Respiratory

Question 1

Learning objectives

Answer 1

Answer

Question 2

Define acute respiratory distress syndrome

Answer 2

• A syndrome of acute and persistent lung inflammation with increased vascular permeability. Characterised by: o Acute onset o Bilateral infiltrates consistent with pulmonary oedema o Hypoxaemia o No clinical evidence of increased left arterial pressure (pulmonary capillary wedge pressure) o ARDS is the severe end of the spectrum of acute lung injury

Question 3

Explain the aetiology / risk factors of acute respiratory distress syndrome

Answer 3

Severe insults to the lungs and other organs leads to the release of inflammatory mediators. These lead to increased capillary permeability, pulmonary oedema, impaired gas exchange and reduced lung compliance . Causes o Sepsis o Aspiration o Pneumonia o Pancreatitis o Trauma/burns o Transfusion o Transplantation (bone marrow and lung) o Drug overdose/reaction There are THREE pathological stages of ARDS: o Exudative o Proliferative o Fibrotic

Question 4

Summarise the epidemiology of acute respiratory distress syndrome

Answer 4

1 in 6000

Question 5

Recognise the presenting symptoms of acute respiratory distress syndrome

Answer 5

• Rapid deterioration of respiratory function • Dyspnoea • Respiratory distress • Cough • Symptoms of CAUSE

Question 6

Recognise the signs of acute respiratory distress syndrome on physical examination

Answer 6

• Cyanosis • Tachypnoea • Tachycardia • Widespread inspiratory crepitations • Hypoxia refractory to oxygen treatment • Signs are usually bilateral but may be asymmetrical in early stages

Question 7

Identify appropriate investigations for acute respiratory distress syndrome and interpret the results

Answer 7

• CXR - bilateral alveolar infiltrates and interstitial shadowing • Bloods - to figure out the cause (FBC, U&Es, LFTs, ESR/CRP, Amylase, ABG, Blood Culture) o NOTE: plasma BNP < 100 pg/mL could distinguish ARDS from heart failure • Echocardiography o Check for severe aortic or mitral valve dysfunction o Low left ventricular ejection fractions = haemodynamic oedema rather than ARDS • Pulmonary Artery Catheterisation o Check pulmonary capillary wedge pressure (PCWP) • Bronchoscopy o If the cause cannot be determined from the history

Question 8

Define Aspergillus Lung Disease

Answer 8

• Lung disease associated with Aspergillus fungal infection NOTE: Aspergillus infection is usually caused by Aspergillus fumigatus

Question 9

Explain the aetiology/risk factors for Aspergillus lung disease

Answer 9

Inhalation of Aspergillus spores can produce THREE different clinical pictures: • Aspergilloma o Growth of an A. fumigates mycetoma ball in a pre-existing lung cavity (e.g. post-TB, old infarct or abscess) • Allergic Bronchopulmonary Aspergillosis (ABPA) o Colonisation of the airways by Aspergillus leads to IgE and IgG-mediated immune responses o Usually occurs in asthmatics o The release of proteolytic enzymes, mycotoxins and antibodies leads to airway damage and central bronchiectasis • Invasive Aspergillosis o Invasion of Aspergillus into lung tissue and fungal dissemination o This occurs in immunosuppressed patients (e.g. neutropenia, steroids, AIDS)

Question 10

Summarise the epidemiology of Aspergillus lung disease

Answer 10

• UNCOMMON • Mainly occurs in the ELDERLY and IMMUNOCOMPROMISED

Question 11

Recognise the presenting symptoms of Aspergillus lung disease

Answer 11

• Aspergilloma o ASYMPTOMATIC o Haemoptysis (potentially massive) • ABPA o Difficult to control asthma o Recurrent episodes of pneumonia with wheeze, cough, fever and malaise • Invasive Aspergillosis o Dyspnoea o Rapid deterioration o Septic picture

Question 12

Recognise the signs of Aspergillus lung disease on physical examination

Answer 12

• Tracheal deviation (only with very large aspergillomas) • Dullness in affected lung • Reduced breath sounds • Wheeze (in ABPA) • Cyanosis (possible in invasive aspergillosis)

Question 13

Identify appropriate investigations for Aspergillus lung disease

Answer 13

• Aspergilloma o CXR • May show a round mass with a crescent of air around it • Usually found in the upper lobes o CT or MRI - may be used if CXR is unclear o NOTE: sputum cultures may be negative if there is no communication between the cavity colonised by Aspergillus and the bronchial tree • ABPA o Immediate skin test reactivity to Aspergillus antigens o Eosinophilia o Raised total serum IgE o Raised specific serum IgE and IgG to A. fumigatus o CXR • Transient patchy shadows • Collapse • Distended mucous-filled bronchi • Signs of complications:  Fibrosis in upper lobes  Bronchiectasis o CT • Lung infiltrates • Central bronchiectasis o Lung Function Tests • Reversible airflow limitation • Reduced lung volumes/gas transfer • Invasive Aspergillosis o Aspergillus is detected in cultures or by histological examination o Bronchoalveolar lavage fluid or sputum may be used diagnostically o Chest CT • Nodules surrounded by a ground-glass appearance (halo sign) • This is caused by haemorrhage into the tissue surrounding the fungal invasion

