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Respiratory System > Structure and function of the airways > Flashcards

Structure and function of the airways Flashcards

1
Q

What is a major risk factor for COPD

A

Smoking

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2
Q

Describe cartillage

A

C-Shaped- offset in places- more densely packed in some areas along the trachea to give a greater tensile strength

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3
Q

Where is cartilage not found

A

Bronchioles or alveoli

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4
Q

Describe the basic functions and anatomy of the lung

A

 The branching of the lungs is dichotomous branching.

 The c-rings of the bronchi and trachea are slightly offset from each other to give greater tensile strength.

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5
Q

Describe the basic functions of the airways

A

Conduit (‘pipes’) to:
conduct O2 to the alveoli
conduct CO2 out of the lung
- gas exchange

Facilitated by:
mechanical stability (cartilage)
control of calibre (smooth muscle)
protection and ‘cleansing’

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6
Q

What is meant by calibre

A

how much the airways are contracted

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7
Q

Describe the basic organisation of the airways

A

Cartilage: c-shaped and offset
Smooth muscle: to control calibre
Submucosal gland: tip embedded in smooth muscle, potentially to cause secretion upon contraction
Systemic circulation: tracheal/bronchial circulation
Basement membrane: separates muscle, vessels and glands from endothelium
Airway epithelium: mainly ciliated with few goblet cells
Mucous: small amount in healthy people (10ml) to trap pathogens - wafted towards back of throat
See diagram!

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8
Q

Describe where mucous is wafted to

A

Wafted towards back of throat- in mucocillliray transport

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9
Q

Outline the organisation of the airways

A

 The c-rings aren’t complete as the are offset (at an angle).
 Below cartilage is a layer of smooth muscle cells with submucosal glands embedded into (when smooth muscle contracts, it squeezes the mucosal glands).
 ~10mL mucous produced per day.
 Goblet cells AND submucosal glands produce mucin.
 Cilia beat METASYNCHRONOUSLY.

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10
Q

Describe the structure of the airway wall

A

Epitehlial lining
Cilia
mucous layer on top of wall

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11
Q

Describe lining cells

A

Ciliated, intermediate, brush, basal

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12
Q

Describe contractile cells

A

Smooth muscle (airway, vasculature)

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13
Q

Describe secretory cells

A

Goblet (epithelium), mucous, serous (glands)

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14
Q

Describe connective tissue

A

Fibroblast, interstitial cell

(elastin, collagen, cartilage)

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15
Q

Describe neuroendocrine

A

Nerves, ganglia, neuroendocrine cells,

neuroepithelial bodies

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16
Q

Describe vascular cells

A

Endothelial, pericyte, plasma cell

(+ smooth muscle)

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17
Q

Describe immune cells

A

Mast cell, dendritic cell, lymphocyte,

eosinophil, macrophage, neutrophil

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18
Q

What is present inside goblet cells

A

Mucin granules- which contain mucin in a hightail condensed form

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19
Q

What is meant by acinus

A

Part of the airway that is involved in gaseous exchange (passage of oxygen from the lungs to the blood and carbon dioxide from the blood to the lungs).
It begins with respiratory bronchioles and subsequent divisions of the airway and alveoli.

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20
Q

Describe the airway submucosal glands ion the human bronchial gland

A 
Mucous cells secrete mucus
  Serous cells secrete antibacterials
       (e.g. lysozyme)
  Glands also secrete water and salts
       (e.g. Na+ and Cl-)
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21
Q

Describe the arrangement of the submucosal glands

A

The arrangement of the human submucosal glands means that with serous cells on the outside, the watery substance that they secrete mixes with the innermost mucous and washes it into a collecting duct.
so the watery serous acini wash more viscous mucus to collecting duct upon contraction

Reducing the viscosity of the mucous is essential in allowing it to move across the cilia

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22
Q

Describe ciliary structure

A

9 pairs of microtubules around the outside- joined by next links
joined to central pari by radial spokes
all surrounded by a cell membrane
each pair of the peripheral microtubules has an outer and inner arm (dynein)

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23
Q

Summarise ciliary structure

A

 Cilia beat in a METACHRONAL rhythm (like a wave).
 The cilia waft the mucous up the respiratory tract using their apical hooks.
 Each individual cilia displays a ‘9+2’ relationship with 9 filaments around 2 central filaments.
o The rods then slide over each other to simulate movement.
 ~200 cilia per cell.
 In COPD patients, you would see a continuous sheet of mucous on the airway but normally, it’s flaked under microscope.

