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RESPIRATORY > ASTHMA > Flashcards

ASTHMA Flashcards

1
Q

What’s the epidemiology of asthma?

A

Affects >300 million people worldwide
12% of the UK population have been diagnosed with asthma at some point
Incidence is higher in children than adults
In early childhood, asthma is more common in boys but by adulthood its more common in girls
It accounts for 2-3% of primary care consultations and 60,000 hopsital admissions a year

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2
Q

What proportion of adult-onset asthma is occupational asthma?

A

Up to 15% - making it the most common industrial lung disease in the developed world

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3
Q

What are the aetiological factors of asthma?

A

Atopy
Hygiene hypothesis
Aspirin-induced asthma
Occupational asthma
Exercise-induced asthma

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4
Q

What is atopy?

A

A genetic predisposition to IgE-mediated allergen sensitivity
Atopic individuals are predisposed to allergic asthma, atopic dermatitis and allergic rhinitis

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5
Q

What is the hygeiene hypothesis?

A

Reduced exposure to infectious pathogens at a young age predisposes individuals to asthma
It’s thought that the developing immune system needs stimuli from infectious agents to adequately develop regulatory T cells and without that stimuli you become more susceptible to allergic disease

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6
Q

What is aspirin-induced asthma?

A

Ingestion of asthma triggers an asthma attack
These pt exhibit Samter’s triad: asthma, aspirin sensitivity and nasal polyps

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7
Q

What is Samter’s triad?

A

Asthma
Aspirin sensitivity
Nasal polyps

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8
Q

What is exercise-induced asthma?

A

In this variant asthma is triggered by strenuous physical activity. The aetiology is complex but exposure to cold air and environmental pollutants contributes.

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9
Q

What is asthma?

A

a chronic inflammatory condition of the airways that causes episodic exacerbations of bronchoconstriction. This causes reversible airway obstruction that typically responds to bronchodilators
This is caused by hypersensitivity of the airways and can be triggered by environmental factors

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10
Q

What are typical triggers of asthma?

A

Infections (particularly viral URTI)
Allergies - pollen, dust mites, pet dander, feathers, pests
Smoke, fumes, pollution
Night time/early morning
Exercise
Cold
Mold/damp
Cleaning and disinfectants
Strong emotions

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11
Q

What are risk factors for developing asthma?

A

Personal or FHx atopy
Male sex for pre-pubertal asthma
Female sex for persistence of asthma from childhood to adulthood
Respiratory infections in infancy
Exposure to tobacco smoke
Premature birth and low birth weight
Obesity
Social deprivation
Exposure to inhaled particulates
Workplace exposure - flour dust, isocyanates etc

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12
Q

Whats the prognosis of asthma?

A

Male children are more likely to grow out of asthma in the transition to adulthood
The earlier the onset of asthma the better the prognosis however early-onset asthma in atopic children may be associated with a worse prognosis

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13
Q

What are complications of asthma?

A

Death
Respiratory complications - irreversible airway changes, pneumonia, pulmonary collapse, respiratory failure, pneumothorax and status asthmaticus
Impaired quality of life e.g. fatigue or underperformance and time off school/work

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14
Q

What is status asthmaticus?

A

repeated asthma attacks without respite, or non-response to appropriate treatment

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15
Q

Outline the pathophysiology of asthma?

A

EARLY PHASE
Type 1 hypersensitivity reaction - initial sensitisation to allergen -> production of CD4 Th2 cells -> release of IL4 and IL5 -> environmental trigger -> cross‐linking of IgE on the mast cell surface -> release of histamine and production of prostaglandins, leukotrienes, and other enzymes -> eosinophils and mast cells release inflammatory mediators in bronchial walls -> inflammation -> smooth muscle in bronchioles spasm and mucus production in airways increases + vasodilation of pulmonary vascular use increases capillary permeability = oedema

