Summary

This document provides an overview of asthma, including its pathophysiology, risk factors, and treatment strategies. Topics such as the respiratory tract, respiration mechanism, and treatment principles are discussed. The document serves as a valuable resource for learning about asthma.

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Asthma Asthma trajectories - Variable pathways – early onset (mostly atopic) - Post puberty – resolution/new development. - Adult onset –late onset asthma. - Why do we need to know this? o People often ask – will my child grow out of their asthma? § T...

Asthma Asthma trajectories - Variable pathways – early onset (mostly atopic) - Post puberty – resolution/new development. - Adult onset –late onset asthma. - Why do we need to know this? o People often ask – will my child grow out of their asthma? § They may or may not. The respiratory tract Respiration – mechanism - Inspiration: contraction of diaphragm and external intercostal muscles increase the thoracic cavity space and decrease intra-pleural pressure- allowing air to rush in due to pressure diEerential. - The diaphragm then relaxes, increasing intra-pleural pressure – triggering passively the process of expiration. - The inspiration-expiration cycle allows gas exchange. Respiration – control - This is managed by the CNS respiratory control system. o The central neural respiratory generator. o The sensory input system (thoracic neural receptors, peripheral (carotid and aortic bodies) and central medullary chemoreceptors), and o The muscular eBector system. ASTHMA PATHOGENESIS AND PATHOPHYSIOLOGY What is asthma? - Asthma is a chronic obstructive lung disease, which can be controlled but not cured. - In clinical practice, i.e., for a diagnosis. Asthma is characterised by both the following: o A respiratory of symptoms (cough, wheeze, dyspnoea, or chest tightness) which vary over time and intensity as well as. o Excessive variation in expiratory airflow function. - Asthma is also associated with airway inflammation and airway hyper-responsiveness. Current understanding of asthma development - Asthma may be a result of gene-environment interactions that occur as early as in-utero. Risk factors that impact onset, development, progression Asthma triggers - House dust mites - Mould - Pets - Pollen - Cigarette smoke - Exercise - Smoke - Chemicals - Stress - Emotions - Hormonal changes (women) - Respiratory infections. (common cold =80% of bad asthma exacerbations) - Weather (e.g. thunderstorms) - Medications, occupational exposures. Asthma pathophysiology - Repeated infections/ exposures disrupt airway epithelial barrier → danger signalling and chemokine secretion. - Immature dendritic cells (DC) recruited to airway mucosa – act as antigen presenting cells (APCs) - Allergen linked APCs then migrate to local lymph nodes and stimulate naïve T helper Cells to diEerentiate to T helper Type 2 (TH2) cells. - Cytokines linked to Th2 cell response drive inflammation (majority of asthma cases) – eosinophils are the main driver. Changing concepts in pathophysiology of asthma. - Even with first episode of asthma, the lung will be damaged and start remodelling it. Counselling on patients to control their asthma using snit-inflammatory is very important as controlling the asthma will at least reduce the amount of remodelling of the lung. Asthma management Asthma Diagnosis - History (family history, symptoms, symptoms pattern) - Physical examination (wheeze) - Considering other diagnoses. - Documenting variable airflow limitation (spirometry – pre-pose bronchodilator variability. Asthma treatment decisions à exacerbation à 위독, 악화 Assessing Asthma control Risk factors for asthma flare-ups. Asthma treatment principles - Bronchodilators (relievers) o Short acting beta agonists (SABAs) o Long-acting beta agonists (LABAs) o Short or long-acting muscarinic antagonists (SAMA/LAMA) - Anti-inflammatory agents (preventers) o Inhaled corticosteroids (ICS) à omnipotent. o Leukotriene receptor antagonists (LTRA) o Targeted biologic agents. - If symptoms more than twice a month à need to be on preventer à inhaled corticosteroids. - Most children can be treated by SABA. à You can add on ICS or montelukast. - No ICS+LABA combination allowed for 1-5 years children. Reliever medications – schedule 3 - Short acting beta 2 agonists (SABAs) o Salbutamol o Terbutaline - Salbutamol - Formulation type: (pressurised metered dose inhaler or pMDI and Autohaler) - Formulation strength: 100 µgs/puE x 200 doses in inhaler. - Time to action: 1-2 minutes. - Elimination half-life: 2.7-5 hours. - Dose: 1-2 puEs (100-200 µgs) every 4-6 hours ONLY when needed or 5-15 minutes pre- exercise. - Inhaler use is important – as inappropriate inhalation technique can lead to systemic absorption. - Precautions o Risk factors for angle – closure glaucoma - inhaled salbutamol may rarely precipitate acute angle-closure crisis, especially if used with ipratropium. - Pregnancy and breastfeeding: safe to use. - Side eBects: o Skeletal muscle tremor, Peripheral arteriole dilation – compensatory in blood pressure, Tachycardia, Headache, Nausea, Insomnia, Hyperactivity in children, Paradoxical bronchospasm (first time use-check), Potentially serious hypokalaemia – more likely with high doses or oral route. pMDIs usage steps The role of spacers – usage steps Reliver medications – schedule 3 (Terbutaline) - Terbutaline formulation: (Dry Powder Inhaler DPI) - Formulation strength: 500 µgs/puE x 120 doses in inhaler. - Time to action: 5-30 minutes. - Elimination half-life: excreted mainly unchanged in the urine. Practically all of an administered dose of terbutaline is eliminated after 72 hours. Duration of action ¬4-5 hours. - Dose: 1–3 inhalations (500–1500 micrograms) when required, or 5–15 minutes before exercise. Repeat 3 or 4 times daily as necessary. - Inhaler use is important – as inappropriate inhalation technique can lead to systemic absorption, or NO DOSE! - Precautions o Risk factors for angle – closure glaucoma - inhaled salbutamol may rarely precipitate acute angle-closure crisis, especially if used with ipratropium. Dry Powder Inhalers- Turbuhalers Teach back method – key steps. Salbutamol vs terbutaline - No clinical diEerence in eEect. - However, for S4 versions terbutaline is no longer subsidised by PBS. - Dry powder inhalers may need a higher inspiratory flow generation (though most people even with severe asthma etc. can use these inhalers). - Dry powder inhalers more environmentally friendly – lower carbon footprint. Key roles for pharmacist SABA use issues - There is increased risk of severe flare-ups in patients using as needed SABAs in the absence of inhaled corticosteroids or with poor adherence to inhaled corticosteroids. à This should be a key discussion point for S3 requests for SABAs. SABA use issues Key roles for pharmacists in dispensing S3 Relievers– no emergency situation. - Check asthma control (how?) - Check if patient has been prescribed preventers (if Sx > 2 per month) - Check patient is adherent to preventers (how?) - Check level of SABA usage (no of puEs/day or cannisters bought per year) – info gathering/pharmacy records if you record sales. - Check if patient knows appropriate technique for using their SABA inhaler. - Check if there may be comorbid conditions (AR, OSA, GORD – refer if needed). - Check if patient has an asthma action plan. Asthma first aid Information gathering à poorly controlled asthma Management options - Provide Reliver PuEer Yes/No. - Demonstrate puEer technique. - Provide Bisolvon Dry Cough Liquid Yes/No –Why? - GP referral Preventer need education. - Awareness about what do in a serious asthma flare-up (including what a serious flare up may be) Suggest Symptom diary for GP visit. - Provide information on asthma management (Asthma Australia) 1800Asthma or 1800 278 462. - Record key counselling provided if possible.

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