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Respiratory 1

oelomar's version from 2018-11-05 17:30


Question Answer
What is the difference between atopic and non-atopic asthma?Atopic = evidence of allergen sensitisation (often in a patient with a history of other atopic disease such as eczema). Non-atopic = no evidence of allergen sensitisation.
Up to 50% of childhood asthma remits in adolescence only to return in adulthood in a significant number of patients. True or false?True.
What can trigger asthma symptoms?Cold air, exercise, emotion, allergens (house dust, pollen, fur) infection, smoking, pollution, aspirin/NSAIDS/beta blockers, GORD.
What are the clinical features of asthma?Episodic expiratory wheezing (inspiratory as well when severe) and episodic shortness of breath, nocturnal cough, symptoms are usually worse at night/morning, increased anterior-posterior diameter of the chest due to air trapping and increase in residual volume. Other signs include eosinophilia in sputum, NO in the breath, and 60% of patients have acid reflux.
How is asthma diagnosed?Diagnosis can be established by a compatible clinical history plus either/or an FEV1 ≥ 15% (and 200 ml) increase following administration of a bronchodilator/trial of corticosteroids.
What will ABGs show in someone exhibiting symptoms of asthma?Mild hypoxia and respiratory alkalosis.


Question Answer
What is “step 1” in the pharmacological management of asthma?Short-acting bronchodilator (most commonly a β2 agonist such as salbutamol).
What is “step 2” in the pharmacological management of asthma?Addition of inhaled corticosteroids (e.g. beclomethasone).
What is “step 3” in the pharmacological management of asthma?Addition of a leukotriene receptor antagonist (LTRA).
What is “step 4” in the pharmacological management of asthma?Addition of inhaled long-acting β2 agonist (LABA). Continue LTRA based on patient's response to LTRA..
What is “step 5” in the pharmacological management of asthma?Continue on short-acting beta-agonist+/-LTRA and switch ICS/LABA for a maintenance and reliever therapy (MART), that includes a low-dose inhaled corticosteroid.
What is “step 6” in the pharmacological management of asthma?SABA +/- LTRA + medium-dose inhaled corticosteroid maintenance and reliever therapy (MART); or consider changing back to a fixed-dose of a moderate-dose inhaled corticosteroid and a separate LABA.
What is “step 7” in the pharmacological management of asthma?SABA +/- LTRA + one of the following options: increase inhaled corticosteroid to high-dose (only as part of a fixed-dose regime, not as a MART); a trial of an additional drug (for example, a long-acting muscarinic receptor antagonist or theophylline); seeking advice from a healthcare professional with expertise in asthma.
What is maintenance and reliever therapy (MART)?A form of combined inhaled corticosteroid and LABA treatment in which a single inhaler, containing both inhaled corticosteroid and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required. MART is only available for inhaled corticosteroid and LABA combinations in which the LABA has a fast-acting component (for example, formoterol).
What constitutes a low, medium, or high-dose of inhaled corticosteroid?<= 400 micrograms budesonide or equivalent = low dose; 400 micrograms - 800 micrograms budesonide or equivalent = moderate dose; >800 micrograms budesonide or equivalent= high dose.


Question Answer
What are the adverse effects of β2 agonists?Tremor, arrhythmia, hypokalaemia.
Theophylline blocks the action of adenosine. True or false?True.
What is ipratropium bromide and how does it relieve asthma symptoms?Ipratropium bromide is a competitive antagonist of muscarinic (acetylcholine) receptors. This prevents bronchoconstriction. Muscarinic antagonists can also be used in COPD.
What is montelukast and what relevance does it have in asthma?A leukotriene receptor antagonist. It can be used in the treatment of asthma, and is especially good in aspirin-induced asthma.
What are the clinical features of an acute severe asthma attack?Patients with acute severe asthma typically have: inability to complete a sentence in one breath; respiratory rate ≥ 25 breaths per minute; tachycardia ≥ 110 beats/min; PEFR < 50% of predicted normal or best.
What are the clinical features of a life-threatening asthma attack?A silent chest, cyanosis or feeble respiratory effort; exhaustion, confusion or coma; bradycardia or hypotension; PEFR < 30% of predicted normal or best (approximately 150 L/min in adults).
How are acute severe attacks of asthma treated?“O SHIP”: Oxygen 40-50%; nebulised 5mg Salbutamol; IV 200mg Hydrocortisone; nebulized Ipratropium 0.5mg; Prednisolone 60mg orally. Discharge with prednisolone 40mg od for 5 days.
When would magnesium sulphate be considered as a treatment for asthma attacks?Consider a single dose of IV magnesium sulphate in life threatening attacks, and patients without a good response to inhaled bronchodilator therapy.
Patients may have to go to hospital during an acute severe asthma attack. When can they be discharged?Patients need to be stable on their normal inhalers for 24 hours before discharge.


