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Yr 3 resp > asthma > Flashcards

asthma Flashcards

1
Q

definition of asthma

A

Chronic inflammatory airway disease

characterized by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation.

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2
Q

aetiology of asthma

A

genetic

  • +ve FH
  • atopy - (tendency of T lymphocyte (Th2) cells to drive production of IgE on exposure to allergens)
  • genetic heterogeneity

env

  • house dust mite
  • pollen
  • pets (urinary protein/fur)
  • cigarette smoke
  • viral resp tract infection
  • aspergillus fumigatus spores
  • occupational allergens (isocyanates, epoxy resins)
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3
Q

pathology of early phase of asthma (1hr)

A

Exposure to inhaled allergens in a presensitized individual results in cross-linking of IgE on the mast cell surface and release of histamine, prostaglandin D2, leukotrienes and TNF-a. T

= these mediators induce smooth muscle contraction (bronchoconstriction), mucous hypersecretion, oedema and airway obstruction.

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4
Q

pathology of late phase of asthma (6-12hr)

A

Recruitment of eosinophils, basophils, neutrophil and Th2 lymphocytes and their products

= perpetuation of the inflammation and bronchial hyper-responsiveness.

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5
Q

structural cells involvement in asthma pathology

A

Structural cells (bronchial epithelial cells, fibroblasts, smooth muscle and vascular endothelial cells),

may also release cytokines, profibrogenic and proliferative growth factors, and contribute to the inflammation and altered function and proliferation of smooth muscle cells and fibroblasts (‘airway remodeling’).

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6
Q

3 factors that contribute to airway narrowing

A

increased mucus production

mucosal swelling/inflamm

bronchoconstriction

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7
Q

epidemiology of asthma

A

either young as part of the ‘atopic triad’

or in adolescence and teenagers

affects 10% children and 5% adults

prevalence increasing

men=women

acute asthma medical emergency 1000-2000 deaths/yr UK

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8
Q

presenting symptoms of asthma

A

wheeze - lower airway obstruction (terminal bronchioles)

tight chest

difficulty breathing

intermittent dysponoea

cough - often nocturnal

sputum

worse:

cold,

exercise,

dust, pollen, fur

emotion

infection

smoking and passive smoking

drugs - B blocker/NSAIDs

worse in morning - diurnal pattern - get peak flow diary

distrubed sleep - severe asthma

reduced exercise tolerance

acid reflux

atopic disease: eczema, hay fever, allergy, FH, uticaria, nasal polyps

pets, carpets, feather bedding, soft furnishings

if symptoms stop at weekends - job trigger - paint sprayers, food processors, welders, and animal handlers) - Ask the patient to measure their peak flow at intervals at work and at home (at the same time of day) to confirm this

days off school

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9
Q

signs of asthma

A

tachypnoea

use of accessory muscles

prolonged expiratory rate

audible wheeze

polyphonic wheeze

hyperinflated chest

hyperresonant percussion

reduced air entry

widespread

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10
Q

moderate asthma exacerbation

A
  • Increasing symptoms
  • PEF 50-75% best or predicted
  • No features of severe asthma
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11
Q

signs in severe asthma attack

A

PEFR <50%

pulse >110/min

RR >25/min

inability to complete sentences

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12
Q

signs of life threatening asthma attack

A

PEFR <33%

cyanosis

PaO2<8kPa but PaCO2 normal SpO2<92%

silent chest

bradycardia, arrhythmia

hypotension

confusion

coma

exhaustion, feeble resp effort

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13
Q

sign of near fatal asthma attack

A

high PaCO2

and/or needing mechanical ventilation with over inflation pressures

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14
Q

investigations for acute asthma

A

peak flow

pulse ox

ABG - normal/low Ox, low CO2 - hyperventilation, if PaCO2 is normal or raised, transfer to high-dependency unit or ITU for ventilation, as this signifies failing respiratory effort

CXR - exclude ddx

FBC - high WCC if infective exacerbation

CRP
UE

blood and sputum cultures

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15
Q

investigations for chronic asthma

A

PEFR monitoring - diurnal of >20% on ≥3d a wk for 2wks.

pul func test (spirometry) - obstructive defect (low FEV1/FVC, high RV), improvement after B agonist

blood - eosinophilia, IgE level, aspergillus Ab tutre

skin prick test - identify allergens

CXR - hyperinflation

histamine or methacholine challenge

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16
Q

management of acute asthma

A

resus, O2 sats, ABG, PEFR

high flow ox

salbutamol - nebulised B2-agonist bronchodilator (5mg initially continuously, then 2-4hrly. Ipratropium (0,5mg qds)

steroid therapy (100–200 mg IV hydrocortisone, followed by 40 mg oral prednisolone for 5–7 days).

