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Phase 1 Med (Liv) > Respiratory (summary sheets) > Flashcards

Respiratory (summary sheets) Flashcards

1
Q

What are the components of the upper respiratory tract?

A
  • The nose
  • Turbinates/Conchae create
  • Paranasal sinuses
  • Pharynx
  • Larynx
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2
Q

What is the most superior portion of the respiratory tract?

A

The nose

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3
Q

What are the functions of the nose?

A
  • Warms inspired air
  • Humidifies air
  • Filters inspired air of pathogens
  • Defence function
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4
Q

How does the nose filter inspired air of pathogens?

A

Using cilia in the nose which traps particulates

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5
Q

How does the defence function of the nose work?

A

Cilia take inhaled particulates backwards to be swallowed

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6
Q

What do the anterior nares do in relation to the defence function of the nose?

A

Opens into the enlarge vestibule (skin lined and has stiff hairs)

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7
Q

What gives the nose a large surface area?

A

It is doubled by turbinates

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8
Q

What are the 3 turbinates/ conchae create?

A

Superior meatus, middle meatus and inferior meatus

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9
Q

Give 3 features of the superior meatus

A
  • Has olfactory epithelium
  • Olfactory nerve penetrates into superior meatus through pores in the cribriform plate
  • Sphenoid sinus drains into it
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10
Q

Give a feature of the middle meatus

A

Some sinuses drain here

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11
Q

Give a feature of the inferior meatus

A

Nasolacrimal duct drains there

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12
Q

Give 2 features of the paranasal sinuses

A
  • Pneumatised areas (a bone that is hollow or contains many air cells) of the frontal, maxillary, ethmoid and sphenoid bones
  • Arranged in pairs
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13
Q

Give 2 features of the frontal sinuses

A
  • Within the frontal bone

- Lie over the orbit

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14
Q

Where are the maxillary sinuses located?

A

Within the body of the maxilla

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15
Q

Which nerve innervates the frontal sinuses?

A

The ophthalmic division of the trigeminal nerve (CN5)

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16
Q

What shape is the maxillary sinus?

A

Pyramidal

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17
Q

Which nerve innervates the maxillary sinus?

A

The maxillary division of the trigeminal nerve (CN5)

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18
Q

Where does the base of the maxillary sinus lie?

A

The lateral wall of the nose

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19
Q

Where does the apex of the maxillary sinus lie?

A

Zygomatic process of the maxilla

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20
Q

Where does the roof of the maxillary sinus lie?

A

Floor of the orbit

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21
Q

Where does the floor of the maxillary sinus lie?

A

Alveolar process

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22
Q

Where does the maxillary sinus open into?

A

The middle meatus

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23
Q

Where is the ethmoid sinuses?

A

Between the eyes

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24
Q

Which nerve innervates the ethmoid sinuses?

A

The ophthalmic and maxillary branches of the trigeminal nerve (CN5)

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25
Q

Where do the ethmoid sinuses open into?

A

The middle meatus

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26
Q

Where is the sphenoid sinuses?

A

Medial to the cavernous sinus and inferior to optic canal, dura and pituitary gland

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27
Q

Name the artery and the 4 cranial nerves which are in the cavernous sinus

A
  • Internal carotid artery
  • Oculomotor never (CN3)
  • Trochlear nerve (CN4)
  • Trigeminal nerve (CN5)
  • Abducens (CN6)
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28
Q

What is the importance of keeping the cavernous sinus functioning?

A

Contains many important structures, nerves for eye movement and heart blood supply

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29
Q

Where do the sphenoid sinuses empty into?

A

The sphenoethmoidal recess, lateral to the attachment of the nasal septum

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30
Q

Which nerve innervates the sphenoid sinus?

A

The ophthalmic branch of the trigeminal nerve (CN5)

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31
Q

The sphenoid sinus is close to which gland?

A

The pituitary gland

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32
Q

What is the pharynx?

A

A fibromuscular tube which takes filtered air from the nose to larynx

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33
Q

What are the cell types in the pharynx?

A

Squamous and columnar ciliated epithelium

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34
Q

Where is the pharynx?

A

Extends from the skull base to C6, where is becomes continuous with the oesophagus

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35
Q

What are the three components of the pharynx?

A

Nasopharynx, oropharynx, laryngopharynx

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36
Q

What is the valvular function of the larynx?

A

Prevents liquids and food from entering the lungs

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37
Q

What is the structure of the larynx?

A
  • Rigid structure
  • Has 9 cartilages
  • Has multiple muscles
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38
Q

What are the 3 paired cartilages in the larynx?

A

Cuneiform, corniculate and arytenoid

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39
Q

What are the 3 unpaired cartilages in the larynx?

A

Epiglottis, thyroid and cricoid

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40
Q

What is the significant feature of the arytenoid cartilages?

A

Rotate on the cricoid cartilage to change the vocal chords

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41
Q

What nerve innervates the larynx?

A

The vagus nerve (CN10) - superior laryngeal and recurrent laryngeal nerve

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42
Q

What are the divisions of the superior laryngeal nerve and what are their functions?

A
  • Internal (for sensation)

- External (motor innervation to the cricothyroid muscle)

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43
Q

What is the function of the recurrent laryngeal nerve?

A

Provides motor innervation for all muscles except the cricothyroid muscle

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44
Q

Where does the left recurrent laryngeal nerve run?

A

Runs laterally to the arch of the aorta, loops under aortic arch, ascends between the trachea and oesophagus

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45
Q

Where does the right recurrent laryngeal nerve run?

A

Loops under the right subclavian artery, then runs up plane between trachea and oesophagus

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46
Q

What is a sign of a tumour/ulcer on/near the recurrent laryngeal nerve?

A

Hoarse voice

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47
Q

What are the components of the lower respiratory tract?

A
  • Trachea
  • Main Bronchi
  • Lobar bronchi
  • Segmental branches
  • Alveoli
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48
Q

What is the main function of the lungs?

A

Gas exchange

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49
Q

What is the gas exchange area per lung?

A

20 m^2 per lung

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50
Q

Define minute volume

A

The volume of air inhaled/exhaled in a minute

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51
Q

Define cardiac output

A

Volume of blood pumped out by the heart a minute

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52
Q

What is the approx value for the minute volume?

A

5 litres

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53
Q

What is the approx value for the cardiac output?

A

5 litres

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54
Q

Where is the trachea?

A

From larynx to carina (C6-T5)

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55
Q

What shape is a cross section of the trachea?

A

Oval

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56
Q

What structure is the cartilage in the trachea?

A

Semi-circular C-shaped hyaline cartilage connected by tracheal muscle

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57
Q

How come the cartilage in the trachea is C-shaped?

A

Increases the flexibility of the trachea

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58
Q

What are the cell types in the trachea?

A

Pseudo-stratified ciliated columnar epithelium

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59
Q

Name a cell type which is present in the trachea?

A

Goblet cells

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60
Q

Which is more mobile: upper trachea or distal trachea?

A

Upper trachea

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61
Q

What is the carina?

A

A ridge of cartilage in the trachea that occurs between the division of the two main bronchi

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62
Q

Where does the main bronchi divide into a left and right bronchus?

A

At the carina, at the level of T5

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63
Q

Which bronchus is more vertically disposed?

A

The right main bronchus

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64
Q

How long is the right main bronchus?

A

1-2.5 cm long

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65
Q

Which artery is the right main bronchus related to?

A

Right pulmonary artery

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66
Q

Which bronchus comes off at more of an angle?

A

Left main bronchus

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67
Q

How long is the left main bronchus?

A

5cm

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68
Q

Which artery is the left main bronchus related to?

A

Aortic arch

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69
Q

Which bronchus are things more likely to get stuck in and why?

A

Right - due to the left being longer and more angled

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70
Q

How many lobes are there in the right lung and what are their names?

A

3 - upper, middle and lower

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71
Q

How many lobes are there in the left lung and what are their names?

A

2 - upper and lower

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72
Q

How does the lobar bronchi divide in the right lung?

A

3 divisions

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73
Q

How does the lobar bronchi divide in the left lung?

A

2 divisions

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74
Q

How many segmental branches are there in the right lung?

A

10

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75
Q

How many segmental branches are there in the left lung?

A

8

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76
Q

What are the divisions after the lobar bronchi?

A
  • Terminal bronchioles
  • Respiratory bronchioles
  • Alveolar ducts (short tubes with multiple alveoli)
  • Alveoli
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77
Q

What is a acinus of the lung?

A

The tissue supplied with air by one terminal bronchiole

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78
Q

What are the 6 cell types present in the alveoli?

