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Year 6 > Resp > Flashcards

Resp Flashcards

1
Q

Question: What are the common features of an acute asthma attack?

A

Answer: Common features include:

Worsening dyspnoea, wheeze, and cough not responding to salbutamol
May be triggered by a respiratory tract infection

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2
Q

Question: How are patients with acute severe asthma stratified?

A

Answer: Patients are stratified into moderate, severe, or life-threatening asthma.

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3
Q

Question: What are the criteria for moderate acute asthma?

A

Answer:

PEFR: 50-75% best or predicted
Speech: Normal
Respiratory rate (RR): < 25 / min
Pulse: < 110 bpm

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4
Q

Question: What are the criteria for severe acute asthma?

A

Answer:

PEFR: 33-50% best or predicted
Speech: Can’t complete sentences
Respiratory rate (RR): > 25 / min
Pulse: > 110 bpm

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5
Q

Question: What are the criteria for life-threatening asthma?

A

Answer:

PEFR: < 33% best or predicted
Oxygen saturation: < 92%
Signs: Silent chest, cyanosis, or feeble respiratory effort
Vital signs: Bradycardia, dysrhythmia, or hypotension
Mental status: Exhaustion, confusion, or coma

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6
Q

Question: What does a normal pCO2 in an acute asthma attack indicate, and how should it be classified?

A

Answer: A normal pCO2 in an acute asthma attack indicates exhaustion and should be classified as life-threatening.

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7
Q

Question: What characterizes near-fatal asthma?

A

Answer: Near-fatal asthma is characterized by a raised pCO2 and/or requiring mechanical ventilation with raised inflation pressures.

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8
Q

Question: What further assessments are recommended by the BTS guidelines for patients with oxygen sats < 92%?

A

Arterial blood gases should be checked.
Chest X-ray is recommended in cases of life-threatening asthma, suspected pneumothorax, or failure to respond to treatment.

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9
Q

Question: When should all patients with life-threatening asthma be admitted to the hospital?

A

Answer: All patients with life-threatening asthma should be admitted immediately.

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10
Q

Question: What are the criteria for admitting patients with severe acute asthma?

A

Failure to respond to initial treatment.
Previous near-fatal asthma attack.
Pregnancy.
Attack occurring despite already using oral corticosteroids.
Presentation at night.

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11
Q

Question: What is the initial oxygen therapy for hypoxaemic patients?

A

Start on 15L of supplemental oxygen via a non-rebreathe mask, which can then be titrated down to maintain SpO2 94-98%.

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12
Q

Question: What is the role of short-acting beta2-agonists (SABA) in acute asthma management?

A

Answer: High-dose inhaled SABA (e.g., salbutamol, terbutaline) is used for bronchodilation. Nebulised SABA is recommended for patients with features of life-threatening asthma.

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13
Q

Question: What corticosteroid regimen is recommended for all patients with acute asthma?

A

Answer: 40-50mg of prednisolone orally (PO) daily, continued for at least five days or until the patient recovers from the attack.

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14
Q

Question: What additional treatments are recommended for severe or life-threatening asthma?

A

Nebulised ipratropium bromide.
IV magnesium sulphate.
IV aminophylline (following consultation with senior medical staff).

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15
Q

Question: What are the criteria for discharging a patient with acute asthma?

A

Stable on discharge medication for 12-24 hours.
Inhaler technique checked and recorded.
PEF >75% of best or predicted.

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16
Q

Question: What is acute bronchitis and how long does it usually last?

A

Answer: Acute bronchitis is a type of chest infection resulting from inflammation of the trachea and major bronchi, often producing sputum. It is usually self-limiting and resolves before 3 weeks, although 25% of patients may have a cough beyond this time.

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17
Q

Question: What is the leading cause of acute bronchitis and during which seasons does it most commonly occur?

A

Answer: Viral infection is the leading cause of acute bronchitis, with around 80% of episodes occurring in autumn or winter.

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18
Q

Question: What are the typical presenting symptoms of acute bronchitis?

A

Cough: may or may not be productive
Sore throat
Rhinorrhoea
Wheeze

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19
Q

Question: What are the common physical examination findings in patients with acute bronchitis?

A

The majority of patients have a normal chest examination, but some may present with:

Low-grade fever
Wheeze

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20
Q

Question: How can you differentiate between acute bronchitis and pneumonia based on history?

A

Answer: In acute bronchitis, sputum, wheeze, and breathlessness may be absent, whereas in pneumonia, at least one of these symptoms tends to be present.

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21
Q

Question: What are the examination findings in acute bronchitis compared to pneumonia?

A

Answer: Acute bronchitis usually lacks other focal chest signs (e.g., dullness to percussion, crepitations, bronchial breathing) and systemic features (malaise, myalgia, fever) that are commonly present in pneumonia.

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22
Q

Question: What investigation is typically used to diagnose acute bronchitis?

A

Answer: Acute bronchitis is usually a clinical diagnosis, but CRP testing may be used if available to guide antibiotic therapy.

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23
Q

Question: What is the general management of acute bronchitis?

A

Answer:

Analgesia
Good fluid intake
Consider antibiotic therapy if the patient:

Is systemically very unwell
Has pre-existing comorbidities
Has a CRP of 20-100 mg/L (offer delayed prescription) or CRP >100 mg/L (offer antibiotics immediately)

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24
Q

Question: What is the first-line antibiotic recommended for acute bronchitis according to the BNF, and what are the alternatives?

A

Answer:

First-line: Doxycycline (not suitable for children or pregnant women)
Alternatives: Amoxicillin

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25
Q

Question: What are the most common bacterial causes of acute exacerbations of COPD?

A

Haemophilus influenzae (most common)
Streptococcus pneumoniae
Moraxella catarrhalis

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26
Q

Question: What are the most important respiratory viruses that cause COPD exacerbations, and what percentage do they account for?

A

Answer: Respiratory viruses account for around 30% of exacerbations, with human rhinovirus being the most important pathogen.

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27
Q

Question: What are the typical features of an acute exacerbation of COPD?

A

Increase in dyspnoea, cough, wheeze
Possible increase in sputum suggestive of an infective cause
Patients may be hypoxic and, in some cases, have acute confusion

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28
Q

Question: According to NICE guidelines from 2010, what is recommended for the management of an acute exacerbation of COPD?

A

Increase the frequency of bronchodilator use, consider nebuliser
Prednisolone 30 mg daily for 5 days
Antibiotics if sputum is purulent or there are clinical signs of pneumonia
First-line antibiotics: amoxicillin, clarithromycin, or doxycycline

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29
Q

Question: What are the admission criteria for acute exacerbations of COPD?

A

Severe breathlessness
Acute confusion or impaired consciousness
Cyanosis
Oxygen saturation < 90% on pulse oximetry
Social reasons (e.g., inability to cope at home)
Significant comorbidity (e.g., cardiac disease, insulin-dependent diabetes)

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30
Q

Question: What is the initial oxygen saturation target for COPD patients at risk of hypercapnia, and what device should be used?

A

An initial oxygen saturation target of 88-92% should be used. A 28% Venturi mask at 4 l/min should be used until blood gas results are available.

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31
Q

Question: What are the nebulised bronchodilators recommended for severe exacerbations of COPD?

A

Beta adrenergic agonists: e.g., salbutamol
Muscarinic antagonists: e.g., ipratropium

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32
Q

Question: What steroid therapy is recommended for acute exacerbations of COPD, and when might IV hydrocortisone be considered?

A

Prednisolone 30 mg orally daily for 5 days
IV hydrocortisone may be considered instead of oral prednisolone in some cases

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33
Q

Question: When might IV theophylline be considered in the management of acute exacerbations of COPD?

A

Answer: IV theophylline may be considered for patients not responding to nebulised bronchodilators.

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34
Q

Question: What type of respiratory failure are patients with COPD prone to develop, and what is a common treatment for it?

A

Answer: Patients with COPD are prone to develop type 2 respiratory failure. Non-invasive ventilation (NIV) may be used, typically with bilevel positive airway pressure (BiPAP).

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35
Q

Question: What is the primary pathological mechanism in Acute Respiratory Distress Syndrome (ARDS)?

A

Answer: ARDS is caused by the increased permeability of alveolar capillaries, leading to fluid accumulation in the alveoli, resulting in non-cardiogenic pulmonary oedema.

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36
Q

Question: What is the approximate mortality rate associated with ARDS?

A

Answer: The mortality rate of ARDS is around 40%.

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37
Q

Question: What are the common causes of ARDS?

A

Infection: sepsis, pneumonia
Massive blood transfusion
Trauma
Smoke inhalation
Acute pancreatitis
COVID-19
Cardio-pulmonary bypass

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38
Q

Question: What are the typical clinical features of ARDS?

A

Dyspnoea
Elevated respiratory rate
Bilateral lung crackles
Low oxygen saturations

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39
Q

Question: What are the key investigations for diagnosing ARDS?

A

Chest x-ray
Arterial blood gases (ABGs)

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40
Q

Question: What are the American-European Consensus Conference criteria for diagnosing ARDS?

A

Acute onset (within 1 week of a known risk factor)
Pulmonary oedema: bilateral infiltrates on chest x-ray (not fully explained by effusions, lobar/lung collapse, or nodules)
Non-cardiogenic: pulmonary artery wedge pressure needed if doubt
pO2/FiO2 < 40 kPa (300 mmHg)

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41
Q

Question: What is the general management approach for ARDS?

A

Oxygenation/ventilation to treat hypoxaemia
General organ support: e.g., vasopressors as needed
Treatment of the underlying cause: e.g., antibiotics for sepsis

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42
Q

Question: Which specific strategies have been shown to improve outcomes in ARDS?

A

Prone positioning
Muscle relaxation

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43
Q

Question: What causes Allergic Bronchopulmonary Aspergillosis (ABPA)?

A

Answer: ABPA results from an allergy to Aspergillus spores.

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44
Q

Question: What clinical history is often associated with ABPA in exam questions?

A

Answer: A history of bronchiectasis and eosinophilia.

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45
Q

Question: What are the typical features of ABPA?

A

Bronchoconstriction: wheeze, cough, dyspnoea (patients may have a previous diagnosis of asthma)
Bronchiectasis (proximal)

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46
Q

Question: What investigations are commonly conducted for ABPA?

A

Eosinophilia
Flitting CXR changes
Positive radioallergosorbent (RAST) test to Aspergillus
Positive IgG precipitins (not as positive as in aspergilloma)
Raised IgE

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47
Q

Question: What is the first-line management for ABPA?

A

Answer: Oral glucocorticoids

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48
Q

Question: What is a potential second-line agent for managing ABPA?

A

Answer: Itraconazole

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49
Q

Question: What is Alpha-1 Antitrypsin (A1AT) deficiency?

