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Pharmacology examII

Causes of Lung Swelling/Inflammation? From mechanical lung trauma;From inhalation of noxious or toxic substances;From respiratory infections & systemic infections producing septicaemia and septic shock leading to ARDS; From allergic or non-allergic stimulation in asthma.
degranulation a cascade of chemical mediators spilling out from the ruptured mast cell :histamine, heparin, leukotrienes, prostaglandins, and thromboxanes
Common early-phase response: Local vasodilatation; Increased vascular permeability; Redness; Wheal formation;
Late-phase response: (to be prevented) Develops 6 to 8 hours later.mucus plugging. An increase in white cells (eosinophils and neutrophils) infiltrate the asthmatic airway. Mediators leukotrienes & prostaglandins are released and cause congestions of airways.
Corticosteroid Mechanism of Action Block or diminish late-phase asthma response (leukotrienes & prostaglandin release).Suppressing the immune response. LESS A/W CONGESTION. Reduce airway inflammation. Together they decrease airway obstruction
Corticosteroids clinical response Increased responsiveness to b-agonists within 2 hrs Increased b-receptor density within 4 hrs Exercise-induced bronchospasm sensitivity decreases after 4 weeks of medication Seasonal bronchial hyper-responsiveness requires at least 1 week to reverse
Adverse Effects of Corticosteroids (Systemic) Appetite stimulation; Stomach irritation; Headache; Mood changes; Exacerbation of acne; Hypokalemia ; Hyperglycemia ; Osteoporosis ; Immuno-suppression; Increased risk of infection; Myopathy of skeletal muscles (weakness)
corticosteroid effect time Objective improvement a minimum of 6-12 hrs Maximum improvement > 1 wk