A
  • Type I pneumocytes
  • Type II pneumocytes (secrete surfactant)
  • Alveolar macrophages
  • Basement membrane
  • Membrane 1 micron thick
  • Columnar ciliated epithelium
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79
Q

Where does the pulmonary plexus lie?

A

Behind each hilum

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80
Q

What does the pulmonary plexus receive innervation from?

A
  • The right and left vagus (CN10)

- The T2-T4 ganglia of the sympathetic trunk

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81
Q

What does sympathetic supply cause in the lung?

A
  • From the sympathetic trunk

- Results in bronchodilation

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82
Q

What does parasympathetic supply cause in the lung?

A
  • From the vagus

- Results in bronchoconstriction

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83
Q

Why is the right lung larger than the left?

A

Due to the silhouette of the heart

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84
Q

How many lobes does the right lung have?

A

3

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85
Q

What are the names of the lobes of the right lung?

A

Superior, middle and inferior

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86
Q

How many lobes does the left lung have?

A

2

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87
Q

What are the names of the lobes of the left lung?

A

Superior and inferior

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88
Q

What is lung pleura and what are the layers?

A
  • 2 main layers of mesodermal origin
  • Visceral and parietal layer s
  • Each a single layer of cells
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89
Q

Where does the visceral layer of the lungs lie?

A

Applied to the lung surface - only have autonomic innervation

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90
Q

Where does the parietal layer of the lungs lie?

A

Applied to the internal chest - has pain sensation via phrenic nerve

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91
Q

Where are the layers of the lung pleura continuous?

A

At the lung root

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92
Q

What are the two blood supplies of the lungs?

A

Bronchial and pulmonary

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93
Q

What vessels are involved in the pulmonary circulation?

A
  • Left and right pulmonary arteries run from the right ventricle
  • Bronchus & pulmonary arteries run together - via the bronchovascular bundle
  • Pulmonary veins run on their own
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94
Q

What is the standard minute volume (lungs)?

A

5 litres of air a minute

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95
Q

Define transpulmonary pressure

A

Difference in pressure between the inside and outside of the lung (alveolar - intrapleural pressure)

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96
Q

Define intrapleural pressure

A

The pressure in the pleural space, also known as intrathoracic pressure

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97
Q

Define alveolar pressure

A

Air pressure in pulmonary alveoli

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98
Q

What is inspiration initiated by?

A

A neurally induced contraction of the diaphragm and the external intercostal muscles located between the ribs

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99
Q

What is the most important inspiratory muscle during normal quiet breathing?

A

The diaphragm

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100
Q

Where are the impulses stimulating contraction of the diaphragm from?

A

Via the phrenic nerve, arises from C3, 4 & 5 (C345 keeps the diaphragm alive)

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101
Q

What does the diaphragm do during inspiration?

A
  • Contracts causing its dome to move downwards

- Enlarges the thorax so increasing the volume

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102
Q

What happens to the intercostal muscles during inspiration?

A
  • Activation of the motor neurones in the intercostal nerves to the EXTERNAL intercostal muscles
  • Causes contractions
  • Results in an upward and outward movement of the rib (further increase in thoracic volume)
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103
Q

What happens as the thorax expands during inspiration?

A
  • The intrapleural pressure is being lowered and the transpulmonary pressure is becoming more positive
  • Results in lung expansion as transpulmonary pressure > elastic recoil of lungs
  • Lung expansion results in the alveolar pressure becoming negative and results in an inward flow
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104
Q

What causes the end of the inspiration?

A
  • The chest wall is no longer expanding but yet to start passive recoil as lungs remain the same size
  • The glottis is open
  • Alveolar pressure = atmospheric pressure
  • Results in no airflow
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105
Q

When does expiration occur?

A

At the end of inspiration

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106
Q

What happens to the intercostal muscles at the end of inspiration/start of expiration?

A
  • The motor neurones to the diaphragm and external intercostal muscles decrease their firing
  • These muscles can relax
  • Diaphragm lowers and flattens
  • Decreases thoracic volume
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107
Q

What happens as the diaphragm and intercostal muscles relax during expiration?

A
  • The lungs and chest walls start to passively collapse due to elastic recoil
  • Muscle relaxation causes the intrapleural pressure to increase, so decreasing the transpulmonary pressure, eventually causing passively collapsing
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108
Q

What happens as the lungs become smaller during expiration?

A

Air in the alveoli becomes temporarily decompressed resulting in an increase in alveolar pressure

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109
Q

Why is expiration at rest passive?

A

Due to it only relying on relaxation of the external intercostal muscles and diaphragm and the elastic recoil of the lungs

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110
Q

What happens during forced expiration?

A
  • The internal intercostal muscles also contract, along with the abdominal muscles
  • This results in the ribs moving downwards and inwards - actively decreasing thoracic volume, increasing intra-abdominal pressure, forcing the relaxed diaphragm further up, further decreasing thoracic volume
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111
Q

What is the airway with the greatest resistance and why?

A

The trachea - has a small surface area meaning it provides more resistance

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112
Q

Define dead space

A

The volume of air not contributing to ventilation

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113
Q

Where does gas exchange take place?

A

Between the alveoli and capillaries

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114
Q

What does bulk from in the airways allow for?

A

Oxygen and carbon dioxide movement - requires a large surface area with minimal distance for gases to move across and adequate perfusion of blood

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115
Q

Where do terminal bronchioles lead to?

A

Respiratory bronchioles, which lead to alveolar ducts & alveoli

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116
Q

Where are the respiratory bronchioles found?

A

In the centre of the acinus

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117
Q

What is the total combined area for gas exchange?

A

40-100m^2

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118
Q

How many alveoli are there per lung?

A

300 million

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119
Q

How many capillaries are there per alveolus?

A

1000

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120
Q

How many layers does the oxygen have to diffuse through to get to the erythrocyte?

A
  • 7
  • Alveolar epithelium
  • Tissue interstitium
  • Capillary endothelium
  • Plasma layer
  • Red cell membrane
  • Red cell cytoplasm
  • Haemoglobin binding
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121
Q

How can the alveoli be the most efficient?

A

If the correct proportion of alveolar airflow (ventilation) and capillary blood flow (perfusion) shows to be available at each alveolus

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122
Q

What is the main effect of ventilation-perfusion inequality?

A

The partial pressure of oxygen is decreased in systemic-arterial blood

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123
Q

What is the natural ventilation-perfusion caused by?

A
  • Gravitational effects
  • The upright posture causes the increase of filling of blood vessels at the bottom of the lung (due to gravity)
  • This contributes to the difference in blood-flow distribution in the lung
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124
Q

What are the two extremes as a direct consequence of V/Q mismatch?

A
  • Ventilated alveoli but no blood supply at all (dead space/wasted ventilation)
  • Adequate blood flow through the areas of the lung but there is no ventilation (shunt) due to collapsed alveoli
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125
Q

What is the mechanism of hypoxic pulmonary constriction?

A
  • A decrease in ventilation within a group of alveoli - as a result of a mucous plug blocking the small airways
  • This decrease in the partial pressure of O2 in the alveoli and nearby blood vessels leads to VASOCONSTRICTION - diverting blood away from the poorly ventilated area
  • This effect is unique to the pulmonary arterial vessels (since in systemic circulation the opposite would occur) - it ensures that blood flow is directed away from diseases areas of the lung toward areas that are well-ventilated
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126
Q

What is the effects of hypoxic pulmonary constriction unique to and why?

A

The pulmonary arterial vessel (since in systemic circulation the opposite would occur)

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127
Q

What is the mechanism of local bronchoconstriction?

A
  • If there is a decrease in blood flow within a lung region, for example, a small blood clot in a pulmonary arteriole
  • The local decrease in blood flow will mean there is less systemic CO2 in the area, resulting in a local decrease of the partial pressure of CO2
  • This results in BRONCHOCONSTRICTION which diverts airflow away to areas of the lung with better perfusion
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128
Q

What is used to greatly improve the efficiency of pulmonary gas exchange?

A

Hypoxic pulmonary constriction & local bronchoconstriction

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129
Q

What is PaCO2?

A

Arterial CO2

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130
Q

What is PACO2?

A

Alveolar CO2

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131
Q

What is PaO2?

A

Arterial O2

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132
Q

What is PAO2?

A

Alveolar O2

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133
Q

What is PIO2?

A

Pressure of inspired O2

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134
Q

What is VA?

A

Alveolar ventilation

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135
Q

What is VCO2?

A

CO2 production

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136
Q

What is the structure of a haemoglobin molecule?