A

Answer: A1AT deficiency is a common inherited condition caused by a lack of a protease inhibitor normally produced by the liver. It protects cells from enzymes such as neutrophil elastase and classically causes emphysema in young, non-smoking patients.

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50
Q

Question: What are the features of A1AT deficiency?

A

Lungs: Panacinar emphysema, most marked in the lower lobes
Liver: Cirrhosis and hepatocellular carcinoma in adults, cholestasis in children

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51
Q

Question: What investigations are used to diagnose A1AT deficiency?

A

A1AT concentrations
Spirometry: Shows an obstructive pattern

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52
Q

Question: What are the management strategies for A1AT deficiency?

A

No smoking
Supportive care: Bronchodilators, physiotherapy
Intravenous alpha1-antitrypsin protein concentrates
Surgery: Lung volume reduction surgery, lung transplantation

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53
Q

Question: What is the threshold for hypoxaemia in ABG interpretation?

A

Answer: A PaO2 less than 10 kPa indicates hypoxaemia.

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54
Q

What are the steps in interpreting ABG

A

Answer: How is the patient? Assess the overall clinical condition of the patient.
Answer: Is the patient hypoxaemic? The PaO2 on air should be >10 kPa.
Answer: Is the patient acidaemic or alkalaemic? Determine if the pH is <7.35 (acidaemia) or >7.45 (alkalaemia).
Answer: Respiratory component: What has happened to the PaCO2?
Answer: Metabolic component: What is the bicarbonate level/base excess?

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55
Q

Question: What indicates acidaemia in ABG interpretation?

A

Answer: A pH less than 7.35 indicates acidaemia.

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56
Q

Question: What indicates alkalaemia in ABG interpretation?

A

Answer: A pH greater than 7.45 indicates alkalaemia.

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57
Q

Question: What does a PaCO2 > 6.0 kPa suggest?

A

Answer: A PaCO2 > 6.0 kPa suggests respiratory acidosis (or respiratory compensation for a metabolic alkalosis).

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58
Q

Question: What does a PaCO2 < 4.7 kPa suggest?

A

Answer: A PaCO2 < 4.7 kPa suggests respiratory alkalosis (or respiratory compensation for a metabolic acidosis).

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59
Q

Question: What does a bicarbonate level < 22 mmol/L or a base excess < -2 mmol/L suggest?

A

Answer: A bicarbonate level < 22 mmol/L or a base excess < -2 mmol/L suggests metabolic acidosis (or renal compensation for a respiratory alkalosis).

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60
Q

Question: What does a bicarbonate level > 26 mmol/L or a base excess > +2 mmol/L suggest?

A

Answer: A bicarbonate level > 26 mmol/L or a base excess > +2 mmol/L suggests metabolic alkalosis (or renal compensation for a respiratory acidosis).

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61
Q

Question: What is the most common form of asbestos-related lung disease?

A

Answer: Pleural plaques are the most common form of asbestos-related lung disease.

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62
Q

Question: Are pleural plaques malignant?

A

Answer: No, pleural plaques are benign and do not undergo malignant change. They do not require follow-up.

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63
Q

Question: How long is the latent period for pleural plaques?

A

Answer: The latent period for pleural plaques is typically 20-40 years after asbestos exposure.

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64
Q

Question: What is pleural thickening in asbestos exposure?

A

Answer: Pleural thickening is a condition that may occur following asbestos exposure and resembles patterns seen after empyema or haemothorax. Its pathophysiology is not fully understood.

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65
Q

Question: What is the typical latent period for asbestosis?

A

Answer: The latent period for asbestosis is typically 15-30 years.

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66
Q

Question: What are the common features of asbestosis?

A

Dyspnoea and reduced exercise tolerance
Clubbing
Bilateral end-inspiratory crackles
Restrictive pattern with reduced gas transfer on lung function tests

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67
Q

Question: How is asbestosis treated?

A

Answer: Asbestosis is treated conservatively, as no interventions offer significant benefit.

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68
Q

Question: What is mesothelioma?

A

Answer: Mesothelioma is a malignant disease of the pleura, often caused by asbestos exposure, particularly crocidolite (blue) asbestos.

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69
Q

Question: What are the common features of mesothelioma?

A

Progressive shortness of breath
Chest pain
Pleural effusion

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70
Q

Question: What is the prognosis for mesothelioma?

A

Answer: The prognosis for mesothelioma is very poor, with a median survival from diagnosis of 8-14 months.

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71
Q

Question: What is the most common form of cancer associated with asbestos exposure?

A

Answer: Lung cancer is the most common form of cancer associated with asbestos exposure.

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72
Q

Question: How does smoking affect the risk of lung cancer in patients exposed to asbestos?

A

Answer: Smoking increases the risk of lung cancer in individuals with asbestos exposure. The combination of asbestos exposure and smoking has a synergistic effect, significantly raising the risk.

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73
Q

Question: What is aspiration pneumonia?

A

Answer: Aspiration pneumonia is a pneumonia that develops as a result of foreign materials (usually oral or gastric contents) entering the bronchial tree, causing inflammation and infection.

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74
Q

Question: What are the common causes of aspiration pneumonia?

A

Common causes include:

Incompetent swallowing mechanisms (e.g., neurological diseases such as stroke, multiple sclerosis, or intoxication)
Iatrogenic causes (e.g., intubation)

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75
Q

Question: What are the risk factors for aspiration pneumonia?

A

Risk factors include:

Poor dental hygiene
Swallowing difficulties
Prolonged hospitalization or surgical procedures
Impaired consciousness
Impaired mucociliary clearance

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76
Q

Question: Which lung lobes are most commonly affected by aspiration pneumonia?

A

Answer: The right middle and lower lung lobes are most commonly affected due to the larger calibre and more vertical orientation of the right main bronchus.

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77
Q

Question: What types of bacteria are implicated in aspiration pneumonia?

A

Both aerobic and anaerobic bacteria can cause aspiration pneumonia.

Aerobic bacteria:

Streptococcus pneumoniae
Staphylococcus aureus
Haemophilus influenzae
Pseudomonas aeruginosa
Klebsiella (often seen in aspiration lobar pneumonia in alcoholics)
Anaerobic bacteria:

Bacteroides
Prevotella
Fusobacterium
Peptostreptococcus

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78
Q

Question: What is asthma?

A

Answer: Asthma is a chronic inflammatory disorder of the airways caused by type 1 hypersensitivity, leading to variable and recurring symptoms such as reversible bronchospasm, airway obstruction, and difficulty breathing.

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79
Q

Question: What are common risk factors for developing asthma?

A

Risk factors include:

Personal or family history of atopy
Maternal smoking, viral infections during pregnancy, low birth weight, not being breastfed
Exposure to allergens (e.g., house dust mite)
Air pollution and the “hygiene hypothesis”
Occupational allergens (e.g., isocyanates, flour)

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80
Q

Question: What are common symptoms of asthma?

A

Cough (often worse at night)
Dyspnoea (difficulty breathing)
Wheeze and chest tightness

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81
Q

Question: What are the signs of asthma on examination?

A

Expiratory wheeze on auscultation
Reduced peak expiratory flow rate (PEFR)

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82
Q

Question: How is asthma diagnosed?

A

Diagnosis is confirmed using spirometry which shows:

Reduced FEV1 (forced expiratory volume in 1 second)
Normal FVC (forced vital capacity)
FEV1/FVC ratio < 70%
Other tests include fractional exhaled nitric oxide (FeNO) to assess inflammation and chest x-ray for older or smoking patients.

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83
Q

Question: What are the main drug classes used in asthma management?

A

Drug classes include:

Short-acting beta-agonists (SABA) (e.g., Salbutamol) – for acute relief
Inhaled corticosteroids (ICS) (e.g., Beclometasone) – for long-term control
Long-acting beta-agonists (LABA) (e.g., Salmeterol) – for maintenance
Leukotriene receptor antagonists (e.g., Montelukast) – oral medication

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84
Q

Question: What is Maintenance and Reliever Therapy (MART)?

A

Answer: MART is a combined therapy of ICS and LABA, where a single inhaler containing both is used for both daily maintenance and symptom relief. It requires a fast-acting LABA (e.g., formoterol).

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85
Q

Question: What is the first-line investigation for suspected asthma in adults according to the 2024 NICE guidelines?

A

The first-line investigations include measuring:

Eosinophil count, or
Fractional exhaled nitric oxide (FeNO)
If eosinophil count is above the reference range or FeNO is ≥ 50 ppb, asthma can be diagnosed without further investigations.

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86
Q

Question: What is the diagnostic threshold for bronchodilator reversibility (BDR) in adults with suspected asthma?

A

Asthma is diagnosed if:

The FEV1 increase is ≥ 12% and 200 mL from the pre-bronchodilator measurement, or
The FEV1 increase is ≥ 10% of the predicted normal FEV1

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87
Q

Question: If spirometry is not available in adults, how can asthma be diagnosed?

A

If spirometry is not available or delayed, peak expiratory flow (PEF) can be measured twice daily for 2 weeks. Asthma is diagnosed if:

PEF variability (amplitude percentage mean) is ≥ 20%

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88
Q

Question: What is the diagnostic threshold for FeNO in children aged 5-16?

A

Answer: Asthma is diagnosed in children aged 5-16 if FeNO is ≥ 35 ppb.

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89
Q

Question: What investigations are used to diagnose asthma in children aged 5-16 if FeNO is not raised?

A

If FeNO is not raised or not available, the following tests are used:

Bronchodilator reversibility (BDR) with spirometry, diagnosing asthma if FEV1 increase is ≥ 12% or ≥ 10% of the predicted normal FEV1.
If spirometry is unavailable, PEF variability (≥ 20%) over 2 weeks may support diagnosis.
Skin prick testing or measuring total IgE levels to assess allergen sensitivity.

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90
Q

Question: How should asthma be diagnosed in children under 5 according to NICE guidelines?

A

In children under 5, diagnosis is challenging. The guidelines suggest:

Treating with inhaled corticosteroids and regular review.
Referral to a specialist if there are 2 or more emergency admissions with wheezing in 12 months.

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91
Q

Question: What role do eosinophils play in asthma?

A

Answer: Eosinophils are involved in type 2 inflammation, releasing cytotoxic proteins that damage epithelial cells and perpetuate inflammation. They are a key marker for disease activity in asthma.

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92
Q

Question: What does FeNO reflect in asthma diagnosis?

A

Answer: FeNO reflects the level of nitric oxide produced by airway epithelial cells in response to eosinophilic inflammation, a hallmark of asthma. It is measured non-invasively in parts per billion (ppb).

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93
Q

Question: What is the significance of bronchodilator reversibility (BDR) in asthma diagnosis?

