Week 8 RM - Respiratory Mucosa Flashcards

0
Q

What is the structure and function of the mucosa?

A

Composed of ciliated pseudo stratified epithelia. Cilia are attached to the apical surface of the cells and beat within the airway surface liquid to propel mucous along. Also contains goblet cells which secrete mucus.

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1
Q

What are the three layers of airway mucosa?

A

Mucosa, submucosa and adventitia

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2
Q

What is the role of the submucosa?

A

Composed of connective tissue and contains the seromucosal glands which secrete into the lumen.

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3
Q

What is the role of the adventitia?

A

Outermost layer of connective tissue within the airway which in the upper airways contains the cartilage rings/plates, and in lower airways the smooth muscle.

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4
Q

Where is the airway surface liquid located and what does it do?

A

It is located on the surface of respiratory epithelium from the trachea to the respiratory bronchioles. It is a thinner liquid that allows the cilia to stand up and beat the mucus along the airways towards the pharynx.

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5
Q

What is the normal thickness of the ASL layer, and what occurs when it is too thin?

A

Normal thickness is 5-25 micrometers. If too thin, cilia can’t stand up and won’t work. Mucus build up.

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6
Q

What is ASL secreted by?

A

Glands, serous cells and also plasma squeezed out of capillaries.

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7
Q

What are the three methods of clearing inhaled particles?

A

Nasal conchae
Mucociliary escalator
Alveolar macrophages

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8
Q

What is the mucociliary escalator?

A

Transportation of foreign particles from the bronchiole/bronchi/tracheal level of the airways to the pharynx via the work of the cilia

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9
Q

What is the role of alveolar macrophages?

A

They pass into the alveoli from the pulmonary capillaries and phagocytose particles that have made it past the bronchioles. Destroyed particles delivers to the mucociliary escalator or delivered into the lymphatics

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10
Q

Compare ciliary movement in the trachea with the bronchioles?

A

2cm per minute in the trachea, 1mm per minute in the bronchioles. Movement in the trachea is 20x faster

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11
Q

What is the underlying pathology in primary ciliary dyskinesia? What are the effects?

A

Structural defects with the cilia. This causes lack of ciliary function. Stagnant mucus. Recurrent airway infection. Situs inversus (partially or totalis)

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12
Q

What are some things that inhibit alveolar macrophages?

A
Cigarette smoke
Oxidant gases
Alveolar hypoxia
Corticosteroid
Alcohol
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13
Q

What is a major proteolytic enzyme macrophages use to kill bacteria?

A

Trypsin

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14
Q

Why does cigarette smoke cause damage to the lungs via macrophages?

A

It kills macrophages, which in turn spill our their granules of proteolytic enzymes which digest away lung tissue.

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15
Q

What is the definition of a Chronic Obstructive Airway Disease? What are the two common types of COAD?

A

Associated with the narrowing of, or obstruction of the airways.
Chronic Bronchitis and emphysema

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16
Q

What are the three major ways that airways can become obstructed?

A

Constriction of the smooth muscle surrounding airway
Plugin airway with mucus
Inflammation/swelling of airway mucosa

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17
Q

What other conditions can arise that lead to the narrowing of the airways?

A

Hyper trophy of mucus glands

Oedema in airway wall

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18
Q

What conditions cause narrowing of airways that arise outside of the airway?

A

Destruction of lung parenchyma leads to loss of radial traction
Localised compression of the bronchus due to enlarged lymph nodes/neoplasm
Peri bronchial oedema

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19
Q

What is COPD?

A

Ill defined term related to patients with a mixture of chronic bronchitis and emphysema. Narrowing and inflammation of airways leading to respiratory difficulty

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20
Q

What are the characteristics of chronic bronchitis?

A

Excessive mucus production and excessive expectoration of mucous
Very common in smokers and people from smoggy cities

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21
Q

What are the two most important factors in the pathogenesis of chronic bronchitis?

A

Chronic irritation by inhaled substances

Microbiological infection

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22
Q

What changes occur in the airways in chronic bronchitis?