LATE PHASE - delayed by hours
APCs may present a variety of allergenic antigens to chronically activated T helper cells. These cells then secrete multiple cytokines that maintain and intensify the local inflammatory response. Many other inflammatory cells, including mast cells and eosinophils, will respond to the T cells’ cytokines. These inflammatory cells will produce cytokines, which amplify the cellular response and the inflammatory reaction. There is a migration of inflammatory cells from the circulation into the pulmonary vasculature and the airway submucosa. inflammation = intermittent airflow obstruction

CHRONIC
After persistent chronic inflammation the airways lay down fibrous tissue and overtime airway remodelling occurs and manifests as fixed airway obstruction

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16
Q

Whats the pathophysiology of aspirin-induced asthma?

A

Aspirin inhibits COX-1 which leads to a decrease in prostaglandins and causes an increase in activity in the lipooxygenase pathway which synthesises leukotrienes. = bronchospasms, increased vascular permeability and increased mucin production

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17
Q

What are symptoms of asthma?

A

Cough
Dyspnoea
Chest tightness
Expiratory wheeze

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18
Q

How do asthma symptoms tend to vary throughout the day?

A

They are commonly episodic, diurnal (worse at night/early morning) and triggered by exercise, viral infection and exposure to cold air/allergens

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19
Q

What wheeze is typically heard in asthma?

A

Expiratory polyphonic wheeze - multiple pitches and tones heard over different areas of the lung
Bilateral and wide spread

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20
Q

What are high risk occupations for occupational asthma?

A

Paint spraying or foam moulding using adhesives - isocyanates
Baking - flour
Wood work - wood dust
Welding - fumes, mists
Healthcare settings - latex, vapours from surgical techniques
Agricultural - grain and poultry dusts

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21
Q

What questions can you ask to assess occupational asthma?

A

Are symptoms better on days away from work?
Are symptoms better when on holiday?

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22
Q

What are the NICE guidelines for diagnosing asthma?

A

The advice is to not make a diagnosis clinically without testing once the pt is 5 or older (unlike BTS)

Investigations:
- FeNO
- spirometer with bronchodilator reversibility

And if there is diagnostic uncertainty then peak flow variability and direct bronchial challenge test can be done

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23
Q

What is FeNO?

A

A device that measures fractional exhaled nitric oxide in the breath of pt
One of the type of nitric oxide is inducible and levels tend to rise in inflammatory cells, particularly eosinophils so the levels typically correlate with levels of inflammation
FeNO> 40ppb is considered positive in adults (35 in children)

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24
Q

How is spirometry useful for diagnosing asthma?

A

A decreased FEV1/FVC ratio i.e. <70 (obstructive!)
However a normal spirometry result when the person is asymptomatic does not rule out asthma

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25
Q

How do you carry out spirometry with bronchodilator reversibility?

A

Spirometry is done

You use a reliever inhaler (beta 2 agonist or corticosteroids), wait 15-20 minutes and carry out another spirometry test

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26
Q

How should you interpret the results of bronchodilator revsibility testing?

A

FEV1 improvement of 12% or more, together with an increase in volume of at least 200mL in response to the bronchodilator is a positive result
An improvement of >400mL in FEV1 is strongly suggested of asthma

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27
Q

When should you offer variable peak expiratory flow to help diagnose asthma?

A

If the person has normal spirometry or obstructive spirometry and positive BDR with a FeNO level of 39ppb or less

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28
Q

How do you calculate peak flow expiratory variability?

A

the difference between the highest and lowest readings expressed as a percentage of the average PEF.

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29
Q

How do you use variable peak expiratory flow readings to diagnose asthma?

A

Pt does peak flow readings at least twice a day (morning and evening) for 2-4 weeks

A value of >20% variability is regarded as a positive result

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30
Q

What is a direct bronchial challenge test?

A

Pt inhales nebulised histamine or methacholine which provokes bronchoconstriction
eople with pre-existing airway hyperreactivity, such as asthmatics, will react to lower doses of drug.
A provocative concentration causing a 20% drop in FEV1 of 8mg/ml or less is regarded as a positive result

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31
Q

When is direct bronchial challenge test offered?

