This is a sample of our (approximately) 3 page long Airways Pharmacology notes, which we sell as part of the Respiratory System Notes collection, a 60-70% package written at Bristol University in 2012 that contains (approximately) 49 page of notes across 17 different document.
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Lecture 14 & 15 Airways pharmacology
ASTHMA o What is asthma? Characterised by:
? Wheeze, cough, chest tightness, dyspnoea, airway hyperresponsiveness, inflammation of lungs, variable airflow obstruction o Asthma pathology
* Genetic/ethnic o IgE levels genetically influenced o 50% higher prevalence in black vs. white children
* Environmental o Higher in city than rural dwellers o Passive smoking
? Triggered by...
* Respiratory infections
* Exercise, breathing in cold air
* Exposure to allergens o Pollen/moulds; dust mites/cockroaches; pollution; pets; tobacco smoke
? Pathological process
* Initiation o Allergens stimulate T-cells o Generate B cell activating cytokines, leads to IgE production o Induces expression of IgE receptors (Fc receptor) mainly on mast cells & macrophages
* Early/acute/immediate phase o Release mediators from macrophage/mast cells:
? Histamine; leukotrienes; cytokines; neurokinins; platelet activating factor; prostaglandin o Promote bronchoconstriction (ACUTE ASTHMA ATTACK) o Mediators also attract T cells, neutrophils, platelets and monocytes releasing more spasmogens &
inflammogens o Further exacerbates inflammation and triggers inflammation
* Late phase o Progressive inflammation o Influx TH2 lymphocytes o Activation of Eosinophils releasing toxic proteins o PGE2 from smooth muscle: permeable BVs= OEDEMA o Damage and loss of epithelium o Increased irritant receptor/C fibre accessibility=Bronchial hyperactivity o Subepithelial cell fibrosis o Hypertrophy and hyperplasia of smooth muscle cells
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