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Respiratory > 7. Lung cell biology > Flashcards

7. Lung cell biology Flashcards

1
Q

How does the cross sectional area of the lung increase?

A

Increases peripherally

Largest SA accounted for by respiratory bronchioles and alveoli

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2
Q

What stops the lungs from collapse?

A

Surfactant

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3
Q

How many generations of gas exchange units are there?

A

23

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4
Q

What % of epithelial cells are goblet cells?

A

20%

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5
Q

Which 3 diseases characterise COPD?

A

Bronchitis
Small airways disease
Emphysema

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6
Q

Describe chronic bronchitis

A

Large/central airways affected

Copious mucus production for 3 months of the year. Airways obstructed by mucus and thickened mucosal cell layer.

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7
Q

Describe small airways disease

A

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

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8
Q

Describe 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 SA and elastic recoil.
Loss of vascular tissue.
Gas exchange severely compromised

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9
Q

5 functions of epithelium in the airways

A

Barrier: isolates external environment from host
Produces secretions to facilitate clearance, via mucociliary escalator and protect underlying cells as well as maintain reduced surface tension (alveolae)
Metabolises foreign and host-derived compounds
Releases mediators

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10
Q

How do goblet cells and mucus change in smokers?

A

Goblet cells INCREASE in number (hyperplasia)
Secretions INCREASE in quantity
Secretions are THICKER (more viscoelastic)-traps cigarette smoke particles and harbours microorganisms, enhancing chances of infection

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11
Q

What does mucus contain?

A

Mucin proteins, proteoglycans, GAGs: give viscoelasticity
Serum derived proteins e.g. albumin + alpha-1 antitrypsin + alpha-1 proteinase inhibitor: combat microorganisms
Antiproteases secreted by the epithelia: combat microorganisms
Anti-oxidants from blood: combats inhaled oxidants

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12
Q

What % of epithelial cells are ciliated cells?

A

60-80%

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13
Q

How do ciliated cells change in smokers?

A

Ciliated cell are severely depleted
Beat asynchronously
Ciliated cells found in bronchioles (start moving down airways, blocking smaller airways)
Unable to transport thickened mucus: leads to infection and bronchitis, airways obstructed

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14
Q

Describe intact small airways

A

Alveoli pull on small airway and keep it open

When you breath in, alveoli stretch (full of elastic tissue)

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15
Q

Describe small airways in COPD

A

Walls of alveoli become disrupted, don’t pull out and open airway
In combination with higher secretions, leads to blockage of small airways

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16
Q

What is a stenotic airway? (as would be found in a COPD lung)

A

Stenotic region- doesn’t join up completely

No gas exchange distally to stenotic region as air will not get through it

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17
Q

Give 2 characteristics of small airways.

A 
< 2 mm in diameter
NOT cartilaginous (rely on elastic tissue of alveoli to keep them open in inspiration)
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18
Q

What are clara cells?

A

Non-ciliated secretory epithelia found in the large, central and small airways and bronchi and bronchioles

19
Q

What are Clara cells also known as?

A

Club cells

20
Q

How are clara cells distributed throughout the respiratory system?

A

Increase in proportion distally

21
Q

What is the major role of clara cells?

A

Xenobiotic metabolism

metabolism of foreign compounds deposited by inhalation

22
Q

What are the 2 classes of enzymes produced by Clara cells?

A

Phase 1 and Phase 2

23
Q

What do Phase 1 and Phase 2 enzymes do?

A

Metabolise foreign substances but are also implicated in oncogenesis.
Phase 1 enzymes convert procarcinogens to carcinogens
Phase 2 enzymes conjugate the carcinogens to make them inactive

24
Q

What do Clara cells produce other than phase 1 and phase 2 enzymes?

A

Antiproteases

Lyoszyme.

25
Q

What are the epithelial cells on the surface of alveoli?