Question Answer
What is chronic obstructive pulmonary disease (COPD)?A type of obstructive lung disease characterised by long-term poor airflow (FEV1<80% of predicted & FEV1/FVC<0.7) with little or no reversibility. The term COPD includes the conditions emphysema and chronic bronchitis.
What is emphysema?Emphysema is defined histologically as enlarged airspaces distal to terminal bronchioles, with destruction of alveolar wall.
What is chronic bronchitis?Chronic bronchitis is defined as a productive cough that lasts for three months or more per year for at least two years.
What are the symptoms of COPD?Cough, sputum, dyspnoea, and wheeze.
What are the signs of COPD?Tachypnoea, use of accessory muscles, hyperinflation, decreased cricosternal distance (<3cm), decreased expansion, resonant or hyper-resonant percussion note; wheeze, cyanosis, cor pulmonale.
What will a chest x-ray show in someone with COPD?Flat diaphragms, hyperinflated lungs, and a thin-appearing heart and mediastinum. Parenchymal bullae or subpleural blebs are also seen.
Are haemoglobin and PCV (packed cell volume – same thing as the haematocrit) levels increased or decreased in COPD patients?Increased, as a result of persistent hypoxaemia (secondary polycythaemia).
What will sputum examination show in COPD patients?May show H. influenza (commonest) and Moraxella catarrhalis, as they are the commonest organisms that produce acute exacerbations of COPD.
What is the link between α1-antitrypsin and COPD?α1-antitrypsin is a protease inhibitor which is produced in the liver, secreted into the blood, and diffuses into the lung. Here it inhibits proteolytic enzymes which are capable of destroying alveolar wall connective tissue. Hereditary deficiency of α1-antitrypsin accounts for about 2% of emphysema cases.
When is long-term oxygen therapy offered to COPD patients?When PaO2 is <7.3kPa when breathing air, or when PaO2 is 7.3-8kPa with secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema, or evidence of pulmonary hypertension.


Question Answer
Some COPD patients may be referred to a specialist for consideration of long-term non-invasive ventilation. When would this happen?When the patient is on long-term oxygen therapy and is either hypercapnic or acidotic.
What is seretide a combination of?Fluticasone (glucocorticoid) and salmeterol (long-acting beta2-adrenergic receptor agonist).
When are high concentrations of oxygen especially NOT administered for a COPD patient?When the patient is in type II respiratory failure (i.e. during an acute exacerbation of COPD). In type II respiratory failure the PaCO2 is elevated and the patient is dependent on hypoxic drive. Consequently, giving additional oxygen will nearly always lead to a further rise in the PaCO2. In those at high risk of high carbon dioxide levels, oxygen saturations of 88-92% are recommended.
What is the management of an acute exacerbation of COPD?“O SHIP”: Oxygen – aim for PaO2>7.3kPa with a rise in PaCO2<1.5kPa; nebulised Salbutamol 5mg; IV Hydrocortisone 200mg; Ipratropium 500micrograms/6h; oral Prednisolone 30-40mg. Use antibiotics if evidence of infection. The pH should not be allowed to fall below 7.25; if it does, increased ventilation must be achieved either by artificial ventilation or by using a respiratory stimulant. Non-invasive ventilation (NIV) (usually BiPAP – bilevel positive airway pressure) is the treatment of choice for persistent hypercapnic patients.
What antibiotic therapy is used in COPD patients where there is evidence of an infection?First line therapy is amoxicillin, or if allergic to penicillin, then clarithromycin. Second line is doxycycline.
What is cystic fibrosis?An autosomal recessive disorder in which there is a defect in the cystic fibrosis transmembrane conductance regulator (CFTR) protein, which is a critical chloride channel. CFTR is involved in the production of sweat, digestive fluids, and mucus. When CFTR is defective, secretions which are usually thin become thick.
What are the clinical features of cystic fibrosis?Many, including recurrent lung infections in childhood that become persistent and chronic, severe lung disease, pancreatic dysfunction (resulting in symptomatic steatorrhoea), meconium ileus, and sinusitis. Breathlessness and haemoptysis occur in the later stages airflow limitation and bronchiectasis develop. Males are almost always infertile owing to failure of development of the vas deferens and epididymis. Many patients also suffer from malnutrition due to a combination of malabsorption and maldigestion.
Which bacteria causing lung infections are commonly found in cystic fibrosis patients?Pseudomonas aeruginosa (most common – 70% of adults with CF have Pseudomonas infection in their sputum), Staphylococcus aureus, Haemophilus influenza, Burkholderia cepacia (worse prognosis but less common – discourage CF patients from grouping).
How is cystic fibrosis diagnosed?Clinical history, family history of the disease, a high sweat sodium concentration of >60mmol/L, blood DNA analysis of gene defect, absent vas deferens and epididymis.
Pseudomonas aeruginosa is an aerobic gram-negative rod-shaped bacterium. True or false?True.
What is the link between Pseudomonas aeruginosa and wound and burn infections?Pseudomonas aeruginosa is the most common source of burn infections.


