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Phase 1 Med > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Name four functions of the nasal cavity?

A
  • Warms inspired air
  • Humidifies air
  • Filters inspired air - brush-like hairs/cilia
  • Defence function - cilia take inhaled particles backwards to be swallowed
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2
Q

What is the role of turbinates in the nose?

A

To double the surface area of the nasal cavity

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3
Q

What is found in the superior meatus and what drains here?

A

The olfactory epithelium is found here - olfactory nerves penetrate into superior meatus through pores in the cribriform plate

Sphenoid sinus drains here - sphenoethmoidal recess

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4
Q

What drains into the inferior meatus?

A

Nasolacrimal duct

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5
Q

Name the four pairs of paranasal sinuses

A

Frontal
Maxillary
Ethmoid
Sphenoid

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6
Q

Which nerve innervates the Frontal sinus?

A

Ophthalmic division (V1) of the trigeminal nerve CN5

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7
Q

Which nerve innervates the maxillary sinuses?

A

Maxillary division (V2) of the trigeminal nerve

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8
Q

Where is the base, Apex and roof of the maxillary sinus?

A

Base - lateral wall of the nose
Apex: zygomatic process of the maxilla
Roof: the floor of the orbit

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9
Q

Which meatus do the Maxillary sinuses drain into?

A

Middle meatus

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10
Q

Describe the position and structure of the ethmoid sinuses

A

The ethmoid sinuses are between the eyes and are a labyrinth of air cells

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11
Q

Which nerves innervate the ethmoid sinuses?

A

Ophthalmic (V1) & Maxillary (V2) branches of the trigeminal nerve

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12
Q

Which meatus does the ethmoid sinus drain into?

A

anterior ethmoid - Middle meatus

posterior ethmoid - sphenoethmoidal recess in superior meatus

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13
Q

Which structures are in close proximity to the sphenoid sinus?

A

Cavernous sinus
Optic canal
Dura
Pituitary gland

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14
Q

Which meatus does the sphenoid sinus drain into?

A

Superior meatus through the sphenoethmoidal recess

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15
Q

Which nerve innervates the sphenoid sinus?

A

The ophthalmic (V1) branch of the trigeminal nerve

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16
Q

What is the role of the pharynx?

A

To take filtered air from the nose to the larynx

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17
Q

Where does the pharynx extend from and finish

A

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

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18
Q

Name the three parts of the pharynx

A

nasopharynx, oropharynx, laryngopharynx

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19
Q

What are the functions of the larynx?

A

Valvular function: prevents liquids and food from entering the lungs

Produces vocal sounds - vocal cords

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20
Q

Name the three double and three single cartilages in the larynx

A 
3 paired (cuneiform, corniculate & arytenoid) and 
3 unpaired (epiglottis, thyroid & cricoid)
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21
Q

Which cartilages take part in changing the shape/size of the vocal cords and how do they do this?

A

Arytenoid cartilages rotate on the cricoid cartilage to change vocal cords

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22
Q

What is the nervous innervation of the larynx?

A

Innervated by the Vagus nerve (CNX) - Superior laryngeal & Recurrent laryngeal nerve

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23
Q

Name the branches of the superior laryngeal nerve and their functions

A

internal - sensation ABOVE vocal cords

external - motor innervation to CRICOTHYROID MUSCLE)

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24
Q

Describe the role of the recurrent laryngeal nerve

A

provides motor innervation for ALL muscles except the
cricothyroid muscle
Sensation below the vocal cords

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25
Q

Describe the route that the left recurrent laryngeal nerve takes

A

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

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26
Q

Describe the route of the right recurrent laryngeal nerve

A

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

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27
Q

What might a patient with an ulcer/tumour on or near the recurrent laryngeal nerve present with?

A

Hoarse voice

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28
Q

What is the average minute volume and cardiac output?

A

Minute volume - approx 5 litres

Cardiac Output - approx 5 litres per minute

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29
Q

At what vertebral level does the trachea start and end?

A

From larynx to carina (C6 - T5)

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30
Q

Describe the structure of the trachea?

A

Semicircular hyaline cartilages (C-shaped cartilage increases flexibility of trachea)
connected by tracheal muscle

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31
Q

What is respiratory epithelia?