A
  • Protein made up of 4 subunits bound together
  • Each subunit is a heme group and a polypeptide attached
  • The 4 polypeptides of the molecule are called globin
  • Each of the four heme groups contain one atom of iron to which molecular oxygen binds
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137
Q

What are the two forms that haemoglobin can exist in?

A
  • Hb (deoxyhaemoglobin)

- HbO2 (oxyhemoglobin)

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138
Q

Why is the oxygen-dissociation curve sigmoid shaped?

A
  • Each haemoglobin contains 4 sub-units
  • Each subunit can combine with 1 molecule of oxygen
  • The reactions occur sequentially
  • The binding between oxygen and haemoglobin increases very rapidly as the partial pressure of oxygen is increased
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139
Q

Where does haemoglobin give up its oxygen?

A

In areas of low partial O2 pressure (e.g. metabolically active tissue) where oxygen will diffuse from an area of high concentration to an area of low concentration

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140
Q

What does an increase in temperature do to the oxygen-dissociation curve?

A

Cause the curve to shift to the right

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141
Q

What does a shift to the right on the oxygen-dissociation curve mean?

A

Haemoglobin has less affinity for oxygen

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142
Q

What does a decrease in pH do to the oxygen-dissociation curve?

A

Cause the curve to shift to the right

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143
Q

What does a decrease in temperature do to the oxygen-dissociation curve?

A

Cause the curve to shift to the left

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144
Q

What does a shift to the left on the oxygen-dissociation curve mean?

A

Haemoglobin has more affinity for oxygen

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145
Q

What does an increase in pH do to the oxygen dissociation curve?

A

Cause the curve to shift to the left

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146
Q

What kind of temperature increase will shift the oxygen-dissociation curve?

A

Because of heat produced by tissue metabolism

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147
Q

What kind of pH decrease will shift the oxygen-dissociation curve?

A

Because of elevated CO2 partial pressure (which enters from the tissues) and the release of metabolically produced acids

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148
Q

What happens when haemoglobin is exposed to elevated partial CO2 pressure, reduced pH and increased temperatures?

A
  • As it passes through the tissue capillaries it has a decreased affinity for oxygen
  • Means it gives up more oxygen
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149
Q

What factors about a metabolically active tissue causes a greater oxygen release?

A
  • Greater partial CO2 pressure
  • Lower pH
  • Greater temperature
  • Releases more oxygen so to provide more active cells with additional oxygen
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150
Q

What does carbon monoxide do to the oxygen dissociation curve?

A

Shifts it to the left, so decreasing the unloading of oxygen from haemoglobin in the tissues

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151
Q

What is the equation which links arterial CO2 and alveolar ventilation?

A

PaCO2 = (k x VCO2)/ VA

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152
Q

What are the three ways in which carbon dioxide is carried in the blood?

A
  • Bound to haemoglobin
  • Dissolved in plasma
  • As bicarbonate
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153
Q

What does carbon dioxide binding to haemoglobin form?

A

Carbaminohaemoglobin - deoxygenated haemoglobin has a greater affinity for carbon dioxide than oxygen

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154
Q

How is bicarbonate formed in the erythrocyte?

A
  • Produced with the enzyme carbonic anhydrase in the erythrocyte
  • Rapid dissociation into bicarbonate and H ion
  • Bicarbonate moves into the plasma from the erythrocyte via a transporter, which exchanges one bicarbonate for one chloride ion
  • Bicarbonate leaving the erythrocyte favours the forward reaction
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155
Q

What happens to the remaining hydrogen ion from bicarbonate formation in the erythrocyte?

A
  • Binds to deoxyhaemoglobin
  • As venous blood passes through the lungs, deoxyhaemoglobin becomes converted to oxyhemoglobin
  • In the process, releases the H picked up in the tissues
  • This reacts with bicarbonate to produce carbonic acid
  • Carbonic anhydrase dissociates this to from CO2 & H2O
  • CO2 then diffuses to the alveoli to be expired
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156
Q

What happens when venous blood reaches the lungs?

A
  • The blood partial CO2 pressure is higher than alveolar partial CO2
  • A net diffusion of CO2 from the blood to the alveoli occurs
  • The loss of CO2 causes H ions and bicarbonate to produce H2CO3, which then dissociate back into CO2 & H2O
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157
Q

Why are the bodies acids and bases regulated?

A

The ensure for optimal function e.g. for enzymes

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158
Q

What is the normal pH of the blood?

A

Around 7.4 (7.35-7.45)

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159
Q

How is the acid-base balance regulated?

A

By mechanisms which generate, buffer and eliminate acids and bases

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160
Q

Are the bodies acids and bases weak or strong?

A

Weak

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161
Q

How is the pH of bodily fluids maintained?

A
  • Intracellular & extracellular buffers
  • The lungs eliminating CO2
  • Renal bicarbonate reabsorption and hydrogen ion elimination
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162
Q

What is the most important buffer in the body?

A
  • The carbonic acid/bicarbonate buffer

- Works with the lungs to compensate for increased carbonic acid production

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163
Q

What is the phenomenon which occurs when a person HYPOventilates?

A
  • Inadequate ventilation of the alveoli
  • CO2 can’t be excreted and expired adequately
  • Partial pressure of CO2 increases thereby resulting in more carbonic acid being produced
  • Increased hydrogen ion conc. in the blood
  • RESPIRATORY ACIDOSIS
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164
Q

What is the phenomenon which occurs when a person HYPERventilates?

A
  • Decrease arterial partial CO2 pressure
  • Decreased hydrogen ion conc. in the blood
  • RESPIRATORY ALKALOSIS
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165
Q

What is the Henderson-Hasselbach equation?

A
  • pH = 6.1 + log10([HCO3-]/[0.03 x PCO2])
  • 6.1 is the dissociation constant for the bicarbonate buffer system
  • 0.03 x PCO2 is an estimate of H2CO3
  • 0.03 = the blood carbon dioxide solubility co-efficient
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166
Q

What is Dalton’s law?

A
  • Pressure exerted by each gas in a mixture is independent of the pressure exerted by other gases
  • This is due to gas molecules being so far apart from each other
  • Total pressure = sum of partial pressures
  • Partial pressures are directly proportional to its concentration
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167
Q

What is Boyle’s law?

A
  • Pressure of a fixed amount of gas in a container is inversely proportional to container’s volume
  • P1V1 = P2V2
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168
Q

What is Henry’s law?

A
  • Amount of gas dissolved in a liquid is proportional to the partial pressure of gas with which the liquid is in equilibrium
  • At equilibrium the partial pressures of the gas molecules in the liquid and gaseous phases must be identical
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169
Q

What is the alveolar gas equation?

A
  • PAO2 = PiO2 - PaCO2/R

- R = the respiratory exchange ratio - the ratio between the amount of CO2 produced in metabolism and oxygen used

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170
Q

How is pressure in the bronchi calculated?

A

Pressure = flow x resistance

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171
Q

What is the law of Laplace?

A
  • Describes the relationship between pressure (P), surface tension (T) and the radius (r) of an alveolus
  • P = 2T/r
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172
Q

What is lung compliance?

A
  • The change in lung volume caused by a given change in transpulmonary pressure
  • The greater the lung compliance, the more readily the lungs are expanded
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173
Q

Name two determinants of lung compliance

A
  • Stretchability of the lung tissues

- Surface tension of the air-water interfaces of the alveoli

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174
Q

How does the stretchability of the lung tissues affect lung compliance?

A

A thickening and thus a loss in stretchability of the lungs elastic connective tissue results in a decrease in lung compliance

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175
Q

How does surface tension of the air-water interfaces of the alveoli affect lung compliance?

A
  • The surface of alveolar cells are moist, thus alveoli are effectively air-filled sacs lined with water
  • At the interface, attractive forces between the water molecules (surface tension), makes the water lining like a stretched balloon that constantly tends to shrink and resists further stretching
  • The expansion of the lungs requires energy not only to expand the connective tissues, but to overcome surface tension of the water layer lining the alveoli
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176
Q

What is the function of the type II pneumocytes and why is this important?

A
  • Produces surfactant
  • This reduces the cohesive forces between water on the alveolar surface
  • Lowers the surface tension, so increases lung compliance and makes it easier to expand the lungs
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177
Q

When does the amount of surfactant tend to decrease?

A

When breaths are small and constant

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178
Q

What does a deep breath do in terms of surfactant production?