A

Answer: BDR testing evaluates the reversibility of airway obstruction after bronchodilator administration. In asthma, an increase in FEV1 of ≥ 12% and ≥ 200 mL confirms reversible airway obstruction, distinguishing asthma from fixed obstruction (e.g., COPD).

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94
Q

Question: How does peak expiratory flow (PEF) variability help diagnose asthma?

A

Answer: PEF variability reflects diurnal changes in airway calibre due to underlying inflammation and smooth muscle tone. A ≥ 20% variation in PEF between morning and evening supports the diagnosis of asthma.

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95
Q

Question: What is the role of skin prick testing in diagnosing asthma in children?

A

Answer: Skin prick testing for house dust mite is used to identify sensitisation to common allergens, such as house dust mite, which may trigger asthma. Sensitisation supports the diagnosis of allergic asthma.

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96
Q

Question: What is the bronchial challenge test used for in asthma diagnosis?

A

Answer: The bronchial challenge test assesses airway hyperresponsiveness by exposing the airways to a provocative agent (e.g., methacholine or histamine). A significant decline in FEV1 indicates asthma.

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97
Q

Question: What is the first-line treatment for newly diagnosed asthma in adults aged ≥12 according to the 2024 NICE guidelines?

A

Answer: The first-line treatment is a low-dose inhaled corticosteroid (ICS)/formoterol combination inhaler to be taken as needed for symptom relief. This is known as anti-inflammatory reliever (AIR) therapy.

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98
Q

Question: What is the recommended treatment for a patient with newly diagnosed asthma who presents with severe exacerbation or highly symptomatic (e.g., regular nocturnal waking)?

A

Answer: For such patients, start treatment with low-dose Maintenance and Reliever Therapy (MART), which includes a combination of ICS/formoterol for daily maintenance and as needed for symptom relief. Acute symptoms may also require oral corticosteroids.

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99
Q

Question: What does Maintenance and Reliever Therapy (MART) consist of?

A

Answer: MART involves using a combination inhaler containing ICS and formoterol for both daily maintenance therapy and the relief of symptoms as needed, i.e., regularly and as required.

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100
Q

Question: How is asthma management escalated to Step 3 in adults according to the NICE guidelines?

A

Answer: In Step 3, the treatment involves a moderate-dose MART, which is a combination of ICS and formoterol at a higher dose.

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101
Q

Question: What should be done at Step 4 if asthma control is inadequate despite moderate-dose MART?

A

Answer: At Step 4, check fractional exhaled nitric oxide (FeNO) and blood eosinophil count. If either is raised, refer to a specialist. If neither is raised, trial either a leukotriene receptor antagonist (LTRA) or a long-acting muscarinic antagonist (LAMA) alongside moderate-dose MART. If control does not improve, switch to the alternative treatment (LTRA or LAMA).

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102
Q

Question: What is the recommended action if asthma control is still not achieved at Step 5 despite treatment?

A

Answer: Refer the patient to a specialist in asthma care if asthma is not controlled despite treatment with moderate-dose MART and trials of LTRA or LAMA.

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103
Q

Question: What is the recommended treatment for adults with asthma who were previously managed with SABA as required only?

A

Answer: Switch the patient to a low-dose ICS/formoterol combination inhaler used as needed, which is now termed anti-inflammatory reliever (AIR) therapy.

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104
Q

Question: How should patients previously managed with SABA and regular low-dose ICS or LABA be treated according to the new guidelines?

A

Answer: These patients should be transitioned to a regular low-dose ICS/formoterol combination inhaler as Maintenance and Reliever Therapy (MART).

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105
Q

Question: What is the recommended treatment for patients previously managed with moderate-dose ICS and other add-ons like LTRA or LAMA?

A

Answer: These patients should be transitioned to a regular moderate-dose ICS/formoterol combination inhaler as part of MART therapy.

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106
Q

Question: What should be done for patients currently on high-dose ICS for asthma management?

A

Answer: Patients on high-dose ICS should be referred to a respiratory specialist.

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107
Q

Question: What symptoms may suggest that a patient’s asthma is related to their occupation?

A

Answer: Symptoms may worsen at work and improve on weekends or when away from work. Patients may also report concerns that chemicals or substances at work are exacerbating their asthma.

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108
Q

Question: What are some common chemicals associated with occupational asthma?

A

Chemicals commonly associated with occupational asthma include:

Isocyanates (most common cause)
Platinum salts
Soldering flux resin
Glutaraldehyde
Flour
Epoxy resins
Proteolytic enzymes

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109
Q

Question: Which occupations are at higher risk for occupational asthma due to isocyanate exposure?

A

Answer: Occupations at higher risk include spray painting and foam moulding using adhesives, where isocyanates are commonly used.

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110
Q

Question: How can occupational asthma be investigated?

A

Answer: Serial measurements of peak expiratory flow (PEF) are recommended to be taken both at work and away from work to assess variability and identify patterns related to the workplace.

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111
Q

Question: How often should asthma treatment be stepped down, according to the British Thoracic Society (BTS) guidelines?

A

Answer: Asthma treatment should be considered for stepping down every 3 months, or more frequently if the patient has had recent treatment escalation.

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112
Q

Question: What factors should be considered when stepping down asthma treatment?

A

Duration of treatment
Side effects of treatment
Patient preference

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113
Q

Question: When reducing the dose of inhaled steroids, what is the recommended decrease according to the BTS guidelines?

A

Answer: The recommended decrease in inhaled steroids is 25-50% at a time.

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114
Q

Question: How often should stable asthma patients be formally reviewed?

A

Answer: Stable asthma patients should be formally reviewed on an annual basis, although more frequent reviews may be needed after recent treatment escalation.

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115
Q

Question: What is atelectasis?

A

Answer: Atelectasis is a common postoperative complication where basal alveolar collapse leads to respiratory difficulty, often caused by airway obstruction due to bronchial secretions.

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116
Q

Question: When should atelectasis be suspected in a postoperative patient?

A

Answer: Atelectasis should be suspected when a patient presents with dyspnoea and hypoxaemia around 72 hours postoperatively.

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117
Q

Question: What is the management for atelectasis?

A

Positioning the patient upright
Chest physiotherapy, including breathing exercises

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118
Q

Question: What are the most common causes of bilateral hilar lymphadenopathy?

A

Sarcoidosis
Tuberculosis

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119
Q

Question: What are other causes of bilateral hilar lymphadenopathy?

A

Lymphoma or other malignancies
Pneumoconiosis (e.g., berylliosis)
Fungal infections (e.g., histoplasmosis, coccidioidomycosis)

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120
Q

Question: What are the key features of bronchiectasis?

A

Persistent productive cough with large volumes of sputum
Dyspnoea
Haemoptysis

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121
Q

Question: What signs might be observed in a patient with bronchiectasis?

A

Signs include:

Abnormal chest auscultation
Coarse crackles
Wheeze
Clubbing (may be present)

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122
Q

Question: What are the key management strategies for bronchiectasis after assessing for treatable causes?

A

Physical training (e.g. inspiratory muscle training)
Postural drainage
Antibiotics for exacerbations and long-term rotating antibiotics in severe cases
Bronchodilators in selected cases
Immunisations
Surgery in selected cases (e.g., localized disease)

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123
Q

Question: What are the most common organisms isolated from patients with bronchiectasis?

A

Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae

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124
Q

Question: What are the common indications for chest drain insertion?

A

Pleural effusion
Pneumothorax (not suitable for conservative management or aspiration)
Empyema
Haemothorax
Haemopneumothorax
Chylothorax
Some cases of penetrating chest wall injury in ventilated patients

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125
Q

Question: What are the relative contraindications for chest drain insertion?

A

INR > 1.3
Platelet count < 75
Pulmonary bullae
Pleural adhesions

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126
Q

Question: What is the recommended positioning for a patient undergoing chest drain insertion?

A

The patient should be positioned:

In a supine position or at a 45º angle
Forearm behind the head for easy axillary access
Use ultrasound guidance to determine the optimal position, especially for fluid within the pleura

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127
Q

Question: What are the complications that may occur during chest drain insertion?

A

Failure of insertion (e.g., drain in wrong position)
Bleeding (around the site or into the pleural space)
Infection
Penetration of the lung
Re-expansion pulmonary oedema

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128
Q

Question: How is re-expansion pulmonary oedema managed after chest drain insertion?

A

If re-expansion pulmonary oedema is suspected:

Clamp the chest drain
Obtain an urgent chest x-ray
To prevent, avoid rapid fluid output (e.g., no more than 1L in less than 6 hours)

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129
Q

Question: When should a chest drain be removed in cases of fluid drainage or pneumothorax?

A

For fluid drainage: Remove the drain after >24 hours of no output and imaging showing resolution of fluid.
For pneumothorax: Remove when no bubbling is seen and imaging shows resolution.

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130
Q

Question: What are the key features of the ‘safe triangle’ for chest drain insertion?

A

The ‘safe triangle’ for chest drain insertion is located:

In the mid-axillary line at the 5th intercostal space.
Bordered by:
Anterior edge of the latissimus dorsi
Lateral border of the pectoralis major
A line superior to the horizontal level of the nipple
Apex below the axilla

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131
Q

Question: What are the general guidelines for choosing the size of the chest drain based on the indication?

A

Large bore chest drains are preferred for trauma and haemothorax drainage.
Smaller diameter chest drains are used for pneumothorax or pleural effusion drainage.

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132
Q

Question: What are the main differential diagnoses for a cavitating lung lesion on a chest x-ray?

A

Abscess (e.g., Staphylococcus aureus, Klebsiella, Pseudomonas)
Squamous cell lung cancer
Tuberculosis
Wegener’s granulomatosis
Pulmonary embolism
Rheumatoid arthritis
Fungal infections (e.g., Aspergillosis, Histoplasmosis, Coccidioidomycosis)

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133
Q

Question: Which bacterial organisms are commonly associated with lung abscesses causing cavitating lesions?

A

Staphylococcus aureus
Klebsiella
Pseudomonas

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134
Q

Question: Which types of cancer may present with cavitating lung lesions?

A

Answer: Squamous cell lung cancer can present with cavitating lung lesions on a chest x-ray.

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135
Q

Question: What is the relevance of tuberculosis in cavitating lung lesions?

A

Answer: Tuberculosis can lead to cavitating lung lesions, which can be detected on a chest x-ray.

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136
Q

Question: How does Wegener’s granulomatosis present on a chest x-ray?

A

Answer: Wegener’s granulomatosis can present with cavitating lung lesions on a chest x-ray due to granulomatous inflammation in the lungs.

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137
Q

Question: What role does rheumatoid arthritis play in cavitating lung lesions?

A

Answer: Rheumatoid arthritis can cause cavitating lung lesions, especially in the context of rheumatoid nodules or associated interstitial lung disease.

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138
Q

Question: Which fungal infections can lead to cavitating lung lesions?