A

Pseudo-stratified ciliated, columnar epithelium with goblet cells

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32
Q

Why are inhaled foreign object more likely to enter the right lung?

A

Right main bronchus is more vertically disposed and shorter

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33
Q

How many lobar bronchi division are there in the right and left lungs?

A

Right has 3 divisions

Left has 3 division

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34
Q

How many segmental branches does the right and the left lungs have?

A

Right has 10

Left has 8

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35
Q

What is an Acinus?

A

Acinus: the tissue supplied with air by one terminal bronchiole

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36
Q

Name the two predominant cells found in the alveoli

A

Type 1 pneumocytes

Type 2 pneumocytes

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37
Q

What is the role of type 2 pneumocytes?

A

Secretes surfactant to reduce surface tension

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38
Q

What is the nervous innervation of the lung?

A

The pulmonary plexus lies behind each hilum - right and left vagus nerve and T2-T4 ganglia of sympathetic trunk

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39
Q

What does sympathetic innervation and parasympathetic innervation cause in the lung?

A

Sympathetic (from sympathetic trunk) - results in bronchodilation
- Parasympathetic (from vagus) - results in bronchoconstriction

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40
Q

Which trilaminar layer does the pleura arise from?

A

Mesoderm ( splanchnic lateral plate mesoderm)

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41
Q

Where is the visceral pleura found and describe its innervation

A

applied to the lung surface - only has autonomic innervation

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42
Q

Where is the parietal pleura found and describe its innervation

A

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

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43
Q

Name the different types of blood supply to the lungs

A

Bronchial and pulmonary circulation

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44
Q

Define transpulmonary pressure

A

difference in pressure between the inside and

outside of the lung (alveolar pressure - intrapleural pressure)

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45
Q

Define intrapleural pressure

A

The pressure in the pleural space

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46
Q

Define alveolar pressure

A

Air pressure in pulmonary alveoli

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47
Q

Which muscle is the most important during inspiration?

A

Diaphragm

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48
Q

Which muscles contract during inspiration?

A

Diaphragm and the external intercostals

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49
Q

Which nerve innervates the diaphragm?

A

Phrenic nerve

which arises form C3,4 & 5 (C3,4,5 keeps the diaphragm alive!):

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50
Q

Briefly describe the process of inspiration

A

1) Diaphragm contracts - moves down increasing thoracic volume
2) External intercostals contract - ribs move up and out - increasing volume
3) negative pressure in the lungs causes inwards airflow

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51
Q

Briefly describe the process of expiration at rest?

A

1) Diaphragm and external intercostals relax
2) Elastic recoil - pressure increases as volume decreases
3) lungs passively collapse
4) airflow outwards

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52
Q

Briefly describe the extra processes of forced expiration

A

1) Internal intercostals and abdominal muscles also contract
2) ribs move down and in
3) abdominal muscles force the diaphragm higher up into the thorax - further reducing volume
4) Greater volume of air expired

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53
Q

Which part of the airways has the greatest resistance?

A

Trachea - it is a single ( not branched) and long structure which contributes to increased resistance

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54
Q

Define dead space and how much in total?

A

The volume of air not contributing to gas exchange

150mls anatomical and 25mls alveolar

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55
Q

Define anatomical dead space

A

The volume of air that cannot reach the alveoli

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56
Q

Does a red blood cell come into contact with just one alveoli?

A

No, can come into contact with many alveoli

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57
Q

What is V/Q mismatch?

A

Incorrect proportion of ventilation and capillary perfusion available to each alveolus

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58
Q

What is the main effect of ventilation-perfusion mismatch

A

Decreased partial pressure of oxygen in systemic arterial blood

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59
Q

Why is there naturally some V/Q mismatch in healthy people

A

Gravitational effects cause increase filling of blood vessels at the bottom of the lung due to gravity

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60
Q

Describe what occurs when there is a high V/Q ratio and what can it be caused by?

A

ventilated alveoli but no blood supply at all (known as dead space
or wasted ventilation) due to a blood clot for example

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61
Q

Describe what occurs when there is a low V/Q ratio and what can it be caused by?

A

There may be adequate blood flow through the areas of the lung but there is no ventilation (this is termed shunt) due to collapsed alveoli

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62
Q

What is the bodies response when there is reduced ventilation to a group of alveoli?

