Asthma Flashcards

1
Q

Three typical features of asthma

A

Airflow limitation that is usually reversible spontaneously or with treatment

Airway hyper-responsiveness (AHR)

Bronchial inflammation with T lymphocytes, mast cells, eosinophils.

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2
Q

Pathophysiology in asthma.

A

T lymphocytes, eosinophils and mast cells

Plasma exudation

Oedema

Smooth muscle hypertrophy

Matrix deposition

Mucus plugging

Epithelial damage

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3
Q

What is the most common association to childhood-asthma?

A

Often accompanied by asthma and reacts to allergens.

They have a wheezing illness with inhaled allergic triggers.

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4
Q

Is middle aged onset of asthma usually allergic?

A

No, it can be, but it often starts by getting triggered due to respiratory infection.

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5
Q

Give causes of developing asthma in non-atopic individuals in middle age.

A

Infection

Occupational agents such as toluene diisocyanate

Intolerance to NSAIDs such as aspirin and ibuprofen

B-blockers

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6
Q

How are IgE levels related to asthma?

A

In atopic asthma elevated serum IgE levels are linked to airway hyper-responsiveness.

However elevated IgE levels cannot confirm diagnosis of asthma.

Non-elevated levels of IgE does not exclude asthma.

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7
Q

Genetic factors of asthma.

A

No single gene for asthma but several, in combination with environmental factors might influence its development.

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8
Q

Environmental factors of asthma.

A

Early childhood exposure to allergens and maternal smoking has a major influence on IgE production.

Hygiene hypothesis

Dirtier environment might be protective

Aspergillus fumigatus

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9
Q

Give examples of precipitating factors of asthma.

A

Occupational sensitisers

Cold air and exercise

Atmospheric pollution and irritant dusts

Vapours and fumes

Diet

Emotion

Drugs

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10
Q

Occupational sensitisers are divided into two groups.

Which?

A

Low-molecular-weight (Non-IgE)

High-molecular weight (IgE)

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11
Q

Give examples of LMW non IgE occupational sensitisers.

A

Isocyanates

Colophony fumes

Wood dust

Drugs

Bleaches and dyes

Complex metal salts like nickel, platinum and chromium.

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12
Q

Which occupations might be exposedto isocyanates?

A

Polyurethane varnishes

Industrial coatings

Spray painting

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13
Q

What occupations might be exposed to colophony fumes?

A

Soldering/welders

Electronics industry

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14
Q

Give examples of HMW (IgE) occupational sensitisers.

A

Allergens from animals and insects

Antibiotics

Latex

Proteolytic enzymes

Complex salts of platinum

Acid anhydrides and polyamine hardening agents

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15
Q

What can decrease the risk of developing some forms of occupational asthma?

A

Not smoking/stop smoking

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16
Q

Explain the difference in developing asthma due to exposure to occupational sensitisers in atopic vs non-atopic asthma.

A

Atopic asthma has a more rapid onset due to the development of IgE antibody.

Non-atopic can develop asthma but does so more slowly, and need longer exposure.

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17
Q

Explain the effects of weather and exercise on asthma.

A

Prolonged exercise can induce an asthma attack, this is commonly after the exercise itself.

Also inhalation of cold and dry air can set off an attack.

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18
Q

What is exercise-induced asthma driven by?

A

Release of histamine, prostaglandins and leukotrienes from mast cells, as well as stimulation of neural reflexes.

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19
Q

Explain triggers of asthma found out in the open air.

A

Tobacco smoke

Car exhaust fumes

Solvents

Strong perfumes

High concentrations of airborne dust

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20
Q

Give examples of food which have shown to be protective against asthma.

A

Fresh fruit and vegetables.

Possible due to greater consumption of anti-oxidants.

Genetic variation in antioxidant enzymes is associated with more severe asthma.

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21
Q

Give examples of drugs that can trigger an asthma attack.

A

NSAIDs such as aspirin, indometacin and ibuprofen.

