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asthma Flashcards

1
Q

how is asthma an obstructive resp disease?

A

inflam mechanism
bronchioles constrict - narrowing of airways
makes it more difficult to get air in and out

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2
Q

describe the prevalence of asthma?

A

increasing across developing world
linked to modern lifestyles - potentially lacking exposure

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3
Q

what is meant be atophy?

A

allergy

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4
Q

what type of hypersensitivity is asthma?

A

type 1

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5
Q

how does type 1 hypersensitivity work?

A
  • Allergen is presented to mast cell after entering cell and passing through epithelial
  • Ig receptor in mast cell receives antigen from allergen
  • Triggers response of mast cell degranulation mediator release
  • Inflammation cycle induced – release of histamine, proteinoids (lipid mediators), platelet activating factor and leukotrienes
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6
Q

what are TH2 a response to?

A

helminth infection

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7
Q

describe an asthmatic airway?

A
  • Inflamed wall and thickened
  • Tightened smooth muscle
  • Air trapped in alveoli
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8
Q

name some causes of asthma

A

environmental allergens
genetic susceptibility

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9
Q

how can cigarette smoke affect asthmatics?

A

could be beneficial in children - exposure to pollutant
but bad in asthmatics

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10
Q

is asthma episodic?

A

yes - variability of all symptoms and broader history

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11
Q

what does spirometry?

A

forced expiratory volume - forces all out

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12
Q

what does peak flow meter measure?

A

measures how fast you can blow
usually more later in the day - treatment can improve peak flow - reduced the variability

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13
Q

what are tests involved in asthma?

A

spirometry
peak flow meter
exhaled nitric oxide
methacholine challenge test - can induce asthma symptoms - see effect
skin prick test - allergies

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14
Q

define asthma

A

heterogenous diseases usually characterised by chronic airway inflammation. Defined by history of respiratory symptoms such as wheeze, SoB, chest tightness and cough that vary over time in intensity together with variable expiratory airflow limitation.

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15
Q

how is asthma linked to genetic deposition?

A

concordance is higher in monozygotic twins than dizygotic twins
having a parent with asthma increases risk and having two parents have a further increased risk

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16
Q

what allergies are associated with asthma?

A

dust mites
pets

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17
Q

what is basic management of asthma?

A

regular inhaled steroids - preventer and reliver
beta agonist reliver - SABA

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18
Q

what is SABA

A

short acting beta agonist

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19
Q

what is the most common chronic childhood disease?

A

asthma

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20
Q

what is the most common childhood asthma symptom?

A

wheeze

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21
Q

what conditions are common alongside asthma?

A

eczema, hayfever

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22
Q

what are the risk factors for adults to have asthma?

A

family history, exposure to allergens – dust mites, pets, tobacco smoke, history of atopic diseases, smoking (tobacco and E-cigarettes), obesity, GORD – chronic irritation and inflammation of airways following exposure to gastric contents

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23
Q

what are the symptoms in adults’ asthma?

A
  • Recent upper respiratory infections can make symptoms worse
  • Dyspnoea: caused by exposure to allergen, cold air, tobacco smoke
  • Cough: caused by exposures and can disrupt sleep
  • Expiratory wheezes: polyphonic, high pitched expiratory wheezes
  • Nasal polyposis; small growths inside nose
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24
Q

what are first line investigations of asthma?

A
  • FEV1/ FVC ratio - <80% via spirometry
  • Peak flow – long term daily PEFR can help detect early changes in disease states or to evaluate responses to changes in therapy
  • CXR: indicate pathologies – can show acute exacerbation or pneumothorax
  • FBC: test for eosinophils/ neutrophils (helminths- TH2 inappropriate response – atopy) and infection
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25
Q

what are second line investigations for asthma?

A
  • Bronchial challenge test – if spirometry and peak expiratory flow may not show reversibility and variability.
  • IgE- allergens
  • Skin prick testing – allergens
  • Fractional exhaled nitric oxide – reflective of degree of eosinophilic inflammation
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26
Q

what is a gas transfer test?

A

measures how eell lungs can take up oxygen from air
compares partial pressure

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27
Q

what is bronchial hyperresponsiveness?

