Asthma Flashcards
Outline the aims of asthma control. Outline the steps of asthma control.
Aims:
- minimise symptoms (day & night)
- minimal need for reliever medication
- no exacerbations
- no limitation of physical activity
- normal lung function (FEV1 & PEFR > 80% of predicted)
- Short-acting beta-2 agonists (SABAs)
- Inhaled corticosteroids
- Long-acting beta-2 agonists (LABAs)
- Leukotriene receptor antagonists/methylxanthine/long-acting anti-cholinergic (M3)
- Oral corticosteroids
What should be done before initiating new drug therapy in asthma?
Check compliance with existing therapies
Check inhaler technique
Eliminate trigger factors
What is the first step in asthma control? What is its mechanism of action? When is it indicated?
Short-acting beta-2 agonists (SABAs)
e.g. salbutamol, terbutaline
Indicated for mild, intermittent asthma
Acts on airway smooth muscle & inhibits mast cell degranulation
Symptom relief (reversal of bronchoconstriction)
Use as required (regular use reduces asthma control by increasing mast cell degranulation in response to allergens)
Give some examples of ADRs associated with beta-2 agonists.
- tachycardia
- palpitations
- tremor
What is the second stage of asthma control? What is its mechanism of action? When is it indicated? What are the aims of treatment?
Inhaled corticosteroids
Reduce eosinophilic inflammation (therefore patients respond better if they have eosinophilic asthma)
- up-regulates beta-2 receptors, inhibition of inflammation & inflammatory mediators (induces apoptosis)
Indicated when:
- using beta-2 agonist 3+ times/wk
- symptoms 3+ times/wk
- waking 1+ times/wk
- exacerbation requiring oral steroids in last 2yrs (point of consideration)
Aims:
- improve symptoms
- improve lung function
- reduce exacerbations
- prevent death
Outline the pharmacokinetics and pharmacodynamics of inhaled corticosteroids.
10um particles enter mouth and oropharynx —> absorbed in gut —> inactivated in the liver (first pass) —> systemic circulation
1-5um particles settle in small airways —> absorbed in lungs —> systemic circulation
0.5um particles too small (inhaled to alveoli and exhaled without being deposited in lungs)
Few systemic ADRs as metabolised in lungs and poorly absorbed
What is the third step in asthma control? When is it indicated?
Long-acting beta-2 agonists (LABAs) e.g. salmeterol, formoterol
Indicated when not controlled on 400ug/day of inhaled corticosteroids (flat dose-response curve, therefore no improvement when increasing dose), nocturnal asthma
note: co-prescribed with inhaled steroids (not anti-inflammatory on their own - COPD can be used on their own) —> combination inhalers increase compliance, cheaper, safer, etc.
Subsequently:
- if control is inadequate increase the concentration of inhaled steroid
- if no response, stop LABA and institute leukotriene receptor antagonist/theophylline
What is the fourth step of asthma control? What is their mechanism of action?
High dose inhaled corticosteroids (biopsy to check if non-eosinophilic asthma)
OR leukotriene receptor antagonists
(leukotrienes released by mast cells & eosinophils; cause bronchoconstriction, mucus secretion, mucosal oedema, inflammatory cell recruitment)
OR methyxantine e.g. theophylline
(inhibits TNF-alpha & leukotriene synthesis)
OR long-acting anti-cholinergic (M3) e.g. tiotropium bromide
(reduced smooth muscle contraction & mucus secretion; reduces exacerbations in COPD & asthma)
Give some examples of ADRs associated with leukotriene receptor antagonists.
- angioedema
- dry mouth
- anaphylaxis
- fever
- arthralgia
- gastric disturbances
What is the fifth step of asthma control? When is it indicated?
Oral corticosteroids
OR anti-IgE (prevents IgE binding to allow cross-linking and activation of mast cells)
Indicated in exacerbations and residual eosinophilia
What are the different classes of beta-2 agonists? Give examples for each.
RELIEVERS:
- Fast onset, short duration (3-5hrs) e.g. inhaled terbutaline, inhaled salbutamol
- Fast onset, long duration (12hrs) e.g. inhaled formoterol
PREVENTERS:
- Slow onset, short duration e.g. oral terbutaline, oral salbutamol, oral formoterol
- Slow onset, long duration e.g. inhaled salmeterol, oral bambuterol
What are methylxanthines? What is their mechanism of action?Outline their pharmacokinetics. Give some examples of ADRs associated with methylxanthines.
e.g. theophylline, aminophylline
Antagonist adenosine receptors + inhibition of phosphodiesterase in smooth muscle
Poor efficacy
Narrow therapeutic window
ADRs. (freq.):
- nausea
- headache
- reflux
- psychomotor agitation (wringing hands, pacing)
- arrhythmias
- fits
- affected by CYP450 (many drug-drug interactions)
What are some important points to remember regarding inhaler techniques and management of asthma?
Inhaler techniques:
- if patient is unable to use a device satisfactorily, must find an alternative
- assess ability to use an inhaler in clinical reviews
- medication titrated against clinical response to ensure optimum efficacy
Once asthma is controlled, stepping down is recommended (otherwise may receive higher dose than necessary)
Every asthmatic should have a self-management plan with written instructions on when and how to step-up and step-down treatment (better outcomes)
What is required to diagnose an episode of acute, severe asthma in adults?
Any one of:
- unable to complete sentences
- pulse > 110bpm
- resp. rate > 25/min
- peak flow 33%-50% of best/predicted
Give some examples of life-threatening features in an episode of acute, severe asthma.
- spO2 4.5kPa
- silent chest
- cyanosis
- feeble resp. effort
- hypotension
- bradycardia
- arrhythmias
- exhaustion
- confusion
- coma
NEAR FATAL: paCO2 > 6kPa OR mechanical ventilation