A

Hypoxic Pulmonary constriction

Vasoconstriction - Diverting blood away from poorly ventilated area

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63
Q

What is the bodies response when there is reduced perfusion in a group of alveoli?

A

Local bronchoconstriction

diverts airflow away from to areas of the lung with better perfusion

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64
Q

Describe the structure of a Hb molecule

A

Four subunits - two beta and two alpha chains

Four haem groups each with a single Fe2+

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65
Q

Why is the plateau at higher partial pressures of O2 important of the oxygen dissociation curve?

A

Safety factor allowing for normal oxygen saturation of Hb in situations such as high altitude, pulmonary disease and other limitations in lung function

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66
Q

Why is the plateau at higher partial pressures of O2 important of the oxygen dissociation curve?

A

Safety factor allowing for normal oxygen saturation of Hb in situations such as high altitude, pulmonary disease and other limitations in lung function

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67
Q

What changes need to occur for a right shift in the oxygen dissociation curve

A
  • High pH (less acidic)

- Low temp

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68
Q

What does a right shift in the oxygen dissociation curve result in

A

Decreased Hb affinity for O2 so increased O2 unloading at tissues

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69
Q

What does a left shift in the oxygen dissociation curve result in?

A

Increased Hb affinity - less O2 unloading at tissue level

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70
Q

What changes need to occur for a right shift in the oxygen dissociation curve

A

Decreased temp

Increased pH

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71
Q

Does CO have a higher affinity for the oxygen binding sites on Hb

A

Yes - CO has 200 times higher affinity for binding sites compared to O2.

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72
Q

State the equation to calculate the arterial partial pressure of CO2

A

PaCO2 = k V̇CO2 / V̇A

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73
Q

What is the normal pH of blood?

A

7.4 (7.35-7.45)

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74
Q

How does respiratory acidosis arise?

A

Hypoventilation - Inadequate ventilation of alveoli
CO2 cannot be excreted and expired adequately
Partial pressure of CO2 rises and results in more Carbonic acid production and more H+ conc

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75
Q

How does respiratory alkalosis arise?

A

Hyperventilation - increased CO2 excretion - decreased PaCO2 - decreased H+ conc in blood

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76
Q

State Henderson-Hasselbalch’s equation

A

pH=Pka+Log ([A-]/[HA])

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77
Q

Describe Daltons law

A

total pressure of the mixture
is simply the sum of the individual pressures of gases known as partial pressures which are
directly proportional to its concentration

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78
Q

Describe 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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79
Q

Describe Henry’s law

A

The solubility of a gas is proportional to the partial pressure of the gas. S1/P1 = S2/P2.

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80
Q

State the alveolar gas equation

A

PAO2 = PiO2 - PaCO2/R

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81
Q

What equation can we use to calculate pressure

A

Pressure=flow*resistance

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82
Q

Describe Laplace’s law

A

describes the relationship between pressure (P), surface tension
(T) and the radius (r) of an alveolus: P = 2T/r

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83
Q

What is the significance of Laplace’s law

A

It tells us that small alveoli have a greater pressure and so air will move from small alveoli to larger alveoli; uneven aeration. (Surfactant can prevent this).

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84
Q

Define lung compliance

A

A measure of the lung’s ability to stretch and expand

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85
Q

What might cause a decrease in lung compliance

A

Loss in elastic connective tissues

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86
Q

Describe the role of surfactant

A

Reduces surface tension
Increases Lung compliance
Easier to expand lungs

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87
Q

What can we do to increase/stimulate the secretion of surfactant?

A

Take a deep breath - stretches type 2 pneumocyte - stimulates the secretion of surfactant

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88
Q

Define Inspiratory reserve volume

A

The additional volume of air that can be forcibly inhaled after a tidal volume inspiration.

89
Q

Define Expiratory reserve volume

A

The additional volume of air that can be forcibly exhaled after a tidal volume expiration.

90
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

91
Q

Define vital capacity

A

The maximum volume of air that can be exhaled after a maximal inhalation. (ERV + TV + IRV)

92
Q

Define functional residual capacity

A

Amount of air remaining in the lungs after a

normal tidal expiration (RV + ERV)

93
Q

Define inspiratory capacity

A

The maximum volume of air that can be forcibly inspired - IC = TV + IRV.

