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Respiratory > Cell Biology > Flashcards

Cell Biology Flashcards

1
Q

How does alveolar positioning maximise airway SA?

A

fold round onto the large airways to give economy of space

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2
Q

At which generation do the alveolar sacs end ?

A

generation 23

the cross sectional area of the lung increases peripherally

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3
Q

At which generation are the terminal bronchioles located?

A

5-16

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4
Q

What comprises the lung lining liquid?

A

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

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5
Q

Why do lungs collapse in premature birth?

A

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

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6
Q

What 3 things does COPD consist of?

A

emphysema
bronchitis
small airways disease

advanced COPD - large holes, loss of elasticity

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7
Q

Function of epithelium?

A
  • 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
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8
Q

Pathology of COPD?

A

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

cannot clear mucous efficiently

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9
Q

Goblet cells?

A
  • 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)
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10
Q

Cilia?

A 
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
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11
Q

What holds an intact airway open?

What happens in COPD?

A

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
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12
Q

How does increased small airways disease influence lung function?

A

exacerbates it

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13
Q

What classifies small airways?

A

less than 2mm and no cartilaginous material

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14
Q

What enriches terminal respiratory bronchioles?

A

club cell - non ciliated secretory bronchiolar epithelial cell

  • in small airways
  • secretory granules
  • xenobiotic metabolism (break down enzymes and organisms) (detoxification)
  • secretory
  • repair cells
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15
Q

Cilia in smaller airways?

A

shorter

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16
Q

What influences COPD onset?

A

genetics and environment (smoking)

17
Q

What 2 cells make up alveolar surface?

A

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

18
Q

Function of Type I cell?

A
  • thin, stretched out so covers more of surface (95%)
  • facilitate gas exchange and solute transport across alveolar epithelium
  • strong
19
Q

Function of Type II cell?

A
  • 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
20
Q

Are there ciliated cells in alveoli?

A

no

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

21
Q

What are stromal cells (myofibroblasts)?

A
  • make ECM that cells sit on
  • collage and elastin to give elasticity and compliance
  • divide to repair
22
Q

What is wrong with overdrive of stromal cell proliferation?

A

lead to interstitial fibrosis

  • lungs solid
  • cannot breathe any more
23
Q

Histopathology of emphysema?

A
  • 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
24
Q

What drives gas exchange in alveoli?

A

short diffusion distance

under 1 micrometre thick

25
Q

What happens to repair in alveolar fibrosis?

A
  • 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
26
Q

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

A
  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
27
Q

What can Type II cells do?

A

become myofibroblasts or Type I cells or apoptose

if become myofibroblast (undesirable)

28
Q

What do cigarettes do ?

A

Increased apoptosis/necrosis of epithelium

Block repair processes - no myofibroblasts formed, no transdifferentiation to Type I

29
Q

What are functions of secretory epithelial cells?

A
  • 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
30
Q

What happens after cigarette smoke exposure?

A
  • increased number of inflammatory cells in lung (macrophages and neutrophils) up to 10 fold
FUNCTION
phagocytosis
antimicrobial defence
make antioxidants
xenobiotic metabolism
31
Q

What if more neutrophils than macrophages?

A

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

32
Q

What enzymes do neutrophils and macrophages produce?

A

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
33
Q

What antimicrobial substance do macrophages/neutrophils produce?

A

oxidants

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

34
Q

What do macrophages secrete to regulate their function?

A

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

35
Q

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

A

phase 1 and 2 enzymes needed for xenobiotic metabolism

36
Q

What happens if too much active carcinogen?

A

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

37
Q

What can be seen as high in smokers?

A

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.

Respiratory (7 decks)

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