Question Answer
What is bronchiectasis?Abnormal and permanently widened bronchi or their branches due to inflammatory destruction of airway walls resulting from persistently infected mucus.
What is the most common cause of bronchiectasis?Cystic fibrosis in developed countries. TB is most common cause worldwide.
What is the most common pathogen involved in bronchiectasis?Pseudomonas aeruginosa.
What are the clinical features of bronchiectasis?Cough productive of copious amounts of sputum; haemoptysis (can be massive); clubbing; coarse crackles can be heard over the affected areas, usually at the bases of the lungs; breathlessness may result from airflow limitation.
What investigations can be carried out to help diagnose bronchiectasis?High-resolution CT scanning is the investigation of choice and reveals thickened, dilated bronchi and cysts at the end of the bronchioles. Characteristically the airways are larger than their associated blood vessels. Sputum examination and culture are essential for adequate treatment.
How is bronchiectasis treated?Postural drainage (patients trained by physiotherapists to learn how to do it themselves), antibiotics, bronchodilators (useful in patients with demonstrable airflow limitation), anti-inflammatory agents (inhaled or oral steroids can decrease the rate of progression).
Name some of the complications of bronchiectasis.Pneumonia, pneumothorax, empyema and metastatic cerebral abscess can occur. Severe, life-threatening haemoptysis can also occur.


Question Answer
What are restrictive lung diseases?A category of respiratory disease that restricts lung expansion due to inflammatory and/or fibrosing processes in the alveolar walls, leading to thickening and possible destruction of pulmonary vessels and fibrosis of the interstitium, resulting in decreased lung volume (decrease in total lung capacity and vital capacity), an increased work of breathing, and inadequate ventilation and/or oxygen.
What are the signs/symptoms of restrictive lung disease?The main symptoms are shortness of breath and cough.
What is a normal FEV1/FVC ratio?80%.
What is the FEV1/FVC ratio in obstructive lung diseases?<80%.
What is the FEV1/FVC ratio in restrictive lung diseases?Normal or >80% (because FEV1 and FVC are equally reduced due to fibrosis or other lung pathology (not obstructive pathology)).
What are the CT findings in interstitial lung disease?“Ground glass” in early interstitial lung disease. “Honey combing” is found in late interstitial lung disease, especially in idiopathic pulmonary fibrosis.


Question Answer
What is idiopathic pulmonary fibrosis?A chronic and ultimately fatal disease characterised by a progressive decline in lung function in which the lung tissue scars (fibrosis).
Which group of people is idiopathic pulmonary fibrosis likely to affect?It is relatively rare with a mean onset in the late sixties and is more common in males.
What are the clinical features of idiopathic pulmonary fibrosis?Dyspnoea on exertion, fine bilateral end-inspiratory crackles, non-productive cough, clubbing.
What will a chest x-ray show in people with idiopathic pulmonary fibrosis?Chest x-ray initially shows a ground glass appearance, followed by irregular reticulonodular shadowing and finally a honeycomb lung.
What will a high-resolution CT scan show in people with idiopathic pulmonary fibrosis?Characteristic bilateral changes mainly involving the lower lobes. Note that this is the investigation of choice.
What do blood gas results show in people with idiopathic pulmonary fibrosis?Low PaO2 and normal or low PaCO2 owing to hyperventilation.
How is idiopathic pulmonary fibrosis treated?Supportive treatment includes domiciliary oxygen therapy. In younger patients with severe disease, lung transplantation is offered.
What is the prognosis of idiopathic pulmonary fibrosis?The median survival time is approximately 5 years.

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