Airways Pharmacology Notes
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 pages of notes across 17 different documents.
The original file is a 'Word (Docx)' whilst this sample is a 'PDF' representation of said file. This means that the formatting here may have errors. The original document you'll receive on purchase should have more polished formatting.
Airways Pharmacology Revision
The following is a plain text extract of the PDF sample above, taken from our Respiratory System Notes. This text version has had its formatting removed so pay attention to its contents alone rather than its presentation. The version you download will have its original formatting intact and so will be much prettier to look at.
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
• Respiratory infections
• Exercise, breathing in cold air
• Exposure to allergens o Pollen/moulds; dust mites/cockroaches; pollution; pets; tobacco smoke
• 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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