A
  • Stretches type II pneumocytes

- Stimulates the secretion of surfactant

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179
Q

Define inspiratory reverse volume

A

Amount of air in excess tidal inspiration that can be inhaled with maximum effort

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180
Q

Define expiratory reverse volume

A

Amount of air in excess tidal expiration that can be exhaled with maximum effort

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181
Q

Define residual volume

A

Amount of air remaining in the lungs after maximum expiration; keeps alveoli inflated between breaths and mixes with fresh air on next inspiration

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182
Q

Define vital capacity

A

Amount of air that can be exhaled with maximum effort after maximum inspiration (ERV + TV + IRV); used to assess strength of thoracic muscles as well as pulmonary function

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183
Q

Define functional residual capacity

A

Amount of air remaining in the lungs after a normal tidal expiration (RV + ERV)

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184
Q

Define inspiration capacity

A

Maximum amount of air that can be inhaled after a normal tidal expiration (TV + IRV)

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185
Q

Define total lung capacity

A

Maximum amount of air the lungs can contain (RV + VC)

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186
Q

Define tidal volume

A

Amount of air inhaled or exhaled in one breath

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187
Q

What is the process for a FEV1 reading?

A

In which a person takes a maximal inspiration and then exhales maximally as fast as possible. The important value is the fraction of the total “forced” vital capacity expired in 1 second

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188
Q

What is the approximate amount that a healthy individual can expire in 1 second?

A

80% of vital capacity

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189
Q

What is the pattern of flow of the breath?

A

Greatest at the start of expiration, it declines linearly with volume

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190
Q

Define FEF25

A

Flow at point when 25% of total volume to be exhaled has been exhaled

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191
Q

Define FVC

A

Forced vital capacity, the total amount of air forcibly expired

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192
Q

How is FEV1 used to detect for abnormal values?

A
  • Result is compared with the predicted values if the FEV1 is 80% of greater than the predicted value = normal
  • If the FEV1 is less than 80% of the predicted value = Low
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193
Q

How is FVC used to detect for abnormal values?

A
  • Result is compared with the predicted values, if the FVC is 80% or greater than the predicted = normal
  • If the FVC is less than 80% of the predicted value = low
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194
Q

How does a low FVC mean?

A

Airways restriction

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195
Q

What is the FEV1/FVC ratio?

A
  • The proportions of FVC exhaled in the 1st second

- FEV1 is divided by FVC

196
Q

How can the FEV1/FVC ratio be used to detect for abnormal values?

A
  • If the ratio is below 0.7 = airway obstruction

- If the ratio is high (normal) but the FVC is low = airway restriction

197
Q

What does a low FEV1/FVC ratio mean?

A

Airway obstruction

198
Q

What does a high FEV1/FVC ratio but a low FVC mean?

A

Airway restriction

199
Q

What is inspiration initiated by?

A

A burst of action potentials in the spinal motor neurones to inspiratory muscles like the diaphragm (the vagus nerve arises from C3, 4 & 5 for the diaphragm)

200
Q

How does expiration occur due to the nervous system?

A
  • Action potentials cease
  • Inspiratory muscles relax
  • Expiration occurs as the elastic lungs recoil
201
Q

Where does control of breathing primarily reside?

A

In the neurones of the medulla oblongata (the same area of the brain that contains the major cardiovascular control centres)

202
Q

What are the two main anatomical components of the medullary respiratory centre?

A
  • The neurones of the dorsal respiratory group (DRG)

- The neurones of the ventral respiratory group (VRG)

203
Q

What is the function of the dorsal respiratory group?

A

These primarily fire during inspiration and have input to the spinal motor neurons that activate respiratory muscles involved in inspiration - diaphragm and external intercostal muscles

204
Q

What is the function of the ventral respiratory group?

A
  • The other main complex of neurones in the respiratory centre
  • Contains expiratory neurones that appear to be most important when large increases in ventilation are required
  • During active expiration, motor neurones activated by the expiratory output of the VRG cause the expiratory muscles to contract
  • During quiet breathing the respiratory rhythm generator activates inspiratory neurons in the VRG that depolarise the inspiratory spinal motor neurons, resulting in the inspiratory muscles contracting
205
Q

Where is the respiratory rhythm generator located?

A

The pre-Botzinger complex of neurones in the upper part of the VRG

206
Q

What is the structure and function of the respiratory generator

A

Composed of pacemaker cells and a complex neural network that, acting together, set the basal respiratory rate

207
Q

Where does the medullary inspiratory neurones receive impulses from?

A
  • Receive a rich synaptic input from neurones from various areas in the pons
208
Q

Where is the pons located?

A

Part of the brainstem, just above the medulla

209
Q

What is the function of the apneustic centre?

A
  • Involved in fine tuning the output of the inspiratory neurones of the medulla
  • In continuing to active inspiratory neurones to inhibit expiration
210
Q

What can override the apneustic centre when related to respiration?

A

The pneumotaxic centre

211
Q

Where is the apneustic centre located?

A

The lower pons

212
Q

What is the function of the pneuotexic centre?

A
  • Regulates and may override the activity of the apneustic centre
  • Acts to smooth the transition between inspiration and expiration
  • Also involved in switching off inspiratory neurones to prevent hyper inflation, so allowing expiration
213
Q

Where is the pneumotaxic centre located?

A

The upper pons

214
Q

What are the receptors which are present in the nose, nasopharynx and larynx and what are their functions?

A
  • Chemo and mechano receptors
  • Some appear to sense and monitor flow
  • Stimulation of these receptors appears to inhibit the central controller
215
Q

What are the receptors which are present in the pharynx and what are their functions?

A
  • Appear to be activated by swallowing

- Respiratory activity stops during swallowing thereby protecting against the risk of aspiration of food or liquid

216
Q

What is the function of slowly adapting stretch receptors?

A
  • Maintain a persistent or slowly decaying receptor potential during constant stimulus
  • Initiating action potentials in afferent neurones for the duration of the stimulus
  • Myelinated
217
Q

Where are slowly adapting stretch receptors found?

A

In airways smooth muscle

218
Q

What activates the slowly adapting stretch receptors?

A

Lung distension

219
Q

What happens when there is high activity of the slowly adapting stretch receptors?

A
  • Inhibits further inspiration, thus beginning expiration

- If inflammation is maintained they slowly adapt to low frequency firing

220
Q

What is the function of rapidly adapting stretch receptors?

A
  • Generate a receptor potential and action potentials at the onset of a stimulus but very quickly cease responding
  • Myelinated
221
Q

Where are rapidly adapting stretch receptors found?

A

Between airway epithelial cells

222
Q

What activates rapidly adapting stretch receptors?

A

Lung distension and irritants

223
Q

What happens to the rapidly adapting stretch receptors when there is high activity?

A
  • High activity causes bronchoconstriction
  • Produce a brief burst of activity
  • May be involved in the cough reflex
224
Q

Where are the C-fibre J receptors found?

A
  • In either the capillary walls or the interstitium

- Non-myelinated

225
Q

What stimulates the C-fibre J receptors?

A
  • An increase in lung interstitial pressure caused by the collection of fluid in the interstitium
  • Mainly caused by a pulmonary embolism or left ventricular heart failure
226
Q

What does activity of the C-fibre J receptors cause?

A

Rapid breathing, shallow breathing, bronchoconstriction, cardiovascular depression and a dry cough

227
Q

What does neural input from J receptors give?

A

Gives rise to sensation of pressure in the chest and the feeling that breathing is difficult

228
Q

What chemoreceptors mainly give rise to the automatic control of ventilation at rest?

A

Peripheral (arterial) and central chemoreceptors

229
Q

Where are the peripheral chemoreceptors located?

A
  • High in the neck at the bifurcation of the common carotid arteries
  • In the thorax on the arch of the aorta
  • Carotid bodies and aortic bodies
230
Q

Where are the peripheral chemoreceptors located close to?

A

The arterial baroreceptors and are in intimate contact with arterial blood

231
Q

How are the carotid bodies strategically located?

A

To monitor oxygen supply to the brain

232
Q

What are the peripheral chemoreceptors composed of?

A
  • Specialised receptor cells

- Type II cells

233
Q

What is the function of the specialised receptor cells of the peripheral chemoreceptors?

A
  • Stimulated mainly by a decrease in the arterial partial pressure of oxygen
  • Also by an increase in the arterial H ion concentration
234
Q

What is the function of type II cells of the peripheral chemoreceptors?

A
  • On detection of hypoxia they release stored neurotransmitters that stimulate the carotid sinus nerve
  • These cells provide excitatory synaptic input to the medullary inspiratory neurones
235
Q

What is the predominant peripheral chemoreceptor involved in the control of respiration?

A

The carotid body

236
Q

Are peripheral chemoreceptors sensitive to small reductions of the arterial partial oxygen pressure?

A

No - its only when there is a large dip when they become sensitive

237
Q

Where are the central chemoreceptors located?