A

Answer: Fungal infections such as Aspergillosis, Histoplasmosis, and Coccidioidomycosis can cause cavitating lung lesions.

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139
Q

Question: What are the common causes of lobar collapse on a chest x-ray?

A

Lung cancer (most common cause in older adults)
Asthma (due to mucous plugging)
Foreign body

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140
Q

Question: What are the general signs of lobar collapse on a chest x-ray?

A

Tracheal deviation towards the side of the collapse
Mediastinal shift towards the side of the collapse
Elevation of the hemidiaphragm

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141
Q

Question: How does lung cancer cause lobar collapse?

A

Answer: Lung cancer can obstruct the bronchus, leading to a lobar collapse due to blockage of airflow.

142
Q

Question: How does asthma lead to lobar collapse?

A

Answer: Asthma can lead to lobar collapse due to mucous plugging in the airways, causing obstruction and collapse of the lung segment.

143
Q

Question: How does a foreign body cause lobar collapse?

A

Answer: A foreign body can obstruct an airway, leading to lobar collapse as the affected lung cannot fully expand due to the blockage.

144
Q

Question: What types of cancer are commonly associated with lung metastases?

A

Breast cancer
Colorectal cancer
Renal cell cancer
Bladder cancer
Prostate cancer

145
Q

Question: What are ‘cannonball metastases’?

A

Answer: Cannonball metastases are multiple, round, well-defined lung secondaries, often seen in renal cell cancer. They can also occur due to choriocarcinoma and prostate cancer.

146
Q

Question: In which cancers is lung metastases calcification uncommon?

A

Answer: Calcification in lung metastases is rare except in cases of chondrosarcoma or osteosarcoma.

147
Q

Question: What are the typical radiographic features of cannonball metastases on a chest x-ray?

A

Answer: On chest x-ray, cannonball metastases appear as multiple, well-defined, round nodules distributed in both lung fields. They are most commonly associated with renal cell cancer.

148
Q

Question: What is the most common cause of mediastinal widening on a chest x-ray?

A

Answer: The most common cause of mediastinal widening on a chest x-ray is technical factors, such as patient rotation.

149
Q

Question: What are the potential causes of actual mediastinal widening on a chest x-ray?

A

Vascular problems: Thoracic aortic aneurysm
Lymphoma
Retrosternal goitre
Teratoma
Tumours of the thymus

150
Q

Question: How can a lateral chest x-ray view assist in evaluating mediastinal widening?

A

Answer: A lateral view can help determine whether the mass causing the mediastinal widening is anterior or posterior.

151
Q

Question: What is the preferred method for further investigation if there is doubt about the cause of mediastinal widening?

A

Answer: CT imaging is typically performed if there is any doubt about the cause of mediastinal widening, as it provides more detailed information.

152
Q

Question: What are some features of pulmonary oedema seen on a chest x-ray?

A

Interstitial oedema
Bat’s wing appearance
Upper lobe diversion (increased blood flow to the superior parts of the lung)
Kerley B lines
Pleural effusion
Cardiomegaly (may be seen if the cause is cardiogenic)

153
Q

Question: What are the cardiac causes of clubbing?

A

Cyanotic congenital heart disease (e.g., Fallot’s, TGA)
Bacterial endocarditis
Atrial myxoma

154
Q

Question: What are the respiratory causes of clubbing?

A

Lung cancer
Pyogenic conditions (e.g., cystic fibrosis, bronchiectasis, abscess, empyema)
Tuberculosis
Asbestosis, mesothelioma
Fibrosing alveolitis

155
Q

Question: What are the other causes of clubbing?

A

Crohn’s disease (to a lesser extent UC)
Cirrhosis, primary biliary cirrhosis
Graves’ disease (thyroid acropachy)
Rarely: Whipple’s disease

156
Q

Question: What is the most common cause of COPD?

A

Answer: Smoking is the most common cause of COPD.

157
Q

Question: What is another genetic cause of COPD?

A

Answer: Alpha-1 antitrypsin deficiency is another cause of COPD.

158
Q

Question: What are some occupational and environmental causes of COPD?

A

Cadmium (used in smelting)
Coal
Cotton
Cement
Grain

159
Q

Question: What are the main features of Chronic Obstructive Pulmonary Disease (COPD)?

A

Cough (often productive)
Dyspnoea
Wheeze
In severe cases, right-sided heart failure may develop, leading to peripheral oedema.

160
Q

Question: What investigations are recommended in patients with suspected COPD?

A

Post-bronchodilator spirometry (to show airflow obstruction with FEV1/FVC ratio < 70%)
Chest x-ray (for hyperinflation, bullae, flat hemidiaphragm, and to exclude lung cancer)
Full blood count (to exclude secondary polycythaemia)
BMI calculation

161
Q

Question: How is the severity of COPD classified?

A

Stage 1 - Mild: FEV1/FVC < 0.7, FEV1 > 80%
Stage 2 - Moderate: FEV1/FVC < 0.7, FEV1 50-79%
Stage 3 - Severe: FEV1/FVC < 0.7, FEV1 30-49%
Stage 4 - Very Severe: FEV1/FVC < 0.7, FEV1 < 30%

162
Q

Question: What is the limitation of using peak expiratory flow (PEF) in COPD diagnosis?

A

Answer: PEF is of limited value in diagnosing COPD, as it may underestimate the degree of airflow obstruction.

163
Q

Question: Who should be assessed for long-term oxygen therapy (LTOT) in COPD patients according to NICE guidelines?

A

Very severe airflow obstruction (FEV1 < 30% predicted) or severe obstruction (FEV1 30-49% predicted)
Cyanosis
Polycythaemia
Peripheral oedema
Raised jugular venous pressure
Oxygen saturations ≤ 92% on room air

164
Q

Question: How is the assessment for LTOT performed in COPD patients?

A

Answer: The assessment for LTOT is done by measuring arterial blood gases on 2 occasions, at least 3 weeks apart, in patients with stable COPD on optimal management.

165
Q

Question: What are the criteria for offering LTOT to COPD patients?

A

pO2 < 7.3 kPa (in any patient)
pO2 7.3 - 8 kPa with one of the following:
Secondary polycythaemia
Peripheral oedema
Pulmonary hypertension

166
Q

Question: What does NICE recommend regarding LTOT for patients who continue to smoke?

A

Answer: NICE recommends not offering LTOT to patients who continue to smoke despite being offered smoking cessation advice and treatment, and referral to specialist stop smoking services.

167
Q

Question: What structured risk assessments should be carried out before offering LTOT?

A

Risks of falls from tripping over the equipment
Risks of burns and fires, particularly for people who live in homes with smokers (including e-cigarettes)

168
Q

Question: What general management strategies are recommended for stable COPD according to NICE guidelines?

A

Smoking cessation advice, including offering nicotine replacement therapy, varenicline, or bupropion
Annual influenza vaccination
One-off pneumococcal vaccination
Pulmonary rehabilitation for people who are functionally disabled by COPD (usually MRC grade 3 and above)

169
Q

Question: What is the first-line bronchodilator therapy for stable COPD?

A

Answer: The first-line treatment is a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA).

170
Q

Question: What should be done if a COPD patient remains breathless or experiences exacerbations despite using short-acting bronchodilators?

A

The next step depends on whether the patient has asthmatic features or features suggesting steroid responsiveness.

No asthmatic features/steroid responsiveness: Add a long-acting beta2-agonist (LABA) + long-acting muscarinic antagonist (LAMA).
Asthmatic features/steroid responsiveness: Add LABA + inhaled corticosteroid (ICS). If further exacerbations occur, offer triple therapy (LAMA + LABA + ICS).

171
Q

Question: When is oral theophylline recommended in COPD management?

A

Answer: Theophylline is recommended only after trials of short and long-acting bronchodilators or in patients who cannot use inhaled therapy.

172
Q

Question: When is oral prophylactic antibiotic therapy recommended in COPD?

A

Azithromycin prophylaxis is recommended for select patients who:

Do not smoke
Have optimised standard treatments
Continue to have exacerbations
Have had a CT thorax to exclude bronchiectasis and sputum culture to exclude atypical infections and tuberculosis
Have normal LFTs and an ECG to exclude QT prolongation.

173
Q

Question: What are the indications for using mucolytics in stable COPD?

A

Answer: Mucolytics should be considered in patients with a chronic productive cough and continued if symptoms improve.

174
Q

Question: When are phosphodiesterase-4 (PDE-4) inhibitors recommended for COPD?

A

Answer: PDE-4 inhibitors (e.g., roflumilast) are recommended for patients with severe COPD (FEV1 < 50% predicted) and a history of frequent exacerbations despite triple inhaled therapy (LAMA, LABA, ICS).

175
Q

Question: What is the management for cor pulmonale in stable COPD?

A

For cor pulmonale, features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, and loud P2. Management includes:

Use of loop diuretics for oedema
Consideration of long-term oxygen therapy
ACE inhibitors, calcium channel blockers, and alpha blockers are not recommended.

176
Q

Question: What are the key features of Eosinophilic Granulomatosis with Polyangiitis (EGPA)?

A

Asthma
Blood eosinophilia (e.g., > 10%)
Paranasal sinusitis
Mononeuritis multiplex
pANCA positivity (in 60% of cases)

177
Q

Question: What medication is associated with precipitating the disease in Eosinophilic Granulomatosis with Polyangiitis (EGPA)?

A

Answer: Leukotriene receptor antagonists may precipitate EGPA.

178
Q

Question: What is the cause of Extrinsic Allergic Alveolitis (EAA), also known as hypersensitivity pneumonitis?

A

Answer: EAA is caused by hypersensitivity-induced lung damage due to inhalation of various organic particles, leading to immune-complex mediated tissue damage (type III hypersensitivity) and delayed hypersensitivity (type IV) in the chronic phase.

179
Q

Question: What are some examples of conditions that lead to Extrinsic Allergic Alveolitis (EAA)?

A

Bird fanciers’ lung: Avian proteins from bird droppings
Farmers’ lung: Spores of Saccharopolyspora rectivirgula (from wet hay)
Malt workers’ lung: Aspergillus clavatus
Mushroom workers’ lung: Thermophilic actinomycetes

180
Q

Question: What are the clinical presentations of Extrinsic Allergic Alveolitis (EAA)?

A

Acute (4-8 hours after exposure): Dyspnoea, dry cough, fever
Chronic (weeks to months after exposure): Lethargy, dyspnoea, productive cough, anorexia, weight loss

181
Q

Question: What is the management for Extrinsic Allergic Alveolitis (EAA)?

A

Avoidance of precipitating factors
Oral glucocorticoids for inflammation control

182
Q

Question: What is Granulomatosis with Polyangiitis (formerly Wegener’s Granulomatosis)?

