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A-CCC > GP-respiratory > Flashcards

GP-respiratory Flashcards

1
Q

Asthma definition

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2
Q

presentation of asthma, examination signs and differentials

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3
Q

typical asthma triggers

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4
Q

The NICE guidelines (2020) recommend initial investigations in patients with suspected asthma:

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5
Q

Diagnostic differences between patients over 17years old and those aged 5-16 years

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6
Q

How does spirometry work and which value indicates asthma?

A

test used to establish objective measures of lung function. It involves different breathing exercises into a machine that measures volumes of air and flow rates and produces a report. A FEV1:FVC ratio of less than 70% suggests obstructive pathology (e.g., asthma or COPD).

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7
Q

How does reversibility testing work and which results indicate asthma?

A

involves giving a bronchodilator (e.g., salbutamol) before repeating the spirometry to see if this impacts the results. NICE says a greater than 12% increase in FEV1 on reversibility testing supports a diagnosis of asthma.

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8
Q

How does FeNO testing work and which value indicates asthma?

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Fractional exhaled nitric oxide (FeNO) measures the concentration of nitric oxide exhaled by the patient. Nitric oxide is a marker of airway inflammation. The test involves a steady exhale for around 10 seconds into a device that measures FeNO. NICE say a level above 40 ppb is a positive test result, supporting a diagnosis. Smoking can lower the FeNO, making the results unreliable.

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9
Q

How is peak flow variability measures and which result indicates asthma?

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is measured by keeping a peak flow diary with readings at least twice daily over 2 to 4 weeks. NICE says a peak flow variability of more than 20% is a positive test result, supporting a diagnosis.

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10
Q

Direct bronchial challenge testing: how does it work and which value indicates asthma?

A

opposite of reversibility testing. Inhaled histamine or methacholine is used to stimulate bronchoconstriction, reducing the FEV1 in patients with asthma. NICE say a PC20 (provocation concentration of methacholine causing a 20% reduction in FEV1) of 8 mg/ml or less is a positive test result.

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11
Q

long term drug treatment for asthma

A

Maintenance and reliever therapy (MART)
* a form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required
* MART is only available for ICS and LABA combinations in which the LABA has a fast-acting component (for example, formoterol)

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12
Q

additional management for ashtma

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  • Individual written asthma self-management plan
  • Yearly flu jab
  • Yearly asthma review when stable
  • Regular exercise
  • Avoid smoking (including passive smoke)
  • Avoiding triggers where appropriate
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13
Q

Beta-2 adrenergic receptor agonists MOA and examples

A

are bronchodilators (they open the airways). Adrenalin acts on the smooth muscle of the airways to cause relaxation. Stimulating the adrenalin receptors dilates the bronchioles and reverses the bronchoconstriction present in asthma. Short-acting beta-2 agonists (SABA), such as salbutamol work quickly, but the effects last only a few hours. They are used as reliever or rescue medication during acute worsening of asthma symptoms. Long-acting beta-2 agonists (LABA), such as salmeterol, are slower to act but last longer.

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14
Q

Inhaled corticosteroids (ICS) MOA and example

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such as beclometasone, reduce the inflammation and reactivity of the airways. These are used as maintenance or preventer medications to control symptoms long-term and are taken regularly, even when well.

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15
Q

Long-acting muscarinic antagonists (LAMA) MOA and examples

A

such as tiotropium, work by blocking acetylcholine receptors. Acetylcholine receptors are stimulated by the parasympathetic nervous system and cause contraction of the bronchial smooth muscles. Blocking these receptors dilates the bronchioles and reverses the bronchoconstriction present in asthma.

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16
Q

Leukotriene receptor antagonists MOA and example

A

such as montelukast, work by blocking the effects of leukotrienes. Leukotrienes are produced by the immune system and cause inflammation, bronchoconstriction and mucus secretion in the airways.

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17
Q

Theophylline MOA

A

works by relaxing the bronchial smooth muscle and reducing inflammation. Unfortunately, it has a narrow therapeutic window and can be toxic in excess, so monitoring plasma theophylline levels is required.