94
Q

Define total lung capacity and what equation can we use to calculate this?

A

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

95
Q

Define tidal volume

A

The volume of air moved into or out of the lungs during normal, quiet breathing.

96
Q

What proportion of the vital capacity should be expired in one second for healthy individuals?

A

80%

97
Q

Define forced vital capacity (FVC)

A

The maximum volume of air that can be forcibly exhaled after maximal inhalation. Usually in 6 seconds.

98
Q

Define peak expiratory flow (PEF).

A

The greatest rate of airflow that can be obtained during forced exhalation.

99
Q

How could you diagnose a patient with having an obstructive lung disease?

A

The FEV1/FVC ratio would be less than 70% predicted value.

100
Q

Give two ways in which you could could you diagnose a patient with having an restrictive lung disease?

A
  • The FEV1/FVC ratio would be normal but their FVC value would be very low.
  • FEV1 would be less than 80% of the predicted value
101
Q

Name the two main anatomical components of the medullary respiratory centre

A

Dorsal Respiratory Group

Ventral Respiratory Group

102
Q

Describe the role of the DRG

A

Fire during inspiration and have input to the spinal motor neurons that activate respiratory muscles involved in inspiration - Diaphragm and external intercostals

103
Q

Describe the role of the VRG

A

The VRG contains pre-Botzinger complex, responsible for setting respiratory rhythm upper part of VRG
Contains expiratory neurons which fire during active expiration - cause forced expiratory muscles to contract

104
Q

Name the two areas of the pons involved in controlling respiration and their location

A

Apneustic centre - Lower pons

Pneumotaxic centre - upper pons

105
Q

What is the role of the Apneustic centre

A
  • Fine-tuning output of the inspiratory neurons of medulla
  • Continuing activation of inspiratory neurons, inhibits expiration
  • can be overridden by pneumotaxic centre
106
Q

What is the role of the pneumotaxic centre?

A
  • Overrides the Apneustic centre
  • Establishes smooth transition between inspiration and expiration
  • Switches off inspiratory neurons to prevent hyperinflation
107
Q

Where are SASR (slow adapting stretch receptors) located?

A

Found in the smooth muscle around the airways.

108
Q

What activates SASR?

A

Lung distension.

109
Q

How do SASR respond to activation?

A

They inhibit inspiration and so promote expiration.

110
Q

Where are RASR (rapidly adapting stretch receptors) located?

A

Between airway epithelial cells.

111
Q

What activates RASR?

A

Lung distension and irritants.

112
Q

How do RASR respond to activation?

A

Bronchoconstriction.

113
Q

What activates C fibres J receptors?

A

Increased interstitial fluid volume.

114
Q

How do C fibres J receptors respond to activation?

A

They cause rapid, shallowing breathing. Bronchoconstriction, cardiovascular depression and dry cough

115
Q

Where are central chemoreceptors located?

A

Medulla

116
Q

Where are peripheral chemoreceptors located?

A

Carotid and aortic bodies.

117
Q

What stimulates peripheral chemoreceptors?

A

A decrease in PaO2 and an increase in arterial H+ concentration.

118
Q

What is the dominant peripheral chemoreceptor involved in respiration control?

A

Carotid body input

119
Q

Are the peripheral chemoreceptors sensitive to small reductions of the arterial partial pressure of O2?

A

No

120
Q

What stimulates the central chemoreceptors?

A

An increase in H+ concentration of the CSF through CO2 diffusing through BBB

121
Q

What is the respiratory drive more sensitive to, CO2 or O2?

A

It is very sensitive to CO2 and so CO2 is a greater drive. A small change in PaCO2 results in a large ventilatory change.

122
Q

Define Hypoxia

A

Deficiency of oxygen at the tissue level

123
Q

Name 5 causes of hypoxia.

A

1) hypoventilation - loss of respiratory drive/muscle weakness
2) Diffusion impairment - thickening of the alveolar membranes (pulmonary oedema)
3) Shunting - anatomical abnormality
4) V/Q mismatch can be caused by Pulmonary embolus/oedema
5) Reduced PiO2`

124
Q

What is hypercapnia?