A

Answer: Granulomatosis with Polyangiitis is an autoimmune condition characterized by necrotizing granulomatous vasculitis that affects both the upper and lower respiratory tracts as well as the kidneys.

183
Q

Question: What are the clinical features of Granulomatosis with Polyangiitis?

A

Upper respiratory tract: Epistaxis, sinusitis, nasal crusting
Lower respiratory tract: Dyspnoea, haemoptysis
Kidneys: Rapidly progressive glomerulonephritis (“pauci-immune” in 80% of patients)
Other features: Saddle-shaped nose deformity, vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions

184
Q

Question: What investigations are used for Granulomatosis with Polyangiitis?

A

cANCA positive in >90% of cases
pANCA positive in 25%
Chest x-ray: Can show a wide variety of presentations, including cavitating lesions
Renal biopsy: Epithelial crescents in Bowman’s capsule

185
Q

Question: What is the management for Granulomatosis with Polyangiitis?

A

Steroids (to control inflammation)
Cyclophosphamide (90% response)
Plasma exchange
Median survival: 8-9 years

186
Q

Question: What are the main causes of haemoptysis?

A

Lung cancer - History of smoking, weight loss, anorexia
Pulmonary oedema - Dyspnoea, bibasal crackles, S3
Tuberculosis - Fever, night sweats, anorexia, weight loss
Pulmonary embolism - Pleuritic chest pain, tachycardia, tachypnoea
Lower respiratory tract infection - Acute history of purulent cough
Bronchiectasis - Long history of cough, daily purulent sputum production
Mitral stenosis - Dyspnoea, atrial fibrillation, malar flush, mid-diastolic murmur
Aspergilloma - Past tuberculosis history, severe haemoptysis, chest x-ray shows rounded opacity
Granulomatosis with polyangiitis - Epistaxis, sinusitis, nasal crusting, haemoptysis, glomerulonephritis, saddle-nose deformity
Goodpasture’s syndrome - Haemoptysis, fever, nausea, glomerulonephritis

187
Q

Question: What are the characteristic symptoms of lung cancer causing haemoptysis?

A

History of smoking
Symptoms of malignancy: weight loss, anorexia

188
Q

Question: What are the key signs of pulmonary oedema with haemoptysis?

A

Dyspnoea
Bibasal crackles
S3 heart sound (most reliable signs)

189
Q

Question: What are the characteristic features of tuberculosis causing haemoptysis?

A

Fever, night sweats
Anorexia, weight loss

190
Q

Question: What are the features of pulmonary embolism associated with haemoptysis?

A

Pleuritic chest pain
Tachycardia, tachypnoea

191
Q

Question: What is the clinical presentation of bronchiectasis causing haemoptysis?

A

Long history of cough
Daily purulent sputum production

192
Q

Question: What are the signs and symptoms of mitral stenosis associated with haemoptysis?

A

Dyspnoea, atrial fibrillation
Malar flush on cheeks
Mid-diastolic murmur

193
Q

Question: What are the key features of aspergilloma causing haemoptysis?

A

Often a past history of tuberculosis
Severe haemoptysis
Chest x-ray: Rounded opacity

194
Q

Question: What are the symptoms of Granulomatosis with Polyangiitis causing haemoptysis?

A

Upper respiratory tract: Epistaxis, sinusitis, nasal crusting
Lower respiratory tract: Dyspnoea, haemoptysis
Glomerulonephritis, saddle-nose deformity

195
Q

Question: What are the features of Goodpasture’s syndrome causing haemoptysis?

A

Haemoptysis
Systemically unwell: fever, nausea
Glomerulonephritis

196
Q

Question: What is Idiopathic Pulmonary Fibrosis (IPF)?

A

Answer: IPF is a chronic lung condition characterized by progressive fibrosis of the lung interstitium. It occurs without an identifiable underlying cause, unlike other forms of lung fibrosis which may be secondary to medications, connective tissue disease, or asbestos exposure.

197
Q

Question: What are the common features of Idiopathic Pulmonary Fibrosis (IPF)?

A

Progressive exertional dyspnoea (shortness of breath)
Bibasal fine end-inspiratory crepitations (crackles) on auscultation
Dry cough
Clubbing (nail deformity)

198
Q

Question: What are the diagnostic tests for Idiopathic Pulmonary Fibrosis (IPF)?

A

Spirometry:
Restrictive pattern: FEV1 normal or decreased, FVC decreased, FEV1/FVC increased
Gas exchange: Reduced transfer factor (TLCO)
Imaging:
Chest x-ray: Bilateral interstitial shadowing with ground-glass opacities, progressing to honeycombing
High-resolution CT scan: Preferred for diagnosis
Serology:
ANA positive in 30%, rheumatoid factor positive in 10% (low titres, not necessarily indicative of connective tissue disease)

199
Q

Question: What is the management for Idiopathic Pulmonary Fibrosis (IPF)?

A

Pulmonary rehabilitation
Medications:
Pirfenidone (antifibrotic agent) may be useful for selected patients (evidence-based)
Supplementary oxygen may be required in advanced cases
Lung transplant: Considered for suitable candidates

200
Q

Question: What is the prognosis for Idiopathic Pulmonary Fibrosis (IPF)?

A

Answer: The prognosis is generally poor, with an average life expectancy of around 3-4 years after diagnosis.

201
Q

Question: What is the correct technique for using a metered-dose inhaler (MDI)?

A

Remove the cap and shake the inhaler.
Breathe out gently to empty the lungs.
Place the mouthpiece in your mouth. As you begin to breathe in slowly and deeply, press the canister down to release the medication, and continue inhaling steadily.
Hold your breath for 10 seconds (or as long as comfortable).
Wait for 30 seconds before repeating the process for a second dose (if needed).
Use the inhaler for the number of doses on the label and then start a new inhaler.

202
Q

Question: What are the key features of Klebsiella pneumoniae infections, and who is at higher risk?

A

Gram-negative rod that is part of the normal gut flora.
Commonly causes pneumonia, especially following aspiration.
More common in people with alcoholism and diabetes.
‘Red-currant jelly’ sputum is a characteristic sign.
Affects the upper lobes of the lungs.
Prognosis:
Frequently leads to lung abscess formation and empyema.
Mortality rate: 30-50%.

203
Q

Question: What are the common causes of lung abscess?

A

Aspiration pneumonia (most common)
Haematogenous spread (e.g. from infective endocarditis)
Direct extension (e.g. from an empyema)
Bronchial obstruction (e.g. secondary to a lung tumour)

204
Q

Question: What are the risk factors for developing a lung abscess?

A

Poor dental hygiene
Previous stroke
Reduced consciousness

205
Q

Question: What are the monomicrobial causes of lung abscess?

A

Staphylococcus aureus
Klebsiella pneumoniae
Pseudomonas aeruginosa

206
Q

Question: What are the features of a lung abscess?

A

Subacute pneumonia presentation (symptoms develop over weeks)
Systemic features: Night sweats, weight loss
Other symptoms: Fever, productive cough, foul-smelling sputum
Haemoptysis in some cases
Chest pain and dyspnoea
Signs: Dull percussion, bronchial breathing, clubbing

207
Q

Question: What are the key investigations for diagnosing a lung abscess?

A

Chest x-ray: Fluid-filled space within consolidation, air-fluid level
Sputum and blood cultures to identify causative organism

208
Q

Question: What is the management for a lung abscess?

A

Intravenous antibiotics (first-line treatment)
Percutaneous drainage if not resolving
Surgical resection in very rare cases

209
Q

Question: What is the role of a chest x-ray in investigating lung cancer?

A

Chest x-ray is often the first investigation in suspected lung cancer.
Around 10% of patients diagnosed with lung cancer have a normal chest x-ray

210
Q

Question: What is the investigation of choice for suspected lung cancer?

A

CT scan is the investigation of choice for further investigation of suspected lung cancer.

211
Q

Question: How does bronchoscopy aid in the diagnosis of lung cancer?

A

Bronchoscopy allows a biopsy to be taken for histological diagnosis.
It is sometimes aided by endobronchial ultrasound.

212
Q

Question: What is the role of PET scanning in lung cancer management?

A

PET scanning is typically done in non-small cell lung cancer to establish eligibility for curative treatment.
18-fluorodeoxygenase is preferentially taken up by neoplastic tissue, improving diagnostic sensitivity for local and distant metastasis.

213
Q

Question: What abnormality may be observed in the bloods of a patient with lung cancer?

A

Raised platelets may be seen in the blood tests of patients with lung cancer.

214
Q

Question: What percentage of non-small cell lung cancer patients are suitable for surgery?

A

Only 20% of non-small cell lung cancer patients are suitable for surgery.

215
Q

Question: Why is a mediastinoscopy performed before surgery in non-small cell lung cancer management?

A

Mediastinoscopy is performed to assess mediastinal lymph node involvement, as CT does not always show it accurately.

216
Q

Question: What are the treatment options for non-small cell lung cancer?

A

Treatment options include curative or palliative radiotherapy.
Chemotherapy often has a poor response.

217
Q

Question: What are the contraindications for surgery in non-small cell lung cancer?

A

Stage IIIb or IV (i.e. metastases present)
FEV1 < 1.5 liters (general cut-off for surgery)
Malignant pleural effusion
Tumor near hilum
Vocal cord paralysis
Superior vena cava (SVC) obstruction

218
Q

Question: How is lung function assessed before surgery for non-small cell lung cancer?

A

FEV1 < 1.5 liters is the general cut-off for surgery, but if FEV1 < 1.5 for lobectomy or < 2.0 for pneumonectomy, further lung function tests may be conducted, and surgery could still be considered based on the results.

219
Q

Question: What paraneoplastic features are associated with small cell lung cancer?

A

ADH secretion - hyponatraemia
ACTH secretion (more common features: hypertension, hyperglycaemia, hypokalaemia, alkalosis, and muscle weakness) - cushings, bilateral adrenal hyperplasia and lead to hypokalaemic alkalosis.
Lambert-Eaton syndrome

220
Q

Question: What paraneoplastic features are associated with squamous cell lung cancer?

A

Parathyroid hormone-related protein (PTH-rp) secretion, causing hypercalcaemia
Clubbing
Hypertrophic pulmonary osteoarthropathy (HPOA)
Hyperthyroidism due to ectopic TSH

221
Q

Question: What paraneoplastic features are associated with adenocarcinoma?

A

Gynaecomastia
Hypertrophic pulmonary osteoarthropathy (HPOA)

222
Q

Question: According to the 2015 NICE cancer referral guidelines, when should people be referred using a suspected cancer pathway for lung cancer?

A

If they have chest x-ray findings suggestive of lung cancer.
If they are aged 40 or over with unexplained haemoptysis.

223
Q

Question: When should an urgent chest x-ray be offered to assess for lung cancer in people aged 40 and over, according to NICE guidelines?