A

If diagnostic uncertainty after normal spirometry and either FeNO of 40ppb or more and no variability in peak flow readings OR FeNO of 39ppb or less with variability in peak flow readings

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32
Q

When do you diagnose symptomatic asthmatics?

A

If there is FeNO of 40ppb or more with either positive bronchodilator reversibility, positive peak flow variability or bronchial hyperreactivity
Or if there is FeNO of 25-39ppb and a positive bronchial challenge test
OR if there is a positive bronchodilator reversibility and positive peak flow variability regardless of FeNO level

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33
Q

How is occupational asthma diagnosed?

A

Serial measurements of peak expiratory flow are recommended at work and away from work

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34
Q

What are differential diagnoses for asthma?

A

Bronchiectasis
COPD
Ciliary dyskinesia
Cystic fibrosis
Dysfunctional breathing
Foreign body aspiration
GORD
HF
Interstitial lung disease
Lung cancer
Pertussis
PE
TB
Vocal cord dysfunction
Upper airway cough syndrome

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35
Q

What is complete control of asthma defined as?

A

No daytime symptoms.
No night-time waking due to asthma.
No need for rescue medication.
No asthma attacks.
No limitations on activity including exercise.
Normal lung function (FEV1 and/or PEF > 80% predicted or best)
Minimal SE from meds

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36
Q

How should you assess a persons baseline asthma status before starting treatment?

A

Using a validated questionnaire such as the Asthma Control Questionnaire or the Asthma Control Test, and/or lung function tests

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37
Q

When should you arrange specialist referral for asthma?

A

If occupational asthma is suspected
If a direct bronchial challenge test is needed for diagnosis
If pt needs prophylactic oral antibiotics
If pt experiences 2 asthma attacks within 12 months

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38
Q

How should you manage new asthma diagnosis non-pharmacologically?

A

Assess person’s baseline asthma status using a questionnaire
Provide self management education and a personalised asthma action plan
Ensure pt has all routine vaccinations
Provide information about sources of information and support
Advise pt to avoid asthma triggering factors
Provide advice on weight loss and smoking cessation
Assess for presence of anxiety or depression
Ensure pt has their own peak flow meter

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39
Q

What is a personalised asthma action plan?

A

It’s a sheet that explains medications, how to cut risk of asthma attack, what to do if asthma symptoms get worse and the emergency action to take if you’re having an asthma attack
The pt takes it to all asthma appointments

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40
Q

Where can you direct patients for advice, support and information on asthma?

A

British Lung Foundation
Asthma UK
NHS

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41
Q

What medical management is given for new diagnosis of asthma?

A

1- SABA when needed
2 - add low-dose ICS daily
3 - SABA + low dose ICS + Leukotriene receptor antagonist
4 - SABA + low-dose ICS + LABA + LTRA
5 - SABA +/- LTRA + maintenance and relieve therapy
6- SABA +/- LTRA + medium dose ICS MART
7 - SABA +/- LTRA + (increase ICS to highest dose or trials an additional drug or seek advice from specialist)

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42
Q

After any medication adjustments in asthma how long should you wait to review the response to treatment?

A

4-8 weeks

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43
Q

How can you use the frequency of SABA use to determine asthma control?

A

Good asthma control is associated with little need for use of a SABA
Anyone prescribed more than 1 SAVA a month should have their asthma control and symptoms assessed urgently

44
Q

Who should you prescribe prevent or therapy for in asthma?

A

Anyone using inhaled SABA 3 times a week or more
Anyone who has asthma symptoms 3 times a week or more
Anyone woken at night by asthma symptoms once weekly or more
Anyone who has had an asthma attack requiring treatment with oral corticosteroids in the past 2 years

45
Q

Why may Pts who are current/pervious smokers require a higher dose of inhaled corticosteroids therapy?

A

As smoking decreases the effectiveness of ICS therapy

46
Q

How often should ICS be used when managing asthma?

