnal waking, exacerbations):

Commence MART Therapy

MART (Maintenance And Reliever Therapy) is a treatment strategy for asthma that combines a single inhaler containing both a maintenance (preventer) medication and a reliever (rescue) medication into one device.

So, it is taken regularly for maintenance, and then taken again PRN if required - e.g. if symptoms occur.

The combination inhaler (like in AIR therapy) is with a combined ICS/LABA (budesonide / formoterol)

Start with low-dose Maintenance and Reliever Therapy (MART)

Question 20

Step 3

Increase to moderate-dose MART

i.e. increase the dose of the steroid component of the MART.

Step 4

If still uncontrolled despite adherence:

Check FeNO and blood eosinophil count:
If raised → Refer to asthma specialist

If normal → 8-12 week trial of either..

Leukotriene receptor antagonist (LTRA e.g. montelukast) OR

Long-acting muscarinic antagonist (LAMA e.g. Glycopyrronium, Aclidinium)

Most commonly, MSRA questions focus on the first few steps in the management of chronic asthma as above. Further management includes…

Answer 20

Step 5

If symptoms persist:

Switch between LTRA and LAMA before stopping.

If uncontrolled despite trials → Refer to specialist

Question 21

Important: Existing Asthma Patients (Switching from Older Regimens)

Answer 21

Important: Existing Asthma Patients (Switching from Older Regimens)

SABA-only users → Switch to as-needed AIR therapy.

Switch to a low-dose MART if symptoms are uncontrolled in patients on low dose inhaled corticosteroid based therapy:
Low-dose ICS
Low-dose ICS/LABA
Low-dose ICS + LTRA

Switch to a medium-dose MART if symptoms are uncontrolled in patients on medium dose inhaled corticosteroid based therapy:

Moderate-dose ICS
Moderate dose ICS/LABA
Moderate dose ICS + LTRA/LAMA

If uncontrolled on high-dose ICS → Refer to asthma specialist.

Question 22

Indicators of Uncontrolled Asthma

Answer 22

Any exacerbation needing oral steroids

Frequent symptoms (e.g., using reliever inhaler ≥3 days/week, nocturnal waking ≥1/week)

Important note: A personalised asthma action plan should be provided to all patients.

Inhaler doses:

‘low dose’ = equivalent of 400mcg of budesonide

‘medium dose’ = equivalent of 400-800mcg of budesonide

‘high dose’ = equivalent of > 800mcg of budesonide

Question 23

Occupational Asthma

Answer 23

Occupational asthma might be suggested by

Adult-onset asthma
Symptoms which are noticeably worse at work
Symptoms which improve significantly following a vacation/weekend etc.

Common causes & high risk occupations

Painting - especially if using isocyanates containing spray paint/adhesives
Baking

Working with animals
Welding
Laboratory work

Diagnosis: Refer patient to respiratory specialist + serial PEFR measurements.

Question 24

Acute Asthma

Classification

Answer 24

PEFR
Speech
HR
RR
SaO2

Moderate
50-75%
Normal
< 110bpm
< 25 breaths pm
> 92%

Severe
33-50%
Incomplete sentences
> 110bpm
>25 breaths pm
> 92%

Question 25

Life threatening

Answer 25

Life threatening PEFR < 33% or silent chest Oxygen saturations < 92% or cyanosed Bradycardia Arrhythmia Hypotensive Evidence of fatigue - Poor respiratory effort, exhausted, normal PCO2 on ABG

Question 26

Near fatal Hypercapnia – intubation required

Question 27

Acute asthma mng

Answer 27

Management A-E management, O2 to maintain sats of 94-98% Nebulised SABA (salbutamol/terbutaline) Nebulised SAMA (ipratropium) via nebuliser Steroids - prednisolone 40-50mg or IV hydrocortisone if unable to take PO If life threatening features are present: 1.Discuss with senior/ITU team 2.Consider IV magnesium sulphate (1.2-2g over 20 minutes) 3.Consider back-to-back salbutamol nebulisers

Question 28

Atelectasi Atelectasis refers to the partial or complete collapse of a lung or a lobe of a lung, leading to reduced gas exchange and respiratory function. It can be caused by various underlying conditions and is common in hospital settings.

