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Asthma- With CKS Guideline

17 October 2018 18:20

Chronic (Obstructive Lung Disease) Respiratory Condition - Airway inflammation and Hyper Responsiveness

• Bronchoconstriction
• Inflammation
• It is IgE mediated

Acute asthma exacerbation is a term used to describe the onset of severe asthma symptoms, which can be life-threatening.


Characterised by
1. Cough, wheeze, chest tightness, SOB
2. Symptoms triggered by Allergies , Allergen
3. Decreased Lung sounds
4. Hyper resonance


→ Respiratory Examination- Presence of the signs and symptoms

○ Check for possible occupational asthma
○ Personal/family history of other atopic conditions, particularly atopic eczema/dermatitis and/or allergic rhinitis.
→ Results of fractional exhaled nitric oxide (FeNO) testing
○ used to confirm eosinophilic airway inflammation to support an asthma diagnosis in people aged 17 years and
older. This test may be available in some primary care practices or may require referral to a specialist centre

→ Spirometry : ( Affected by treatment of corticosteriods)

○ objective tests to detect airway obstruction,( symptomatic, over the age of 5)
○ FEV1/ FVC ratio normally >70%


Asthma is both Reversible and Inducible -

Reverse with Beta agonist - Bronchodialtor
Inducible with ACH agonist

TX and Management

Step 1=SABA FEV1- 80%

Step 2 = SABA+ ICS (beclometasone 200 mc/d) given via spacer PO or IV (FEV 80%)
Step 3 = SABA + LABA + ↑ Beclometasone 800mcg/d--- Leukotrine receptor antagonist may be tried (FEV 1
Step 4 = 2000mcg/d Beclometasone (<60%)
Step 5 ------

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Describe the mechanism of action of drugs commonly used to treat acute severe asthma?

 Drugs used to treat asthma generally target the bronchoconstriction, inflammatory response and hyper reactivity.


 Beta agonists bind to the Gs protein of adrenergic B2 receptors and increase adenylyl cyclase and cAMP, causing smooth
muscle relaxation.
→ May be rapid onset---> short acting (salbutamol) or slower onset, longer acting (salmeterol – more lipophilic which
reduces the rate of diffusion away from the target site).
○ SE include tremor and hypokalaemia.

 Muscarinic antagonists bind to the M3 receptor of bronchial smooth muscle, blocking the Gq protein and the associated
increase in phospholipase C and intracellular Ca that would normally accompany its activation.
→ This causes smooth muscle relaxation.
→ Generally do not provide sufficient relief on their own, but in conjunction with beta agonists can improve symptoms.
→ May be short acting (ipratropium) or long acting (tiotropium)
○ SE---> Can cause dry mouth.

 Methylxanthines (theophylline)
→ Act via inhibition of PDE5 and subsequent increase in cAMP----> Bronchodilation, as well as possible adenosine
receptor antagonism.
→ Narrow therapeutic window and risk of arrhythmias and seizure at higher doses – rarely used today.

 Inhaled adrenaline activates beta receptors to provide a similar effect to the beta agonists.
→ also causes alpha agonism, constricting the bronchial mucosa to reduce airway resistance.


 Corticosteroids - bind to the cell nucleus to inhibit the transcription of genes that encode for inflammatory mediators.
→ Multiple side effects associated including HTN, diabetes, oral candidiasis and gastric ulcers.

 Antileukotrienes (montelukast) Competitive antagonist at leukotriene receptors LTD4 and LTE4, reducing leukotriene-
mediated bronchoconstriction and inflammatory mediator release

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mediated bronchoconstriction and inflammatory mediator release

 Anti-IgE antibodies (omalizumab).

→ Rarely used; monoclonal antibodies again IgE that reduce the binding of Ige to mast cells and basophils to prevent the
allergic reaction.
→ Possible increased incidence of malignancy.

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