A

If they have 2 or more of the following unexplained symptoms:
Cough
Fatigue
Shortness of breath
Chest pain
Weight loss
Appetite loss
Or, if they have ever smoked and have 1 or more of these symptoms.

224
Q

Question: What additional scenarios should lead to consideration of an urgent chest x-ray for lung cancer in people aged 40 and over?

A

Persistent or recurrent chest infection
Finger clubbing
Supraclavicular or persistent cervical lymphadenopathy
Chest signs consistent with lung cancer
Thrombocytosis

225
Q

Question: What are the two main classifications of lung cancer, and how are they differentiated?

A

Small Cell Lung Cancer (SCLC): Accounts for ~15% of cases, has a worse prognosis.
Non-Small Cell Lung Cancer (NSCLC): Includes several subtypes with different management and prognosis.

226
Q

Question: What is the most common type of lung cancer, and what factors contribute to its increase?

A

Adenocarcinoma is the most common type of lung cancer.
It has increased due to the rise in the use of low-tar cigarettes.
Adenocarcinoma is often seen in non-smokers, making up 62% of cases in never smokers (compared to 18% for squamous cell carcinoma).

227
Q

Question: What are some characteristics of squamous cell carcinoma of the lung?

A

Squamous cell carcinoma often presents with cavitating lesions, which are more common than in other types of lung cancer.

228
Q

Question: What other types are included in non-small cell lung cancer (NSCLC)?

A

Large cell carcinoma
Alveolar cell carcinoma: Not related to smoking
Bronchial adenoma: Mostly carcinoid tumors

229
Q

Question: What are some conditions causing upper zone fibrosis in the lungs?

A

Hypersensitivity pneumonitis (extrinsic allergic alveolitis)
Coal worker’s pneumoconiosis (progressive massive fibrosis)
Silicosis
Sarcoidosis
Ankylosing spondylitis (rare)
Histiocytosis
Tuberculosis
Radiation-induced pulmonary fibrosis (following breast or lung cancer radiotherapy)

230
Q

Question: What are some conditions causing lower zone fibrosis in the lungs?

A

Conditions causing lower zone fibrosis include:

Idiopathic pulmonary fibrosis (IPF)
Most connective tissue disorders (except ankylosing spondylitis), e.g., SLE
Drug-induced: amiodarone, bleomycin, methotrexate
Asbestosis

231
Q

Question: What is the acronym for remembering causes of upper zone fibrosis?

A

C: Coal worker’s pneumoconiosis
H: Histiocytosis / Hypersensitivity pneumonitis
A: Ankylosing spondylitis
R: Radiation
T: Tuberculosis
S: Silicosis / Sarcoidosis

232
Q

Question: What are the common features of mesothelioma?

A

Dyspnoea, weight loss, chest wall pain
Clubbing
30% present as painless pleural effusion
Only 20% have pre-existing asbestosis
History of asbestos exposure in 85-90%
Latent period of 30-40 years

233
Q

Question: What are the basic facts about mesothelioma?

A

Malignancy of mesothelial cells of the pleura
Metastases to contralateral lung and peritoneum
Right lung affected more often than the left

234
Q

Question: How is mesothelioma diagnosed?

A

Chest x-ray (showing pleural effusion or pleural thickening)
Pleural CT to assess further
Pleural fluid sent for MC&S, biochemistry, and cytology (cytology is only helpful in 20-30%)
Local anaesthetic thoracoscopy for cytology-negative exudative effusions (diagnostic yield ~95%)
Image-guided pleural biopsy if nodularity is seen on CT

235
Q

Question: What is the management and prognosis for mesothelioma?

A

Symptomatic management
Industrial compensation
Chemotherapy, surgery if operable
Prognosis is poor with a median survival of 12 months

236
Q

Question: What are the key features of microscopic polyangiitis?

A

Renal impairment: raised creatinine, haematuria, proteinuria
Fever
Other systemic symptoms: lethargy, myalgia, weight loss
Rash: palpable purpura
Respiratory symptoms: cough, dyspnoea, haemoptysis
Mononeuritis multiplex

237
Q

Question: What are the key indications for non-invasive ventilation (NIV)?

A

COPD with respiratory acidosis (pH 7.25-7.35)
Type II respiratory failure secondary to chest wall deformity, neuromuscular disease, or obstructive sleep apnoea
Cardiogenic pulmonary oedema unresponsive to CPAP
Weaning from tracheal intubation

238
Q

Question: What are the predisposing factors for Obstructive Sleep Apnoea/Hypopnoea Syndrome (OSAHS)?

A

Obesity
Macroglossia (e.g., acromegaly, hypothyroidism, amyloidosis)
Large tonsils
Marfan’s syndrome

239
Q

Question: What are the common consequences of Obstructive Sleep Apnoea/Hypopnoea Syndrome (OSAHS)?

A

Daytime somnolence (sleepiness)
Compensated respiratory acidosis
Hypertension

240
Q

Question: How is sleepiness assessed in patients with OSAHS?

A

Epworth Sleepiness Scale - Questionnaire completed by the patient and/or partner
Multiple Sleep Latency Test (MSLT) - Measures time to fall asleep in a dark room using EEG criteria

241
Q

Question: What diagnostic tests are used for Obstructive Sleep Apnoea/Hypopnoea Syndrome (OSAHS)?

A

Sleep studies (polysomnography):
From pulse oximetry monitoring at night to full polysomnography measuring EEG, respiratory airflow, thoraco-abdominal movement, snoring, and pulse oximetry.

242
Q

Question: What is the first-line treatment for moderate or severe OSAHS?

A

Continuous Positive Airway Pressure (CPAP)

243
Q

Question: What management options are available if CPAP is not tolerated or for mild OSAHS?

A

Intra-oral devices (e.g., mandibular advancement) may be used for mild OSAHS without daytime sleepiness.

244
Q

Question: What is the initial oxygen administration for critically ill patients (e.g., anaphylaxis, shock) according to the British Thoracic Society (BTS) guidelines?

A

Reservoir mask at 15 l/min for critically ill patients (e.g., anaphylaxis, shock).

245
Q

Question: What are the oxygen saturation targets for acutely ill patients?

A

94-98% for acutely ill patients.

246
Q

Question: What are the oxygen saturation targets for patients at risk of hypercapnia (e.g., COPD patients)?

A

88-92% for patients at risk of hypercapnia.

247
Q

Question: What should be the oxygen target for stable COPD patients with no prior history of respiratory acidosis?

A

28% Venturi mask at 4 l/min to achieve an oxygen saturation of 88-92%.

248
Q

Question: What should be the oxygen target for COPD patients if the pCO2 is normal?

A

Adjust target oxygen saturation to 94-98%.

249
Q

Question: In which conditions should oxygen therapy not be used routinely if there is no evidence of hypoxia?

A

Myocardial infarction and acute coronary syndromes
Stroke
Obstetric emergencies
Anxiety-related hyperventilation

250
Q

Question: How are pleural effusions classified based on protein concentration?

A

Transudate: < 30g/L protein
Exudate: > 30g/L protein

251
Q

Question: What are the common causes of transudative pleural effusion?

A

Heart failure (most common transudate cause)
Hypoalbuminaemia
Liver disease
Nephrotic syndrome
Malabsorption
Hypothyroidism
Meigs’ syndrome

252
Q

Question: What are the common causes of exudative pleural effusion?

A

Pneumonia (most common exudate cause)
Tuberculosis
Subphrenic abscess
Connective tissue diseases:
Rheumatoid arthritis
Systemic lupus erythematosus
Neoplasia:
Lung cancer
Mesothelioma
Metastases
Pancreatitis
Pulmonary embolism
Dressler’s syndrome
Yellow nail syndrome

253
Q

Question: What are the common features of pleural effusion?

A

Answer:

Symptoms:
Dyspnoea
Non-productive cough
Chest pain
Examination findings:
Dullness to percussion
Reduced breath sounds
Reduced chest expansion

254
Q

Question: What imaging should be performed for pleural effusion?

A

Chest x-ray (posterior-anterior (PA) view) should be performed in all patients.
Ultrasound is recommended to increase the likelihood of successful pleural aspiration and detect pleural fluid septations.
Contrast CT is increasingly used to investigate the underlying cause, especially for exudative effusions.

255
Q

Question: What are the steps for pleural aspiration and fluid analysis?

A

Ultrasound is recommended to guide the procedure and reduce complications.
A 21G needle and 50ml syringe should be used.
Fluid should be sent for:
pH
Protein
Lactate dehydrogenase (LDH)
Cytology
Microbiology

256
Q

Question: What are Light’s criteria for distinguishing between transudate and exudate in pleural fluid?

A

If the protein level is between 25-35 g/L, Light’s criteria should be applied. An exudate is likely if at least one of the following criteria is met:

Pleural fluid protein / serum protein > 0.5
Pleural fluid LDH / serum LDH > 0.6
Pleural fluid LDH is more than two-thirds the upper limit of normal serum LDH.

257
Q

Question: What are some characteristic pleural fluid findings and their causes?

A

Low glucose: rheumatoid arthritis, tuberculosis
Raised amylase: pancreatitis, oesophageal perforation
Heavy blood staining: mesothelioma, pulmonary embolism, tuberculosis

258
Q

Question: When is a chest tube indicated for pleural infection?

A

Purulent or turbid/cloudy fluid: chest tube for drainage.
If the fluid is clear but the pH is less than 7.2 in patients with suspected pleural infection, a chest tube should be placed.

259
Q

Question: What are the management options for recurrent pleural effusion?

A

Recurrent aspiration
Pleurodesis
Indwelling pleural catheter
Drug management: opioids to relieve dyspnoea and alleviate symptoms

260
Q

Question: What is the most common cause of pneumonia in clinical practice?

A

Bacterial infection is the most common cause of pneumonia, with Streptococcus pneumoniae accounting for 80% of cases.

261
Q

Question: What are some common causes of pneumonia?

A

Bacterial:
Streptococcus pneumoniae
Haemophilus influenzae (common in COPD patients)
Staphylococcus aureus (post-influenza)
Mycoplasma pneumoniae (atypical, dry cough)
Legionella pneumophila (associated with air conditioning units)
Klebsiella pneumoniae (common in alcoholics)
Pneumocystis jiroveci (seen in HIV patients)

Viral

Fungal: e.g., Pneumocystis jiroveci

262
Q

Question: What is the distinction between community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP)?

A

CAP: Pneumonia acquired outside of a hospital.
HAP: Pneumonia that occurs 48 hours or more after admission to the hospital.
The causative organisms and first-line antibiotics differ for each.

263
Q

Question: What are common symptoms and signs of pneumonia?