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24
Q

Describe ciliary beating

A

leading edge of mucous moved by cilia, before they move back to move next field of mucous - synchronised rhythm of beating to move mucous - metasychronal rhythm

25
Q

What are the functions of the airway epithelium

A

Secretion of mucins, water and electrolytes
components of ‘mucus’ (+ plasma, mediators etc)
Movement of mucus by cilia – mucociliary clearance
Physical barrier
Production of regulatory and inflammatory mediators:
NO (by nitric oxide synthase, NOS)
CO (by hemeoxygenase, HO)
Arachidonic acid metabolites, e.g. prostaglandins (COX)
Chemokines, e.g. interleukin (IL)-8
Cytokines, e.g. GM-CSF
Proteases

26
Q

What may play a role in ciliary beating

A

NO- abundant in epithelia

27
Q

What may CO be designed for

A

to kill bacteria

28
Q

How do we visualise smooth muscle

A

actin fluorescence

29
Q

What are the functions of airway smooth muscle cells

A

Regulates:
 Tone- airways calibre (contraction and relaxation)
 Secretion – Up-regulated a lot by inflammation. (Mediators
Cytokines
Chemokines)
 Structure- hypertrophy and proliferation
With respiratory disease, more inflammation and smooth muscle hypertrophy/proliferation which increases contractile forces of smooth muscle meaning more secretions are made.

30
Q

What is seen in asthma

A

plasma exudation

31
Q

Describe the secretory function of smooth muscle in inflammation

A

Bacterial products and cytokines released from inflammation
undergoes hypertrophy and proliferation - may not contract harder but massive increase in secretion to produce mediators, cytokines and chemokines (recruit inflammatory cells); upregulate NOS and COX enzymes to produce NO and prostaglandins;

32
Q

How do humans differ from animals

A

Humans have sensory nerves to open airways compared to the sympathetics of animals
NO producing pathway- vasorelaxtion- dilating the airways
Hormonal pathway from adrenaline too
One cell- produces a whole range of different mediators with a variety of effects, chemotaxis and neuronal modulation
histamine relaxes SM

33
Q

Outline the trachea-bronchial circulation

A

1-5% of cardiac output
Blood flow to airway mucosa = 100-150 ml/min/100g tissue
(amongst the highest to any tissue)
Bronchial arteries arise from many sites on:
aorta, intercostal arteries and others
Blood returns from tracheal circulation via systemic veins
Blood returns from bronchial circulation to both sides of
heart via bronchial and pulmonary veins

34
Q

How well perfused is the airway mucosa

A

 Blood flow to the airway mucosa = 100-150mL/min/100gTissue – The HIGHEST to any tissue.
o I.E. It’s VERY WELL perfused with blood.

35
Q

Describe the subepithelial microvascular network

A

plexuses of arteries, capillaries and veins supply airways

36
Q

What are the functions of the trachea-bronchial circulation

A

Good gas exchange (airway tissues and blood)
Contributes to warming of inspired air
Contributes to humidification of inspired air
Clears inflammatory mediators
Clears inhaled drugs (good/bad, depending on drug)
Supplies airway tissue and lumen with inflammatory
cells
Supplies airway tissue and lumen with proteinaceous
plasma

37
Q

What are airways distal to the terminal bronchiole supplied by

A

Alveolar wall capillaries only
For this reason, a pulmonary embolus may result in infarction of the tissues supplied by the alveolar wall capillaries, shown as wedge-shaped opacity on the lung periphery of chest X-ray

38
Q

Describe plasma exudation

A

post-capillary venules have gaps that leak plasma gently to bathe tissue; can be stimulated to leak more by inflammatory mediators (e.g. Histamine and platelet activating factors) and C-fibre nerves ( sensory nerve)

39
Q

Describe the mechanism of plasma exudation

A

 When the endothelial cells contract, they pull away from each other and form a gap which plasma leaks from.
 This system can become exaggerated in disease.
 The endothelial cells are served by (pseudo) sensory nerves (they also have MOTOR function).
 In asthma for example, histamines and platelet activating factor (PAF) are produced which trigger the sensory nerves thus exaggerating the plasma exudation.

40
Q

How does Evans blue dye appear with PAF

A

Evans blue dye
autofluoresence
(orange colour)- leaves with plasma exudate

41
Q

Summarise the controls of airway function

A 
Nerves:
       parasympathetic (cholinergic)
       (sympathetic – adrenergic?)
       sensory
  Regulatory and inflammatory mediators:
        histamine
        arachidonic acid metabolites
             (e.g. prostaglandins, leukotrienes)
        cytokines
        chemokines
  Proteinases (e.g. neutrophil elastase)
  Reactive gas species (e.g. O2-, NO)
42
Q

Describe innervation of the airways

A

sensory vagus via nodose ganglion to brain stem
constriction- Parasympathetic
(cholinergic)
‘Motor’ pathway passes from brain stem (vagus)
NOT SNS nerves to open airways, instead nitric oxide producing pathway (due to vasorelaxant properties) to dilate airways; adrenal glands can produce adrenaline to induce relaxation