Beta-blockers

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22
Q

In what patients are NSAID intolerance especially prevalent in?

A

Patients with both asthma and nasal polyps

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23
Q

Why might beta-blockers trigger an asthma attack?

A

Airways have direct parasymp innervation elliciting bronchoconstriction.

There is no direct sympathetic innervation of bronchial smooth muscle.

This means that when bronchoconstriction happens due to parasymp, bronchodilation is critically dependent on circulating adrenaline.

Inhibition of b1 can therefore be very serious.

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24
Q

Clinical features of asthma.

A

Wheezingattacks and episodic dyspnoea.

The symptoms are usually worst during night, especially when uncontrolled.

Bilateral widespread polyphonic wheeze

Shows a diurnal variation.

Cough is common, cough is more common at night.

Triggers to asthma attack or worsening asthma are usually appearing.

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25
Q

Investigations of asthma

A

Lung function test

Histamine or methacholine bronchial provocation/challenge test

Trial of corticosteroids

Exhaled nitric oxide

Blood and sputum tests

CXR

Skin tests

Allergen provocation tests

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26
Q

What lung function tests might be done in asthma?

A

PEFR

Spirometry

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27
Q

Explain PEFR testing in asthma.

A

PEFR measurements on waking, prior to taking a bronchodilator, before bed, and after taking a bronchodilator.

This shows the variable airflow limitation.

Diurnal variation in PEFR is a good measure of asthma activity.

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28
Q

Explain spirometry in asthma.

A

Especially good for assessing variability.

An improvement in FEV1 or PEFR following inhalation of a bronchodilator can diagnose asthma.

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29
Q

How much of an improvement in FEV1 or PEFR is needed to support a diagnosis of asthma?

A

Improvement in FEV1 of 12% or more and increase in volume of 200 ml or more

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30
Q

Explain a trial of corticosteroids as an investigation in asthma.

A

Prednisolone 30 mg orally should be given daily for 2 weeks.

Lung functions are measured before and after the course.

An improvement of 15% in FEV1 confirms the presence of reversible element.

It indicates that the administration of inhaled steroids will prove beneficial for the patient.

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31
Q

Explain exhaled nitric oxide in asthma.

A

A measure of airway inflammation.

Can also be used to assess corticosteroid response.

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32
Q

CXR findings on investigating asthma.

A

No diagnostic features.

Overinflation is characteristic during an acute episode or in chronic severe disease.

CXR is more helpful in excluding pneumothorax, and allergic bronchopulmonary aspergillosis.

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33
Q

Explain skin-prick tests in asthma.

A

Should be performed to help identify allergic trigger factors.

It is not diagnostic on its own.

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34
Q

When might allergen provocation test be done in asthma?

A

To investigate patients with suspected occupational asthma.

Not ordinary.

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35
Q

Explain how to diagnose asthma in adults.

A

It is a mix of clinical features, past medical history and family history.

Also triggers should be evaluated and classical diurnal variation.

A lung function test (spirometry) and PEFR.

PEFR can be done in a calender for the patient to record it during the day.

Trial of corticosteroids or beta-agonists is usually done to see improvement.

eNO can support diagnosis.

If all else fails bronchial challenge test is definitive.

36
Q

Explain how to diagnose severe asthma.

A

Based on signs such as using your reliever inhaler more than three times a week.

Need for tablet steroid therapy three days or longer, two or more times per year.

Needing steroid tablets every day.

Symptoms when an attack occurs.

How many A&E visits

If it severely affects your life.

Then usual tests are carried out as well.

37
Q

What are the aims of treatment in asthma?

A

Abolish symptoms

Restore normal or best possible lung function

Reduce risk of severe attacks

Enable normal growth to occur in children

Minimise absence from school or employment

38
Q

How are the aims of asthma treatment achieved?

A

Education for both family and patient

Participation of both patient and family in treatment

Avoidance of triggers

Use of the lowest effective doses possibly needed.

39
Q

How can extrinsic factors be controlled?