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18
Q

Maintenance and reliever therapy (MART) MOA

A

Involves a combination inhaler containing an inhaled corticosteroid and a fast and long-acting beta-agonist (e.g., formoterol). This replaces all other inhalers, and the patient uses this single inhaler both regularly as a preventer and also as a reliever when they have symptoms.

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19
Q

definition of low, moderate and high dose inhaled corticosteroids

A
  • <= 400 micrograms budesonide or equivalent = low dose
  • 400 micrograms - 800 micrograms budesonide or equivalent = moderate dose
  • > 800 micrograms budesonide or equivalent= high dose.
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20
Q

Bronchiectasis definition

A

Bronchiectasis involves permanent dilation of the bronchi, the large airways that transport air to the lungs. Sputum collects and organisms grow in the wide tubes, resulting in a chronic cough, continuous sputum production and recurrent infections.

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21
Q

Bronchiectasis causes

A
  • post-infective: tuberculosis, measles, pertussis, pneumonia
  • cystic fibrosis
  • bronchial obstruction e.g. lung cancer/foreign body
  • immune deficiency: selective IgA, hypogammaglobulinaemia
  • allergic bronchopulmonary aspergillosis (ABPA)
  • ciliary dyskinetic syndromes: Kartagener’s syndrome, Young’s syndrome
  • yellow nail syndrome
  • Alpha-1-antitrypsin deficiency
  • Connective tissue disorders (e.g., rheumatoid arthritis)

TOM TIP: Yellow nail syndrome is characterised by yellow fingernails, bronchiectasis and lymphoedema. Patients are stable and have good clinical signs, making it a good choice for OSCEs. As it is rare, examiners will score high marks if you can combine these features and name the diagnosis.

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22
Q

Bronchiectasis features

A

Key presenting symptoms are:

Shortness of breath
Chronic productive cough: large amount of sputum
Recurrent chest infections
Weight loss
Haemoptysis

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23
Q

Signs of bronchiectasis on examination include:

A

Signs of bronchiectasis on examination include:

  • Sputum pot by the bedside
  • Oxygen therapy (if needed)
  • Weight loss (cachexia)
  • Finger clubbing
  • Signs of cor pulmonale (e.g., raised JVP and peripheral oedema)
  • Scattered crackles throughout the chest that change or clear with coughing
  • Scattered wheezes and squeaks
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24
Q

bronchiectasis CXR

A

Chest x-ray showing tramlines, most prominent in the left lower zone

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25
Q

Bronchiectasis CT

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CT chest showing widespread tram-track and signet ring signs

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26
Q

Bronchiectasis investigations

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27
Q

Most common organisms isolated from patients with bronchiectasis:

A

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

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28
Q

Bronchiectasis management

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29
Q

definition of COPD

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30
Q

COPD presentation

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A typical presentation of COPD is a long-term smoker with persistent symptoms of:

  • Shortness of breath
  • Cough
  • Sputum production
  • Wheeze
  • Recurrent respiratory infections, particularly in winter
  • in severe cases, right-sided heart failure may develop resulting in peripheral oedema

TOM TIP: COPD does NOT cause clubbing, haemoptysis (coughing up blood) or chest pain. These symptoms should be investigated for a different cause, such as lung cancer, pulmonary fibrosis or heart failure.

31
Q

MRC dyspnoea scale: components and what it is used for

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32
Q

COPD diagnosis

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Diagnosis is based on the clinical presentation and spirometry results.

Spirometry will show an obstructive picture with a FEV1:FVC ratio of less than 70%. There is little or no response to reversibility testing with beta-2 agonists (e.g., salbutamol). Reversible obstruction is more suggestive of asthma.

