Asthma is grouped by severity
1) Asthma treatment adrenoreceptor agonists
Leukotriene receptor antagonists take longer to show effects
2) Sympathomimetic agents reliever or bronchodilator
Muscarinic antagonists prevent contraction for airway smooth muscle
1) Steroids decrease creation of the inflammatory mediators
Muscarinic antagonists are an alternative to Beta 2 agonists
2) Inhaled corticosteroids block release of inflammatory mediators
Corticosteroids are for long term maintenance
3) Steroids prevent mast cell activation
Leukotriene receptor antagonists are for long term maintenance
Steroids block asthmatic airways from lymphocytes, eosinophils and mast cells
Steroids can enter cell membrane by dissolving in fats, oils, or lipids
Steroids block creation of inflammatory cytokines in immune cells
Corticosteroids stop creation of prostaglandin and leukotriene
Steroids in mast cells, they increase the production of annexin-1 proteins that inhibit the enzyme phospholipase A2. This stops the conversion of membrane phospholipid into arachidonic acid and decreases the synthesis of leukotrienes and prostaglandins.
Corticosteroids also downregulate the enzyme cyclooxygenase-2, which reduces the production of prostaglandins
Finally, they also inhibit the proliferation of Th2 cells, which reduces the production of IL-4 and IL-5, further reducing the activity of mast cells and eosinophils.
Histamine produced by basophils and mast cells
Histamine increases flow to capillaries to white blood cells
Histamine cause local inflammation
Histamine cause widened blood vessels
Four types of histamine receptors H1, H2, H3, H4
First generation H1 blockers block H1 receptors
First generation H1 blockers block receptors in the brain which can cause drowsiness
Second generation H1 produce less side effects