A

In children sublingual allergen immunotherapy can be done to reduce sensitivity to house dustmites

Active and passive smoking should be avoided.

Avoid beta-blockers in tablets or eye-drops.

Avoid NSAIDs, COX-2i might be better tolerated.

40
Q

How to diagnose asthma in children under 5.

A

Treat symptoms based on clinical judgement and observations.

If they still have symptoms when they reach 5 yo, they should be able to carry out objective tests.

If they still are not able to do so continue as before and review in 6 to 12 months and try the tests again.

41
Q

When should a FeNO test be offered in adults?

A

When there is normal spirometry or non-reversible spirometry with bronchodilators.

42
Q

What is a positive FeNO test in children and adults?

A

Children = 35 ppb or more

Adults = 40 ppb or more

43
Q

When should a bronchial test challenge be done?

A

Normal spirometry and…

FeNO level of 40 ppb or more and no variability in peak flow readings or

FeNO level of 39 ppb or less with variability in peak flow readings.

44
Q

What is a positive bronchodilator reversibility test in adults?

A

Improvement in FEV1 of 12% or more and increase in volume of 200 ml or more

45
Q

What is a positive BDR result in children?

A

Improvement in FEV1 of 12% or more.

46
Q

What is a positive peak flow variability in adults and children?

A

20% or more

47
Q

What is a positive bronchial challenge test in adults?

A

Provocative concentration of methacholine causing a 20% fall in FEV1 (PC20) of 8 mg/ml or less

48
Q

What is a positive bronchial challenge test in children?

A

It is not performed in children.

49
Q

Explain the diagnostic algorithm of asthma.

A
50
Q

Algorithm for objective tests in children 5-16.

A
51
Q

Algorithm for objective tests in patients 17 or older.

A
52
Q

Give examples of why asthma might not be controlled.

A

Alternative diagnoses

Lack of adherence

Suboptimal inhaler technique

Smoking

Occupational exposures

Environmental exposures

Psychosocial factors

53
Q

Explain the pharmacological treatment pathway in newly diagnosed asthma in adults (17 and older)

A

If there is an infrequent short-lived wheeze and normal lung function offer a SABA alone. Bold means symptom relief.

If asthma is uncontrolled for 4 to 8 weeks or if initial symptoms indicate maintenance therapy right away…

Offer low dose of ICS with a SABA.

If asthma is uncontrolled for 4 to 8 weeks…

Low dose ICS, LTRA and a SABA.

If asthma is uncontrolled for 4 to 8 weeks…

Low dose ICS, LABA, SABA +/- LTRA.

If asthma is uncontrolled for 4 to 8 weeks…

Low dose ICS, LABA within MART regimen +/- LTRA and Low dose ICS, LABA within MART regimen.

If asthma is uncontrolled for 4 to 8 weeks…

Moderate ICS dose, LABA either within MART regimen or as a fixed dose +/- LTRA and Low dose ICS, LABA within MART regimen or consider changing to SABA.

If asthma is uncontrolled for 4 to 8 weeks…

High dose ICS, LABA as fixed dose, +/- LTRA + SABA

or

Continuing moderate ICS dose with another treatment such as LAMA or theophylline + SABA or low dose ICS with LABA within MART regimen.

or

Refer to specialist

54
Q

Explain the pharmacological treatment pathway in newly diagnosed patients 5-16 yo.

A

Infrequent and short lived wheeze and normal lung function used SABA alone.

If asthma is uncontrolled for 4 to 8 weeks or if the initial symptoms suggest maintenance treatment…

Paediatric low dose of ICS and SABA

If asthma is uncontrolled for 4 to 8 weeks…

Paediatric low dose of ICS, LTRA and SABA

If asthma is uncontrolled for 4 to 8 weeks…

Paediatric low dose of ICS, LABA and stop LTRA. Also give SABA.

If asthma is uncontrolled for 4 to 8 weeks…

Paediatric low dose of ICS, LABA within a MART regimen, paediatric low dose of ICS, LABA within a MART regimen.