A

The medulla

238
Q

What is the function of the central chemoreceptors?

A

Provide excitatory synaptic input into the medullary inspiratory neurones

239
Q

What are the central chemoreceptors stimulated by?

A
  • An increase of hydrogen ions of the CSF
  • As the blood-brain barrier is pretty impermeable to H+, changes to the H+ in the blood are poorly reflected in the CSF
  • However, CO2 readily diffuses into the CSF and blood partial pressure CO2 influences the H+ levels, enabling the central chemoreceptors to detect changes
240
Q

What happens if there is an increase in arterial partial CO2 pressure?

A
  • Some of the extra CO2 will diffuse into the CSF
  • Bicarbonate and hydrogen ions will form in the CSF
  • More H ions - enables the central chemoreceptors to detect pH change
  • Increase in ventilation by stimulating the medullary inspiratory neurones
241
Q

Define hypoxia

A

A deficiency of oxygen at the tissue level

242
Q

What is the most common type of hypoxia?

A

Hypoxemia - in which the arterial partial O2 pressure is reduced

243
Q

What are the most common causes of hypoxia?

A
  • Hypoventilation
  • Diffusion impairment
  • Shunting
  • Ventilation perfusion mismatch
244
Q

What is hypoventilation and what does it cause?

A
  • Results in an increased arterial partial CO2 pressure
  • Failure to ventilate the alveoli properly
  • Caused by muscular weakness (MND), obesity and loss of respiratory drive
245
Q

What is diffusion impairment and what does it cause?

A
  • Results from the thickening of the alveolar membranes or a decrease in their SA
  • Causes the blood partial O2 pressure and alveolar partial O2 pressure to not equilibrate
  • Caused by pulmonary oedema, anaemia and interstitial fibrosis
246
Q

What is shunting and what does it cause?

A
  • An anatomical abnormality of the cardiovascular system that causes mixed venous blood to bypass ventilated alveoli in passing from the right side of the heart to the left side
  • An intrapulmonary defect in which mixed venous blood perfuses unventilated alveoli
247
Q

What is ventilation-perfusion mismatch and what does it cause?

A
  • Occurs in COPD
  • Arterial partial CO2 pressure may be normal or increased
  • Can be caused by a pulmonary embolism, asthma, pneumonia & pulmonary oedema
248
Q

What is the most common cause of hypoxemia?

A

Ventilation-perfusion mismatch

249
Q

Define hypercapnia

A

Carbon dioxide retention and an increased arterial partial CO2 pressure

250
Q

What is the principle cause of hypercapnia?

A
  • Hypoventilation

- Can sometimes be caused by ventilation-perfusion mismatch depending on how much ventilation is stimulated

251
Q

What are the features of type I respiratory failure?

A
  • pO2 is low
  • pCO2 is low or normal
  • With type I = 1 change
252
Q

What is the most common cause of type I respiratory failure?

A

Pulmonary embolism

253
Q

What are the features of type II respiratory failure?

A
  • pO2 is low
  • pCO2 is high
  • With type II = 2 changes
254
Q

What is the most common cause of type II respiratory failure?

A

Hypoventilation

255
Q

What is the unique dual blood supply of the lungs?

A

The pulmonary circulation (the main circulation) & the bronchial circulation

256
Q

Where does the pulmonary circulation come from?

A

The right ventricle

257
Q

What percentage of the cardiac output does the pulmonary circulation get from the right ventricle

A

100%

258
Q

What is the erythrocyte transit time in the pulmonary circulation?

A

5 seconds

259
Q

How many capillaries is there in the pulmonary circulation?

A

280 billion

260
Q

What percentage of the left ventricular output does the bronchial circulation get?

A

2%

261
Q

What are 3 features of the pulmonary artery?

A
  • Vessel wall is thin
  • Minor muscularisation
  • No need for redistribution
262
Q

What are 3 features of a systemic (everywhere except pulmonary) artery?

A
  • Vessel wall is thick
  • Significant muscularisation
  • Redistribution is required
263
Q

Which system has a greater pressure - pulmonary or systemic?

A

Systemic

264
Q

What does the autonomic system compromise of?

A
  • The parasympathetic (normal physiological conditions, rest & digest)
  • The sympathetic (fight or flight)
  • The enteric (GI tract)
265
Q

What components of the autonomic system serve most organs?

A

The sympathetic and parasympathetic

266
Q

What is the neurotransmitter of the parasympathetic nervous system?

A

Acetylcholine

267
Q

How does the parasympathetic nervous system innervate the lungs?

A

Via the vagus

268
Q

What does the vagus innervate in the lungs?

A

The vasculature, glands and airways

269
Q

What is the intrinsic tone of airways of the lungs governed by?

A

The parasympathetic system

270
Q

How does acetylcholine interact with the lungs?

A

Interacts with the muscarinic cholinergic receptors on the muscle to provide a general level of intrinsic muscle tone

271
Q

What does too much parasympathetic activation of the lungs cause?

A

Bronchoconstriction

272
Q

What is the neurotransmitter of the sympathetic nervous system?

A

Noradrenaline

273
Q

How does the sympathetic nervous system innervate the lungs?

A

Via the sympathetic trunk

274
Q

What does the sympathetic nervous system innervate in the lungs?

A

The vasculature and the glands

275
Q

What is the indirect influence of the sympathetic system on airways tone?

A
  • Sympathetic activation caused Nad to be released to the adrenal glands
  • Can result in the release of adrenaline (from the adrenal medulla)
  • This binds to the beta-2-adrenoreceptors on the muscles of the airways
  • Results in bronchodilation
276
Q

What are cholinergic neurones?

A

Neurones which release acetylcholine

277
Q

What is the link with neurones and Alzheimer’s?

A

Neurones associated with the ACh system degenerate in people with Alzheimer’s

278
Q

What do nicotinic receptors respond too?

A

ACh & Nicotine

279
Q

What are nicotinic receptors stimulated by?

A

Both sympathetic and parasympathetic - but mainly the latter

280
Q

Where are nicotinic receptors found?

A

In post-ganglionic receptors & in the neuro-muscular junction

281
Q

How does the depolarisation if the nicotinic receptors work?

A
  • Contains a ligand-gated channel which is permeable to both Na and K ions, but as Na has a larger electrochemical driving force, the net effect of opening these channels is depolarisation
282
Q

Is the muscarinic receptor sympathetic or parasympathetic?

A

Parasympathetic

283
Q

How many types of muscarinic receptors are there?

A
  • 5
  • M1-M5
  • M3 is involved with the lungs
284
Q

What is the involvement of the M3 receptors with the airways?

A
  • ACh binds to the M3 receptor
  • Receptor couples with Gq protein
  • Gq protein activates phospholipase C
  • PLC catalyses the breakdown of a plasma membrane phospholipid to diacylglycerol and inositol triphosphate
  • DAG acts as a second messenger and activates protein kinase C
  • IP3 binds to ligand-gated Ca receptors located on the ER of the bronchial cells, which open, resulting in Ca release, stimulating bronchoconstriction
285
Q

What happens when acetylcholine binds to a M3 receptor?

A

Bronchoconstriction

286
Q

What is a adrenergic neurone?

A

A neurone which releases NAd

287
Q

What are the types of alpha-adrenergic receptors?

A

Alpha-1 & alpha-2

288
Q

What is the function of an alpha-1 adrenergic receptor?

A

Acts postsynaptically to either stimulate/inhibit the activity of different types of K channels

289
Q

What is the function of an alpha-2 adrenergic receptor?

A

Acts presynaptically to inhibit noradrenaline release

290
Q

How do beta-adrenergic receptors act?

A

Via stimulatory G proteins to increase cAMP in the postsynaptic cell

291
Q

What are the three types of beta-adrenergic receptors?

A
  • Beta-1 (heart)
  • Beta-2 (lungs)
  • Beta-3 (adipose)
292
Q

What happens if adrenaline or noradrenaline binds to a beta-2-adrenoreceptor in the lungs?

A

Bronchodilation

293
Q

What are the two types of receptor ligand?

A

Agonist and antagonist

294
Q

What is an agonist receptor ligand?

A

A compound that binds to a receptor and activates it, demonstrates affinity and efficacy

295
Q

What is an antagonist receptor ligand?

A

A compound that blocks the effect of an agonist by competing with a chemical messenger for its binding site - but does not activate signalling normally - thus blocking its action, has affinity but zero efficacy

296
Q

What is affinity, in terms of receptors?

A
  • The degree to which a particular messenger binds to its receptor
  • Shown by both antagonists and agonists
297
Q

What is efficacy, in terms of receptors?