Question 14

Define asthma

Answer 14

• Chronic inflammatory airway disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation

Question 15

Explain the aetiology / risk factors of asthma

Answer 15

Genetic Factors o Family history o Atopy (tendency for T lymphocytes to drive production of IgE on exposure to allergens) Environmental Factors o House dust mites o Pollen o Pets o Cigarette smoke o Viral respiratory tract infections o Aspergillus fumigatus spores o Occupational allergens

Question 16

Summarise the epidemiology of asthma

Answer 16

• Affects 10% of children • Affects 5% of adults • Prevalence appears to be increasing

Question 17

Recognise the presenting symptoms of asthma

Answer 17

• Episodic history • Wheeze • Breathlessness • Cough (worse in the morning and at night) IMPORTANT: ask about previous hospitalisation due to acute attacks - this gives an indication of the severity of the asthma Precipitating Factors o Cold o Viral infection o Drugs (e.g. beta-blockers, NSAIDs) o Exercise o Emotions Check for history of atopic disease (e.g. allergic rhinitis, urticaria, eczema)

Question 18

Recognise the signs of asthma on physical examination

Answer 18

• Tachypnoea • Use of accessory muscles • Prolonged expiratory phase • Polyphonic wheeze • Hyperinflated chest Severe Attack o PEFR < 50% predicted o Pulse > 110/min o RR > 25/min o Inability to complete sentences Life-Threatening Attack o PEFR < 33% predicted o Silent chest o Cyanosis o Bradycardia o Hypotension o Confusion o Coma

Question 19

Identify appropriate investigations for asthma and interpret the results

Answer 19

ACUTE o Peak flow o Pulse oximetry o ABG o CXR - to exclude other diagnoses (e.g. pneumonia, pneumothorax) o FBC - raised WCC if infective exacerbation o CRP o U&Es o Blood and sputum cultures CHRONIC o Peak flow monitoring - often shows diurnal variation with a dip in the morning o Pulmonary function test o Bloods - check: • Eosinophilia • IgE level • Aspergillus antibody titres o Skin prick tests - helps identify allergens

Question 20

Generate a management plan for asthma

Answer 20

ACUTE o ABCDE o Resuscitate o Monitor O2 sats, ABG and PEFR o High-flow oxygen o Salbutamol nebulizer (5 mg, initially continuously, then 2-4 hourly) o Ipratropium bromide (0.5 mg QDS) o Steroid therapy • 100-200 mg IV hydrocortisone • Followed by, 40 mg oral prednisolone for 5-7 days o If no improvement –> IV magnesium sulphate o Consider IV aminophylline infusion o Consider IV salbutamol o Anaesthetic help may be needed if the patient is getting exhausted o IMPORANT: a normal PCO2 is a BAD SIGN in a patient having an asthma attack • This is because during an asthma attack they should be hyperventilating and blowing off their CO2, so PCO2 should be low • A normal PCO2 suggests that the patient is fatiguing o Treat underlying cause (e.g. infection) o Give antibiotics if it is an infective exacerbation o Monitor electrolytes closely because bronchodilators and aminophylline causes a drop in K+ o Invasive ventilation may be needed in severe attacks o DISCHARGE when: • PEF > 75% predicted • Diurnal variation < 25% • Inhaler technique checked • Stable on discharge medication for 24 hours • Patient owns a PEF meter • Patient has steroid and bronchodilator therapy • Arrange follow-up CHRONIC THERAPY o Start on the step that matches the severity of the patient’s asthma o STEP 1 • Inhaled short-acting beta-2 agonist used as needed • If needed > 1/day then move onto step 2 o STEP 2 • Step 1 + regular inhaled low-dose steroids (400 mcg/day) o STEP 3 • Step 2 + inhaled long-acting beta-2 agonist (LABA) • If inadequate control with LABA, increase steroid dose (800 mcg/day) • If no response to LABA, stop LABA and increase steroid dose (800 mcg/day) o STEP 4 • Increase inhaled steroid dose (2000 mcg/day) • Add 4th drug (e.g. leukotriene antagonist, slow-release theophylline or beta-2 agonist tablet) o STEP 5 • Add regular oral steroids • Maintain high-dose oral steroids • Refer to specialist care • Advice o Teach proper inhaler technique o Explain important of PEFR monitoring o Avoid provoking factors

Question 21

Identify the possible complications of asthma and its management

Answer 21

• Growth retardation • Chest wall deformity (e.g. pigeon chest) • Recurrent infections • Pneumothorax • Respiratory failure • Death

Question 22

Summarise the prognosis for patients with asthma

Answer 22

• Many children improve as they grow older • Adult-onset asthma is usually chronic

Question 23

Define bronchiectiasis

Answer 23

Lung airways disease characterised by chronic bronchial dilation, impaired mcuociliary clearance and frequent bacterial infections

Question 24

Explain the aetiology/risk factors for bronchiectasis

Answer 24

Chronic lung inflammation leads to fibrosis and permanent dilation of the bronchi. This leads to pooling of mucus, which predisposes to further cycles of infection, damage and fibrosis of bronchial walls Causes of bronchiectasis: Idiopathic (50%) Post-infectious (e.g. pneumonia, whooping cough, TB) Host-defence defects (e.g. Kartagener’s syndrome, cystic fibrosis) Obstruction of bronchi (e.g. foreign body, enlarged lymph nodes) GORD Inflammatory disorders (e.g. rheumatoid arthritis)

