lung cell biology

Question 1

common lung problems

Answer 1

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

Question 2

folding round of tubules

Answer 2

surface area massive in small space

Question 3

cross sectional area increases peripherally - 23 generations

Answer 3

diagram from slide 5

Question 4

lung lining liquid

Answer 4

important surface layer of lung - secretions involved in lung defence; phospholipid-rich surfactant stops lung collapsing

Question 5

COPD

Answer 5

bronchitis, small airways disease, emphysema

Question 6

5 functions of epithelium

Answer 6

forms continuous barrier, produces secretions to facilitate clearance and protect undelying cells and maintain surface tension, metabolises foreign and host-derived compounds, releases mediators, triggers lung repair process

Question 7

effect of COPD on human airway epithelium

Answer 7

increased goblet cell numbers (hyperplasia - can become cancerous) and increased mucus secretion

Question 8

goblet cells

Answer 8

more in large, then central, then small airways, 20% of epithelial cells, synthesise and secrete mucus

Question 9

smokers goblet cell

Answer 9

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

Question 10

ciliated cells

Answer 10

more in large, then central, then small airways, 60-80% of epithelial cells, beat metasynchronously

Question 11

smokers ciliated cells

Answer 11

severely depleted, beat asynchronously, found in bronchioles, unable to transport thickened mucus - obstruction of airways and bronchitis

Question 12

intact alveolar walls hold airway open

Answer 12

in COPD, copious secretions disrupts alveolar walls and more secretions causes blockages in small airways

Question 13

why does fibrosis occur

Answer 13

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

Question 14

stenotic bronchiolar airway in COPD

Answer 14

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

Question 15

effect of COPD

Answer 15

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

Question 16

club cells

Answer 16

secretory granules for detoxifying club cells, rich in bronchiolar regions and protect and repair/progenitor cells - 20% small airway epithelia

Question 17

effect of smoking in susceptible subjects’ alveoli

Answer 17

emphysema - holes in alveoli

Question 18

surface of lung

Answer 18

alveolar type 2 (sythesises and secretes surfactant; twice as many as type 1), type 1 (very thin - fascilitates gas exchange and solute transport across alveoli; cover most of surface)

Question 19

what stores surfactant prior to release

Answer 19

lamellar bodies

Question 20

type 2 cells

Answer 20

progenitor cells, precursor of type 1

Question 21

alveoli

Answer 21

type 1, type 2 (like club - do detoxification in alveoli), capillary endothelium, no ciliated cells so many macrophages - phagocytic so engulf particles deposited here - migrate into lymphatics or mucocilliary transport; stroma cells (myo) fibroblasts - make ECM - give elasticity and compliance, divide to repair

Question 22

emphysema

Answer 22

reduced/damaged alveoli

Question 23

alveolar epithelial-endothelial barrier

Answer 23

very thin (<1um) type 1 cell wall for efficient gas exchange

Question 24

alveolar fibrosis

Answer 24

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

Question 25

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

Answer 25

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

Question 26

AT2 can become myofibroblast worsening problem

Answer 26

instead of apoptosis

Question 27

cigarette smoke

Answer 27

block repair, transdifferentiation and proliferation - cell death

Question 28

functions of all secretory cells (goblet, club, type II)

Answer 28

secrete protective lining layer to trap deposited particles –
surfactant and mucus, synthesise and release antioxidants eg glutathione, superoxide dismutase, synthesise and secrete antiproteinases – eg secretory leukoproteinase inhibitor (SLPI), release lysosyme, carry out xenobiotic metabolism (eg process and detoxify
foreign compounds such as carcinogens in cigarette smoke), contain cytochrome P450, phase I & II enzymes etc

Question 29

infection in lung/smokers

Answer 29

more neutrophils present (than macrophages) - phagocytosis, antimicrobial defence, synthesise antioxidants, xenobiotc metabolism

Question 30

neurtophils

Answer 30

in respiratory units, 10%, increase in smokers if infection, in airways of non-smokers, more macrophages, in smokers, more neutrophils (both increase but neutrophils much bigger increase as lots of bacteria in airways as not being cleared)

Question 31

proteinases

Answer 31

serine and merrallo released from neutrophils and macrophages - dissolve lungs if too many; activate each other and cytokines, chemokines and pro-inflammatory mediators

Question 32

oxidants from neutrophils and macrophages

Answer 32

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

Question 33

macrophages secrete mediators

Answer 33

chemoattractants and cytokines - attract more inflammatory cells during infection or after toxicant/microbial depositionl growth factors and proteases trigger growth and repair by other cells

Question 34

club, type II and macrophages

Answer 34

contain phase I and II enzymes; phase I convert procarcinogen to carcinogen in lung, phase II normally make them water soluble and excreted in metabolite, but if pathway overload or inactivated causes DNA binding, adduct formation and no repair so mutation