Answer 28

Pathophysiology Atelectasis results from the loss of lung volume due to the collapse of alveoli. This can occur due to either obstruction of the airways (obstructive atelectasis) or compression of lung tissue (non-obstructive atelectasis). Obstructive Atelectasis: Blockage of the airways by mucus, foreign bodies, tumours, or post-surgical changes. Non-Obstructive Atelectasis: Compression of the lung tissue by pleural effusions, pneumothorax, or tumours.

Question 29

Clinical Features If atelectasis is severe, it may cause shortness of breath, hypoxia, and respiratory distress if significant lung volume is affected. O/E: Reduce breath sounds over affected area. It is common post-operatively and can also be caused by infection This may be mentioned as a clue in vignettes. Presentation: Shortness of breath and hypoxia 72hrs post-op Management Prevention: Early mobilisation, chest physiotherapy. Treatment: Addressing the underlying cause (e.g., clearing airway obstruction, draining effusions). Supportive Care: Supplemental oxygen, bronchodilators, and positive pressure ventilation if necessary.

Answer 29

Investigation Findings Chest X-ray may demonstrate: Increased opacification - The affected area appears denser due to collapsed alveoli filled with fluid or collapsed lung tissue. Loss of volume: Reduction in lung volume in the affected area, leading to crowding of adjacent structures such as bronchi and blood vessels. Focal or Lobar Collapse: Depending on the extent, atelectasis can involve a segment (segmental atelectasis) or an entire lobe (lobar atelectasis) of the lung.

Question 31

Bronchiectasis Bronchiectasis is a chronic lung condition, characterised by irreversible damage to the bronchial wall, which results in permanent airway dilatation. The damaged and dilated bronchi are at increased risk of colonisation which further worsens airway inflammation. Clinical features Symptoms Chronic cough with copious mucopurulent sputum Haemoptysis Dyspnoea TATT, weight loss

Answer 31

Examination findings Coarse bilateral crepitations - especially in lower zones Rhonchi, wheeze, inspiratory squeaks. Nasal polyps Finger clubbing Causes of bronchiectasis Post-infectious bronchiectasis TB Pneumonia Childhood infections - measles, pertussis Cystic fibrosis Kartagener’s syndrome (Triad of primary ciliary dyskinesia + situs inversus + chronic sinusitis) Rheumatoid arthritis Respiratory disease - COPD or asthma which is poorly controlled or with frequent exacerbations Bronchial obstruction – cancer Yellow nail syndrome – thickened discoloured nails, bronchiectasis, pleural effusions and sinusitis Immunodeficiency – IgA deficiency, hypogammaglobulinaemia

Question 32

Investigations bronchiectasis Typical investigation findings include Sputum cultures - patients may be colonised/infected with atypical organisms, identification & sensitivities are therefore important. Spirometry - obstructive airway disease (Fev1% < 0.7) XR – tramlines - thickened, non-tapering airway walls HRCT chest – NICE “the most frequently used imaging test to establish the diagnosis of bronchiectasis” Signet ring sign - dilated airways which are seen in the transverse plane. The airway lies adjacent to an artery, which looks like a ring.

Answer 32

Management Conservative measures Pulmonary rehabilitation/respiratory physiotherapy which might include inspiratory muscle training and postural drainage techniques to relieve mucus production. Medical management Vaccinations - annual influenza + once only pneumococcal as per COPD Antibiotics Patients with 3 or more exacerbations may be appropriate for prophylactic ABx Azithromycin / erythromycin are appropriate If pseudomonas colonisation - first line treatment is inhaled colistin Bronchodilators - LABA (salmeterol/formoterol) may benefit patients with shortness of breath LTOT can be considered if PaO2 < 7.3 / SaO2 < 88%

Question 34

Infective exacerbations of Bronchiectasis Clinical features Change to cough/sputum - increased volume, purulence etc. Shortness of breath Systemic features - fatigue/lethargy /fever/haemoptysis Causes Haemophilius influenzae – most common Others: Pseudomonas, klebsiella, streptococcus pneumonia

Answer 34

Management Admit for IV antibiotics if: hypoxia, confusion, dyspnoea, fever > 38 degrees Send sputum culture before starting antibiotics (but do not delay treatment whilst a/w results) Antibiotics according to sensitivities (7-14 days) Before sensitivities are back/ no prior sensitivities - NICE suggests following local protocols or antibiotics including: 1.Amoxicillin, clarithromycin, doxycycline 2.Consider co-amoxiclav, levofloxacin if high risk.