If asthma is uncontrolled for 4 to 8 weeks…

Paediatric moderate dose of ICS, LABA within a MART regimen or as a fixed dose, paediatric low dose of ICS, LABA within a MART regimen or change to SABA.

If asthma is uncontrolled for 4 to 8 weeks…

Refer to specialist

or

Paediatric high dose of ICS and LABA as a fixed dose + SABA

or

Paediatric moderate dose of ICS and trial of treatment of e.g. theophylline + SABA or low dose ICS with a LABA within a MART regimen.

55
Q

Explain the pharmacological treatment pathway in suspected asthma in children under 5.

A

Symptoms that do not indicate immediate maintenance therapy use SABA alone.

If asthma is uncontrolled for 4 to 8 weeks or if symptoms indicate need for immediate maintenance therapy…

8 week trial dose of paediatric low dose of ICS + SABA

If symptoms did not resolve consider alternative diagnoses.

If symptoms did resolve, but reverted after more than 4 weeks after the trial ended then repeat the 8 week trial.

If symptoms did resolve but reverted before 4 weeks after the trial ended…

Paediatric low dose of ICS and SABA

If asthma is uncontrolled for 4 to 8 weeks…

Paediatric low dose of ICS and LTRA + SABA

If asthma is uncontrolled for 4 to 8 weeks…

Stop LTRA but continue with paediatric low dose of ICS + SABA and refer to specialist.

56
Q

Give examples of SABAs

A

Salbutamol

Terbutaline

Should only be used as a reliever

57
Q

How are SABAs prescribed?

A

Two puffs as required

58
Q

Give examples of LABAs.

A

Salmeterol

Formoterol

Given once or twice daily

59
Q

Give exampels of inhaled corticosteroids.

A

Beclometasone (most common)

Budesonide

Fluticasone propionate

Fluticasone furoate

Mometasone furoate

Triamcinolone

60
Q

Side effects of inhaled ICS.

A

Oral thrush (rinse mouth after use)

Hoarseness of voice

Subcapsular cataract formation

Osteoporosis.

61
Q

What can be given as steroid sparing agents in steroid-dependent asthmatics?

A

Methotrexate

Ciclosporin

Nowadays biologic monoclonal antibodies are now preferred.

62
Q

Give an example of a SAMA.

A

Ipratropium used in acute severe exacerbations of asthma.

63
Q

Give examples of LAMAs.

A

Tiotropium

Aclidinium

64
Q

Give examples of other anti-inflammatory drugs in asthma.

A

Sodium cromoglicate

Nedocromil sodium.

65
Q

How does sodium cromoglicate and nedocromil sodium work?

A

Prevents activation of mast cells, eosinophils and epithelial cells.

However not lymphocytes.

This is through blocking a specific chloride channel preventing calcium influx.

These drugs are not routinely used

66
Q

Give examples of monoclonal antibodies that can be used in asthma.

A

Omalizumab

Mepolizumab

Reslizumab

Benralizumab

67
Q

Explain use and action of omalizumab.

A

Chelates free IgE and downregulates the number and activity of mast cells and basophils.

It is given subcut every 2-4 weeks depending on total serum IgE levels and body weight.

Can be cost-effective in patients with frequent exacerbations requiring oral corticosteroids.

68
Q

Explain the use and action of mepolizumab, reslizumab and benralizumab..

A

Acts against IL-5 or its receptor.

Can be effective in eosinophilic asthma.

69
Q

What is a novel non-pharmacological management of asthma?

A

Bronchial thermoplasty.

70
Q

Explain how bronchial thermoplasty works.

A

Novel approach in moderate to severe persistent asthma.

Uses radiofrequency radiation to heat the bronchial wall and reduce the mass of airway smooth muscle, decreasing bronchoconstriction.

71
Q

What are asthma exacerbations most commonly caused by?

A

Lack of adherence

Respiratory virus infections

Exposure to an allergen or triggering drug.

