- throughout lungs (20% epithelium) but more in large than small airways - make and secrete mucus - number doubles in smokers, secretions increase and are more viscoelastic --> harbour microorganisms so increase chance of infection (bronchitis)

Cell Biology Flashcards by Salma Khan

How does alveolar positioning maximise airway SA?

fold round onto the large airways to give economy of space

How well did you know this?

Not at all

Perfectly

At which generation do the alveolar sacs end ?

generation 23

the cross sectional area of the lung increases peripherally

How well did you know this?

Not at all

Perfectly

At which generation are the terminal bronchioles located?

5-16

How well did you know this?

Not at all

Perfectly

What comprises the lung lining liquid?

surfactant - phospholipid rich substance to prevent lung collapse and stick together
secretions - lung defense

How well did you know this?

Not at all

Perfectly

Why do lungs collapse in premature birth?

type 2 cells that make surfactant do not appear till late in gestation (after 24wks)

How well did you know this?

Not at all

Perfectly

What 3 things does COPD consist of?

emphysema
bronchitis
small airways disease

advanced COPD - large holes, loss of elasticity

How well did you know this?

Not at all

Perfectly

Function of epithelium?

continuous barrier
secretions to aid mucociliary clearance of debris, pathogens, protection, maintain reduced surface tension
metabolise foreign and host derived compounds
release mediators
repair/regeneration

How well did you know this?

Not at all

Perfectly

Pathology of COPD?

increase goblet cell numbers (hyperplasia) can become cancerous
increased mucus secretion
fewer cilia

cannot clear mucous efficiently

How well did you know this?

Not at all

Perfectly

Goblet cells?

throughout lungs (20% epithelium) but more in large than small airways
make and secrete mucus
number doubles in smokers, secretions increase and are more viscoelastic –> harbour microorganisms so increase chance of infection (bronchitis)

How well did you know this?

Not at all

Perfectly

Cilia?

60-80% of epithelium
in smokers:
- severely depleted
- asynchronous beat 
- found in bronchioles (further down airways) where they block smaller airways 
- cannot transport thicker mucus
- infection (bronchitis) and obstruction

How well did you know this?

Not at all

Perfectly

What holds an intact airway open?

What happens in COPD?

intact alveolar wall with elastic tissue

broken alveolar attachments so inspiration will not inflate alveoli
abnormal epithelium, excess mucus, hypertrophy of submucosal glands
fibrosis in attempt to repair tissue but irreversible damage
inflammatory cells accumulate

How well did you know this?

Not at all

Perfectly

How does increased small airways disease influence lung function?

exacerbates it

How well did you know this?

Not at all

Perfectly

What classifies small airways?

less than 2mm and no cartilaginous material

How well did you know this?

Not at all

Perfectly

What enriches terminal respiratory bronchioles?

club cell - non ciliated secretory bronchiolar epithelial cell

in small airways
secretory granules
xenobiotic metabolism (break down enzymes and organisms) (detoxification)
secretory
repair cells

How well did you know this?

Not at all

Perfectly

Cilia in smaller airways?

shorter

How well did you know this?

Not at all

Perfectly

What influences COPD onset?

genetics and environment (smoking)

What 2 cells make up alveolar surface?

Type II epithelial cell
Type I cell (95% of surface)
ratio 1:2

Function of Type I cell?

thin, stretched out so covers more of surface (95%)
facilitate gas exchange and solute transport across alveolar epithelium
strong

Function of Type II cell?

small secretory cuboidal cell that makes surfactant to prevent alveolar collapse on expiration
contain lamellar bosies that store surfactant before release onto air-liquid interface
cells in corners of alveoli, embedded in interstitium
repair/progenitor cells for T1 also (stem cells)
detoxification

Are there ciliated cells in alveoli?

macrophages compensate by engulfing pathogens/particles and migrating via mucociliary escalator / lymphatics

What are stromal cells (myofibroblasts)?

make ECM that cells sit on
collage and elastin to give elasticity and compliance
divide to repair

What is wrong with overdrive of stromal cell proliferation?

lead to interstitial fibrosis

lungs solid
cannot breathe any more

Histopathology of emphysema?

alpha 1 antitrypsin deficiency WITH smoking are more prone to emphysema because A1A made in liver inhibits neutrophil elastase made by neutrophils –> deficiency destroys functioning of lung
fibroblasts attempt to repair but lead to fibrotic rigid regions

What drives gas exchange in alveoli?

short diffusion distance

under 1 micrometre thick

What happens to repair in alveolar fibrosis?

- type II cells dont differentiate to type I cells - gas exchange severely affected - fibroblasts proliferate to myofibroblasts which cause Type II cells to release factors that stimulate fibroblast proliferation to create ECM and to prevent Type II cells from converting to Type I

Role of stromal cell (fibroblasts) in lung repair and fibrosis?

1. epithelial cells try to repair and differentiate to Type I cells 2. abnormal repair - due to elevated growth factors Type I cell death, Type 2 cells not converted and proliferated --> reduced gas exchange 3.fibroblasts proliferate to give lots of connective tissue

What can Type II cells do?

become myofibroblasts or Type I cells or apoptose if become myofibroblast (undesirable)

What do cigarettes do ?

Increased apoptosis/necrosis of epithelium | Block repair processes - no myofibroblasts formed, no transdifferentiation to Type I

What are functions of secretory epithelial cells?

- secrete protective layer to trap debris/pathogens (surfactant, mucus) - make antioxidants (glutathione, superoxide dismutase) - synthesis and secrete antiproteinases (SLPI - superior leukoproteinase inhibitor (SLP1) - release lysozyme - carry out xenobiotic mechanism to detoxify foreign compounds such as carcinogens - contain cytochrome P450

What happens after cigarette smoke exposure?

- increased number of inflammatory cells in lung (macrophages and neutrophils) up to 10 fold ``` FUNCTION phagocytosis antimicrobial defence make antioxidants xenobiotic metabolism ```

What if more neutrophils than macrophages?

if lung infection has reached alveoli ``` mainly macrophages (90%) neutrophils up to 10% but can be up to 30% (smoker with infection) ``` 70: 30 macrophage to neutrophil ratio in non smokers and reverse in COPD - lots of neutrophils as bacteria not being removed by cilia

What enzymes do neutrophils and macrophages produce?

serine proteinases (neutrophil elastase) and mettalloproteinases (MMP9, Zn/metal at reactive site) - Excess of these and lack of antiproteinase can digest lung and lead to holes - activate other proteinases and inactivate antiproteinase - activate cytokines/chemokines/proinflammatory mediators

What antimicrobial substance do macrophages/neutrophils produce?

oxidants interact with proteins and lipids make highly reactive peroxides inactivate alpha 1 antitrypsin fragment connective tissue

What do macrophages secrete to regulate their function?

secrete mediators (chemoattractants/cytokines like IL8) to attract more inflammatory cells in infection/after toxicant/microbial deposition also make GFs to help repair of tissue

What do club cells, type II cells and macrophages contain?

phase 1 and 2 enzymes needed for xenobiotic metabolism

What happens if too much active carcinogen?

active carcinogen made by Phase 1 enzyme in lung cells --> this in normal metabolism is mate water soluble and excreted by Phase 2 enzymes but if overloaded with carcinogen/inactive enzyme --> no metabolism --> DNA binding, adduct forms, no repair, mutation

What can be seen as high in smokers?

adducts precursor to lung cancer DNA adduct is a segment of DNA bound to a cancer-causing chemical. This process could be the start of a cancerous cell, or carcinogenesis.