Question 35

Cystic Fibrosis Aetiology A genetic condition of autosomal recessive inheritance Mutation affecting the long arm of chromosome 7 in the CFTR gene (deletion of phenylalanine at delta F508)

Answer 35

Clinical Features Neonates: Neonatal jaundice / meconium ileus Failure to thrive due to malabsorption Constipation, rectal prolapse Short stature with delayed puberty Bronchiectasis - chronic, productive cough, copious mucus, recurrent chest infections Diabetes mellitus Nasal polyps Fertility - Reduced in females, males are infertile Investigations 1.Infant screening - blood spot immunoreactive trypsin test 2.Sweat test - the gold standard diagnostic test Pilocarpine injection + electrical stimulation to small area of skin - encourages sweating - [chloride] are measured Chloride > 60 mmol/L - CF is probable Chloride 30-59 mmol/L - CF is possible - requires further testing (e.g. genetics) 3.Alternatively - Gene testing can be used for confirmation

Question 36

Bronchiectasis Patients with cystic fibrosis are often colonised by staph aureus, pseudomonas aerguinosa, aspergillus + burkholderia cepcia Nb. Burkholderia cepacia colonisation is a contraindication to lung transplantation

Answer 36

Management Cystic fibrosis is managed by the MDT. Specific treatment measures include: 1.High calorie diet with high fat intake 2.Orkambi (lumacaftor/ivacaftor) Indicated in patients with homozygous delta F508 mutations Increases functional CFTR proteins.

Question 37

Primary Ciliary Dyskinesia Aetiology Autosomal recessively inherited condition Dysfunction of the dynein arm (drive the ‘beating’ of cilia) - results in inefficient/less motile cilia

Answer 37

Clinical Features Bronchiectasis Subfertility - impaired sperm motility/fallopian tube cilia etc. Situs inversus - in combination, PCD, SI and chronic sinusitis are termed Kartagener's syndrome Chest/abdominal organs arranged in 'mirror image' Dextrocardia – Qs may hint quiet heart sounds/small volume complexes on ECG

Question 39

COPD COPD is a chronic lung disease characterised by irreversible airway obstruction and chronic respiratory symptoms such as shortness of breath, cough and sputum production. The term COPD encompasses both emphysema and chronic bronchitis (cough for > 3 months over 2 years in a row). Patients with COPD often present with exacerbations, characterised by a rapid deterioration in symptoms, precipitated by a respiratory tract infection. Causes Smoking – the commonest cause of COPD Alpha-1 antitrypsin deficiency Other: the C’s of COPD - cotton, coal, cadmium, cement

Answer 39

Investigations and Diagnosis A diagnosis of COPD should be considered in all patients who are > 35 years of age AND History of smoking AND Chronic symptoms/ recurrent chest infections Investigations Post-bronchodilator spirometry: Fev1/FVC < 70% (with no significant reversibility) FBC: Polycythaemia, ?eosinophil count (see management) CXR BMI calculation (BODE index)

Question 40

Classification-severity COPD

Answer 40

Classification - Severity The severity of COPD can be categorised as mild, moderate, severe or very severe. This classification is according to the Fev1 (of predicted) Fev1 > 80% = mild Fev1 50-79% = moderate Fev1 30-49% = severe Fev1 < 30% = very severe Severity may also be classified according to symptom burden, using tools such as CAT or mmrc.

Question 41

Management COPD General measures Smoking cessation Annual influenza vaccine Once only pneumococcal vaccine Pulmonary rehabilitation (mmrc 3 and above)

Answer 41

Pharmacological Management - Choice of Inhaler GOLD Guidance - updated in 2023 The GOLD Guidelines for COPD Management changed in 2023, and are summarised below. See page 35 for visual summary: https://goldcopd.org/wp-content/uploads/2023/03/POCKET-GUIDE-GOLD-2023-ver-1.2-17Feb2023_WMV.pdf The choice of pharmacological therapy/inhalers is guided by three things: Symptom burden - mmrc/CAT History of moderate exacerbations - infrequent (0 of 1) or frequent (2 or more, or 1 leading to admission) Steroid responsive COPD - see below

Question 42

Factors to consider when choosing whether to add ICS to long-acting bronchodilators

Answer 42

Strongly in favour Exacerbations: History of hospitalisations with ECOPD 2 or more moderate exacerbations per year Blood eosinophils > 300 cells/ uL History of asthma Favours use Exacerbations - 1 moderate ECOPD per year Blood eosinophils > 100 cells/ uL Against use History of pneumonia or mycobacterial infection Blood eosinophils < 100 cells/ uL