A
  • Describes how well a ligand activates a receptor

- Antagonists results in no conformational change to receptor shape when it binds

298
Q

Name two agonist receptors

A
  • Muscarine binds to muscarinic acetyl choline receptor (mAChR)
  • Nicotine binds to nicotinic acetyl choline receptor (nAChR)
299
Q

Name a antagonist receptor

A

Atropine binds to muscarinic acetyl choline receptor (mAChR) - reverses effect of acetyl choline e.g. use to help people poisoned with sarine (from homeland)

300
Q

How do beta agonists work as medication?

A

Want to increase bronchodilation (sympathetic)

301
Q

How do muscarinic antagonists work as medication?

A

Want to decrease bronchoconstriction (parasympathetic)

302
Q

What is the neurotransmitter, receptor and effect of the parasympathetic system in the lungs?

A
  • Neurotransmitter = ACh
  • Receptor = Muscarinic 3
  • Effect = Constriction
303
Q

What is the neurotransmitter, receptor and effect of the sympathetic system in the lungs?

A
  • Neurotransmitter = NAd which acts on adrenal glands to release adrenaline
  • Receptor = Beta-2-adrenoreceptor
  • Effect = Dilation
304
Q

What is the non-immune host mechanisms of lung defence?

A

Barrier function, leucocyte recruitment, cytokine and growth factors

305
Q

What is the structure of the epithelium of the lungs?

A
  • Tissue composed of cells that line the cavities and surfaces of structures throughout the body
  • Lies on top of connective tissue - the two layers are separated by a basement membrane
306
Q

What is respiratory epithelium?

A

Ciliated pseudostratified columnar epithelium

307
Q

What are the functions of the respiratory epithelium?

A
  • Serve to moisten and protect the airways
  • Functions as a barrier to potential pathogens and foreign particles
  • Prevents infection and tissue injury by action of the mucociliary escalator
308
Q

What doe the skin, salivary and lacrimal glands secrete?

A
  • Antimicrobial chemicals e.g.
  • Antibodies
  • Lysozymes
  • Lactoferrin
309
Q

What is a lysozyme?

A

An enzyme which destroys bacterial cell walls

310
Q

What is lactoferrin?

A

An iron-binding protein which prevents bacteria from obtaining the iron they require to function properly

311
Q

Where is the respiratory tract secretes mucus?

A

The respiratory epithelium and upper gastrointestinal tract

312
Q

What is significant about the mucus secreted by the respiratory tract?

A
  • Contains antibodies
  • It is also very sticky - particles adhere to it and are reverted from entering the blood
  • They are either swept by ciliary action up to the pharynx and then swallowed, or are phagocytosed by macrophages
313
Q

Name 3 other chemical barriers produced by respiratory epithelia

A
  • Anti-fungal peptides
  • Anti-microbial peptides
  • Huge amount of non-pathogenic bacterial flora in the deep of the lungs - helps keep the immune system primed for pathogens
314
Q

Name the 2 physical defence mechanisms

A

Coughing and mucus

315
Q

Is a cough voluntary or reflexively?

A

Either

316
Q

Where are the receptors for the cough reflex?

A

In the larynx, trachea and bronchi

317
Q

What causes a deep inspiration for the cough reflex?

A

The receptors stimulating the medullary inspiratory neurones

318
Q

What happens during a cough?

A
  • The epiglottis is closed
  • The vocal cords shut tightly to entrap air within the lung
  • The abdominal muscles contract forcefully, pushing against the diaphragm
  • The internal intercostal muscles also contract forcefully
  • Pressure in the lungs rise
  • Positive intrathoracic pressure causes narrowing of the trachea
  • Vocal cords and epiglottis suddenly open widely
319
Q

What is the purpose of coughing as a defence mechanism?

A

Particles & secretions are moved from smaller to larger airways, and aspiration of materials into the lungs is also prevented

320
Q

What is airway mucus?

A

A viscoelastic gel containing water, carbohydrate, proteins and lipids

321
Q

What is airway mucus a secretory product of?

A

The goblet cells of the airway surface epithelium and submucosal glands

322
Q

What is the protective role of airway mucus?

A

It protects the epithelium from foreign material and fluid loss

323
Q

How is airway mucus transported from the lower respiratory tract to the pharynx?

A

By airflow and the mucociliary clearance/escalator

324
Q

How does the mucociliary escalator bring up mucus?

A

Does this continuously by cilia beating in directional waves up the airway

325
Q

How does airway mucus protect the epithelium and what does it consist of?

A
  • By being in physical contact with it

- Has a superficial gel/mucous layer and a liquid/periciliary (surfactant) fluid layer which bathes the epithelial cells

326
Q

How can the epithelium repair itself after injury?

A

Due to the fact that epithelium exhibits a level of functional plasticity

327
Q

What are neutrophils & macrophages?

A

Phagocytes, some are antigen presenting cells

328
Q

What are lymphocytes?

A

They make antibodies, kill diseased cells and decide what sort of antibodies to make

329
Q

What is humoural immunity?

A
  • Things that are in the blood/plasma NOT cells
  • Immunoglobulins
  • Complement (formation of the membrane attack complex)
  • Surfactant proteins
  • Cytokines
330
Q

What are cytokines?

A

Proteins which allow leukocytes and tissue cells to talk to each other

331
Q

What is innate immunity?

A
  • Immediate
  • Doesn’t require prior exposure to recognise that something is wrong
  • Mainly involves phagocytosis of bacteria and rapid responses to viruses
332
Q

What is adaptive immunity?

A
  • Hypersensitivity is more prevalent in adaptive

- The formation of immunological memory

333
Q

What is the purpose of inflammation?

A

The local response to infection or injury

334
Q

What are the main functions of innate immunity?

A
  • Destroy or inactivate foreign invaders

- Set the stage for tissue repair

335
Q

What are the key mediators in innate immunity?

A

Cells that function as phagocytes - the most important of which being neutrophils, macrophages and dendritic cells

336
Q

What are the basic stages of innate immunity?

A
  • Bacteria are introduced to a wound
  • Chemical mediators cause vasodilation & capillary permeability; chemoattractants recruit neutrophils to the area
  • Diapedesis (passage of leukocytes out of the blood and into the surrounding tissue) results in neutrophils entering tissue where they engulf and phagocytose bacteria
  • Capillaries return to normal as neutrophils continue to clear the infection
337
Q

How is acute inflammation initiated in the lung?

A
  • Initiated by the tissues, typically by specialist tissue resident macrophages including:
  • Kupffer cells
  • Alveolar macrophages
338
Q

How do macrophages respond to pathogens or tissue?

A

By recognising:

  • Pathogen associated molecular patterns (PAMPs)
  • Damage associated molecular patterns (DAMPs)
339
Q

How do PAMPs and DAMPs work?

A

They recognise new pathogens that haven’t been seen before by using patterns recognition receptors which are part of innate immunity which recognise common antigens on bacteria

340
Q

Where are Toll-like receptors expressed?

A

In the plasma & endosomalw membranes of macrophages and dendritic cells amongst others

341
Q

How do Toll-like receptors work?

A
  • The proteins recognise and bind to PAMPs
  • When binding of a TLR occurs on the plasma membrane of a macrophage, there is stimulation of the activity of the immune cells involved in the innate immune response (e.g. neutrophils)
342
Q

What are the functions of alveolar macrophages?

A
  • Phagocytosis
  • Secrete cytokines
  • Activation and differentiation of helper T cells
343
Q

What is the origin of alveolar macrophages?

A
  • Arise from monocytes (enter tissues and transform into macrophages - produced in the bone marrow)
  • Long lived
344
Q

What is the role of monocytes linked to phagocytes?

A

High phagocytic capacity - bacteria and apoptotic cells

345
Q

What is the role of monocytes relating to ATP?

A

Intermediate ATP production

346
Q

Which cells of the respiratory system has a high susceptibility to apoptosis?

A

Monocytes

347
Q

What is the role of tissue macrophage linked to phagocytes?

A

High-intermediate phagocytic capacity

348
Q

What is the role of tissue macrophages relating to ATP?

A

High ATP generation

349
Q

Which cells of the respiratory system has a low susceptibility to apoptosis?

A

Tissue macrophage

350
Q

What are the functions of the alveolar macrophage?

A
  • Resident phagocyte of the lungs
351
Q

What part of the respiratory system co-ordinates the inflammatory response?

A

Alveolar macrophages - cytokine production

352
Q

What induces and clear apoptotic cells of the alveolar macrophage?

A

Alveolar macrophages

353
Q

What is the level of the response of the alveolar macrophage?