Question 25

Summarise the epidemiology of bronchiectasis

Answer 25

Most often arises initially in CHILDHOOD Incidence has decreased with the use of antibiotics 1/1000 per year

Question 26

Recognise the presenting symptoms of bronchiectasis

Answer 26

Productive cough with purulent sputum or haemoptysis Breathlessness Chest pain Malaise Fever Weight loss Symptoms usually begin after an acutre respiratory illness

Question 27

Recognise the signs of bronchiectasis on physical examination

Answer 27

Clubbing Coarse crepitations (usually at lung bases) - these shift with coughing Wheeze

Question 28

Identify appropriate investigations for bronchiectasis

Answer 28

Sputum Culture and sensitivity Common organisms: Pseudomonas aeruginosa Haemophilus influenzae Staphylococcus aureus Streptococcus pneumoniae Klebsiella Mycobacteria CXR Dilated bronchi (may be seen as parallel lines going from the hilum to the diaphragm (tramline shadows)) Fibrosis Atelectasis Pneumonic consolidations May be normal High resolution CT Best diagnostic method for bronchiectasis Shows dilated bronchi with thickened walls Bronchography - rarely used Others: swear electrolytes (for cystic fibrosis), serum Ig, mucociliary clearance study

Question 29

Generate a management plan for bronchiectasis

Answer 29

Treat acute exacerbations with TWO IV ANTIBIOTICS, which cover Pseudomonas aeruginosa Prophylactic antibiotics should be considered in patients with frequent exacerbations (\>3/year) Inhaled corticosteroids (e.g. fluticasone) - reduces inflammation and volume of sputum but does NOT affect the frequency of exacerbations or lung function Bronchodilators - considered in patients with responsive disease Maintain hydration Flu vaccination Physiotherapy - enables sputum and mucus clearance. This can reduce frequency of acute exacerbations and aid recovery. Bronchial artery embolisation - if life-tthreatening haemoptysis due to bronchiectasis Surgical - localised resection, lung or heart-lung transplantation

Question 30

Identify the possible complications of bronchiectasis

Answer 30

Life-threatening haemoptysis Persistent infections Empyema Respiratory failure Cor pulmonale Multi-organ abscesses

Question 31

Summarise the prognosis for patients with bronchiectasis

Answer 31

Most patients continue to have symptoms after 10 years

Question 32

Define chronic obstructive pulmonary disease (COPD)

Answer 32

Chronic, progressive lung disorder characterised by airflow obstruction, with the following: Chronic Bronchitis - Chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years. Emphysema - Pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles.

Question 33

Explain the aetiology / risk factors of chronic obstructive pulmonary disease (COPD)

Answer 33

Bronchial and alveolar damage is caused by environmental toxins (e.g. cigarette smoke) RARE CAUSE: a1 antitrypsin deficiency Though this is rare, consider it in young patients, who have never smoked, presenting with COPD type symptoms (and may have accomopanying symptoms of cirrhosis) Chronic Bronchitis Narrowing of the airways resulting in bronchiole inflammation (bronchiolitis) Bronchial mucosal oedema Mucous hypersecretion Squamous metaplasia Emphysema Destruction and enlargement of alveoli Leads to loss of elasticity that keeps small airways open in expiration Progressively larger spaces develop called bullae (diameter \> 1cm)

Question 34

Summarise the epidemiology of chronic obstructive pulmonary disease (COPD)

Answer 34

Very Common (8% prevalence) Presents in middle age or later More common in males - this may change because there has been a rise in female smokers

Question 35

Recognise the presenting symptoms of chronic obstructive pulmonary disease (COPD)

Answer 35

Chronic cough Sputum production Breathlessness Wheeze Reduced exercise tolerance

Question 36

Recognise the signs of chronic obstructive pulmonary disease (COPD) on physical examination

Answer 36

Inspection Respiratory distress Use of accessory muscles Barrel-shaped over-inflated chest Decreased cricosternal distance Cyanosis Percussion Hyper-resonant chest Loss of liver and cardiac dullness Auscultation Quient breath sounds Prolonged expiration Wheeze Rhonchi - rattling, continuous and low-pitched breath sounds that sounds a bit like snoring. They are often caused by secretions in larger airways or obstructions. Sometimes crepitations Signs of CO2 retention Bounding pulse Warm peripheries Asterixis LATE STAGES: signs of right heart failure (cor pulmonale) Right ventricular heave Raised JVP Ankle oedema

Question 37

Identify appropriate investigations for chronic obstructive pulmonary disease (COPD) and interpret the results

Answer 37

Spirometry and Pulmonary Function Tests Shows obstructive picture Reduced PEFR Reduced FEV1/FVC Increased lung volumes Decreased carbon monoxide gas transfer coefficient CXR May appear NORMAL Hyperinflation (\> 6 anterior ribs, flattened diaphragm) Reduced peripheral lung markings Elongated cardiac silhouette Bloods FBC - increased Hb and haematocrit due to secondary polycythaemia ABG - may show hypoxia, normal/raised PCO2 ECG and Echocardiogram check for cor pulmonale Sputum and Blood Cultures - useful in acute infective exacerbations a1 antitrypsin levels - useful in young patients who have never smoked