A

Initially twice daily
Adjust the dose over time aiming for the lowest dose required for effective control and once good control is established, once-daily ICS can be considered as maintenance therapy

47
Q

If the persons asthma is not adequately controlled with low dose ICS and you are considering an add-on therapy… what should you consider first?

A

Recheck adherence, inhaler technique and elimination of trigger factor

48
Q

When and how is a leukotriene receptor antagonist taken?

A

At night (leukotrienes are produced in greater amounts at night, reduces side effects affecting pt and stops symptoms waking the pt at night)
Oral therapy

49
Q

What is MART?

A

Maintenance and relieve therapy (combination inhaler that contains LABA and ICS)

50
Q

What additional drugs can be added on to standard asthma therapy?

A

Muscarinic receptor antagonist
Theophylline
Oral steroid therapy

51
Q

What is theophylline?

A

A xanthine that competitively inhibits phosphodiesterases resulting in bronchodilation

52
Q

When should you consider decreasing maintenance therapy?

A

Once a persons’ asthma has been controlled with their currently maintencing therapy for at least 3 months

53
Q

How should you reduce maintencing therapy for asthma?

A

Stop or reduce dose of medicines in an order that takes into account the clinical effectiveness when introduced, side effects and the person’s preference.
Reductions in ICS dose should be slow as people deteriorate at different rates. Dose reductions should be considered every three months, decreasing by 25-50% each time. Only consider stopping ICS treatment completely for people who are using low dose ICS alone as maintenance therapy and are symptom-free.

54
Q

How often should people with asthma be followed up?

A

Annually at least
More regularly if undergoing treatment adjustment

55
Q

What factors should you consider when deciding on a delivery system for inhaled asthma medication?

A

Age 5-12 a spacer is recommended
Consider the ability of the person to develop and maintain an effective technique
Consider suitability to their lifestyle e.g. portability and lifestyle
Consider their preference for and willingness to use a particular device
Consider the meds and dose i.e. a spacer should be used by all people on high-dose inhaled corticosteroids, and by most elderly people using PMDIs.

56
Q

What is PMDI?

A

Pressurised metered-dose inhalers

57
Q

What are DPIs?

A

Dry-powder inhalers

58
Q

What are spacers?

A

plastic devices with a mouthpiece at one end and a hole for a pressurized metered-dose inhaler (pMDI) to be inserted at the other.
They increase the proportion of the drug delivered to the airways and reduce the amount of drug deposited in the oropharynx thereby reducing local adverse effects and reducing the amount of systemic absorption

59
Q

How should you wash a spacer?

A

Wash monthly in detergent
Allow to air dry (as static causes drug to stick to sides)

60
Q

How often should plastic spacers be replaced?

A

At least every 12 months
Most advise every 6 month s

61
Q

What happens at an asthma follow up?

A

Monitor number of asthma tracks, oral corticosteroid use, time off job/school due to asthma
Monitor nocturnal symptoms
Monitor adherence - review prescription refill frequency
Possession of asthma action plan
Monitor tobacco smoke exposure

Monitor sympmttic asthma control using a questionnaire, lung function, bronchodilator overuse, smoking status, posit limit of occupational asthma
Assess the risk of future asthma attacks

Monitoring if on long term steroid tablets

62
Q

Who should you consider prophylactic oral macro lines for?

A

People 50-70 who have ongoing symptoms despite high-dose ICS, who have suffered 1 exacerbation requiring oral steroids in the past year

63
Q

What oral macrolide therapy can be offered for prophylaxis?

A

Treatment with azithromycin 500 mg three times per week, should be considered for a minimum of 6–12 months

64
Q

What should be done before commencing prophylactic oral macrolides?

A

Ensure optimisation of other asthma therapy
ECG to assess QTc
LFTs baseline
Counselling on potential adverse effects

65
Q

What are potential adverse effects of oral macrolides?

A

GI upset
Hearing disturbance
Balance disturbance
Cardiac effects - arrhythmias due to QT prolongation
Microbiological resistance
Liver dysfunction

66
Q

What should be monitored when taking oral macrolides?

