respiratory cell biology Flashcards
respiratory disease pathophysiology: summarise the pathophysiological mechanisms of lung disease including changes in control mechanisms and altered functions of airway cells
5 common lung problems and knock on effects
asthma, smoking, cancer, cough, COPD, knock on effect with atherosclerosis and heart rate variability
3 types of COPD
bronchitis, small airways disease, emphysema
effect of COPD on human airway epithelium (goblet cells)
increased goblet cell numbers (hyperplasia so can become cancerous) and increased mucous secretion (volume and viscosity)
features of smokers goblet cell (similar to COPD)
numbers at least doubles, secretions increase and are more viscoelastic - traps microorganisms, enhancing infection risk
features of smokers ciliated cells
severely depleted, beat asynchronously, found in bronchioles and smaller airways, unable to transport thickened mucous - obstruction of airways and bronchitis and enhanced infection risk
effect of COPD on alveolar walls holding airway open
not intact; copious secretions disrupt alveolar walls and more secretions cause blockages in small airways
why does fibrosis occur in epithelial alveolar cells and what does it lead to
attempt to repair tissue of destroyed alveoli in small, bronchiolar airway, so no chance of repair; many inflammatory cells also present - emphysema
stenotic bronchiolar airway in COPD-affected epithelial cells and what does it lead to
no gas exchange happens distally to stenotic region as gas can’t get through - small airway disease
effect of COPD on structure and blockages of airways
decreased elasticity of supporting structure, plugging, inflammatory narrowing and obliteration of small airways, destruction of peribronchiolar support
what is the effect of smoking in susceptible subjects’ alveoli
emphysema - holes in alveoli, causing reduction in number of useful alveoli
alveolar fibrosis: how does it arise (type I and II pneumocytes)
type 2 divide to repair, don’t differentiate into type 1, so gas exchange severely affected, increased fibroblasts and collagen deposition
effect of increased fibroblasts and collagen deposition on alveolar epithelial-endothelial barrier
normally very thin (<1um) type 1 cell wall for efficient gas exchange; now thicker so less efficient
role of stromal cell (fibroblast) in lung repair and fibrosis
epithelia try to repair and divide; abnormal type 1 cell death and remains as type 2 cells
instead of undergoing apoptosis, what can type II pneumocytes become
myofibroblasts, worsening problem as deposit more collagen and contribute to fibrosis
effect of cigarette smoke
block repair, transdifferentiation and proliferation - cell death
in smokers, are macrophages or neutrophils more abundant and why
more neutrophils (both increase but neutrophils much bigger increase as lots of bacteria in airways as not being cleared)
effect of more oxidants from neutrophils and macrophages
generate highly reactive peroxides, interact with proteins and lipids, fragment connective tissue
effect of more chemoattractants and cytokines from neutrophils and macrophages
attract more inflammatory cells during infection
3 diseases causing loss of airway control and what are they characterised by
asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF) - characterised by airway inflammation leading to obstruction due to airway remodelling
airway remodelling
hypertrophy of submucosal glands, airway smooth musce and goblet cells occur - mucous plugs form, remodelling airways
pathophysiology of asthma
airway epithelia become fragile → sensory nerves exposed → increased airway responsiveness to stimuli → stimulation of sensory nerves → activate cholinergic reflex → bronchoconstriction and mucous secretion, with an influx of inflammatory cells producing mediators