A
  • Meant to destroy bacteria swiftly and with little help

- Macrophage can illicit a huge response by calling neutrophils - causing pneumonia

354
Q

What percentage of white blood cells are neutrophils?

A

70%

355
Q

How many neutrophils can be made per minute?

A

80 million

356
Q

Where are neutrophils produced?

A

Bone marrow

357
Q

What is the purpose of the granules in neutrophils?

A

Released to help combat infection through degranulation

358
Q

What do primary granules of the neutrophils contain?

A
  • Enzymes to carry out anti-microbial activity
  • Elastase (breaks down elastin in lung - enables neutrophil to migrate through lung)
  • Anti-bacterial proteins
359
Q

What is the function of elastase?

A

Breaks down elastin in the lung, so enables neutrophil to migrate through lung

360
Q

What do secondary granules of the neutrophils contain?

A
  • Receptors
  • Lysozymes
  • Collagenase
361
Q

What is the function of lysozyme?

A

Enzyme that breaks down bacterial cell walls

362
Q

What is the function of collagenase?

A

Enzyme which breaks down collagen, allows neutrophils to penetrate hard to reach mollagenised areas

363
Q

How do neutrophils recognise the threat at hand?

A
  • Recognises bacterial structure
  • Has receptors to detect host mediators
  • Recognises host opsonins
364
Q

What is a host opsonin?

A

Any substance that binds a microbe to a phagocyte and promotes phagocytosis

365
Q

What is the process of the activation of neutrophils?

A
  • They are often in the switched off state
  • Activated via stimulus response coupling
  • Signal transduction pathways involving calcium, protein kinases, phospholipase and G proteins
366
Q

What is the process of adhesion of neutrophils?

A
  • Becomes loosely tethered to endothelial cells of blood vessels. This exposes the neutrophil to chemoattractants being released in the area
  • These act on the neutrophil to induce the rapid appearance interns, which bind tightly to their matching molecules on the surface of endothelial cells - meaning tight binding
367
Q

What is the process of migration/chemotaxis of neutrophils?

A
  • A narrow projection is placed between two endothelial cells, where the neutrophil squeezes through and gets into the interstitial fluid
  • Neutrophils follow a chemotactic gradient to the area of the pathogens
368
Q

What is the process of phagocytosis of neutrophils?

A
  • There is contact between the phagocyte and microbe. The major trigger in this is the interaction of phagocyte receptors
  • Chemical factors can bind the phagocyte tightly to the microbe and enhances phagocytosis
  • When the phagocyte engulfs the microbe it is trapped in a internal sac called a phagosome isolating the microbe within the neutrophil
369
Q

What is the process of bacterial killing of neutrophils?

A
  • The phagosome membrane then makes contact with the lysosome to make a phagolysosome
  • The microbe is broke down
370
Q

What is the general process of necrosis?

A
  • Cells swell, then lyse, so other enzymes are released
  • Can cause damage to surrounding tissues
  • Results in inflammation and phagocytosis of necroses cell
371
Q

What is the general process of apoptosis?

A
  • More controlled
  • Cell is turned off and packaged to the be phagocytose by neutrophils
  • No surrounding tissue damage
372
Q

What system does initial responses to pathogens use?

A

Innate (e.g. phagocytosis)

373
Q

What system does later responses to pathogens use?

A

Adaptive

374
Q

What are the cells of the adaptive immune system?

A
  • T-cells
  • B-cells
  • Macrophages
375
Q

What are T cells?

A
  • Type of lymphocyte

- Involved in cell-mediated immunity and the direct killing of cells

376
Q

Where are T cells made?

A

Made in bone marrow, mature in thymus

377
Q

What is the function of the cytotoxic T cell?

A

They travel to the location of their target, bind to them via antigens on these target and directly kill by secreted chemicals

378
Q

What is the function of T helper cells?

A

Assist in the activation and function of B cells, macrophages and cytotoxic T cells

379
Q

What is the function of B cells?

A
  • Type of lymphocyte
  • Involved in antibody production (when activated it causes them to differentiate into plasma cells which secrete antibodies)
380
Q

Where are B cells made?

A

Made in bone marrow, stored in secondary lymphoid organs

381
Q

What are the 5 types of antibody?

A

IgA, IgD, IgE, IgG and IgM

382
Q

Which antibody is made to things we are allergic to?

A

IgE

383
Q

What is the most abundant type of antibody?

A

IgG

384
Q

Which antibody is made at the beginning of infection?

A

IgM

385
Q

What are the functions of the adaptive immune response?

A
  • The recognition of specific non-self antigens
  • Generation of responses tailored to eliminate specific pathogens or pathogen- infected cells
  • Development of immunological memory
386
Q

What is hypersensitivity?

A

The over-reaction by the immune system to things you don’t need to react to

387
Q

What is a type I sensitivity reaction?

A
  • Allergic, acute
  • Examples - acute anaphylaxis, hay fever
  • Immediate & acute
388
Q

What is a type II sensitivity reaction?

A
  • IgG bound to cell surface antigens/IgM
  • Examples - Transfusion reactions, autoimmune disease
  • Fairly quick
389
Q

What is a type III sensitivity reaction?

A
  • Immune complexes, activation of complement/IgG

- Examples - SLE, post-strep GN

390
Q

What is a type IV sensitivity reaction?

A
  • T cell mediated delayed type hypersensitivity (DTH)

- Examples - TB & contact dermatitis

391
Q

What happens in anaphylaxis?

A
  • Severe hypotension
  • Vasodilation
  • Bronchoconstriction (causing mucous hypersecretion)
392
Q

What does histamine do in a type I sensitivity reaction?

A

They initiate a local inflammatory response

393
Q

What are the structural and functional changes with ageing in the lung?

A
  • Delayed response to hypercapnia and hypoxia - increased vulnerability to ventilatory failure
  • FEV and FVC decreases, so FEV1/FVC decreases, so reading may come across as obstructive
394
Q

What is a cause of impaired gas exchange?

A

Due to changes in the shape of the thorax

395
Q

What happens to costal cartilage in impaired gas exchange?

A

Becomes stiffer - harder to breathe

396
Q

What happens to respiratory muscle in impaired gas exchange?

A

Decreases in mass - less effective

397
Q

What happens to type IIA muscle fibres in impaired gas exchange?

A

Reduce - thus get more tired while breathing = breathe less/less efficiently

398
Q

What happens to muscle fibres in impaired gas exchange?

A

Denervation - less contraction, thus less potent inspiration

399
Q

What happens to elastic recoil in impaired gas exchange?

A

It is lost

400
Q

What happens to elastin fibres in impaired gas exchange?

A

In the alveoli and respiratory bronchioles they degenerate and rupture

401
Q

What happens to V/Q mismatch in impaired gas exchange?

A

Increases

402
Q

What happens to the alveolar surface area in impaired gas exchange?

A

Reduces

403
Q

What happens to lung capillary and blood flow in impaired gas exchange?

A

Reduces

404
Q

What happens to oxygen saturation with normal ageing?

A

Declines. Not important until times of demand

405
Q

What happens to the immune system function in impaired gas exchange and what happens?

A
  • Decreases
  • Glandular epithelia cells decrease thus less protective mucus
  • Decrease sputum clearance
  • Less effective mucociliary system
406
Q

Define PiO2

A

Pressure of inspired oxygen (can change)

407
Q

Define FiO2

A

Fraction of inspired oxygen (0.21 - never changes)

408
Q

What is the Pigas equation?

A

Pigas = Patm x Figas

409
Q

What is extremely high altitude?

A

18,000 feet

410
Q

What is PaCO2 directly proportional to?

A

1/alveolar ventilation

411
Q

How can PAO2 be calculated?

A
  • PAO2 = PiO2 - (PaCO2/R)
  • R = respiratory quotient (CO2 produced/O2 consumed)
  • A = alveolar
  • a = arterial
412
Q

What is respiratory quotient and what is it’s normal value?

A
  • CO2 produced/O2 consumed

- 0.8 with normal diet

413
Q

How can PaO2 be calculated?

A
  • PaO2 = PAO2 - (A-aDO2)
  • A = alveolar
  • a = arterial
  • A-aD = arterial-alveolar difference (usually 1kPa due to ventilation-perfusion mismatch)
414
Q

What is the normal blood PaO2 at sea level?

A

10.5 - 13.5 kPa

415
Q

What is the normal blood PaCO2 at sea level?

A

4.5 - 6.0 kPa

416
Q

What is the normal blood pH at sea level?

A

7.36 - 7.44

417
Q

What happens to pressure as altitude rises?