If no improvement: IV magnesium sulphate. Consider IV aminophylline infusion or IV salbutamol, or ipratropium

Monitor oxygen saturation, heart rate, and respiratory rate.

Summon anaesthetic help if patient is getting exhausted (PCO2 increasing)

treat underlying casue

AB if chest infection - purulent sputum, abnormal CXR, raised WCC, fever

Monitor electrolytes closely (bronchodilators and aminophyline reduce K+

May need ventilation in severe attacks. If not improving or patient tiring, involve ITU early.

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17
Q

when can you discharge - asthma

A

PEF>75% within 1h of initial treatment can be discharged if no other reason to admit. otherwise:

  • when PEF >75% predicted, best diurnal variation <25%, inhaler technique checked, stable on discharge med for 24hr

patient owns a PEF meter and has steroid (oral and inhaled) and bronchodilator therapy.

Arrange follow-up. - GP in 2 days, resp clinic in 4wks

18
Q

theory of chronic asthma stepwise therapy

A

start on step appropriate to symptoms then either up or down (if control good for >3mo) to control symptoms

treatment reviewed every 3-6mo

rescue courses of prednisolone can be delivered at any time

19
Q

step 1 - chronic asthma therapy

A

Inhaled short-acting b2-agonist as needed. If used >1/day, or night symptoms move to Step 2.

20
Q

step 2 - chronic asthma therapy

A

As Step 1 plus regular inhaled low-dose steroids (400 mcg/day) eg beclometasone 200–800mcg/day (or fluticasone, budesonide or mometasone)

21
Q

step 3 chronic asthma management

A

As Step 2 plus inhaled long-acting b2-agonist (LABA) (eg salmeterol 50mcg/12h by inhaler).

If inadequate control with LABA, increase steroid dose (800 mcg/day).

If benefit from LABA but control still inadequate – continue LABA and ICS and consider trial of other therapy – Leukotrine receptor antagonists, theophylline or Long-acting muscarinic receptor antagonists

If no response to LABA, stop and increase steroid dose (800 mcg/day).

22
Q

step 4 chronic asthma management

A

increase Inhaled steroid dose (2000 mcg/day),

add a fourth drug, e.g. leukotriene receptor antagonist, SR theophylline or modified release b2-agonist tablet.

Refer patient to specialist care – although specialist care is mentioned in step 4, this may be required earlier and is ALWAYS indicated if there has been a recent severe or life-threatening exacerbation. In these cases follow-up is recommended for at least one year!

23
Q

step 5 chronic asthma management

A

Addition of regular oral steroids (prednisolone) once daily at lowest possible dose.

Maintain high-dose inhaled steroid 20000mg/day

Consider other treatments to minimize the use of oral steroids.

Refer for specialist care

24
Q

advice for asthmatics

A

educate on inhaler technique

routine monitoring of peak flow (twice daily)

develop an individualised management plan, emphasis on avoidance of provoking factors

quit smoking

weight loss

self-management by altering their medication in the light of symptoms or PEF.

Give specific advice about what to do in an emergency; provide a written action plan.

Consider teaching relaxed breathing to avoid dysfunctional breathing

25
Q

mechanism of B agonists

A

B2-adrenoceptor agonists

relax bronchial sm - raise in cAMP, act in minutes

Salbutamol is best given by inhalation (aerosol, powder, nebulizer), but may also be given PO or IV

SE: tachyarrhythmias, low K+, tremor, anxiety.

Long-acting inhaled B2-agonist (eg salmeterol, formoterol) can help nocturnal symptoms and reduce morning dips:

  • alternative to increasing steroids when symptoms are uncontrolled
  • SE as salbutamol, paradoxical bronchospasm
26
Q

mechanism of corticosteroids

A

inhale to avoid systemic effects eg beclometasone via spacer (or powder), but may be given PO or IV.

act over days to reduce bronchial mucosal inflammation

rinse mouth after use to avoid oral candidiasis

Oral steroids are used acutely (high-dose, short courses, eg prednisolone 40mg/24h PO for 7d) and longer term in lower dose (eg 5–10mg/24h) if control is not optimal on inhalers.