A

increase in sensitivity to a wide variety of airway narrowing stimuli - seen in asthma and COPD

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28
Q

what is hypersensitvity?

A

exaggerated or inappropriate immunological response in a persons response to an antigen/ allergen

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29
Q

how is asthma a type 1 hypersensitivity?

A

has an exaggerated IgE response

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30
Q

why might asthmatic wheeze?

A

may result from localised or diffuse airway narrowing or obstruction
- bronchoconstriction, mucosal oedema, external compression

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31
Q

what is a bronchospasm?

A

when muscles lining bronchi tighten

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32
Q

what is an adverse reaction to salbutamol

A

fine tremor, nervous tension and tachycardia

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33
Q

what is salbutamol?

A

short acting beta 2 adrenergic agonist

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34
Q

what is salmeterol?

A

long acting beta 2 adrengic agonist

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35
Q

why are steroids useful in asthmatics?

A

increase airway calibre by reducing bronchial inflammatory reactions eg oedema and mucus hypersensitivty - modifies allergic reactions

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36
Q

how do you perform a peak flow test (step by step)

A
  1. Stand up and take deep breath (arms open)
  2. Lips form a tight seal around plastic
  3. Like a dart blowing
  4. Do not obstruct tab that moves
  5. Best out of 3 attempts
  6. Monitor throughout the day – diaries – will show diurnal characteristics (helps diagnose asthma)
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37
Q

how do you perform a spirometry test?

A
  1. Deep breath in and blow out as fast and hard as you can
  2. Keep going until thee is nothing left
38
Q

what conditions are contra-indicated from performing a spirometry test?

A

angina, heart problems, recent concussion, uncontrolled high or hypotension, pulmonary hypertension, PE, pneumothorax, recent surgery, late term pregnancy, aneurysms

39
Q

what is a normal FEV1/FVC ratio?

A

70-80%

40
Q

what would a score of <80% in FEV1/FVC indicate?

A

restrictive respiratory disease

41
Q

what are examples of obstructive respiratory diseases?

A

COPD, asthma, bronchiectasis, airway obstruction eg foreign body

42
Q

what are examples of restrictive respiratory diseases?

A

CF, idiopathic pulmonary fibrosis, ILD - sarcoidosis

43
Q

why would obstructive resp diseases have reduced FEV1?

A

airway collapsed causing significant reduction in ability to blow air out as hard as possible

44
Q

why would obesity trigger restricted respiration?

A

the fat compresses resp system - extra thoracic pressure

45
Q

in a flow volume loop, how would restricted ventilation look like?

A

shorter slope but follows same shape as normal

46
Q

what shape curve on a flow volume loop look like?

A

concave

47
Q

what are the goals of asthma management?

A
  • Aim to control symptoms – including nocturnal and exercise- induced
  • Prevent exacerbations and need for rescue medication
  • Achieve best possible lung function – aim for PEFR >80% predicted
  • Minimise side effects
  • Maintain patients on lower dosage as possible
  • Investigate reasons for poor control eg poor inhaler technique
  • Patient education and empowerment is key
48
Q

what colour inhaler is salbutamol and what type?

A

blue - SABA

49
Q

what colour and type of inhaler is beclomethasone?

A

brown and ICS

50
Q

what type of inhaler is salmetorol?

A

green and LABA

51
Q

what type of inhaler is fostair and colour?

A

LABA/ICS and pink

52
Q

what colour and type of inhaler is seretide?

A

purple and LABA/ICS

53
Q

how would use an inhaler?

A
  1. Hold inhaler upright, remove cap and shake well
  2. Stand/ sit up and tilt chin upwards
  3. Breath out fully
  4. Place lips around mouthpiece to get a good seal
  5. Breath in slowly and steadily, whilst simultaneously pressing the cannister on the inhaler
  6. Continue to breathe in slowly – until lungs feel full
  7. Remove inhaler from your mouth and seal lips
  8. Hold you breath for 10 seconds and gently breathe out
  9. Then wash mouth after – reduce risk of getting oral thrush
54
Q

who should be offered an inhaler spacer?

A

all patients

55
Q

which symptoms within asthmatics require admitting to ICU?