Question 38

Generate a management plan for chronic obstructive pulmonary disease (COPD)

Answer 38

STOP SMOKING Bronchodilators Short acting beta 2 agonists (e.g. salbutamol) Anticholinergics (e.g. ipratropium bromide) Long acting beta 2 agonists (if \> 2 exacerbations per year) Steroids Inhaled beclamethasone considered in all patients with FEV1 \< 50% of predicted OR \> 2 exacerbations per year Regular oral steroids should be avoided if possible Pulmonary rehabilitation Oxygen therapy Only for those who stop smoking Indicated if: PaO2 \< 7.3 kPa on air during a period of clinical stability PaO2: 7.3 - 8 kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension Treatment of Acute Exacerbations 24 % O2 via Venturi mask Increase slowly if no hypercapnia and still hypoxic (do an ABG) Corticosteroids Start empirical antibiotic therapy if evidence of infection Respiratory physiotherapy to clear sputum Non-invasive ventilation may be necessary in severe cases Prevention of infective exacerbations: pneumococcal and influenza vaccination

Question 39

Identify the possible complications of chronic obstructive pulmonary disease (COPD) and its management

Answer 39

Acute respiratory failure Infections Pulmonary hypertension Right heart failure Pneumothorax (secondary to bullae rupture) Secondary polycythaemia

Question 40

Summarise the prognosis for patients with chronic obstructive pulmonary disease (COPD)

Answer 40

High morbidity 3 year survival of 90% if \< 60 yrs, FEV1 \> 50% predicted 3 year survival of 75% if \> 60 yrs, FEV1: 40 - 49% predicted

Question 41

Define extrinsic allergic alveolitis

Answer 41

Interstitial inflammatory disease of the distal gas-exchanging parts of the lung caused by inhalation of organic dusts. Also known as hypersensitivity pneumonitis.

Question 42

Explain the aetiology/risk factors for extrinsic allergic alveolitis

Answer 42

Inhalation of antigenic dusts induce a hypersensitivity response in susceptible individuals Antigenic dusts include microbes and animal proteins Examples: Famer's Lung - caused by mouldy hay containing thermophilic actinomycetes Pigeon Fancier's Lung - caused by blood on bird feathers and excreta Maltworker's Lung - caused by barley or maltlings containing Aspergillus clavatus

Question 43

Summarise the epidemiology of extrinsic allergic alveolitis

Answer 43

Uncommon 2% of occupational lung disease 50% of reported cases affect farm workers Geographical variation

Question 44

Recognise the presenting symptoms of extrinsic allergic alveolitis

Answer 44

Acute Present 4-12 hrs after exposure REVERSIBLE episodes of: Dry cough Dyspnoea Malaise Fever Myalgia Wheeze and productive cough may develop if repeat high-level exposure CHRONIC Slowly increasing breathlessness Decreased exercise tolerance Weight loss Exposure is usually chronic, low-level and there may be no history of previous acute episodes IMPORTANT: make sure you get a full occupational history and enquire about hobbies and pets

Question 45

Recognise the signs of extrinsic allergic alveolitis on physical examination

Answer 45

ACUTE Rapid shallow breathing Pyrexia Inspiratory crepitations CHRONIC Fine inspiratory crepitations Clubbing (rare)

Question 46

Identify appropriate investigations for extrinsic allergic alveolitis

Answer 46

Bloods FBC - neutrophilia, lymphopenia ABG - reduced PO2 + PCO2 Serology Test for IgG to fungal or avian antigens NOTE: these are not diagnostic because you may find these in normal individuals CXR Often NORMAL in acute episodes Fibrosis may be seen in chronic cases High Resolution CT-Thorax Detects early changes May show patchy 'ground glass' shadowing and nodules Pulmonary Function Tests Restrictive defect (low FEV1, low FVC) Preserved or increased FEV1/FVC ratio Reduced total lung capacity Bronchoalveolar Lavage Increased cellularity Lung biopsy can also be performed

Question 47

Define idiopathic pulmonary fibrosis

Answer 47

Inflammatory condition of the lung resulting in fibrosis of the alveoli and interstitium. Previously known as cryptogenic fibrosing alveolitis.

Question 48

Explain the aetiology/risk factors of idiopathic pulmonary fibrosis

Answer 48

Occurs in genetically predisposed individuals Recurrent injury to alveolar epithelial cells results in secretion of cytokins and growth factors This leads to fibroblast activation, recruitment, proliferation, differentiations into myofibroblasts and increased collagen synthesis and deposition Certain drugs can produce similar illness (e.g. methotrexate, amiodarone) Histological Patterns Interstitial pneumonia Risk factors Smoking Occupational exposure to metal or wood Chronic microaspiration Animal or vegetable dusts

Question 49

Summarise the epidemiology of idiopathic pulmonary fibrosis

Answer 49

Rare 6/100,000 More common in males

Question 50

Recognise the presenting symptoms of idiopathic pulmonary fibrosis

Answer 50

Gradual-onset, progressive dysponea on exertion Dry irritating cough No wheeze Symptoms may be preceded by a viral-type illness Fatigue and weight loss are common IMPORTANT: take a full occupational and drug history

