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Respiratory system > Lung cell biology > Flashcards

Lung cell biology Flashcards

1
Q

What are the divisions of the airways`

A 
0 Trachea
1 bronchi
4 bronchioles 
14 terminal bronchioles 
15 transitional bronchioles 
16 respiratory bronchioles 
19 alveolar ducts 
23 alveolar sacs
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2
Q

What is epithelium?

A

Forms continous barrer isolating extenral from internal
Produces secretions to protect cells and reduce surface tension
Metabolise foreign and host derived compounds
Release mediators
Trigger lung repair process

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3
Q

Where are goblet cells found?

A

Large, small, airways

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4
Q

What percentage of epithelial cells are goblet cells?

A

In healthy lung 20% of epithelial cells

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5
Q

What is the effect of smoking on goblet cell numbers

A

(at least doubles in smokers, thicker and increased secretions, more viscoelastic)

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6
Q

What is the function of goblet cells?

A

Traps smoke carticles and trap and harour microporganisms isncreaisng chance of infection
Sythesisze and secrete mucus
‘thin’ sol phase overlays cells, thick gel phase at air interface.

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7
Q

What does the mucus in goblet cells contain?

A

Mucin proteins, proteoglycans and gycosaminoglycans,

Give mucus viscoelasticity

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8
Q

What combats microorgsnisms and phagocyte roteases in mucus?

A

albumin and alpha 1-antitrypsin, also called alpha 1-proteinase inhibitor,
Inhibit polymorphonuclear neutrophil proteases

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9
Q

What combats inhaled oxidants?

A

Antioxidants from the blood and synthesised by epithelial cells and phagocytes – uric acid and ascorbic acid (blood), glutathione (cells)

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10
Q

Where are cilia found

A
  • Large, central, small airwas,
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11
Q

What proportion of epithelial cells is cilia?

A
  • 80% of epithelial cells
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12
Q

How do cilia beat?

A
  • Beat metasynchroulsy
  • Tips of cilia in sol phase of mucus pushes mucus towards epiglottis
  • Expectorated
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13
Q

How does smoking affect cilia?

A
  • Depleted in smokers with bronchitis
  • Asynchrous
  • Found in bronchioles which blocks smaller airways
  • Unable to transort thickeend mucus
  • Reduced musuc clearance
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14
Q

How are smaller airways held open?

A
  • Intact alveolar walls hold airways open
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15
Q

Where are Clara cells found?

A
  • Mosdt conducting and transitional airways

- Increase in proportion distally e.g bronchi and bronchioles

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16
Q

What is the function of Clara cells?

A
  • Xenobiotic metabolism

- Metablism of foreign compounds deposited by inhallation

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17
Q

What are phase I and phase 2 enzymes?

A

Phase 1: cytocrhome P450 oxidases

  • Metabolise foeigh compounds
  • Enables phase 2 enzymes to neutralise toxic aganet
  • May often activate precarcinogen to carcinogen

Phase 2: glutathione S-transferase

  • Enables conjugation of BPDE to small molcule
  • Neutralises it’s activtiy
  • Some don’t have it
  • If also smoker may increase
18
Q

What else do phase 1 and phase 2 enzymes secrete?

A
  • Lots of proteases
  • Lysosyme
  • Antioxidants
19
Q

What is the normal ratio of Type 1 to Type 2 cells?

A

1:2

Less type 1 in smokers

20
Q

What is the function of type 2 epithelial cells?

A
  • Synthesise and secrete pulmonary surfactant ( immunological functions)
  • Precursor of alveolar epithelial type I cells. Divide and differentiate to replace damaged type I cells.
  • Synthesise and secrete anti-proteases
  • Found in alveoli
  • Carry out xenobiotic metabolism
21
Q

What is the funciton of type 1 epithelial cells?

A

thin but strong to allow gas exchange

(95%) of alveolar surface

22
Q

How are carcinogens made in the lungs?

A
  1. Smoke contains procarcinogens
  2. Club cells, type 2 cells, macrophagesc ontain phase 2 and phase 2 enzymes used in detoxification
  3. Lung cells contain hase 1 enzymes which activste compound
  4. Compound becomes more carcinogenic,
  5. Phase 2 enzymes make them water soluble and they are exreted
  6. If more carcinogens than phase 2 enzymes can deal with you get DNA binding, adduct formtion, no repair and mutation
23
Q

What a proportion of lungs is alveolar macrophages in a normal person and in a smoker ?