A
  • Persistent/ worsening hypoxia
  • Hypercapnia
  • Acidosis
  • Exhaustion
  • Feeble respiration
  • Deterioration PEF
  • Reduced GCS
  • Confusion
  • Resp arrest
56
Q

how would you classify moderate asthmatics?

A

PEFR 50-75%, increasing symptoms, no severe factors, speaking full sentences

57
Q

how would you classify severe astmatics?

A

PEFR 33-50%, resp rate >25, HR>110, inability to complete sentence within a breath

58
Q

how would you classify life threatening asthma?

A

PEFR <33%, sPO2 <92%, silent chest, altered consciousness

59
Q

how would you classify near fatal asthmatics?

A

raised pCO2, mech ventilation

60
Q

what is the aims of asthma management?

A
  1. achieve control
  2. Maintain control
  3. Optimise inhaler technique
  4. Support compliance – avoid triggers and self management & education
61
Q

how do you achieve control within asthma management?

A

make sure diagnosis is correct, smoking cessation, annual flu/ pneumococcal vax (prone to infections), weight loss, breathing exercise programme, reduce exacerbations/ hospital admissions

62
Q

what is the mechanism of SABA?

A
  • Selective B2 agonist – bronchodilators eg salbutamol
  • Stimulates adenylate cyclase
  • Increase cAMP production
  • Phosphorylates myosin kinase, relaxes smooth muscle to achieve bronchodilation
  • cAMP production also causes mast cell membrane stabilization to stop histamine release to prevent bronchoconstriction
63
Q

what are the characteristics of beta 2 agonists?

A
  • salbutamol and terbutaline
  • short acting
  • onset of action is rapid (5-15 mins)
  • produce bronchodilation for up to 6 hrs
64
Q

what is the route of SABA?

A
  • inhaler, nebuliser, IV and oral
65
Q

what are the side effects of SABA?

A
  • tremor – fine skeletal tremor from stimulation of B2 adrenoreceptors within muscles
  • tachycardiac and palpitations – possible arrhthymias
  • hypokalaemia – more potassium uptake into cells
  • cautions – prolonged QT, decreased K
66
Q

what is the action of inhaled steroids?

A
  • most effective class of drug for chronic asthma
  • some improvement in symptoms within 24hrs
  • max effect after 1-2 weeks
  • short term and long term anti-inflam effects
  • suppresses inflammation and immune response
67
Q

when should you use ICS?

A

new data says to start immediately when you start SABA - low dose
use when using SABA >3x weekly/ asthma symptoms present >3x week/ woken at nightly once a week

68
Q

what are examples of ICS?

A

beclomethasone, budesonide, ciclesonide, fluticasone

69
Q

do ICS have systemic effects?

A

no as they are inhaled - local

70
Q

what is the pharmacology behind ICS?

A
  • minimal absorption across mucosal surface
  • rapid inactivation if absorbed
71
Q

how do you take prednisolone?

A

oral

72
Q

what route is hydrocortisone taken?

A

IV

73
Q

what are the side effects of steriods?

A
  • oral candidiasis: steroid depositing in oropharyngeal area. Prevented by spacer device (larger particles are prevented) or gargling after use
  • dysphonia: (hoarseness) – caused by deposition on inhaled steroid on vocal cords and myopathy of laryngeal muscles. Occurs in 1/3 patients using inhaled corticosteroids- less troublesome if using with breath-actuated delivery
74
Q

give examples of long acting beta 2 agonists- controllers?

A

salmeterol
formoterol

75
Q

how does LABA compare to SABA?

A

LABA longer acting than SABA - up to 12 hrs
slower onset than SABA
LABA must be taken alongside ICS

76
Q

what is considered when choosing an inhaler device?

A
  • Compliance eg arthritic hands may not be able to push button down
  • Needs assessed by competent HCP
  • Titrated against clinical response to ensure optimum efficacy
  • Patient specific plan – increase/ decrease
  • Reassess inhaler technique within asthma review
  • Spacers tend to be more useful within children but should be offered to all
  • Dry powder inhaler is most eco-friendly , metered dose inhaler is least eco-friendly
77
Q

what is within a combination inhaler?