Question 51

Recognise the signs of idiopathic pulmonary fibrosis on physical examination

Answer 51

Clubbing (50%) Bibasal fine late inspiratory crackles Signs of right heart failure in advanced stages of disease

Question 52

Identify appropriate investigations for idiopathic pulmonary fibrosis

Answer 52

Bloods ABG Normal in early disease PO2 decreases with exercise Normal PCO2, which rises in late stage disease ANA and Rheumatoid Factor 1/3 of patients are positive for ANA or RF CXR Usually NORMAL at presentation Early disease may show ground glass shadowing Later stage disease shows reticulonodular shadowing, signs of cor pulmonale and, eventually, honeycombing High-resolution CT More sensitive in early disease than CXR Pulmonary Function Tests Restrictive features (reduced FEV1 and FVC, with preserved or increased FEV1/FVC) Decreased lung volumes Decreased lung compliance Decreased total lung capacity Bronchoalveolar Lavage - excludes infections and malignancy Lung biopsy - gold standard for diagnosis Echocardiography - to check for pulmonary hypertension

Question 53

Define obstructive sleep apnoea

Answer 53

A disease characterised by recurrent prolapse of the pharngeal airway and apnoea (cessation of airflow for \>10s) during sleep, followed by arousal from sleep. Also known as Pickwickian syndrome

Question 54

Explain the aetiology/risk factors of obstructive sleep apnoea

Answer 54

Occurs due to narrowing of the upper airways because of the collapse of soft tissues of the pharnx This is due to decreased tone of the pharyngeal dilators during sleep Associated with: Weight gain Smoking Alcohol Sedative use Enlarged tonsils and adenoids in children Macroglossia Marfan's syndrome Craniofacial abnormalities

Question 55

Summary the epidemiology of obstructive sleep apnoea

Answer 55

Common 5-20% of men \>35 years 2-5% of women \>35 years Prevalence increases with age

Question 56

Recognise the presenting symptoms of obstructive sleep apnoea

Answer 56

Excessive daytime sleepiness Unrefreshing or restless sleep Morning headaches Dry mouth Difficulty concentrating Irritability and mood changes Partner reporting snoring, noctural apnoeic episodes or noctural choking

Question 57

Recognise the signs of obstructive sleep apnoea on physical examination

Answer 57

Large tongue Enlarged tonsils Long or thick uvula Retrognathia (pulled back jaws) Neck circumference More than 42cm or 40cm in males and females respectively Obesity Hypertension

Question 58

Identify appropriate investigations for obstructive sleep apnoea

Answer 58

Sleep study Monitor airflow, respiratory effort, pulse oximetry and heart Bloods TFTs ABG

Question 59

Define pneumoconiosis

Answer 59

Fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts Types: Simple: Coalworker's pneumoconiosis or silicosis (symptom-free) Complicated: pneumoconiosis results in loss of lung function Asbestosis: a pneumoconiosis in which diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos

Question 60

Explain the aetiology/risk factors for pneumoconiosis

Answer 60

Caused by inhalation of particles of: Coal dust, silica, asbestos Risk factors: Occupational exposure (coal mining, quarrying, iron and steel foundries, stone cutting, sandblasting, insulation industry, plumbers, ship builders) Risk is dependent on extent of exposure and the size/shape of particles Individual susceptibility is also important Co-factors such as smoking and TB also contribute

Question 61

Summarise the epidemiology of pneumoconiosis

Answer 61

Incidence is increased in developing countries Disability and mortality from asbestosis will continue to increase for the next 20-30 years

Question 62

Recognise the presenting symptoms of pneumoconiosis

Answer 62

Occupational history is very important Asymptomatic - picked up on routine CXR Symptomatic - insidious onset shortness of breath, dry cough, black sputum (melanoptysis) - produced occasionally in coalworker's pneumoconiosis Pleuritic chest pain (due to acute asbestos pleurisy) - in patients exposed to asbestos

Question 63

Recognise the signs of pneumoconiosis on physical examination

Answer 63

Examination may be normal Coalworker's pneumoconiosis and silicosis: Decreased breath sounds Asbestosis: End-inspiratory crepitations Clubbing Signs of pleural effusion or right heart failure (cor pulmonale)

Question 64

Identify appropriate investigations for pneumoconiosis

Answer 64

CXR Simple: micronodular mottling Complicated: Nodular opacities in upper lobes Micronodular shadowing Eggshell classification of hilar lymph nodes (characteristic of silicosis) Bilateral lower zone reticulonodular shadowing and pleural plaques (in asbestosis) CT Scan - fibrotic changes can be visualised early Lung Function tests - restrictive pattern

Question 65

Define pneumonia

Answer 65

Infection of distal lung parenchyma. It can be categorised in many ways: Community-acquired Hospital-acquired/nosocomial Aspiration pneumonia Pneumonia in the immunocomprised Typical Atypical (Mycoplasma, Chlamydia, Legionella)