A

The mucosal layer thickens, goblet cells proliferate.
Submucosal layer thickens greatly, hyper trophy of mucous glands
More mucus is secreted in an attempt to protect the airway from irritants and pathogens, which leads to narrowing

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23
Q

What does the Reid index indicate?

A

The ratio of the diameter of airway in comparison to the diameter of mucous glands. Hyper trophy of glands common in CB and will deliver abnormal Reid index score.

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24
Q

What changes occur in respiratory bronchioles in chronic bronchitis?

A

Migration of goblet cells, and production of mucus in small airways where it does not normally occur.

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25
Q

Why does chronic bronchitis have a ‘double threat’ effect on airways?

A

It has two ways which it narrows. Inflammation of the mucosa and submucosa. Increased mucous within airway.

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26
Q

What is a pink puffer and what are the characteristics of this type of patient?

A

Usually typical of emphysema patient. Over distension of lungs. Little cough evident. No peripheral oedema. Normal JVP. Normal concentrations of oxygen and CO2. This patient will have a high respiratory rate

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27
Q

What is a blue blaster and what are the characteristics of this patient?

A

Typical of chronic bronchitis. History of recurrent infections. Frequent cough, sputum. Hypercapnia and cyanosis. Can have peripheral edema

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28
Q

What are some treatment options for CB?

A

Expectoration of sputum to relieve occluded airways
Increased water intake to decreased mucus viscosity
Nebulising bronchodilators
B2 agonists (may not be effective)
Corticosteroids

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29
Q

What is cystic fibrosis?

A

Genetic mutation of the CFTR gene which leads to a lack of function of chloride/sodium transport

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30
Q

What are some pulmonary symptoms of CF?

A

Bronchiectasis: localised irreversible dilation of bronchial tree, chronic purulent sputum expectoration. Airways become floppy and easily occluded
Inflammation of the bronchioles

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31
Q

Where is the CFTR protein found in healthy people?

A

Epithelial cells in many places, lungs, pancreas, airway mucosa

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32
Q

Apart from chloride transport, what other ion does CFTR influence the movement of?

A

Sodium

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33
Q

In the lungs, what affect does CFTR have on ENaCs?

A

Inhibition of sodium movement into cells

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34
Q

Why do CFTR mutations result in thick, viscous mucous?

A

The absence of functional CFTR leads to decreased inhibition of ENaCs, which cause greater amounts of sodium absorption. This draw water from mucus into cell, following the sodium. This dehydrates the mucus and makes it stickier and more viscous.

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35
Q

Why is the ASL decreased in CF?

A

Water is drawn away from the ASL layer back into the muscosal cells due to the increased sodium absorption

How well did you know this?
1
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3
4
5
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36
Q

What is the major differences in classes 1-3 and 4-6?

A

Classes 4-6 have some form of functional CFTR, whereas the other classes it is either completely non functioning or missing entirely

37
Q

Why is infection and inflammation common in CF?

A

Incompetent mucociliary escalator function. Mucus builds up and infections cause inflammation of the airways. Mucus build up obstructs airways. Hypertrophic of mucus glands results from the recurrent infections.

38
Q

Clinical symptoms of CF?

A

Four crackles and Rhonchi in breath sounds
Consolidation, fibrosis and cystic changes
High concentration of sodium and chloride in sweat
High levels of immunoreactive trypsinogen

39
Q

What are the principle organ affected in CF?

A

Lungs and pancreas

40
Q

What affect does CF have on the pancreas?

A

Impedes the delivery of digestive enzymes to the small intestines which means that often CF patients will be less able to absorb nutrients and fats from food, and will be underweight and undernourished.

41
Q

What effect does a decreased elastic recoil in CF patients have?

A

Makes exhalation active/forced.

42
Q

What is FEV1?

A

Function expiration volume in one second. It is essentially the patient trying to blow out as much air as they can in a one second timeframe. It will be reduced in CF patients as they can have bronchioles collapsing following expiration

43
Q

What is the most major factor in the clinical course of CF?

A

The class of mutation to which the patient falls in. Variable onset of clinical symptoms generally correlates with the level of functioning CFTR.

