respiratory cell biology

Question 1

5 common lung problems and knock on effects

Answer 1

asthma, smoking, cancer, cough, COPD, knock on effect with atherosclerosis and heart rate variability

Question 2

3 types of COPD

Answer 2

bronchitis, small airways disease, emphysema

Question 3

effect of COPD on human airway epithelium (goblet cells)

Answer 3

increased goblet cell numbers (hyperplasia so can become cancerous) and increased mucous secretion (volume and viscosity)

Question 4

features of smokers goblet cell (similar to COPD)

Answer 4

numbers at least doubles, secretions increase and are more viscoelastic - traps microorganisms, enhancing infection risk

Question 5

features of smokers ciliated cells

Answer 5

severely depleted, beat asynchronously, found in bronchioles and smaller airways, unable to transport thickened mucous - obstruction of airways and bronchitis and enhanced infection risk

Question 6

effect of COPD on alveolar walls holding airway open

Answer 6

not intact; copious secretions disrupt alveolar walls and more secretions cause blockages in small airways

Question 7

why does fibrosis occur in epithelial alveolar cells and what does it lead to

Answer 7

attempt to repair tissue of destroyed alveoli in small, bronchiolar airway, so no chance of repair; many inflammatory cells also present - emphysema

Question 8

stenotic bronchiolar airway in COPD-affected epithelial cells and what does it lead to

Answer 8

no gas exchange happens distally to stenotic region as gas can’t get through - small airway disease

Question 9

effect of COPD on structure and blockages of airways

Answer 9

decreased elasticity of supporting structure, plugging, inflammatory narrowing and obliteration of small airways, destruction of peribronchiolar support

Question 10

what is the effect of smoking in susceptible subjects’ alveoli

Answer 10

emphysema - holes in alveoli, causing reduction in number of useful alveoli

Question 11

alveolar fibrosis: how does it arise (type I and II pneumocytes)

Answer 11

type 2 divide to repair, don’t differentiate into type 1, so gas exchange severely affected, increased fibroblasts and collagen deposition

Question 12

effect of increased fibroblasts and collagen deposition on alveolar epithelial-endothelial barrier

Answer 12

normally very thin (<1um) type 1 cell wall for efficient gas exchange; now thicker so less efficient

Question 13

role of stromal cell (fibroblast) in lung repair and fibrosis

Answer 13

epithelia try to repair and divide; abnormal type 1 cell death and remains as type 2 cells

Question 14

instead of undergoing apoptosis, what can type II pneumocytes become

Answer 14

myofibroblasts, worsening problem as deposit more collagen and contribute to fibrosis

Question 15

effect of cigarette smoke

Answer 15

block repair, transdifferentiation and proliferation - cell death

Question 16

in smokers, are macrophages or neutrophils more abundant and why

Answer 16

more neutrophils (both increase but neutrophils much bigger increase as lots of bacteria in airways as not being cleared)

Question 17

effect of more oxidants from neutrophils and macrophages

Answer 17

generate highly reactive peroxides, interact with proteins and lipids, fragment connective tissue

Question 18

effect of more chemoattractants and cytokines from neutrophils and macrophages

Answer 18

attract more inflammatory cells during infection

Question 19

3 diseases causing loss of airway control and what are they characterised by

Answer 19

asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF) - characterised by airway inflammation leading to obstruction due to airway remodelling

Question 20

airway remodelling

Answer 20

hypertrophy of submucosal glands, airway smooth musce and goblet cells occur - mucous plugs form, remodelling airways

Question 21

pathophysiology of asthma

Answer 21

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