airways function Flashcards
C-shape
allows oesophagus to run down back of trachea; slightly off-set to confer greater tensile strength
functions of conduit airways
conduct O2 to alveoli, conduct CO2 out of lung (gas exchange)
how is it facilitated
mechanical stability (cartilage), control of calibre (smooth muscle), protection and ‘cleansing’
organisation of airway structures
outside cartilage - smooth muscle - submucosal gland with tip in smooth muscle - systemic circulation - airway epithelium (ciliated (bend left and right) and goblet cells - mucociliary transport) - mucus in airway lumen
human airway epithelium (EM)
mucin granules in goblet cells contain mucin in highly condensed form, ciliated cell have high mt to ensure beating; as soon as mucin secreted it takes on water and expands massively
acini
functional mucus secreting units into collecting duct - wafted onto lumen surface by cilia
mucous and serous acini
serous acini on outside secrete antibacterials (e.g. lysozyme - more water based); wash mucus into collecting duct
ciliary structure
apical hooks, rods slide over each other to allow movement; 9+2 arrangement
metachronal rhythm
layer of mucus; leading edge; field of cilia will move leading edge a little way along; cilia then move back and waft again after other cilia have moved
mucus flakes
so much mucus can’t see cilia
airway epithelium functions
Secretion of mucins, water and electrolytes (components of ‘mucus’ + plasma, mediators etc), movement of mucus by cilia – mucociliary clearance, physical barrier, production of regulatory and inflammatory mediators
regulatory and inflammatory mediators
NO (by nitric oxide synthase, NOS), CO (by hemeoxygenase, HO), arachidonic acid metabolites (e.g. prostaglandins - COX), chemokines (e.g. interleukin - (IL)-8), cytokines (e.g. GM-CSF), proteases
airway smooth muscle functions
structure, tone (airway calibre - contraction and relaxation), secretion (mediators, cytokines, chemokines)
under chronic airway inflammation
structure - hypertrophy due to proliferation, massive increase in secretion to engage in inflammatory response and inflammatory cell recruitment
tracheo-bronchial circulation
systemic; perfusion through airway mucosa is highest in body; massive input and output
tracheo-bronchial circulation
slide 22
subepithelial microvascular network
below epithelium is plexus of capillaries, veins and arteries - massive bloodflow for good gas exchange
tracheo-bronchial circulation functions
good gas exchange (airway tissues and blood), contributes to warming of inspired air, contributes to humidification of inspired air, clears inflammatory mediators, clears inhaled drugs (good/bad, depending on drug), supplies airway tissue and lumen with inflammatory cells, supplies airway tissue and lumen with proteinaceous plasma
mechanism of plasma exudation in airways
endothelial cell gaps leak plasma out to bathe tissue; C-fibre nerve, inflammatory mediators make it more leaky; Evans blue dye shows experimentally as binds to albumin (platelet activating factor - inflammatory mediator)
control of airway function
nerves (parasympathetic (cholinergic) and sympathetic – adrenergic, sensory), regulatory and inflammatory mediators (histamine, arachidonic acid metabolites (e.g. prostaglandins, leukotrienes), cytokines, chemokines
Proteinases (e.g. neutrophil elastase)
Reactive gas species (e.g. O2-, NO)
innervation of airways
if obstruction in airway, contrict airway by parasympathetic motor pathway, no sympathetic nerves to relax airway so NO relaxation - speeds up cilia and is vasorelaxant (same as blood vessels); adrenaline also induces relaxation
cholinergic mechanisms in airways
sensory nerves - CNS - parasymp. - parasymp. ganglion - ACh - mucus to allow open more easily, vasodilation
regulatory-inflammatory cells in airways: cells
eosinophil, neutrophil, macrophage, mast cell, T lymphocyte, structural cells (smooth muscle)
regulatory-inflammatory cells in airways: mediators
complexity: cells produce more than one mediator and these do more than one thing
regulatory-inflammatory cells in airways: effect of mediators
smooth muscle (airway, vascular: contraction, relaxation), secretion (mucins, water, etc), plasma exudation, neural modulation, chemotaxis, remodelling
loss of airway control
asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF) - characterised by airway inflammation leading to obstruction due to airway remodelling
asthma
clinical syndrome - increased airway responsiveness to variety of stimuli causing airway obstruction; varies over short periods of times and is reversible; symptoms are dyspnoea, wheezing and cough; lumen filled with mucus plug; more goblet cells; fragile epithelium; thickening of basement membrane; hypertrophy of smooth muscle and submucosal glands; vasodilation; massive cellular infiltrate (mainly eosinophils); airway wall thrown into folds - bronchoconstriction
asthma theory
epithelial fragility - exposes sensory nerves - stimulated - set up cholinergic reflex - bronchoconstriction and mucus secretion - excessive mucus in airway lumen; influx of inflammatory cells - mediators released - remodelling so submucosal glands and smooth muscle undergo hypertophy, vasodilation, bronchoconstriction