A

90% of phagocytic cells

Increase 5-10x in smoker

24
Q

What is the role of alveolar macrophages?

A
  • phagocytose debris and microorganisms.
  • Use cytokines to recruit pro inflammatory cells and molecules
  • proteases to digest unwanted debris, attack organic material
  • oxidants during phagocytosis and on activation to kill infecting organisms etc
  • antioxidants such as glutathione to neutralise oxidative molecules that might be inhaled or generated during infection etc
  • Contain enzymes that metabolise toxicants (xenobiotic metabolism)
25
Q

What is the proportion of polymorphonuclear neutrophils in smokers and on smokers?

A
  • 5% of lower respiratory tract phagocytes
  • Increase 5-10x proportion in msokers

Macrophage: neutrophil ratio

70: 30 in non smokers
30: 70 in COPD

26
Q

What is the function of polymorphonuclear neutrophils?

A
  • Secretory
  • Store high levels of proteases
  • Released
  • Also release oxidative molecules (hydroxyl anions) during activation
27
Q

What occurs during COPD?

A
  • Walls of alveoli become distrupted due to secretions
  • Alveoli can’t open
  • Small airways may also become blocked
    Fibrosis occurs in an attemt to repair tissue
    • Airways can’t reverse dmagae
    • Lots of inflammatory cells
  • Stenotic region: not joined to rest of airways due to firbrosis
28
Q

What are resiratory bronchioles enriched with?

A

Secretory club cells

29
Q

What is the funciton of Club cells?

A
  • Contain secretory granules
  • Important in symbiotic metabolism (imortant for enzymes)
  • Deotification
  • Repair/progintor cells
30
Q

What is the effect of smoking on ciliate and club cells?

A

Increased brnchiolar ciliated cells
Club cells lower

Alveolar surface made of 2 types of cells

31
Q

What is the function of stromal cells (myofibroblasts)?

A
  • Make ECM
  • Collagen, elastin, elasticity, compliance
  • Repair
32
Q

What is the histopathology of alveolar fibrosis?

A
  • Increased type 2 (don’T differentiate into type 1)
  • Increased firboblasts
  • Increased collagen deposition
33
Q

What is the histpathology of abnormal repair?

A
  • Type 1 cells proliferation
  • Stromal cell roliferation
  • Connective tissue synthesis
34
Q

What is the function of serin and metalloproteinases?

A
  • Released by airways
  • Substrates: proteinases, connective tissue, elastin, collagen,
  • Activate other roteinases
  • Inactivate antiproteinases
  • Activaste cytokines/chemokines and othe pro inflammatory mediators
35
Q

What is the function of serin and metalloproteinases?

A
  • Generate hioghly reactive peroxides
  • Interact with proteins and lipids
  • Inactivate alpha 1 antitrypsin
  • Grament connective tissue
36
Q

What proportion of COPD affects smokers?

A

15-20%

37
Q

What is chronic bronchitis?

A

large/central airways affected, copious mucus production for three months of the year. Airways obstructed by mucus and thickened mucosal cell layer.

38
Q

What is small airways disease?

A

small airways become blocked/obstructed due to mucus secretion and stenosis/narrowing of airway wall due to fibrosis

39
Q

What is emphysema?

A

destruction of the respiratory tissue (especially the respiratory bronchioles of smokers) by proteolytic enzymes leads to loss of connective tissue scaffold, basement membrane “cement” and normal cell organisation. Loss of surface area and elastic recoil. Loss of vascular tissue. Gas exchange severely compromised. Affects fewer, about 10% of smokers.

40
Q

How do CYPIA1 polymorphism cause carcinogen production?

A
  • high levels of carcinogenic BPDE are generated.
  • insufficiently inactivated by conjugation e.g. with glutathione by glutathione transferase, as happens with the null phenotype i.e. no glutathione transferase,
  • chances of DNA adduct formation with BPDE increases massively – 40-fold increase in chance of a smoker getting lung cancer.

Respiratory system (20 decks)

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