This is an extract of our Airways Pharmacology document, which we sell as part of our Respiratory System Notes collection written by the top tier of Bristol University students.
The following is a more accessble plain text extract of the PDF sample above, taken from our Respiratory System Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:
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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