43
Q

Summarise the cholinergic mechanisms

A

Irritants activate sensory nerves (via Vagus and nodose ganglion to CNS)
Central cholinergic reflex down Vagus PSNS nerve to PSNS ganglion
Postganglionic neurones lead to muscarinic receptors that:
Cause vasodilation
Cause airway constriction
Cause submucosal glands to secrete mucous

44
Q

Describe the roles of the vagus nerve in airway function

A

 Cholinergic Nerves are the most important pathways.
o The cholinergic reflex can trigger bronchoconstriction if an allergen is detected (e.g. peanut).
 MOST animals have PNS pathways causing constriction and SNS causing relaxation but humans DON’T.
o CONSTRICTION via PNS nerves (the cholinergic reflex).
o DILATION via adrenaline from adrenal gland AND NO in nervous pathway – work together.
Note that the contraction and secretion is under the cholinergic reflex control (reacts in response to ACh

45
Q

List some regulatory inflammatory cells in the airways

A 
Eosinophils
Neutrophils
Macrophages
Mast cells
T lymphocyte 
\+ ‘Structural’ cells
(e.g. smooth muscle)
46
Q

List some inflammatory mediators

A 
Histamine
Serotonin
Adenosine
Prostaglandins
Leukotrienes
Thromboxane
PAF
Endothelin
Cytokines
Chemokines
Growth factors
Proteinases
Reactive gas
   species
47
Q

List some effects of these inflammatory mediators

A 
Smooth muscle
   (airway, vascular:
    contraction, relaxation)
Secretion
   (mucins, water, etc)
Plasma exudation
Neural modulation
Chemotaxis
Remodelling
48
Q

What is key to remember about inflammatory mediators

A

Cells produce more than
one mediator
Mediators do more than
one thing

49
Q

List some diseases associated with loss of airway control

A

Asthma, chronic obstructive pulmonary disease (COPD)

and cystic fibrosis (CF)

50
Q

Describe the epidemiology of these conditions

A

Asthma – ~5% of population (industrialised countries)
COPD – 4th cause of death in UK and USA
CF – lethal autosomal recessive gene defect (~1:20 gene
frequency; affects ~1:2000 Caucasians): CFTR

51
Q

What are these diseases caused by

A

These common conditions are characterised by airway inflammation and airway obstruction due to airway remodelling- they are no longer fit for purpose
can also cause airway remodelling

52
Q

Describe asthma

A

A clinical syndrome characterised by increased airway
responsiveness to a variety of stimuli
(→ airways obstruction)
Airflow obstruction varies over short periods of time
and is reversible
(spontaneously or with drugs)
Dyspnoea, wheezing and cough
(varying degrees - mild to severe)
Airway inflammation → re-modelling

53
Q

Describe the histology of asthma pathology: airway inflammation

A 
‘Mucus’ plug
In lumen
Basement
membrane
thickening
Epithelial
‘fragility’
Cellular
infiltration
Vasodilation
(‘congested’
vessels)
Airway wall thrown into folds 
smooth muscle hypertrophy, increased gland size
54
Q

Describe the cellular infiltration in asthma

A

inflammatory cells in submucosa

eosinophil is the primary inflammatory cell

55
Q

What are antigens to asthmatics

A

Cold air, small molecular weight particles, emotions (laughing, crying)- generally inocuous thins

56
Q

Summarise the pathology of asthma

A

 Airway obstruction varies over short periods of time and is reversible (due to adrenaline).
 Characterised by dyspnoea, wheezing and coughing.
 Airway inflammation leads to remodelling.
 EOSINOPHILS are the major player and act fast to form mucous plugs made of eosinophils.
 HISTOLOGY: epithelial fragility, thickening of the basement membrane and prominent blood vessels.
 Mucous plug combined with bronchoconstriction can cause full obstruction of breathing.

57
Q

outline the pathophysiology of asthma

A

Epithelial fragility exposes sensory nerve- making it more sensitive to activation. Activation leads to bronchoconstriction (hypertrophy/hyperplasia of SMC), vasodilation and Mucus
hypersecretion
(Hypertrophy/
Hyperplasia).
Infiltration of inflammatory mediators- vast array of effects such as re-modelling of the airways with hypertrophied submucosal glands and airway smooth muscle and general inflammation
leads to plasma exudation, sub epithelial fibrosis and goblet cell hypertrophy
 PAF causes plasma exudation.
 ATP causes goblet cell exocytosis.
histamine (causes plasma exudation and airway constriction)

58
Q

How do animals and humans differ in airway innervation

A

Both have adrenaline to cause dilation
We have motor nerves containing NO for dilation
Animals have sympathetic innervation (cervical thoracic ganglion)

Respiratory System (23 decks)

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