A

LFTs before treatment, 1 month after and every 6 months
ECG 1 monther after to check for new QTc prolongation - if present treatment should be stopped

67
Q

What is the ‘Royal College of Physicians 3 questions’?

A

A simple questionnaire to check asthma control

Ask these:
Have you had difficulty sleeping because of asthma sympotms?
Have you had your usually asthma symptoms during the day?
has your asthma interfered with your usual activities?

68
Q

What are examples of delivery devices for asthma?

A

Metered dose inhalers
Dry powder inhaler
Soft mist inhaler
Spacers
Nebulisers

69
Q

What is a metered dose inhaler?

A

a device that delivers a specific amount of medication to the lungs, in the form of a short burst of aerosolized medicine that is usually self-administered by the patient via inhalation. It is the most commonly used delivery system for treating asthma, chronic obstructive pulmonary disease

70
Q

What is a dry powder inhaler?

A

a device that delivers medication to the lungs in the form of a dry powder - medication is commonly held either in a capsule for manual loading or in a proprietary form inside the inhaler

71
Q

What are soft mist inhalers?

A

release medication in a fine mist that comes out more slowly and lasts longer in the air than the aerosol produced by MDIs and DPIs which means more meds gets into the lungs

72
Q

What is a nebuliser?

A

drug in liquid form is converted into a mist using a nebuliser machine with compressed air.

73
Q

What are examples of SABAs?

A

salbutamol
terbutaline sulfate
All utero l

74
Q

What are examples of ICS used?

A

Budenoside
Beclometasone dispropionate
Fluticasone
Mometasone

75
Q

What are examples of leukotriene receptor antagonists?

A

Montelukast
Zafirlukast

76
Q

What are examples of LABAs?

A

Salmeterol
Formeterol fumarate
Olodaterol

77
Q

What are examples of MART regimens?

A

Budenoside with formoterol
Beclometasone with formoterol

78
Q

What are examples of LAMAs?

A

Tiotropium
Glycopyrronium
Aclidinium

79
Q

What are examples of monoclonal antibodies that may be used in asthma management?

A

omalizumab, mepolizumab, benralizumab, reslizumab and dupilumab

80
Q

What are the characteristics of acute asthma attacks?

A

Worsening of normal symptoms that is not responding to treatment
Often triggered by a respiratory tract infection

81
Q

What are characteristics of moderate acute asthma attack?

A

PEFR 50-75% best/predicted
Normal speech
RR<25
Pulse <110

82
Q

What are characteristics of severe acute asthma attack?

A

PEFR 33-50% best/predicted
Can’t complete sentences
RR >25
Pulse >110

83
Q

What are characteristics of life-threatening acute asthma attack?

A

PEFR <33% best/predicted
Ox sats <92%
Silent chest, cyanosis, feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma

Note: a pt having any one of the life-threatening features should be treated as having a life-threatening attack

84
Q

Which asthmatic patients should be admitted to hospital?

A

Anyone with features of life threatening asthma exacerbations
Anyone with any feature of severe asthma attack persisting after initial bronchodilator treatment
Anyone with a moderate asthma exacerbation with worsening symptoms despite initial bronchodilator treatment and/or who have had a previous near-fatal asthma attack.

85
Q

What is near-fatal asthma?

A

Characterised by a raised pCO2 and/or requiring mechanical ventilation with raised inflation pressures

86
Q

What investigations should be done for an acute asthma attack?

A

Oxygen sats, HR, RR
PEFR
ABG
FBC and CRP - look for a precipitating cause e.g. infection
CXR - if life threatening, suspected pneumothorax, failure to respond to treatment

87
Q

How should an acute asthma tack be managed?