Question 43

Patients are categorised as Group A, B or E

Answer 43

Group E - any patients with 2 or more exacerbations, or 'steroid responsive COPD' (as above) Consider LABA + LAMA + ICS Group A - mild symptoms (CAT < 10) and infrequent exacerbations (0 or 1) “A bronchodilator” Group B - more severe symptoms (CAT > 10, mmRC > 2) and infrequent exacerbations (0 or 1) LABA + LAMA

Question 44

NICE Guidance - Last updated in 2019 NICE - Classify patients as steroid responsive (asthmatic) COPD or non-steroid (non-asthmatic) responsive COPD as follows: Steroid responsive COPD is suggested by the following features: History of asthma / atopy Bloods: Eosinophilia Diurnal variation of PEFR of 20% or more or Fev1 variation day-to-day of 400ml

Answer 44

Step 1: NICE “If the person is breathless and has exercise limitation” Reliever: SABA or SAMA Step 2: NICE “If the person continues to be limited by symptoms or exacerbations” Add maintenance therapy, continue reliever Steroid responsive COPD – LABA + ICS + continue reliever (SABA or SAMA) Non-steroid responsive COPD – LABA + LAMA + continue reliever (SABA) Step 3: NICE “if the person continues to have day-to-day symptoms adversely affecting QOL” For both steroid-responsive and non-asthmatic COPD - LABA + LAMA + ICS + reliever (SABA)

Question 45

Additional considerations COPD mng

Answer 45

Theophyline PO Antibiotics: Azithromycin can be used for patients fitting the following criteria: NON-smokers with exacerbations CT thorax shows no evidence of bronchiectasis ECG shows no long QTc (exacerbated by azithromycin) Sputum sample shows no atypical growth Mucolytics – carbocisteine Cor pulmonale (suggested by peripheral oedema, raised JVP, right ventricular heave, loud P2) – loop diuretics Oral phosphodiesterase-4 inhibitors - Roflumilast - consider for severe disease LTOT

Question 46

LTOT LTOT has been demonstrated to significantly improve survival of patients with advanced COPD. Indications for assessment Severe or very severe (Fev1<49%) COPD Symptoms/signs of cor pulmonale Polycythaemia Saturations < 92% on room air Assessment: 2 x arterial blood gas (at least 3 weeks apart)

Answer 46

Indications for LTOT Offer LTOT for > 15 hours / day if: PaO2 < 7.3kpa PaO2 7.3-8.0kpa AND polycythaemia/cor pulmonale/ pulmonary hypertension Contraindications: Patient continues to smoke

Question 47

Infective exacerbation of COPD Aetiology

Answer 47

Aetiology The most common bacterial cause is HAEMOPHILIUS INFLUENZE Others include strep pneumoniae, Moraxella catarrhalis. Viral causes account for 30% - rhinovirus Management Prednisolone 30mg OD for 5 days Antibiotics – if evidence of pneumonia, or purulent sputum Amoxicillin / clarithromycin / doxycycline

Question 48

Niv indication

Answer 48

Non invasive ventilation Indications COPD with T2RF + respiratory acidosis T2RF secondary to neuromuscular disease / chest wall deformity / OSA Cardiogenic pulmonary unresponsive to CPAP Weaning from endotracheal intubation

Question 49

Lung Cancer Suspected Lung Cancer - Red flags & NICE 2WW Criteria Refer patients for a 2 week wait suspected cancer appointment if: CXR suggestive of lung cancer Unexplained haemoptysis in a patient > 40yrs Arrange an urgent CXR (performed within 2 weeks) in patients who are age > 40 with any 2 of the following unexplained symptoms: If they are or have ever been a smoker Cough SOB Unexplained tiredness Chest pain Weight loss Reduced appetite

Answer 49

Consider an urgent CXR in patients aged 40 or more with one of the following: Recurrent chest infections Examination findings: Supraclavicular lymphadenopathy/persistent cervical LN, finger clubbing or chest signs consistent with lung ca. Thrombocytosis Investigations CXR - 10% of patients with lung cancer have a normal CXR CT chest - Diagnostic investigation of choice Bronchoscopy for biopsy +/- EBUS PET scan 18-fluorodeoxygenase uptake Used in non-small cell lung cancer (NSCLC) to determine eligibility for treatment with curative intent