A
  • ICS and LABA (controller) to reduce inflammation
  • Combining the two medications may increase the widening of the airways more than separately
78
Q

why might a combination inhaler be more beneficial?

A
  • More convenient for patient – only one device – better compliance
  • The combination ensures the LABA inhaler is not be used alone
79
Q

what is the action of LTRA?

A
  • Eg montelukast (singulair) and zafirlukast (accolate)
  • Inhibits leukotriene induced bronchoconstriction by blocking leukotriene receptor
80
Q

when would LTRA be used?

A
  • Most useful in mild-moderate asthma, exercise induced asthma and asthma provoked by NSAIDs including aspirin
81
Q

what are the side effects of LTRA?

A
  • GI disruption
  • Dry mouth and thirst
  • Hypersensitivity reactions linked to anaphylaxis, angioedema and skin rashes
82
Q

give a brief overview of xolair?

A
  • Used in severe and persistent asthma that cannot be controlled
  • Via SC injection
  • Binds specifically to IgE and removes it from circulation – leads to a reduction to IgE receptors on mast cell, basophils and dendritic cells
  • Treatment gradually reduces airways inflammation – peak response is 12-16weeks after starting
  • SPECIALIST
83
Q

what is the management in acute asthma that doesnt require hospitalisation?

A
  • SABA via large volume spacer to relive acute symptoms
  • Adult: 4 puffs initially followed by 2 puffs every 2 minutes and up to 10 puffs
  • Consider advising quadrupling ICS at the onset of an asthma attack for up to 14 days in order to reduce pf needing prescribed oral steroids
84
Q

what is the acute management of asthma that requires hospital admission?

A
  • Asses severity – mild/ moderate/ severe/ life threatening – start bronchodilator immediately
  • Oxygen – administer if required – target for 94-98% adults
  • Bronchodilator – nebuliser/ inhaler – salbutamol or ipratropium
  • Observations- completing observations and assessments
  • Steroids – administer systemic corticosteroids (IV hydrocortisone) within first hour of treatment
  • IV aminophylline (broke n down theophylline)
  • Repeatedly reassessing – response to treatment and either continuing treatment or adding on treatments until acute asthma is controlled or patient is sent to ICU
  • Observe patient for at least an hour after dyspnoea has resolved, providing post-acute care and arranging follow up
85
Q

how do you classify moderate acute asthma?

A
  • Increasing symptoms
  • PEF> 50-75%
  • No features of severe
86
Q

how do you classify acute severe asthma?

A
  • PEF 33-50%
  • Resp rate >25/ min
  • Heart rate > 110/min
  • Inability to complete a sentence within a breath
87
Q

how do you classify life threatening asthma?

A
  • PEF <33%
  • SpO2 <92% - need ABG checked
  • PaO2 <8kPa
  • Normal PCO2 – over compensation
  • Altered consciousness
  • Exhaustion
  • Arrhythmia
  • Hypotension
  • Cyanosis
  • Silent chest
  • Poor resp effort
88
Q

when would you use steroid therapy?

A

all cases of acute asthma. Continue prednisolone 40-50mg daily for at least 5 days or until recovery

89
Q

when would you use agonist bronchodilators?

A

high dose as first line in acute exacerbations. IV if can not be inhaled. In life threatening – nebuliser. In severe – initial bolus dose and then continuous nebuliser if needed

90
Q

when would you use magnesium within asthma management?

A

senior specialist. Used in life threatening cases where PEF<50%. Bronchodilation achieved by blocking calcium channels in smooth muscle membrane. Can cause AV block so needs ECG monitoring, does have hypotensive effects

91
Q

when do you refer to ICU within asthma management?

A
  • Requiring ventilatory support
  • Severe/ life threatening asthma failing to respond to meds
  • Deteriorating PEF
  • Persistent/ worsening hypoxia
  • Hypercapnia
  • ABG shows acidosis
  • Exhaustion, feeble respiration
  • Drowsiness, confusion, altered conscious state
  • Respiratory arrest – not breathing
92
Q

what is the asthma management pneumonic?

A

O SHIT ME – oxygen, salbutamol, hydrocortisone, ipratropium, theophylline, magnesium, escalate early

respiratory (10 decks)

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