A

Answer:

Symptoms:
Cough
Sputum
Dyspnoea
Chest pain (pleuritic)
Fever
Signs:
Fever
Tachycardia
Reduced oxygen saturation
Reduced breath sounds
Bronchial breathing

264
Q

Question: What are the key investigations in pneumonia?

A

Chest x-ray: The classical finding is consolidation.
Blood tests:
Full blood count (neutrophilia in bacterial infections)
Urea and electrolytes (check for dehydration)
CRP (raised in infection)
Arterial blood gases: If oxygen saturation is low or if the patient has respiratory disease (e.g., COPD).

265
Q

Question: What is the management for pneumonia?

A

Antibiotics: To treat the underlying infection.
Supportive care:
Oxygen therapy (if hypoxaemic)
Intravenous fluids (if hypotensive or dehydrated)

266
Q

Question: What is the CRB-65 score used for in pneumonia management?

A

The CRB-65 score is used to assess the severity and risk of mortality in community-acquired pneumonia.
Criteria:

C: Confusion (mental test score ≤ 8/10)
R: Respiration rate ≥ 30/min
B: Blood pressure (systolic ≤ 90 mmHg or diastolic ≤ 60 mmHg)
65: Age ≥ 65 years
Management:

Score 0: Home care with oral antibiotics (e.g., amoxicillin).
Score 2 or more: Hospital assessment required.

267
Q

Question: What is the role of the CRP test in pneumonia management according to NICE?

A

CRP < 20 mg/L: Do not routinely offer antibiotics.
CRP 20-100 mg/L: Consider a delayed antibiotic prescription.
CRP > 100 mg/L: Offer antibiotic therapy.

268
Q

Question: What investigations should be done for pneumonia in intermediate or high-risk patients?

A

Chest x-ray
Blood and sputum cultures
Pneumococcal and Legionella urinary antigen tests
CRP monitoring to assess treatment response

269
Q

Question: What is the recommended first-line treatment for low-severity community-acquired pneumonia?

A

Amoxicillin is first-line.
If penicillin allergic, use a macrolide or tetracycline.
5-day course of antibiotics is recommended.

270
Q

Question: What is the recommended management for moderate and high-severity community-acquired pneumonia?

A

Dual therapy with amoxicillin and a macrolide.
7-10 day course of antibiotics.
For high-severity, consider beta-lactamase stable penicillin (e.g., co-amoxiclav, ceftriaxone, or piperacillin-tazobactam) with a macrolide.

271
Q

Question: What are the discharge criteria for pneumonia according to NICE?

A

Do not discharge if any of the following occur in the past 24 hours:
Temp > 37.5°C
Respiratory rate ≥ 24/min
Heart rate > 100 beats/min
Systolic BP ≤ 90 mmHg
Oxygen saturation < 90%
Abnormal mental status
Inability to eat without assistance.

272
Q

Question: When should a repeat chest x-ray be done after pneumonia treatment?

A

A repeat chest x-ray should be done 6 weeks after clinical resolution to ensure consolidation has resolved and rule out underlying abnormalities (e.g., lung cancer).

273
Q

Question: What happens in the pathophysiology of pneumonia?

A

In pneumonia, pathogens enter the lower respiratory tract, triggering an inflammatory cascade. Neutrophils migrate to the infected alveoli, releasing cytokines that activate the immune response and induce fever. This leads to fluid and pus accumulation in the alveoli, impairing gas exchange and causing hypoxia.

274
Q

Question: What is pneumothorax?

A

Pneumothorax is a condition characterized by the accumulation of air in the pleural space, causing partial or complete collapse of the affected lung.

275
Q

Question: What are the types of spontaneous pneumothorax?

A

Primary spontaneous pneumothorax (PSP): Occurs without underlying lung disease, often in tall, thin, young individuals, and is associated with the rupture of subpleural blebs or bullae.
Secondary spontaneous pneumothorax (SSP): Occurs in patients with pre-existing lung disease, such as COPD, asthma, cystic fibrosis, lung cancer, and Pneumocystis pneumonia. It is also associated with connective tissue diseases like Marfan’s syndrome.

276
Q

Question: What is traumatic pneumothorax?

A

Traumatic pneumothorax occurs due to penetrating or blunt chest trauma, leading to lung injury and air accumulation in the pleural space.

277
Q

Question: What is iatrogenic pneumothorax?

A

Iatrogenic pneumothorax occurs as a complication of medical procedures such as thoracentesis, central venous catheter placement, non-invasive ventilation, or lung biopsy.

278
Q

Question: What is a tension pneumothorax?

A

A tension pneumothorax is a severe form of pneumothorax where air accumulates and cannot escape, causing displacement of mediastinal structures and resulting in severe respiratory distress and haemodynamic collapse.

279
Q

Question: What is catamenial pneumothorax?

A

Catamenial pneumothorax occurs in 3-6% of spontaneous pneumothoraces in menstruating women and is thought to be caused by endometriosis within the thorax.

280
Q

Question: What are the clinical features of pneumothorax?

A

Symptoms: Sudden onset of dyspnoea and pleuritic chest pain.
Signs:
Hyper-resonant lung percussion
Reduced breath sounds
Reduced lung expansion
Tachypnoea
Tachycardia

281
Q

Question: What are the signs of tension pneumothorax?

A

Respiratory distress
Tracheal deviation away from the side of the pneumothorax
Hypotension

282
Q

Question: What is the first step in managing pneumothorax according to the BTS guidelines?

A

The first step is assessing whether the patient is symptomatic. If there are no significant symptoms or physiological compromise, conservative care is recommended.

283
Q

Question: What are the high-risk characteristics for pneumothorax that require more aggressive intervention?

A

Haemodynamic compromise (suggesting a tension pneumothorax)
Significant hypoxia
Bilateral pneumothorax
Underlying lung disease
≥ 50 years with a significant smoking history
Haemothorax

284
Q

Question: What are the management options for a symptomatic pneumothorax with no high-risk characteristics?

A

Conservative care
Ambulatory device (e.g., Rocket® Pleural Vent®)
Needle aspiration

285
Q

Question: When should a chest drain be inserted for a pneumothorax?

A

A chest drain should be inserted if needle aspiration is unsuccessful or if the patient has high-risk characteristics.

286
Q

Question: How is safety for intervention in pneumothorax determined?

A

Safety is typically assessed by the size of the pneumothorax on chest X-ray (≥ 2cm laterally or apically) or any size on CT scan that can be safely accessed with radiological support.

287
Q

Question: What is the management approach for persistent or recurrent pneumothorax?

A

For persistent air leak or insufficient lung reexpansion despite chest drain insertion, or recurrent pneumothorax, video-assisted thoracoscopic surgery (VATS) is considered for mechanical/chemical pleurodesis and bullectomy.

288
Q

Question: What discharge advice is given to pneumothorax patients regarding smoking?

A

Patients should avoid smoking to reduce the risk of further episodes, as the lifetime risk of pneumothorax is much higher in smokers (10%) compared to non-smokers (0.1%).

289
Q

Question: What is the fitness to fly recommendation after pneumothorax treatment?

A

Patients can travel by air 2 weeks after successful drainage if no residual air is present. The previous recommendation of 6 weeks has been updated to 1 week post check X-ray.

290
Q

Question: What is the characteristic finding in obstructive lung disease on pulmonary function tests?

A

FEV1: Significantly reduced
FVC: Reduced or normal
FEV1/FVC ratio: Reduced

291
Q

Question: What is the characteristic finding in restrictive lung disease on pulmonary function tests?

A

FEV1: Reduced
FVC: Significantly reduced
FEV1/FVC ratio: Normal or increased

292
Q

Question: What are some examples of obstructive lung diseases?

A

Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans

293
Q

Question: What are some examples of restrictive lung diseases?

A

Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome (ARDS)
Infant respiratory distress syndrome
Kyphoscoliosis (e.g., ankylosing spondylitis)
Neuromuscular disorders
Severe obesity

294
Q

Question: What are the common causes of respiratory acidosis?

A

COPD
Decompensation in other respiratory conditions (e.g., life-threatening asthma, pulmonary oedema)
Neuromuscular disease
Obesity hypoventilation syndrome
Sedative drugs (e.g., benzodiazepines, opiate overdose)

295
Q

Question: What are common causes of respiratory alkalosis?

A

Anxiety leading to hyperventilation
Pulmonary embolism
Salicylate poisoning (mixed respiratory alkalosis and metabolic acidosis)
CNS disorders (e.g., stroke, subarachnoid haemorrhage, encephalitis)
Altitude
Pregnancy

296
Q

Question: What is tidal volume (TV) and its average volume?

A

The volume inspired or expired with each breath at rest.
500 ml in males, 350 ml in females.

297
Q

Question: What is inspiratory reserve volume (IRV) and its average volume?

A

The maximum volume of air that can be inspired at the end of a normal tidal inspiration.
2-3 L.

298
Q

Question: What is expiratory reserve volume (ERV) and its average volume?

A

The maximum volume of air that can be expired at the end of a normal tidal expiration.
750 ml.
Significantly reduced in obesity due to abdominal fat mass pushing against the diaphragm.

299
Q

Question: What is residual volume (RV) and its average volume?

A

The volume of air remaining after maximal expiration.
1.2 L.
Increases with age.

300
Q

Question: What is functional residual capacity (FRC) and how is it calculated?

A

The volume in the lungs at the end-expiratory position.
FRC = ERV + RV.

301
Q

Question: What is vital capacity (VC) and its average volume?

A

The maximum volume of air that can be expired after maximal inspiration.
5 L (4,500 ml in males, 3,500 ml in females).
Decreases with age.
VC = inspiratory capacity + ERV.

302
Q

Question: What is total lung capacity (TLC)?

A

The sum of vital capacity + residual volume.

303
Q

Question: How is physiological dead space (VD) calculated?

A

VD = tidal volume * (PaCO2 - PeCO2) / PaCO2
Where:
PaCO2 = partial pressure of CO2 in arterial blood
PeCO2 = partial pressure of CO2 in expired air

304
Q

Question: In which conditions is an immediate antibiotic prescribing approach considered for respiratory tract infections?

A

Children < 2 years with bilateral acute otitis media.
Children with otorrhoea (discharge from the ear) and acute otitis media.
Patients with acute sore throat/pharyngitis/tonsillitis who meet 3 or more Centor criteria.

305
Q

Question: What are the Centor criteria for determining whether to prescribe antibiotics for acute sore throat/pharyngitis/tonsillitis?

A

Tonsillar exudate
Tender anterior cervical lymphadenopathy or lymphadenitis
History of fever
Absence of cough

306
Q

Question: When is an immediate antibiotic prescribing policy recommended for patients with respiratory tract infections according to NICE?