33
Q

investigations for COPD

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34
Q

how to assess severity of COPD

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35
Q

examination signs in COPD

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36
Q
  • COPD causes
A

o Smoking
o Fumes & dust at work e.g. cadmium dust & fumes, silica dust
o Alpha-1 antitrypsin deficiency
Airway narrowing - Result of hypertrophy/hyperplasia mucus secreting glands

37
Q

COPD RF

A
  • Cigarette smoking
  • Occupational exposure (dust, particles)
  • Air pollution
  • Advanced age
  • Genetic factors (α1-antitrypsin deficiency)
  • White ancestry
38
Q

COPD differentials

A
  1. Asthma
  2. Congestive heart failure
  3. Bronchiectasis
  4. Lung cancer
39
Q

COPD long term management

A

Oral prophylactic antibiotic therapy
azithromycin prophylaxis is recommended in select patients
* patients should not smoke, have optimised standard treatments and continue to have exacerbations
* other prerequisites include a **CT thorax **(to exclude bronchiectasis) and sputum culture (to exclude atypical infections and tuberculosis)
* LFTs and an ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval

Phosphodiesterase-4 (PDE-4) inhibitors NICE
oral PDE-4 inhibitors such as roflumilast reduce the risk of COPD exacerbations in patients with severe COPD and a history of frequent COPD exacerbations
NICE recommend if:
* the disease is severe, defined as a forced expiratory volume in 1 second (FEV1) after a bronchodilator of less than 50% of predicted normal, and
* the person has had 2 or more exacerbations in the previous 12 months despite triple inhaled therapy with a long-acting muscarinic antagonist, a long-acting beta-2 agonist and an inhaled corticosteroid

Cor pulmonale
* features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2
* use a loop diuretic for oedema, consider long-term oxygen therapy

40
Q

Cor pulmonale definition and causes

A
41
Q

Cor pulmonale symptoms

A

Often patients with early cor pulmonale are asymptomatic. Symptoms of cor pulmonale include:

Shortness of breath
Peripheral oedema
Breathlessness of exertion
Syncope (dizziness and fainting)
Chest pain

42
Q

signs of Cor pulmonale

A
  • Hypoxia
  • Cyanosis
  • Raised JVP (due to a back-log of blood in the jugular veins)
  • Peripheral oedema
  • Parasternal heave
  • Loud second heart sound
  • Murmurs (e.g., pan-systolic in tricuspid regurgitation)
  • Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)
43
Q

management of cor pulmonale

A

Treating the symptoms (e.g., diuretics for oedema) and the underlying cause.
Long-term oxygen therapy is often used.
The prognosis is poor unless there is a reversible underlying cause.

44
Q

Acute exacerbation of COPD presentation

A

Acute exacerbations:
* increase in dyspnoea, cough, wheeze
* may be an increase in sputum suggestive of an infective cause
* may be hypoxic and in some cases have acute confusion

45
Q

ABG results in acute exacerbation of COPD

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46
Q

Investigations for acute exacerbations of COPD

A

ABG first

47
Q

target O2 sats for COPD patients and rules for O2 therapy

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48
Q

The most common infective causes of COPD exacerbations are:

A

bacteria
* Haemophilus influenzae (most common cause)
* Streptococcus pneumoniae
* Moraxella catarrhalis

respiratory viruses
* account for around 30% of exacerbations
* human rhinovirus is the most important pathogen

49
Q

Management of acute exacerbations of COPD

A

the BNF recommends one of the following oral antibiotics first-line: amoxicillin or clarithromycin or doxycycline.

50
Q

NICE Clinical Knowledge Summaries recommend admission for COPD exacerbation if any of the following criteria are met

A

NICE Clinical Knowledge Summaries recommend admission if any of the following criteria are met (please see the link for the full list)
* severe breathlessness
* acute confusion or impaired consciousness
* cyanosis
* oxygen saturation less than 90% on pulse oximetry.
* social reasons e.g. inability to cope at home (or living alone)
* significant comorbidity (such as cardiac disease or insulin-dependent diabetes)

51
Q

Severe exacerbations of COPD management

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52
Q

How are patients with COPD assessed for O2 therapy? Criteria for receiving long term oxygen therapy

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53
Q

Non-invasive ventilation explanation for COPD.
Criteria for getting it.
Monitoring investigations

A
54
Q

how does FVC change in asthma and COPD?