44
Q

What is the largest cause of death for CF patients?

A

Recurrent pulmonary infections - 80-90% of all deaths

45
Q

What are the three layers of airway mucosa?

A

Mucosa, submucosa and adventitia

46
Q

What is the structure and function of the mucosa?

A

Composed of ciliated pseudo stratified epithelia. Cilia are attached to the apical surface of the cells and beat within the airway surface liquid to propel mucous along. Also contains goblet cells which secrete mucus.

47
Q

What is the role of the submucosa?

A

Composed of connective tissue and contains the seromucosal glands which secrete into the lumen.

48
Q

What is the role of the adventitia?

A

Outermost layer of connective tissue within the airway which in the upper airways contains the cartilage rings/plates, and in lower airways the smooth muscle.

49
Q

Where is the airway surface liquid located and what does it do?

A

It is located on the surface of respiratory epithelium from the trachea to the respiratory bronchioles. It is a thinner liquid that allows the cilia to stand up and beat the mucus along the airways towards the pharynx.

50
Q

What is the normal thickness of the ASL layer, and what occurs when it is too thin?

A

Normal thickness is 5-25 micrometers. If too thin, cilia can’t stand up and won’t work. Mucus build up.

51
Q

What is ASL secreted by?

A

Glands, serous cells and also plasma squeezed out of capillaries.

52
Q

What are the three methods of clearing inhaled particles?

A

Nasal conchae
Mucociliary escalator
Alveolar macrophages

53
Q

What is the mucociliary escalator?

A

Transportation of foreign particles from the bronchiole/bronchi/tracheal level of the airways to the pharynx via the work of the cilia

54
Q

What is the role of alveolar macrophages?

A

They pass into the alveoli from the pulmonary capillaries and phagocytose particles that have made it past the bronchioles. Destroyed particles delivers to the mucociliary escalator or delivered into the lymphatics

55
Q

Compare ciliary movement in the trachea with the bronchioles?

A

2cm per minute in the trachea, 1mm per minute in the bronchioles. Movement in the trachea is 20x faster

56
Q

What is the underlying pathology in primary ciliary dyskinesia? What are the effects?

A

Structural defects with the cilia. This causes lack of ciliary function. Stagnant mucus. Recurrent airway infection. Situs inversus (partially or totalis)

57
Q

What are some things that inhibit alveolar macrophages?

A
Cigarette smoke
Oxidant gases
Alveolar hypoxia
Corticosteroid
Alcohol
58
Q

What is a major proteolytic enzyme macrophages use to kill bacteria?

A

Trypsin

59
Q

Why does cigarette smoke cause damage to the lungs via macrophages?

A

It kills macrophages, which in turn spill our their granules of proteolytic enzymes which digest away lung tissue.

60
Q

What is the definition of a Chronic Obstructive Airway Disease? What are the two common types of COAD?

A

Associated with the narrowing of, or obstruction of the airways.
Chronic Bronchitis and emphysema

61
Q

What are the three major ways that airways can become obstructed?

A

Constriction of the smooth muscle surrounding airway
Plugin airway with mucus
Inflammation/swelling of airway mucosa

62
Q

What other conditions can arise that lead to the narrowing of the airways?

A

Hyper trophy of mucus glands

Oedema in airway wall

63
Q

What conditions cause narrowing of airways that arise outside of the airway?

A

Destruction of lung parenchyma leads to loss of radial traction
Localised compression of the bronchus due to enlarged lymph nodes/neoplasm
Peri bronchial oedema

64
Q

What is COPD?

A

Ill defined term related to patients with a mixture of chronic bronchitis and emphysema. Narrowing and inflammation of airways leading to respiratory difficulty

65
Q

What are the characteristics of chronic bronchitis?

A

Excessive mucus production and excessive expectoration of mucous
Very common in smokers and people from smoggy cities

66
Q

What are the two most important factors in the pathogenesis of chronic bronchitis?

A

Chronic irritation by inhaled substances

Microbiological infection

67
Q

What changes occur in the airways in chronic bronchitis?