A

The patient is systemically very unwell.
There are signs suggestive of serious illness or complications (e.g. pneumonia, mastoiditis, abscesses).
The patient is at high risk of complications due to comorbidities (e.g. heart, lung, renal, liver diseases, immunosuppression, cystic fibrosis, premature birth).
Patients are older than 65 years with acute cough and two or more risk factors, or older than 80 years with acute cough and one or more risk factors.

307
Q

Question: What are the risk factors for prescribing antibiotics to older patients with acute cough?

A

For patients older than 65 years with acute cough and two or more of the following, or older than 80 years with acute cough and one or more of the following:

Hospitalisation in the previous year
Type 1 or type 2 diabetes
History of congestive heart failure
Current use of oral glucocorticoids

308
Q

Question: What duration do respiratory tract infections typically last, according to NICE guidelines?

A

Acute otitis media: 4 days
Acute sore throat/pharyngitis/tonsillitis: 1 week
Common cold: 1 1/2 weeks
Acute rhinosinusitis: 2 1/2 weeks
Acute cough/acute bronchitis: 3 weeks

309
Q

Question: What is sarcoidosis, and what is its hallmark feature?

A

Sarcoidosis is a multisystem disorder of unknown aetiology characterized by the formation of non-caseating granulomas. It is more common in young adults and individuals of African descent.

310
Q

Question: What are the acute features of sarcoidosis?

A

Erythema nodosum
Bilateral hilar lymphadenopathy (BHL)
Swinging fever
Polyarthralgia

311
Q

Question: What are the insidious features of sarcoidosis?

A

Dyspnoea
Non-productive cough
Malaise
Weight loss

312
Q

Question: What ocular and skin features are associated with sarcoidosis?

A

Ocular: Uveitis
Skin: Lupus pernio

313
Q

Question: Why does hypercalcaemia occur in sarcoidosis?

A

Hypercalcaemia occurs because macrophages within the granulomas cause an increased conversion of vitamin D to its active form, 1,25-dihydroxycholecalciferol.

314
Q

Question: Is there a single diagnostic test for sarcoidosis?

A

No, there is no single diagnostic test for sarcoidosis. The diagnosis is still largely clinical.

315
Q

Question: What is the role of ACE levels in diagnosing sarcoidosis?

A

ACE levels have a sensitivity of 60% and specificity of 70%. They are not reliable for diagnosing sarcoidosis but may help in monitoring disease activity.

316
Q

Question: What may routine blood tests show in patients with sarcoidosis?

A

Routine blood tests may show hypercalcaemia (seen in 10% of patients) and a raised ESR (erythrocyte sedimentation rate).

317
Q

Question: How is sarcoidosis staged on a chest x-ray?

A

Stage 0: Normal
Stage 1: Bilateral hilar lymphadenopathy (BHL)
Stage 2: BHL + interstitial infiltrates
Stage 3: Diffuse interstitial infiltrates only
Stage 4: Diffuse fibrosis

318
Q

Question: What spirometry finding may be seen in sarcoidosis?

A

Spirometry may show a restrictive defect in sarcoidosis.

319
Q

Question: What does a tissue biopsy show in sarcoidosis?

A

A tissue biopsy typically shows non-caseating granulomas.

320
Q

Question: What is the primary treatment for sarcoidosis?

A

The primary treatment for sarcoidosis is steroids (e.g., prednisone).

321
Q

Question: When are steroids indicated in the management of sarcoidosis?

A

Stage 2 or 3 disease with symptoms (e.g., dyspnoea, cough)
Asymptomatic stable Stage 2 or 3 disease with mildly abnormal lung function (no treatment required)
Hypercalcaemia
Involvement of eye, heart, or nervous system

322
Q

Question: What is the management approach for asymptomatic stable Stage 2 or 3 sarcoidosis?

A

For asymptomatic stable Stage 2 or 3 sarcoidosis with only mildly abnormal lung function, no treatment is required.

323
Q

Question: What percentage of patients with sarcoidosis experience remission without treatment?

A

Approximately two-thirds of people with sarcoidosis experience remission without treatment.

324
Q

Question: What factors are associated with a poor prognosis in sarcoidosis?

A

Factors associated with a poor prognosis in sarcoidosis include:

Insidious onset and symptoms lasting > 6 months
Absence of erythema nodosum
Extrapulmonary manifestations (e.g., lupus pernio, splenomegaly)
CXR Stage III-IV features (advanced disease)
Black African or African-Caribbean ethnicity

325
Q

Question: What is a characteristic feature of Chronic Obstructive Pulmonary Disease (COPD)?

A

Chronic obstructive pulmonary disease is invariably seen in smokers. It often presents with a chronic productive cough and features of right heart failure may be seen.

326
Q

Question: Which features are characteristic of Heart Failure causing chronic shortness of breath?

A

Characteristic features of heart failure include:

History of ischaemic heart disease or hypertension
Orthopnoea and paroxysmal nocturnal dyspnoea
Bibasal crackles and a third heart sound (S3) for left-sided failure
Peripheral oedema and a raised JVP for right-sided failure

327
Q

Question: What symptoms are typical of Asthma?

A

Asthma typically presents with cough, wheeze, and shortness of breath. Symptoms often worsen at night and may be precipitated by cold weather or exercise. It is associated with hay fever and eczema.

328
Q

Question: What are the characteristic features of Aortic Stenosis?

A

Characteristic features of aortic stenosis include:

Chest pain, shortness of breath, and syncope in symptomatic patients
An ejection systolic murmur radiating to the neck
Narrow pulse pressure

329
Q

Question: What are the features of Recurrent Pulmonary Emboli?

A

Features of recurrent pulmonary emboli include:

History of predisposing factors (e.g., malignancy)
Pleuritic chest pain and haemoptysis (symptoms can be vague)
Tachycardia and tachypnoea in acute situations
Symptoms of right heart failure in severe cases

330
Q

Question: What are common presentations of Lung Cancer?

A

Common presentations of lung cancer include:

Seen in smokers
Haemoptysis, chronic cough, or unresolving infection
Systemic symptoms such as weight loss and anorexia

331
Q

Question: What are the typical findings in Pulmonary Fibrosis?

A

Pulmonary fibrosis typically presents with:

Progressive shortness of breath as the only symptom
Fine bibasal crackles
Restrictive pattern on spirometry

332
Q

Question: What symptoms and history are associated with Bronchiectasis?

A

Bronchiectasis is associated with:

Large amounts of purulent sputum
History of previous infections (e.g., tuberculosis, measles), bronchial obstruction, or ciliary dyskinetic syndromes (e.g., Kartagener’s syndrome)

333
Q

Question: How does Anaemia present in terms of chronic shortness of breath?

A

Anaemia may present with:

History of gastrointestinal symptoms
Pallor on examination

334
Q

Question: How does Obesity contribute to chronic shortness of breath?

A

Obese patients tend to be more short of breath due to the increased work of activity.

335
Q

Question: What is Silicosis?

A

Silicosis is a fibrosing lung disease caused by the inhalation of fine particles of crystalline silicon dioxide (silica). It is a risk factor for developing tuberculosis because silica is toxic to macrophages.

336
Q

Question: Which occupations are at risk of developing Silicosis?

A

Occupations at risk include:

Mining
Slate works
Foundries
Potteries

337
Q

Question: What are the characteristic features of Silicosis?

A

Upper zone fibrosing lung disease
‘Egg-shell’ calcification of the hilar lymph nodes

338
Q

Question: What is Tension Pneumothorax?

A

Tension pneumothorax is a life-threatening condition characterized by the accumulation of air in the pleural space under positive pressure, leading to the collapse of the lung on the affected side and a shift of the mediastinum towards the contralateral side, resulting in impaired venous return to the heart and reduced cardiac output.

339
Q

Question: What are the causes of Tension Pneumothorax?

A

Traumatic: Penetrating or blunt chest trauma
Iatrogenic: Thoracentesis, central venous catheter placement, positive pressure mechanical ventilation
Spontaneous: Particularly in those with underlying lung diseases (e.g., COPD or cystic fibrosis) or ruptured lung blebs.

340
Q

Question: What is the pathophysiology of Tension Pneumothorax?

A

Tension pneumothorax develops when air enters the pleural space and is unable to escape, creating a one-way valve effect. This leads to:

Increased intrapleural pressure exceeding atmospheric pressure throughout the respiratory cycle.
Lung collapse: Decreased functional residual capacity and impaired gas exchange.
Mediastinal shift: Pressure pushes the mediastinum towards the contralateral side, compressing the opposite lung.
Impaired venous return: Compression of the great veins reduces venous return to the heart, diminishing cardiac output.
Reduced cardiac filling: Pressure on the heart and reduced venous return impairs right and left ventricular filling, lowering cardiac output and systemic blood pressure.

341
Q

Question: What are the clinical features of Tension Pneumothorax?

A

Features include:

Acute onset of dyspnoea
Pleuritic chest pain
Tachypnoea
Signs:

Hyperresonance on percussion, diminished breath sounds on the affected side.
Tracheal deviation away from the affected side
Shock signs: Hypotension and tachycardia in severe cases.

342
Q

Question: How should Tension Pneumothorax be managed?

A

Management involves decompression of the pleural space:

Needle thoracostomy: Insert a cannula into the second intercostal space in the midclavicular line on the affected side.
Chest drain (tube thoracostomy): Place in the safe triangle of the chest for continuous drainage of air.

343
Q

Question: What does the transfer factor (TLCO) describe?

A

The transfer factor describes the rate at which a gas, typically carbon monoxide, diffuses from the alveoli into the blood. It is used to assess the efficiency of gas exchange in the lungs.

344
Q

Question: What are the causes of a raised TLCO?

A

Asthma
Pulmonary haemorrhage (e.g., granulomatosis with polyangiitis, Goodpasture’s syndrome)
Left-to-right cardiac shunts
Polycythaemia
Hyperkinetic states
Male gender, exercise

345
Q

Question: What are the causes of a lower TLCO?

A

Pulmonary fibrosis
Pneumonia
Pulmonary emboli
Pulmonary oedema
Emphysema
Anaemia
Low cardiac output

346
Q

Question: How does KCO relate to age and other factors?

A

KCO (transfer coefficient) tends to increase with age. Some conditions may cause an increased KCO despite a normal or reduced TLCO, including:

Pneumonectomy/lobectomy
Scoliosis/kyphosis
Neuromuscular weakness
Ankylosis of costovertebral joints (e.g., ankylosing spondylitis)

347
Q

when should you give standby meds for copd

A

short course of oral corticosteroids and oral antibiotics to keep at home if: NICE
have had an exacerbation within the last year
understand how to take the medication, and are aware of associated risks and benefits
know to when to seek help and when to ask for replacements once medication has been used

348
Q

When would you give ipratropium bromide in acute management of asthma

A

in severe/life threatening cases

349
Q

What is tiotropium

A

lama

350
Q
A

Year 6 (10 decks)

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