72
Q

Features of moderate acute asthma.

A

Increasing symptoms;

Peak flow > 50-75% best or predicted;

No features of acute severe asthma.

73
Q

Features of acute severe asthma.

A

Any one of the following:

Peak flow 33-50% best or predicted;

Respiratory rate ≥ 25/min;

Heart rate ≥ 110/min;

Inability to complete sentences in one breath.

74
Q

Features of life-threatening asthma attack.

A

Peak flow < 33% best or predicted;

Arterial oxygen saturation (SpO2) < 92%;

Partial arterial pressure of oxygen (PaO2) < 8 kPa;

Normal partial arterial pressure of carbon dioxide (PaCO2) (4.6–6.0 kPa);

Silent chest;

Cyanosis;

Poor respiratory effort;

Arrhythmia;

Exhaustion;

Altered conscious level;

Hypotension.

75
Q

Features of near-fatal acute asthma.

A

Raised PaCO2 and/or the need for mechanical ventilation with raised inflation pressures.

PaO2 <8kPa despite treatment with O2

Low and/or falling arterial pH

76
Q

Treatment pathway of acute severe asthma.

A

Supplementary O2 to stay between 94-98% SpO2.

Salbutamol 5mg (or terbutaline 10mg) nebulised with O2

IV hydrocortisone 100mg or oral Prednisolone 40-50mg.

Nebulised Ipratropium bromide can be given in acute severe or life-threatening along with SABA, or if SABA does not give enough of a bronchodilation. 0.5 mg/6h nebulised

IV magnesium sulfate can be given .

In worst case scenarios IV aminophylline can also be given.

Ventilation is required for patients deteriorating past this regime.

CXR can be helpful to rule of pneumothorax.

77
Q

What organism is acute bronchitis in previously healthy subjects?

A

Usually viral.

78
Q

What organisms are common in sequel to a viral infection in smokers and COPD?

A

S. pneumoniae

H. influenzae

79
Q

Clinical features of acute bronchitis.

A

Irritating, non-productive cough, together with discomfort behind the sternum.

Chest tightness

Dyspnoea

Wheezing.

Cough can become productive later on.

80
Q

Treatment of acute bronchitis.

A

Otherwise healthy adults the disease improves spontaneously usually in 4-8 days without serious illness.

Antibiotics are however often given, although their purpose is not always clear.

81
Q

Acute asthma management (according to workbook)

A

ABCDE

SpO2 of 94-98%

ABG if sats are <92%

5 mg nebulised Salbutamol

40mg oral Prednisolone STAT (IV hydrocortisone if PO not possible)

82
Q

Management of severe acute asthma treatment (according to workbook)

A

Nebulised ipratropium bromide 500 micrograms

Consider back to back salbutamol

83
Q

Management of life-threatening or near fatal asthma (according to workbook).

A

Urgent ITU or anaesthesist assessment

Urgent portable CXR

IV aminophylline

Consider IV salbutamol if nebulised route is ineffective.

84
Q

Criteria for safe asthma discharge after exacerbation.

A

PEFR >75% within an hour of treatment can be dischared if there are no other reasons to admit.

Stop regular nebulisers for 24 hours prior to discharge

Inpatient asthma nurse review to reassess inhaler technique and adherence

Provide PEFR meter and written asthma action plan

5 days oral prednisolone

GP follow up within 2 working days

Resp clinic follow up within 4 weeks

For severe or worse, also consider psychosocial factors.

85
Q

Criteria for discharge of an asthma patient.

A

Been stable on discharge medication for 24h

Had inhaler technique checked

PEFR >75 predicted or best with diurnal variability <25%

Steroid inhaled and oral + bronchodilator therapy up to date

Their own PEF meter and written management plan

GP appointment within 2d

Resp clinic appointment within 4wks.

86
Q

What is the MART regime?

A

A combination inhaler containing a low dose inhaled corticosteroid and a fast acting LABA.

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.