Question 66

Explain the aetiology/risk factors of pneumonia

Answer 66

Community-Acquired Streptococcus pneumoniae (70%) Haemophilus influenzia Moraxella catarrhalis (occurs in COPD patients) Chlamydia pneumonia Chlamydia psittaci (causes psittacosis) Mycoplasma pneumonia Legionella (air conditioning) Staphylococcus aureus Coxiella burnetii (causes Q fever) TB Hospital-Acquired Gram-negative enterobacteria (Pseudomonas, Klebsiella) Anaerobes (due to aspiration pneumonia) Risk factors Age Smoking Alcohol Pre-existing lung disease (COPD) Immunodeficiency Contact with patients with pneumonia

Question 67

Summarise the epidemiology of pneumonia

Answer 67

5-11/1000 Community-acquired pneumonia is responsible for \>60,000 deaths per year in the UK

Question 68

Recognise the presenting symptoms of pneumonia

Answer 68

Fever Rigors Sweating Malaise Cough Sputum Breathlessness Pleuritic chest pain Confusion (in severe cases or in the elderly) Atypical Pneumonia Symptoms: Headache Myalgia Diarrhoea/abdominal pain Dry cough

Question 69

Recognise the signs of pneumonia on physical examination

Answer 69

Pyrexia Respiratory distress Tachypnoea Tachycardia Hypotension Cyanosis Decreased chest expansion Dull to percuss over affected area Increased tactile vocal fremitus over affected area Bronchial breathing over affected area Coarse crepitations on affected side Chronic suppurative lung disease (empyema, abscess) --\> clubbing

Question 70

Identify appropriate investigations for pneumonia

Answer 70

Bloods FBC - raised WCC U&Es LFT Blood cultures ABG Blood Film - Mycoplasma causes red cell agglutination CXR Lobar or patchy shadowing Pleural effusion NOTE: Klebsiella often affects upper lobes May detect complications (e.g. lung abscess) Sputum/Pleural Fluid - MC&S Urine - Pneumococcus and Legionella antigens Atypical Viral Serology Bronchoscopy and Bronchoalveolar Lavage - if Pneumocystis carinii pneumonia is suspected, or if pneumonia fails to resolve

Question 71

Generate a management plan for pneumonia

Answer 71

Assess severity using the British Thoracic Society Guidelines Start empirical antibiotics Oral Amoxicillin (0 markers) Oral or IV Amoxicillin + Erythromycin (1 marker) IV Cefuroxime/Cefotaxime/Co-­‐amoxiclav + Erythromycin (\> 1 marker) Add metronidazole if: Aspiration Lung abscess Empyema Switch to appropriate antibiotic based on sensitivity Supportive treatment Oxygen IV fluids CPAP, BiPAP or ITU care for respiratory failure Surgical drainage may be needed for lung abscesses and empyema Discharge planning If two or more features of clinical instability are present (e.g. high temperature, tachycardia, tachypnoea, hypotension, low oxygen sats) there is a high risk of re-admission and mortality Consider other causes if pneumonia is not resolving Prevention Pneumococcal vaccine Haemophilus influenzae type B vaccine These are only usually given to high risk groups (e.g. elderly, splenectomy)

Question 72

Identify the possible complications of pneumonia

Answer 72

Pleural effusion Empyema Localised suppuration (e.g. abscess) Symptoms of abscesses: Swinging fever Persistent pneumonia Copious/foul-smelling sputum Septic shock ARDS Acute renal failure Extra complications of Mycoplasma pneumonia Erythema multiforme Myocarditis Haemolytic anaemia Meningoencephalitis Transverse myelitis Guilliain-Barre syndrome

Question 73

Summarise the prognosis for patients with pneumonia

Answer 73

Most resolve within treatment within 1-3 weeks Severe pneumonia has a high mortality The CURB-65 score is used to assess the severity of pneumonia: Confusion \<8 AMTS Urea \> 7 mmol/L Respiratory rate \>30/min Blood pressure: systolic \< 90 mmHg or diastolic \< 60 mmHg Age \> 65 years

Question 74

Define pneumothorax

Answer 74

Air in the pleural space There are some other variants in which other substances are found in the pleural space: Haemothorax - blood Chylothorax - lymph

Question 75

Explain the aetiology/risk factors of pneumothrax

Answer 75

Spontaneous Occurs in people with typically normal lungs Typically in tall, thin males It is probably caused by the rupture of a subpleural bleb Secondary Occurs in patients with pre-existing lung disease (e.g. COPD, asthma, TB) Traumatic Caused by penetrating injury to the chest Often iatrogenic (e.g. during jugular venous cannulation, thoracocentesis) Risk factors Collage disorders (e.g. Marfan's syndrome, Ehler's-Danlos syndrome)

Question 76

Summarise the epidemiology of pneumothorax

Answer 76

Annual incidence: 9/100,000 Mainly in 20-40 years old 4 x more common in males

Question 77

Recognise the presenting symptoms of pneumothorax

Answer 77

May be asymptomatic if the pneumothorax is small Sudden-onset breathlessness Pleuritic chest pain Distress with rapid shallow breathing in tension pneumothorax

Question 78

Recognise the signs of pneumothorax on physical examination

Answer 78

There may be no signs if the pneumothorax is small Signs of respiratory distress Reduced expansion Hyper-resonance to percussion Reduced breath sounds Tension pneumothorax Severe respiratory distress Tachycardia Hypotension Cyanosis Distended neck veins Tracheal deviation away from the side of the pneumothorax