A

Oxygen if hypoxaemic
High dose SABA nebuliser every 15-30 minutes
40-50mg oral prednisolone daily for at least 5 days or IV hydrocortisone 100mg six hourly
Ipratropium bromide nebulisers 0.5mg 4-6 hourly if severe/life threatening or not respond at to above
IV magnesium sulphate if severe/life-threatening
IV aminophylline may be considered by senior staff

88
Q

What are discharge criteria for acute asthma attack?

A

been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
inhaler technique checked and recorded
PEF >75% of best or predicted

89
Q

Whats the duration of action of salbutamol?

A

Onset : 15 minutes
Duration: 4-6 hours

90
Q

Whats the duration of action of terbutaline?

A

Onset: 15 mins
Duration: up to 6 hours

91
Q

What are side effects for beta-2-adrenergic agonists

A

Arrhythmias and palpitations
Headache
Tremor
Nausea
Muscle cramps

SABAs and LABAs both cause thee SE but they tend to be more severe with LABAs.
LABAs when used as mono therapy can also increase the risk of asthma exacerbations and even death.

92
Q

Whats the onset and duration of action of tiotropium?

A

Onset: within 30 minutes
Peak effect 3-4 hours
Duration of 24 hours

93
Q

What are the cautions associated with beta-2-adrenergic agonists?

A

CVD - they can increase HR and BP
Diabetes - they can cause hyperglycaemia
Pregnancy - may affect foetal HR but generally ok to use
Hyperthyroidism - can worsen symptoma
Hypokalaemia - can cause hypokalaemia so may worsen this

94
Q

Whats the onset and duration of tiotropium (LAMA)?

A

Onset: within 30 mins
Peak: 3-4 hours
Duration >24 hours

95
Q

Whats the onset and duration of ipratropium (SAMA)?

A

Onset: 1-2 hours
Duration: 4-6 hours

96
Q

Whats the moa of beta-2-adrenergic agonists?

A

They bind to beta-2-adrenergic receptors in the smooth muscle cells of the airways leading to activation of adenylate cyclase = increased levels of cAMP = activates protein kinase A = relaxation of smooth msucle cells = bronchodilator and improved airflow

In addition, they can also inhibit the release of inflammatory mediators

97
Q

Whats the moa of Muscarinic antagonists?

A

They block the action of acetylcholine on muscarinic receptors located in smooth muscle cells of the airways = prevents contraction of smooth muscle cells = bronchodilation and improved airflow

Muscarinic antagonists also inhibit the production and release of mucus by the cells lining the airways, which can help to reduce airway obstruction and improve breathing.

98
Q

What are SE for antimuscarinics?

A

Arrhythmias
Constipation
Cough
Dizziness
Dry mouth
Blurred vision
Urinary retention
Headache
Nausea

99
Q

What medical conditions might you not want to prescribe anti Muscarinics for?

A

Bladder outflow obstruction e.g. prostatic hyperplasia
Narrow angle glaucoma - can increase pressure in eye
Urinary retention - may worsen it
GI obstruction - can slow down gut motility
Myasthenia gravis - can worsen symptoms
Severe hepatic impairment

100
Q

What are side efefcts of inhaled corticosteroids?

A

Headache
Oral candidiasis
Pneumonia
Altered taste
Voice alteration
Skin thinning
Osteoporosis
Adrenal suppression

101
Q

how does magneiusm suylphate work for asthma?

A

The bronchodilator effects of MgSO4 are attributed to the blockade of calcium channels in the airway smooth muscles and a reduction in airway excitability.

102
Q

What cytokines are most prevalent in asthma?

A

IL-4 - facilitates class switching to IgE
IL-5 - facilitates release of eosinophils
IL-13 - stimulates mucus production

103
Q

What might you see on CXR in asthma?

A

Normal or hyperinflation

104
Q

What might you see on FBC in asthma?

A

Eosinophilia

105
Q

How does smoking affect asthma?

A

Increases the risk of asthma flare-ups
Increases the risk of COPD
Reduces the probability of achieving good asthma control
Reduces therapeutic response in inhaled corticosteroids
Accelerates long-term decline in lung function

RESPIRATORY (22 decks)

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