A

Pressure decreases (not a linear relationship)

418
Q

Does the value for FiO2 change at different altitudes?

A

It remains constant at around 0.21

419
Q

What happens to PiO2 with altitude?

A

Falls with altitude

420
Q

What is the normal response to altitude on the lungs?

A
  • Hypoxia leads to hyperventilation
  • Increased minute ventilation
  • Lowers PaCO2
  • Alkalosis initially & tachycardia
421
Q

How can respiratory alkalosis be compensated for?

A

By renal bicarbonate excretion

422
Q

When diving, how far does it take to drop one atmosphere?

A

Every 10 meters, it drops one atmosphere

423
Q

What is Boyle’s law?

A
  • At a constant temperature, the absolute pressure of a fixed amount of gas is inversely proportional to its volume
  • P1V1 =P2V2
424
Q

What is Henry’s law and how does it relate to descent?

A
  • The amount of gas dissolved in a liquid at a given temperature is directly proportional to the partial pressure of the gas
  • Thus proportionally more gas dissolves in the tissues at depth
425
Q

What may happen in relation to the lungs with free diving?

A
  • Aponea
  • Bradycardia
  • Peripheral vasoconstriction
426
Q

What is the purpose of the lungs in the foetus?

A

No purpose

427
Q

What is the respiratory tract derived from in embryo?

A

The foregut (anterior out pouching) endoderm and associated mesoderm

428
Q

Which part of the respiratory tract is derived from the endoderm?

A

Epithelial lining of trachea, larynx, bronchi and alveoli

429
Q

Which part of the respiratory tract is derived from the splanchnic mesoderm?

A

Cartilages, muscle, connective tissue of tract & visceral pleura

430
Q

When do the lung buds develop in embryo?

A
  • During the 4th week

- Initially appears as the respiratory diverticulum

431
Q

What is the respiratory diverticulum?

A

A ventral outgrowth of foregut endoderm

432
Q

When do the left and right bronchi develop in embryo?

A

During week 5 of development

433
Q

When to terminal bronchioles give way to terminal sacs in embryo?

A

Week 16

434
Q

When are alveolar sac, type I & II pneumocytes developed in embryo?

A

Week 24+

435
Q

What happens in weeks 5-17 in embryo (respiratory)?

A
  • Major airways defined
  • Nests of angiogenesis
  • Smaller airways down to respiratory bronchioles
436
Q

What happens in weeks 16-24 in embryo (resp)?

A
  • Terminal bronchioles

- Alveolar ducts

437
Q

What happens in weeks 24-40 in embryo (resp)?

A

Alveolar budding, thinning ad complexification

438
Q

How does the foetal circulation work?

A
  • Shunting of blood from right to left

- Higher vascular resistance in the lungs meaning higher pressure in right side (supplies lungs)

439
Q

Where does right-to-left shunting happen?

A

Through the foramen ovale

440
Q

What is the main purpose of the systemic circulation?

A

To deliver oxygen to hypoxic tissue

441
Q

Name 3 vasodilators

A
  • Hypoxia
  • Acidosis
  • Carbon dioxide
442
Q

Why do arteries dilate in hypoxia?

A

So more oxygen can be provided to tissues

443
Q

Why is there vasoconstriction when there are high levels of oxygen?

A

As not as much oxygen is required

444
Q

In systemic circulation, is oxygen a vasodilator or vasoconstrictor?

A

Vasoconstrictor

445
Q

What is the purpose of pulmonary circulation?

A

Pick-up oxygen from oxygenated lung

446
Q

What are the vasoconstrictors in pulmonary circulation and why?

A
  • Hypoxia
  • Acidosis
  • Blood will be shunted away to alveoli with better ventilation
447
Q

In pulmonary circulation, is oxygen a vasodilator or vasoconstrictor and why?

A
  • Vasodilator

- Dilation will mean more oxygen can be picked up

448
Q

What is the process of birth and the lungs?

A
  • Fluid in lungs is squeezed out by birth process
  • Adrenaline released due to stress = increased surfactant
  • Air inhaled
  • Oxygen vasodilators pulmonary arteries
  • Umbilical arteries and ductus arteriosus constrict becoming the medial umbilical ligaments & ligament arteriosum
449
Q

When does the production of surfactant in the lungs begin?

A
  • Produced by type 2 pneumocytes from 34 weeks gestation

- Production rapidly increases 2 weeks prior to birth

450
Q

What are the functions of the respiratory system?

A
  • Filtration, humidification & warming
  • Olfaction and tased
  • Gas transport/exchange
  • Protection against infection
  • Speech
451
Q

Where does the respiratory epithelium line?

A

The tubular portions of the respiratory tract

452
Q

What is respiratory epithelium?

A

Pseudostratified ciliated columnar epithelial cells interspersed with goblet cells

453
Q

What are the 4 main functions of the nose?

A
  • Filtration
  • Humidification
  • Warming
  • Olfaction
454
Q

What is the epithelium of the nose?

A
  • Keratinising & non-keratinising squamous epithelium

- Respiratory epithelium

455
Q

What is the structure of the lamina of the nose?

A
  • Richly vascular
  • Contains seromucinous glands
  • Vascular so it can rapidly warm and humidify air
456
Q

Where does olfaction happen in the nose?

A

Roof of nasal cavity, extending down septum and lateral wall

457
Q

What is the structure of the epithelium of the olfactory portion of the nose?

A
  • Pseudostratified columnar epithelium of olfactory cells
  • Serous glands of Bowman
  • Richly innervated lamina propria
458
Q

What are the main functions of the nasopharynx?

A
  • Gas transport
  • Humidification
  • Warming
  • Olfaction
459
Q

What is the epithelium of the nasopharynx?

A

Respiratory epithelium

460
Q

Give 3 functions of the nasal sinuses

A
  • Lower the weight of the skull
  • Add resonance to voice
  • Humidify & warm inspired air
461
Q

What is the epithelium of the nasal sinuses?

A

Respiratory epithelium

462
Q

What is the structure of the larynx?

A
  • A cartilaginous box

- Loose fibrocollagenous storm with seromucinous glands

463
Q

What is the function of the larynx?

A

Voice production

464
Q

What is the epithelium of the larynx?

A

Respiratory epithelium

465
Q

What is the function of the vocal chords?

A

Voice production

466
Q

What is the structure of the vocal cords?

A
  • Stratified squamous epithelium overlying loose irregular fibrous tissue (Reinke’s space)
  • Almost no lymphatics
467
Q

What is the function of the trachea?

A

Conducts air to and from the lungs

468
Q

What is the epithelium of the trachea?

A

Respiratory epithelium

469
Q

What is posterior to the trachea?

A

The tracheal muscle

470
Q

What are the glands in the trachea?

A

Seromucinous glands in submucosa

471
Q

What is the general structure of the trachea in terms of cartilage?

A

C-shaped cartilaginous rings

472
Q

What is the most numerous cell in the terminal bronchioles?

A

Clara cells

473
Q

What is the function of Clara cells?

A

Secretory

474
Q

What is the first part of the distal respiratory tract?

A

Respiratory bronchioles

475
Q

What is the function of the respiratory bronchioles?

A

Gas exchange as well as transport

476
Q

What do the respiratory bronchioles link?

A

The terminal bronchioles and alveolar ducts

477
Q

What is the epithelial structure of the respiratory bronchioles?

A

Cuboidal ciliated epithelium

478
Q

What is the structure of the smooth muscle of the respiratory bronchioles?

A

Spirally-arranged (also no cartilage)

479
Q

How many alveoli are present per lung?

A

150-400 million

480
Q

What is the structure of type 1 pneumocytes?

A

Flattened cells, flattened nucleus, few organelles - main gas exchangers

481
Q

What is the structure of type 2 pneumocytes?

A

Rounded cells, round nucleus, rich in mitochondria, smooth and rough ER

482
Q

Which cells produce surfactant in the lungs?

A

Type 2 pneumocytes

483
Q

What is the structure of alveolar macrophages?

A

Luminal cells, also present in the interstitium

484
Q

What is the function of the alveolar macrophages?

A
  • Phagocytose particulates including dust and bacteria

- Enter lymphatics or leave via mucociliary escalator

485
Q

What is the structure of the alveoli blood-air barrier?

A
  • 1 pneumocyte thick
  • Fused basement membrane of pneumocyte and capillary
  • Vascular endothelial cell
486
Q

What is the structure of the visceral pleura?

A
  • Flat mesothelial cells
  • Loose fibrocollagenous tissue
  • Irregular external elastic layer
  • Interstitial fibrocollagenous layer
  • Irregular internal elastic layer

Phase 1 Med (Liv) (13 decks)

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