Asthma Treatment PDF
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South College
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Summary
This document provides an overview of asthma, discussing its causes, pathophysiology, and protective and risk factors, as well as treatment options. It also covers chronic and acute asthma, and examines clinical presentations and related lab values.
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Introduction Corticosteroids Global Initiative for Asthma (GINA) sets guidelines yearly ▪ Glucocorticoids: immune system o Gene...
Introduction Corticosteroids Global Initiative for Asthma (GINA) sets guidelines yearly ▪ Glucocorticoids: immune system o Generally: asthma is reversible ▪ Mineralocorticoids: BP/electrolytes o 80-90% of Asthma related deaths are preventable o Mucus production: goblet cells Etiology o Airway smooth m.: hypertrophy/hyperplasia o Genetic, environment, and altered immune response (T-helper o Neurogenic inflammation: stimulation of nonmyelinated C fibers cells) of afferent system to induce release of substance P and o Protective Factors: neurokinin A which releases NO Being the younger sibling o Vasoactive intestinal peptide (VIP): degrading VIP induces Natural birth, breastfeeding bronchoconstriction Pig/cattle farming Drugs and Asthma ("This is def on the exam.") Foodborne illness o Estrogen: a decrease in estrogen can cause an exacerbation of High burden helminth asthma s/s Healthy diet, low pollution There is evidence that this can be absent when given o Risk Factors: with progesterone Being the older sibling o Aspirin: can cause bronchospasm/constriction; to tx this give ICSs C-section, formula Feeding o Non-selective B-blocker: can attach to any B receptor and prevent Sheep farming bronchospasm reversal RSV NE and E act on B-cells Low burden helminths B1 (Heart), B2 (lung), B3 (fat cells) Smoking, obesity Clinical Presentation Pathophysiology o Chronic Asthma lab: FEV1/FVC ratio is normally 0.75-0.80 o IgE mediated rection binding to mast cells to release histamine Dx when spirometry shows obstruction with reversibly Mediators induce microvasc. leakage and exudative following inhaled B2 agonist plugs o Acute Severe Asthma: FEV1 is less than 40% of predicted vales Recruitment of eosinophils and basophils o Exercise induces asthma: FEV1 drops 10% from baseline, with Activation of T-cells return w/n 30 min ▪ Th2 cells produce cytokines (IL-4, 5, and 13) o Nocturnal asthma: night s/s that are worsened by other things that mediate allergic inflammation and inhibit production of Th1 cytokines o In Neonates: the cord blood is skewed to Th2 and should be corrected w/n first 6 mns (daycare, sibling) o Exercise Induced: osmotic stimuli leads to degranulation o Inflammatory mediators Arachidonic acid and metabolites -- steroids block PLA ▪ Prostaglandins ▪ Thromboxane ▪ Leukotrienes -- montelukast (Singulair) blocks LTs D and E Chronic Asthma Acute Asthma Treatment ≥6y Risk Factors for Death: o All pt need to have a fast-relief inhaler o Overuse of SABA (> 1 canister/month) B2-agonists (±ICS) or MART o No use of ICS o ICS is preferred long-term control o Poor medication adherence For those who are inadequately controlled on low-dose o Lack of written action plan ICS: increase dose or add in LABA In Hospital Tx o Additional Drugs: montelukast (Singulair) o Same as out-pt with addition of oxygen therapy (maybe Heliox) o Assess pt every 3mns o With severe s/s (HR ≥120, RR ≥30, PEF ≤50%) consider IV Mg, IV Step down ICS by 25-50% at 3 month intervals steroids, and high-dose ICS Treatment