Question 50

Small cell lung cancer Pathology APUD cells (high Amine Precursor Uptake Decarboxylase Management Surgery if very early (T2aN0M0) Most patients are managed with a combination of chemotherapy + radiotherapy

Answer 50

Paraneoplastic features SIADH ---> Presenting with unexplained hyponatraemia ACTH ---> Presenting with features of cushing's syndrome, hypokalaemic alkalosis, bilateral adrenal hyperplasia (BAH), LEMS - Antibodies vs voltage gated calcium channels —> presenting with Lambert-Eaton myasthenic syndrome Proximal muscle weakness (e.g. difficulty getting up from chair/climbing stairs) Weakness improves with muscle use (in contrast to myasthenia gravis) Diagnosis: Nerve conduction studies

Question 52

Complications – Superior Vena Cava Obstruction (SVCO) SVCO is an oncological emergency Common causes include

Answer 52

Small cell LC Lymphoma Clinical features SOB Facial swelling/plethora Pemberton’s sign - bilateral arm elevation worsens facial plethora and SOB, headache Headache Raised JVP, distended chest veins Management Dexamethasone Balloon venoplasty/stenting Chemotherapy / Radiotherapy

Question 53

Non-small cell lung cancer NSCLCs include Squamous cell lung cancer Lung adenocarcinoma Large cell lung cancer Carcinoid lung cancer (1%)

Answer 53

Squamous cell cancer Clinical & Paraneoplastic Features Hypertrophic pulmonary osteoarthropathy (HPOA) - painful inflammation and swelling of the ankles and wrists, finger clubbing. PTH related peptide release ---> hypercalcaemia TSH release ---> hyperthyroidism

Question 54

Adenocarcinoma Most common type of lung cancer in non-smokers Clinical & Paraneoplastic Features HPOA Gynaecomastia Large cell cancer Anaplastic, poorly differentiated, poor prognosis Paraneoplastic features B-hcg positive

Answer 54

Management of NSCLC Most cases of NSCLC are managed with palliative radiotherapy as there is usually a poor response to chemotherapy. 20% of patients are suitable for surgical management, though contraindications include: Tip: '3 cancer characteristics, 2 complications, 1 investigation' Cancer characteristics: malignancy near hilum, malignant pleural effusion present, stage 3b/4 Complications: superior vena cava obstruction (SVCO) or vocal cord paralysis Fev1 < 1.5

Question 55

Carcinoid lung cancer

Answer 55

Rare - 1% of cases of lung cancer Most bronchial adenomas are carcinoid Cell origin: APUD (same as small cell) Investigations: Bronchoscopy - cherry red ball Carcinoid syndrome is rare, and more commonly associated with liver metastasis

Question 56

Lung function test

Answer 56

Spirometry Basics FEV1 (Forced Expiratory Volume in 1 second): The volume of air that can be forcibly exhaled in 1 second. Normal Value: FEV1 > 80% of predicted FVC (Forced Vital Capacity): The total volume of air that can be forcibly exhaled after full inspiration. Normal Value: FVC > 80% of predicted FEV1/FVC Ratio: A calculated ratio used to diagnose obstructive and restrictive airway diseases. Normal Value: FEV1/FVC ratio > 0.7

Question 57

Restrictive Airway Disease Causes: Pulmonary fibrosis, asbestosis, sarcoidosis, ARDS, kyphoscoliosis, neuromuscular disorders Spirometry Findings: FEV1: Reduced FVC: Significantly reduced FEV1/FVC Ratio: Normal or increased

Answer 57

Obstructive Airway Disease Causes: Asthma, COPD, bronchiectasis, bronchiolitis obliterans Spirometry Findings: FEV1: Reduced FVC: Normal or reduced FEV1/FVC Ratio: Reduced (< 0.7)

Question 58

Transfer Factor Transfer Factor (TLCO or DLCO): Measures the rate at which gas diffuses from the alveoli into the blood. KCO (Corrected Transfer Factor): TLCO adjusted for alveolar volume. Causes of Low Transfer Factor Pulmonary fibrosis Pneumonia Pulmonary embolism (PE) Pulmonary oedema Emphysema Anaemia

Answer 58

Causes of High Transfer Factor Asthma Pulmonary haemorrhage (e.g., granulomatosis with polyangiitis/Wegener's) Polycythaemia Hyperkinetic states (e.g., Graves' disease, pregnancy) Left-to-right cardiac shunt