27
Q

mechanism of aminophylline

A

(Metabolized to theophylline)

inhibit phosphodiesterase = reduced bronchoconstriction by increased cAMP

prophylaxis, at night PO - prevent morning dipping

useful as an adjunct if inhaled therapy is inadequate

In acute severe asthma, it may be given IVI.

narrow therapeutic ratio, causing arrhythmias, GI upset, and fi ts in the toxic range.

  • check levels, do ECG monitoring and check plasma levels after 24h if IV therapy is used.
28
Q

mechanism of anticholinergics

A

ipratropium, tiotropium

reduce muscle spasm synergistically with B2 agonists

not recommended for chronic asthma

29
Q

mechanism for cromoglicate

A

mast cell stabaliser

May be used as prophylaxis in mild and exercise-induced asthma (always inhaled), especially in children.

It may precipitate asthma

30
Q

mechanism of leukotriene receptor atagonists

A

(Eg oral montelukast, zafi rlukast.)

Block the effects of cysteinyl leukotrienes in the airways by antagonizing the CystLT1

31
Q

mechanism of anti-IgE monoclonal Ab

A

Omalizumab 36 may be of use in highly selected patients with persistent allergic asthma.

Given as a subcutaneous injection every 2–4 wks depending on dose.

Specialists prescribe only.

32
Q

drugs used in acute asthma

A

Salbutamol (B2-agonist). SE: tachycardia, arrhythmias, tremor, low K+.

Hydrocortisone and prednisolone (steroid; reduces inflammation).

aminophylline

  • less frequently, not routinely recommended in current BTS guidelines, but may be initiated by respiratory team or ICU
  • inhibits phosphodiesterase; increase [cAMP]
  • SE: raised pulse, arrhythmias, nausea, seizures. - monitor ECG
  • Aim for plasma concentration of 10–20mcg/mL (55–110μmol/L). Serious tox icity (low BP arrhythmias, cardiac arrest) can occur at concentrations ≥25mcg/mL.
  • Measure plasma K+: theophyllines may cause low K+.
  • Don’t load patients already on oral preparations.
33
Q

complications of asthma

A

growth retardation

chest wall deformity (pigeon chest)

recurrent infections

pneumothorax

resp failure

death

34
Q

prognosis for asthma

A

Many children improve as they grow older. Adult-onset asthma is usually chronic.

35
Q

why are quiet breath sounds a bad sign

A
  • patient may have blocked off large areas of the lung and may be getting tired. If not acted on, respiratory arrest may ensue rapidly.
  • You would expect to hear widespread wheeze in most asthmatics with active disease
    • increased pulse and respiratory rate are an additional concern in the presence of a ‘silent’ chest
36
Q

why is normal PaCO2 concerning in an asthma attack

A
  • would expect it to be low
  • if normal/high – fail to keep up and soon go into worse resp failure
37
Q

effect of adding LABA and montelukast

A
  • halve the rate of exacerbation and their effects are additive.
38
Q

SE of long term oral steroids

A
  • Cataracts
  • Weight gain
  • Candida
  • Osteoporosis
  • Dm
  • some risk of these side effects in asthmatics requiring frequent ‘short’ courses of oral steroids for exacerbations, although this is rare
39
Q

how do you avoid candidiasis in pts using inhaled steroids

A

spacer device, rinses their mouth out with water after using the inhaler or cleans their teeth.

Cleaning of teeth also provides a useful memory trigger to aid concordance as most inhaled steroid regimes are twice daily inhalations, and most people clean their teeth twice a day

40
Q

when do you give AB in asthma

A
  • not routine
  • unless signs of a bacterial infection (purulent productive cough, fever, leukocytosis, raised CRP, chest x-ray signs).
  • A positive sputum culture in the presence of consolidation on a chest x-ray would require antibiotic treatment.
41
Q

what is sufficient asthma control

A
  • No daytime symptoms
  • No night time waking due to asthma
  • No rescue med needed
  • Ne exacerbations
  • No limitations in daytime activity including exercise
  • Normal lung function (FEV1 and/or PEF >80% predicted or best) with minimal side effects
42
Q

In females established on inhaled corticosteroids (ICS) what advice should you give

A

o The most recent revision of the BTS/SIGN guidance suggest continuing with short acting beta-2 agonists and inhaled corticosteroids as normal during pregnancy.

o Oral steroids should still be used if needed for asthma exacerbations during pregnancy

o Women with asthma should be advised of the importance of good control of their asthma during pregnancy to avoid problems for both mother and baby.

Yr 3 resp (19 decks)

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