A

The mucosal layer thickens, goblet cells proliferate.
Submucosal layer thickens greatly, hyper trophy of mucous glands
More mucus is secreted in an attempt to protect the airway from irritants and pathogens, which leads to narrowing

68
Q

What does the Reid index indicate?

A

The ratio of the diameter of airway in comparison to the diameter of mucous glands. Hyper trophy of glands common in CB and will deliver abnormal Reid index score.

69
Q

What changes occur in respiratory bronchioles in chronic bronchitis?

A

Migration of goblet cells, and production of mucus in small airways where it does not normally occur.

70
Q

Why does chronic bronchitis have a ‘double threat’ effect on airways?

A

It has two ways which it narrows. Inflammation of the mucosa and submucosa. Increased mucous within airway.

71
Q

What is a pink puffer and what are the characteristics of this type of patient?

A

Usually typical of emphysema patient. Over distension of lungs. Little cough evident. No peripheral oedema. Normal JVP. Normal concentrations of oxygen and CO2. This patient will have a high respiratory rate

72
Q

What is a blue blaster and what are the characteristics of this patient?

A

Typical of chronic bronchitis. History of recurrent infections. Frequent cough, sputum. Hypercapnia and cyanosis. Can have peripheral edema

73
Q

What are some treatment options for CB?

A

Expectoration of sputum to relieve occluded airways
Increased water intake to decreased mucus viscosity
Nebulising bronchodilators
B2 agonists (may not be effective)
Corticosteroids

74
Q

What is cystic fibrosis?

A

Genetic mutation of the CFTR gene which leads to a lack of function of chloride/sodium transport

75
Q

What are some pulmonary symptoms of CF?

A

Bronchiectasis: localised irreversible dilation of bronchial tree, chronic purulent sputum expectoration. Airways become floppy and easily occluded
Inflammation of the bronchioles

76
Q

Where is the CFTR protein found in healthy people?

A

Epithelial cells in many places, lungs, pancreas, airway mucosa

77
Q

Apart from chloride transport, what other ion does CFTR influence the movement of?

A

Sodium

78
Q

In the lungs, what affect does CFTR have on ENaCs?

A

Inhibition of sodium movement into cells

79
Q

Why do CFTR mutations result in thick, viscous mucous?

A

The absence of functional CFTR leads to decreased inhibition of ENaCs, which cause greater amounts of sodium absorption. This draw water from mucus into cell, following the sodium. This dehydrates the mucus and makes it stickier and more viscous.

80
Q

Why is the ASL decreased in CF?

A

Water is drawn away from the ASL layer back into the muscosal cells due to the increased sodium absorption

81
Q

What is the major differences in classes 1-3 and 4-6?

A

Classes 4-6 have some form of functional CFTR, whereas the other classes it is either completely non functioning or missing entirely

82
Q

Why is infection and inflammation common in CF?

A

Incompetent mucociliary escalator function. Mucus builds up and infections cause inflammation of the airways. Mucus build up obstructs airways. Hypertrophic of mucus glands results from the recurrent infections.

83
Q

Clinical symptoms of CF?

A

Four crackles and Rhonchi in breath sounds
Consolidation, fibrosis and cystic changes
High concentration of sodium and chloride in sweat
High levels of immunoreactive trypsinogen

84
Q

What are the principle organ affected in CF?

A

Lungs and pancreas

85
Q

What affect does CF have on the pancreas?

A

Impedes the delivery of digestive enzymes to the small intestines which means that often CF patients will be less able to absorb nutrients and fats from food, and will be underweight and undernourished.

86
Q

What effect does a decreased elastic recoil in CF patients have?

A

Makes exhalation active/forced.

87
Q

What is FEV1?

A

Function expiration volume in one second. It is essentially the patient trying to blow out as much air as they can in a one second timeframe. It will be reduced in CF patients as they can have bronchioles collapsing following expiration

88
Q

What is the most major factor in the clinical course of CF?

A

The class of mutation to which the patient falls in. Variable onset of clinical symptoms generally correlates with the level of functioning CFTR.

89
Q

What is the largest cause of death for CF patients?

A

Recurrent pulmonary infections - 80-90% of all deaths