Question 59

Obstructive sleep apnoea (OSA) Obstructive Sleep Apnoea (OSA) is characterised by repeated episodes of partial or complete obstruction of the upper airway during sleep, leading to disrupted sleep, hypoxia and hypercapnia. Pathophysiology Airway Collapse: During sleep, the muscles supporting the soft tissues in the throat relax, causing the airway to narrow or collapse. This leads to intermittent airway obstruction, resulting in apnoea (complete cessation of airflow) or hypopnoea (partial reduction of airflow), with consequent hypoxaemia and hypercapnia. Causes Obesity Anatomical Factors: Enlarged tonsils, adenoids, or macroglossia; small jaw; nasal obstruction.

Answer 59

Clinical Features Daytime Symptoms: Day-time somnolence Morning headaches Night-time Symptoms: Loud snoring Witnessed apnoeas, gasping or choking during sleep Restless, disturbed sleep Investigations Polysomnography: Gold standard to confirm diagnosis and severity. Questionnaires: Epworth Sleepiness Scale (ESS) for assessing daytime sleepiness. Management Continuous Positive Airway Pressure (CPAP) First-line therapy for moderate to severe OSA. If not tolerated, consider intra-oral devices for mandibular advancement Patient must inform the DVLA

Question 60

Occupational Lung Disease Key learning

Answer 60

Sub-types: Coal worker's pneumoconiosis (coal dust), silicosis (silica dust), asbestosis (asbestos). Clinical Features: Delayed onset (over 10 years post-exposure), cough, dyspnoea, lethargy, potential asymptomatic findings on CXR. Investigations: CXR (upper or lower zone fibrosis), spirometry (restrictive pattern), HRCT (fibrosis assessment). Management: Avoid further exposure, smoking cessation, symptomatic relief (oxygen, bronchodilators), pulmonary rehab, compensation referral.

Question 61

Management occupational lung disease No specific curative treatment Avoid further exposure Stop smoking Oxygen and bronchodilators may help Pulmonary rehab Signpost to government compensation schemes Complications Progressive massive fibrosis Respiratory failure requiring long term oxygen Pulmonary hypertension and therefore right heart failure (cor pulmonale)

Answer 61

Other conditions related to occupational exposure Asthma Symptoms may worsen at work and improve at weekends/away on holiday Lung cancer Especially exposure to radon gas and iron oxides Mesothelioma Exposure to asbestos Allergic contact dermatitis Nickel Chromates (leathers) Lanolin (creams/cosmetics) Useful links BMJ Best Practice- Pneumoconioses

Question 62

Management occupational lung disease No specific curative treatment Avoid further exposure Stop smoking Oxygen and bronchodilators may help Pulmonary rehab Signpost to government compensation schemes Complications Progressive massive fibrosis Respiratory failure requiring long term oxygen Pulmonary hypertension and therefore right heart failure (cor pulmonale)

Answer 62

Other conditions related to occupational exposure Asthma Symptoms may worsen at work and improve at weekends/away on holiday Lung cancer Especially exposure to radon gas and iron oxides Mesothelioma Exposure to asbestos Allergic contact dermatitis Nickel Chromates (leathers) Lanolin (creams/cosmetics) Useful links BMJ Best Practice- Pneumoconioses

Question 64

Pleural Effusion An accumulation of fluid within the pleural space. Clinical features Symptoms – shortness of breath, cough, pleuritic chest pain Examination findings Reduced chest expansion on affected side Tracheal deviation away from pleural effusion (if large) Reduced or absent air entry/breath sounds Stony dull percussion Investigations All patients should have CXR (see below) US guided pleural tap is recommended CT can be considered for the diagnosis of exudative causes

Answer 64

Classification - Transudate vs Exudate Pleural effusions can be classified as transudative or exudative based on their biochemical properties. This can help to identify the likely underlying cause. Transudates Pathophysiology Extravasation of fluid through a normal membrane due to increased hydrostatic/oncotic pressures Pleural fluid protein < 30g/L Causes Heart failure Hypoalbuminaemia (liver failure, nephrotic syndrome, malnutrition) Hypothyroidism Meig's syndrome - benign ovarian tumour + ascites + transudative pleural effusion Tip: Causes can be remembered as 'the failures' - heart failure, liver failure, kidney failure (nephrotic syn.), nutritional failure, thyroid failure.