Question 79

Identify appropriate investigations for pneumothorax

Answer 79

CXR It will show a dark area of film with no vascular markings Fluid level may be seen if there is any bleeding ABG - check for hypoxaemia

Question 80

Generate a management plan for pneumothorax

Answer 80

Tension pneumothorax (emergency) Max O2 Insert large bore needle into 2nd intercostal space MCL Up to 2.5L of air can be aspirated Stop if patient coughs or resistance is felt Follow up CXR 2 hours and 2 weeks later Chest Drain with Underwater Seal Performed if: Aspiration fails Fluid in the pleural cavity After decompression of a tension pneumothorax Inserted in the 4th-6th intercostal space midaxillary line Recurrent Pneumothoraces Chemical pleurodesis (fusing of visceral and parietal pleura with tetracycline or calc) Surgical pleurectomy Advice Avoid air travel until follow-up CXR confirms that pneumothorax has resolved Avoid diving

Question 81

Identify the possible complications of pneumothorax

Answer 81

Recurrent pneumothoraces Bronchopleural fistula

Question 82

Summarise the prognosis for patients with pneumothorax

Answer 82

After having one pneumothorax, at least 20% will have another Frequency increased with repeated pneumothoraxes

Question 83

Define pulmonary embolism

Answer 83

Occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the pulmonary vascular system from another site

Question 84

Explain the aetiology / risk factors of pulmonary embolism

Answer 84

Thrombus 95% arise from DVT in the lower limbs Rarely arises in the right atrium (in AF patients) Other causes of embolus: Amniotic fluid Air Fat Tumour Mycotic Risk Factors Surgical patients Immobility Obesity OCP Heart failure Malignanc

Question 85

Summarise the epidemiology of pulmonary embolism

Answer 85

Relatively COMMON (especially in hospitalised patients) Occur in 10 - 20% of patients with confirmed proximal DVT

Question 86

Recognise the presenting symptoms of pulmonary embolism

Answer 86

Depends on the SITE and SIZE of the embolus Small may be ASYMPTOMATIC Moderate Sudden onset SOB Cough Haemoptysis Pleuritic chest pain Large (or proximal) As above and: Severe central pleuritic chest pain Shock Collapse Acute right heart failure Sudden death Multiple Small Recurrent Symptoms of pulmonary hypertension

Question 87

Recognise the signs of pulmonary embolism on physical examination

Answer 87

Severity of PE can be assessed based on associated signs: Small often no clinical signs. There may be some tachycardia and tachypnoea Moderate Tachypnoea Tachycardia Pleural rub Low O2 saturation ( despite O2 supplementation) Massive PE Shock Cyanosis Signs of right heart strain Raised JVP Left parasternal heave Accentuated S2 heart sound Multiple Recurrent PE Signs of pulmonary hypertension Signs of right heart failure

Question 88

Identify appropriate investigations for pulmonary embolism and interpret the results

Answer 88

The Well's Score is used to determine the best investigation for PE Low Probability (Wells 4 or less) - use D dimer High Probability (Wells \> 4) required imaging (CTPA) Additional investigations: Bloods - ABG, thrombophilia screen ECG May be normal May show tachycardia, right axis deviation or RBBB May show S1Q3T3 pattern CXR often NORMAL but helps exclude other diagnoses Spiral CT Pulmonary Angiogram FIRST LINE INVESTIGATION Poor sensitivity for small emboli VERY sensitive for medium to large emboli Ventilation - Perfusion (VQ) Scan Identifies areas of ventilation and perfusion mismatch, which would indicate an area of infarcted lung Pulmonary Angiography Invasive Rarely necessary Doppler US of Lower Limb allows assessment of venous thromboembolism Echocardiography may show right heart strain

Question 89

Generate a management plan for pulmonary embolism

Answer 89

Primary Prevention Compression stockings Heparin prophylaxis for those at risk Good mobilisation and adequate hydration If haemodynamically stable O2 Anticoagulation with heparin or LMWH Switch over to oral warfarin for at least 3 months Maintain INR 2 - 3 Analgesia If haemodynamically UNSTABLE (massive PE) Resuscitate O2 IV fluids Thrombolysis with tPA may be considered if cardiac arrest is imminent Surgical or radiological Embolectomy IVC filters sometimes used for recurrent PEs despite adequate anticoagulation or when anticoagulation is contraindicated

Question 90

Identify the possible complications of pulmonary embolism and its management

Answer 90

Death Pulmonary infarction Pulmonary hypertension Right heart failure

Question 91

Summarise the prognosis for patients with pulmonary embolism

Answer 91

30% mortality in those left untreated 8% mortality with treatment Increased risk of future thromboembolic disease

Question 92

Define sarcoidosis

Answer 92

• Multisystem granulomatous inflammatory disorder

Question 93

Explain the aetiology/risk factors of sarcoidosis

Answer 93

• UNKNOWN • Transmissible agents (e.g. viruses), environmental triggers and genetic factors have all been suggested • Pathogenesis o An UNKNOWN antigen is presented on MHC class 2 complexes on macrophages to CD4+ T-lymphocytes o These accumulate and release cytokines o This leads to the formation of non-caseating granulomas in organs

