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Asthma - Coggle Diagram
Asthma
PATHOPHYSIOLOGY
The person has a trigger for their asthma when a trigger is initiated a signal is sent to the dendrite cells (T2 helper cells) to produce interleukins 4,5 & 13 as they stimulate B bell production.
IGE antibodies attach to receptor mast cells & then due to exacerbation then cause histamines, prostaglandins & leukotrienes to be released, when mast cells degranulates.
Broncho spams occurs as the smooth muscle contracts increasing mucus production in the goblet cells & IGE production occurs as antibodies attach to receptors on mast cells.
Increased fluid cells become oedemic this results in further limits to air flow through the broncho's affecting treatment.
Treatment Nice 245 2024
NEBS - Salbutamol, bronchodilator - beta 2 agonist 5mg every 15/30mins helping constriction of smooth muscle preventing further spams.
o2 Therapy - 94% - 98% for hypoxia increases available o2 helping with demands reducing respiratory effort for patient because of increased o2 helping with pressure in the alveoli.
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Nursing Care
Positioning of Patient, sitting up as much as possible (tripod position) increases the amount of available o2 getting into the lungs and reduce fatigue. Aids treatment by helping patient expel high levels of co2 which had become trapped within the alveoli due to broncho narrowing.
Continuous Monitoring including observations following NEWS2 guidelines which aids treatment and pick up deuteration quickly. Assists with treatment effectiveness and following further treatment pathways.
Patient Clinical History vital to verify asthma history as to triggers, allergies and medication sensitivities. Past episodes with effective treatment used. Family history and regular medication patients takes. Hypersensitivity may have other allergies and more prone to developing asthma.
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Clinical Features
The patient is wheezing due to increased mucus secretion, wall oedema & broncho constriction. Resulting in restriction of airflow in & out of the alveoli, making expiration worse and due to co2 being trapped in the alveoli causing low spo2 leading to hyperinflation (hypoxia).
Gas exchange can't take place & patient then experiences hyperresonance & dyspnea and patient using accessory muscles more to try & expel co2. Resulting in respiratory failure.