A

Type I

Type II

26
Q

Describe type I cells

A 
Very thin (<1um)
Facilitate gas exchange and solute transport
Covers 95% alveolar surface
27
Q

Describe the role of type II cells

A 
Produce SURFACTANT
Synthesise and secrete antiproteases 
Detoxify alveoli
Make up 5% of alveolar surface 
Precursor for Type I cells (pneumocytes)
28
Q

How are alveoli different in emphysema?

A

They have holes in them
Volume of alveoli increases
SA of the alveoli decrease

29
Q

What is the ratio of Type II to Type I cells?

A

2:1

30
Q

What are alveolar type II epithelial cells also known as?

A

Type II pneumocytes

31
Q

Why are there many macrophages in the alveoli? What do they do?

A

No ciliated cells
Macrophages engulf particles deposited in alveoli, can migrate up into airways and onto mucociliary escalator or through lymphatic system

32
Q

What do stromal fibroblasts do?

A

Make ECM
Deposit collagen and elastin to give elasticity and compliance to the alveolus
Divide to repair

33
Q

Describe alveolar fibrosis

A

Gas exchange severely effected
Fibroblasts proliferate and myofibroblasts form
Communicate to Type II cells, which release factors that further stimulate proliferation of fibroblasts
Fibroblasts stimulate Type II cells to remain as Type II cells and not differentiate

34
Q

Describe normal and abnormal repair.

A

Normal repair:
Type I pneumocyte death leads to a release of growth factors that stimulate proliferation and differentiation of type II pneumocytes into Type I
Abnormal repair:
Excess tissue damage leads to more type I pneumocyte death, leads to excess release of growth factors, leads to excessive release of collagen, resulting in irreversible damage/fibrosis

35
Q

What can Type II cells differentiate into?

A

Type I cells

Myofibroblasts

36
Q

Describe the effect of smoking on the proliferation and differentiation of alveolar epithelial cells.

A

Smoking BLOCKS proliferation and differentiation of type II cells into type I cells (transdifferentiation)
Stimulates apoptosis and necrosis of type I and type II cells.
Smoking also blocks communication between type II cells and fibroblasts, thus inhibiting normal repair process.

37
Q

Alveolar macrophages
%
6 Functions

A

Macrophages make up 90% of ALL phagocytes in the lung
Phagocytose cell debris and microorganisms
Recruit other inflammatory cells during infection
Synthesise and secrete proteases
Generate oxidants (in phagocytosis)
Generate anti-oxidants
Contain enzymes that metabolise toxicants

38
Q

Neutrophils in the airways

A

~10% of lung phagocytes
Store high levels of potent proteases in granules, released on activation
Release potent oxidative molecules when activated

39
Q

Macrophage: neutrophil ratio in non smokers and those with COPD

A

Non smokers= 70% : 30%

COPD= 30% : 70%

40
Q

How do numbers of macrophages and neutrophils change in smokers and during infection?

A

Proportions switch over. Numbers of macrophages and neutrophils increases but ratio becomes:
Macrophages: Neutrophils = 30:70
Proportions switch over in the CONDUCTING/LARGE AIRWAYS (not smaller airways). Smaller airways are still dominated by macrophages.
Bronchial lavage will give an indication of the distribution of phagocytes in the larger airways.

41
Q

How does smoking effect number of neutrophils and macrophages?

A

Neutrophils: increase 5-10 fold
Macrophages: increase 5-10 fold

42
Q

What do phagocytes produce that increase alveolar inflammation?

A

Massive increase in the numbers of macrophages and neutrophils and there is an increase in the amount of proteases produced by them.
Secrete serine proteases (e.g. neutrophil elastase) and matrix metalloproteinases, which overwhelm the neutralising capacity of the anti-proteases and causes damage to the alveolar epithelium resulting in inflammation.

43
Q

Describe the normal metabolism of procarcinogens and how this changes in smokers.

A

Normally, phase I enzymes convert the procarcinogen to a carcinogen and the phase II enzymes conjugate it so it becomes water soluble and can be excreted
Smoking can overload the safe removal pathway so the carcinogen may bind to DNA and cause mutations.

Respiratory (21 decks)

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