A

COPD and asthma have reduced FEV1/FVC ratio but FVC may be normal

55
Q

the step-down treatment of asthma: how to reduce ICS

A

In the step-down treatment of asthma, aim for a reduction of 25-50% in the dose of inhaled corticosteroids

56
Q

when should you step down treatment for asthma?

A

The British Thoracic Society (BTS) guidelines recommend that we should consider stepping down treatment every 3 months or so.

57
Q

Idiopathic lung fibrosis definition and group it affects

A

Idiopathic pulmonary fibrosis (IPF, previously termed cryptogenic fibrosing alveolitis) is a chronic lung condition characterised by progressive fibrosis of the interstitium of the lungs. Whilst there are many causes of lung fibrosis (e.g. medications, connective tissue disease, asbestos) the term IPF is reserved when no underlying cause exists.

IPF is typically seen in patients aged 50-70 years and is twice as common in men.

58
Q

features of idiopathic pulmonary fibrosis

A

progressive exertional dyspnoea
bibasal fine end-inspiratory crepitations on auscultation
dry cough
clubbing

59
Q

idiopathic lung fibrosis investigations and results

A
  • spirometry: classically a restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased)
  • impaired gas exchange: reduced transfer factor (TLCO)
  • imaging: bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’) may be seen on a chest x-ray but high-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF
  • ANA positive in 30%, rheumatoid factor positive in 10% but this does not necessarily mean that the fibrosis is secondary to a connective tissue disease. Titres are usually low
60
Q

Management of idiopathic lung fibrosis

A
  • pulmonary rehabilitation
  • very few medications have been shown to give any benefit in IPF. There is some evidence that pirfenidone (an antifibrotic agent) may be useful in selected patients (see NICE guidelines)
  • many patients will require supplementary oxygen and eventually a lung transplant
61
Q

Prognosis for interstitial lung fibrosis

A

poor, average life expectancy is around 3-4 years

62
Q

CXR of idiopathic pulmonary fibrosis

A
63
Q

CT and CXR of idiopathic pulmonary fibrosis

A
64
Q

Fibrosis predominately affecting the upper zones causes

A

CHARTS
C - Coal worker’s pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis

radiation-induced pulmonary fibrosis
* may develop following radiotherapy for breast or lung cancer
* typically seen between 6 and 12 months following completion of radiotherapy course

65
Q

Lung Fibrosis predominately affecting the lower zones causes

A
  • idiopathic pulmonary fibrosis
  • most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
  • drug-induced: amiodarone, bleomycin, methotrexate
  • asbestosis
66
Q

management options for interstitial lung disease

A

Generally, there is a poor prognosis and limited management options in interstitial lung disease, and treatment is primarily supportive. Options include:

  • Remove or treat the underlying cause
  • Home oxygen where there is hypoxia
  • Stop smoking
  • Physiotherapy and pulmonary rehabilitation
  • Pneumococcal and flu vaccine
  • Advanced care planning and palliative care where appropriate
  • Lung transplant is an option, but the risks and benefits need careful consideration
67
Q

interstitial lung disease definition and some of the conditions it covers

A

Interstitial lung disease includes many conditions that cause inflammation and fibrosis of the lung parenchyma (lung tissue). Fibrosis involves the replacement of elastic and functional lung tissue with non-functional scar tissue.

The conditions we will cover here are:

  • Idiopathic pulmonary fibrosis (the most important to remember)
  • Secondary pulmonary fibrosis
  • Hypersensitivity pneumonitis
  • Cryptogenic organising pneumonia
  • Asbestosis
68
Q

secondary pulmonary fibrosis causes

A
69
Q

hypersensitivity pneumonitis definition, example of specific cause, investigations, management

A
70
Q

cryptogenic organising pneumonia definition, presentation, investigation findings and treatment

A
71
Q

asbestosis definition, consequences, pathophysiology

A

A-CCC (9 decks)

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