Question 94

Summarise the epidemiology of sarcoidosis

Answer 94

• Most common in AFRICANS and SCANDINAVIANS • Can occur at any age but tends to be in adults \> 50 yrs

Question 95

Recognise the presenting symptoms and the signs of sarcoidosis

Answer 95

• General Symptoms o Fever o Malaise o Weight loss o Bilateral parotid swelling o Lymphadenopathy o Hepatosplenomegaly • Pulmonary Symptoms o Breathlessness o Dry cough o Chest discomfort o Minimal clinical signs • Musculoskeletal Symptoms o Bone cysts (e.g. dactylitis) o Polyarthralgia o Myopathy • Eye Symptoms o Keratoconjunctivitis sicca (inflammation of the conjunctivitis and surrounding tissues due to the eyes being dry) o Uveitis o Papilloedema • Skin Symptoms o Lupus pernio (red-blue infiltrations of the nose, cheeks, ears and terminal phalanges) o Erythema nodosum o Maculopapular eruptions • Neurological Symptoms o Lymphocytic meningitis o Space-occupying lesions o Pituitary infiltration o Cerebellar ataxia o Cranial nerve palsies o Peripheral neuropathy • Cardiac Symptoms o Arrhythmia o Bundle branch block o Pericarditis o Cardiomyopathy o Congestive cardiac failure

Question 96

Identify appropriate investigations for sarcoidosis

Answer 96

• Bloods o High serum ACE o High calcium o High ESR o FBC - WCC may be low due to lymphocyte sequestration in the lungs o Immunoglobulins - polyclonal hyperglobulinaemia o LFTs - high ALP + GGT • 24 hr Urine Collection o Hypercalciuria • CXR o Stage 0 - may be clear o Stage 1 - bilateral hilar lymphadenopathy o Stage 2 - stage 1 with pulmonary infiltration and paratracheal node enlargement o Stage 3 - pulmonary infiltration and fibrosis • High-Resolution CT Scan o Check for diffuse lung involvement • Gallium Scan - shows areas of inflammation • Pulmonary Function Tests o Low FEV1 o FVC shows restrictive picture • Bronchoscopy and Bronchoalveolar Lavage o High lymphocytes o High CD4: CD8 ratio • Transbronchial Lung Biopsy (or lymph node biopsy) o Shows non-caseating granulomas consisting of: • Epithelioid cells (activated macrophages) • Multinucleate Langerhans cells • Mononuclear cells (lymphocytes)

Question 97

Define Tuberculosis

Answer 97

Granulomatous disease caused by Mycobacterium tuberculosis Primary TB: initial infection may be pulmonary or more rarely gastro Miliary TB: results from haematogenous dissemination of TB Post-Primary TB: caused by reinfection or reactivation

Question 98

Explain the aetiology/risk factors of tuberculosis

Answer 98

Mycobacterium tuberculosis is an intracellular organism It survives after being phagocytosed by macrophages

Question 99

Summarise the epidemiology of tuberculosis

Answer 99

Annual mortality = 3 million (95% in developing countries) Annual UK incidence = 6000 Asian immigratns are the highest risk group in the UK

Question 100

Recognise the symptoms and signs of tuberculosis

Answer 100

Primary TB: Mostly Asymptomatic Fever Malaise Cough Wheeze Erythema Nodosum Phlyctenular conjuctivits Miliary TB: Fever Weight loss Meningitis Yellow caseous tubercles spread to other organs Post-primary TB Fever/night sweats Malaise Weight loss Breathlessness Cough Sputum Haemoptysis Pleuritic chest pain Signs of pleural effusion Collapse Consolidation Fibrosis Non-pulmonary TB - occurs mainly in the immunocompromised Lymph nodes - suppuration of cervical lymph nodes leading to abscesses or sinuses CNS - meningitis, tuberculoma Skin - lupus vulgaris (jelllylike reddish-brown glistening plaques) Heart - pericardial effusion, constrictive pericarditis GI Subacute obstruction Change in bowel habit Weight loss Peritonitis Ascites Genitourinary UTI symptoms Renal failure Epididymitis Endometrial or tubal involvement Infertility Adrenal insufficiency Bone/Joint - osteomyelitis, arthiritis, vertebral collapse (Pott's disease), spinal cord compression from an abscess

Question 101

Identify appropriate investigations from tuberculosis

Answer 101

Sputum/Pleural Fluid/Bronchial Washings -MC&S Note: culturing TB takes a long time (around 6 weeks) Tuberculin Tests Positive if the patient has had previous exposure to M.tuberculosis or BCG Mantoux Test A purified protein derivative is injected intradermally Erythema occurs after 72 hours Heaf Test Place a drop of PPD on the forearm Fire a spring-loaded needle gun Check again after 3-7 days Graded according to papula size and vesiculation Interferon Gamma Tests Useful in latent TB Exposure of host T cells to TB antigens leads to release of interferon CXR Primary Infection - Peripheral consolidation & Hilar lymphadenopathy Miliary Infection - Fine shadowing Post-Primary - Upper lobe shadowing, Streaky fibrosis and cavitation, Calcification, Pleural effusion, Hilar lymphadenopathy HIV Testing CT, lymph nodes, pleural biopsy, sampling of other affected systems