Question 65

Exudate

Answer 65

Exudates Pathophysiology Increased permeability of pleural surface and blood vessels due to inflammation results in intravascular fluid leak. Pleural fluid protein > 30g/L Exudate = Excess protein Causes Infection (pneumonia, TB) Autoimmune cancer pancreatitis Pulmonary emboli Dressler Yellow nail syndrome Tip: Remember that exudative effusions are typically caused by infectious/ inflammatory conditions.

Question 66

Light’s criteria

Answer 66

Light's criteria If pleural fluid protein is 25-35, Light’s criteria can be used to differentiate between transudative and exudative effusions. Any one of the following indicates an EXUDATE: Pleural fluid LDH > 2/3rds the upper limit of normal serum LDH (or > 0.6 actual serum LDH) Pleural fluid protein / serum protein > 0.5

Question 67

Empyema

Answer 67

Empyema A pleural effusion in the presence of sepsis/pneumonia is an indication for pleural fluid sampling. If the fluid is turbid/cloudy or the pH is < 7.2 this indicates an Empyema Management - chest drain & antibiotics

Question 68

Pneumothorax Background A pneumothorax is defined as the pathological presence of gas in the pleural space (between the parietal and visceral pleura) of the lung. This can result in abnormal pressure on the lung which causes it to collapse.

Answer 68

A spontaneous pneumothorax is one which occurs in the absence of trauma. Primary vs Secondary A primary pneumothorax is occurs in the absence of underlying lung disease A secondary pneumothorax occurs in the presence of underlying lung disease Small vs Large Small pneumothorax = < 2cm from lung edge to thoracic wall (at hilar level) Large pneumothorax = > 2cm from lung edge to thoracic wall (at hilar level)

Question 69

Secondary pneumothorax - causes Long-term smokers aged > 50 (as per BTS guidelines) Asthma COPD Tuberculosis Bronchiectasis, inc. CF Interstitial lung disease

Answer 69

Clinical Features Symptoms - Sudden onset pleuritic chest pain and shortness of breath Respiratory distress (tachypnoea, accessory muscle use) Reduced breath sounds or absent air entry on the affected side Reduced chest expansion on the affected side Percussion can be hyperresonant. Investigations 1st LINE: PA CXR If further evaluation is required – CT thorax – gold standard

Question 70

Management The British Thoracic Society updated their guidance on management in 2023, with the below algorithm. In summary.. If the patient is asymptomatic - manage conservatively with regular follow up If the patient symptomatic, determine whether they have high-risk characteristics. If high-risk pneumothorax - chest drain insertion is 1st line If low-risk - consider the patient's preferences: Rapid symptom relief - Needle aspiration or chest drain Procedure avoidance - consider conservative management with follow up

Answer 70

Other management Patients admitted/those who are symptomatic should be treated with high flow oxygen (NRBM 15L/min) - as pneumothoraces resolve 3-4x as quickly than on room air alone (fixed O2 concentration if pt has COPD). Patients must be advised to permanently avoid scuba diving (unless they have pleurectomy + CT) Aspiration Aspiration is with a 16-18G cannula

Question 71

Chest drain insertion

Answer 71

Relative contraindications: INR > 1.3, platelet count < 75, pulmonary bullae/pleural adhesions 5th intercostal space, mid axillary line Complications: re-expansion pulmonary oedema Cough / short of breath after chest drain? Clamp the drain and perform CXR Remove the drain once it is no longer bubbling or CXR shows resolution and the patient is coughing

Question 72

Tension Pneumothorax A medical emergency in which the pleural leak acts like a one-way valve, resulting in increasing pressure on the lung and resultant collapse. Increasing pressures result in mediastinal shift and haemodynamic instability. Management: immediate needle decompression - large bore (14-16G) needle into 4/5th ICS at the mid-axillary line, or alternatively 2nd intercostal space MCL.

Answer 72

References and further reading Management of spontaneous pneumothorax: British Thoracic Society pleural disease guideline 2010. Andrew MacDuff,1 Anthony Arnold,2 John Harvey,3. https://www.bsuh.nhs.uk/library/wp-content/uploads/sites/8/2020/06/BTS-pneumothorax-guideline.pdf British Thoracic Society Guideline for Pleural Disease (2023). Mark Roberts, Najib Rahma, Nick Maskell, Anna Bibby, Kevin Blyth, John Corcoran et al. https://doi.org/10.1136/thorax-2023-220304. https://thorax.bmj.com/content...