A

Increased arterial partial pressure of CO2

125
Q

What is type 1 respiratory failure and what are its causes?

A

• pO2 (partial O2 pressure) is low
• pCO2 (partial CO2 pressure) is low or normal
• Pulmonary embolism (a form of ventilation-perfusion mismatch) most commonly
causes Type 1

126
Q

What is type 2 respiratory failure and what are its causes?

A
  • pO2 is low - Hypoxia
  • pCO2 is high - Hypercapnia
  • Hypoventilation causes Type 2 - muscle weakness, loss of respiratory drive
127
Q

What is the parasympathetic neurotransmitter in the lungs?

A

Acetylcholine.

128
Q

What is the sympathetic neurotransmitter in the lungs?

A

Noradrenaline.

129
Q

Name 2 receptors for Ach.

A

Muscarinic (G protein coupled) and Nicotinic (ligand gated ion channels).

130
Q

What is the effect of Ach on the pulmonary vessels?

A

Bronchoconstriction and vasodilation.

131
Q

What is the effect of noradrenaline on the pulmonary vessels?

A

Bronchodilation and vasoconstriction.

132
Q

Which receptor does Ach bind to for controlling muscle tone?

A

Muscarinic (M3) Cholinergic receptors

133
Q

How does noradrenaline lead to indirect bronchodilation?

A
  • Noradrenaline acts on the adrenal glands
  • Adrenal glands release adrenaline
  • Binds to Beta-2-adrenoreceptors
  • causes bronchodilation
134
Q

What are the neurons called that release acetylcholine and noradrenaline

A

Acetylcholine - chollinergic

Noradrenaline - adrenergic

135
Q

How do bronchodilators work?

A
  • beta-2 agonists - wants to increase bronchodilation

- muscarinic antagonists - wants to decrease bronchoconstriction

136
Q

What is the function of the epithelial barrier in host defence?

A

Moistens and protects airways.

Functions as a barrier to pathogens and foreign matter.

137
Q

Name 4 non-immune host defense mechanisms.

A
  1. Mucus.
  2. Muco-cilliary escalator.
  3. Epithelium.
  4. Cough.
138
Q

What is the muco-ciliary escalator?

A

Mucosal secretions from goblet cells and submucosal glands trap particulate matter. The beating cilia transport the mucus up the respiratory tract. This acts to prevent infection.

139
Q

What is coughing?

A

An explosive expiration that acts to clear foreign matter from the airways. It is an important defence mechanism

140
Q

What nerves does the efferent limb of the cough reflex include?

A

Recurrent laryngeal and spinal nerves.

141
Q

What nerves does the afferent limb of the cough reflex include?

A

Receptors within the sensory distributions of Cn 5, 9 and 10.

142
Q

Why do you see decreased immune function in an ageing lung?

A

There is less protective mucus and sputum clearance is less effective.

143
Q

What is the function of mucus?

A

It protects the epithelium from foreign material and from fluid loss.

144
Q

What is mucus composed of?

A

Water, carbohydrates, lipids and proteins.

145
Q

What mechanism moves airway mucus up into the throat?

A

Muco-ciliary escalator.

146
Q

What is the consequence of mucus plugs in the lungs?

A

Airway obstruction which can ultimately lead to death.

147
Q

briefly describe the process of inflammation

A
  • Bacteria enter a wound
  • Chemical mediators cause vasodilation & increase capillary permeability
  • Diapedesis - passage of neutrophils/monocytes out of blood into tissue
  • phagocytosis occurs
  • Capillaries return to normal as neutrophils continue to clear the infection
148
Q

How do we recognise pathogens we have nerve seen before?

A

Pattern recognition receptors - PRRs.

149
Q

What are alveolar macrophages derived from?

A

Monocytes. They are the resident phagocyte in the lungs and they coordinate inflammatory response.

150
Q

What are the main cells involved in chronic inflammation?

A

Mononuclear cells e.g. monocytes, macrophages, lymphocytes, plasma cells.

151
Q

What is the main cell involved in acute inflammation?

A

Neutrophils! Also eosinophils and basophils.

152
Q

What is the function of helper T cells?

A

they secrete cytokines to attract macrophages and neutrophils etc.

153
Q

What is the most abundant WBC?

A

Neutrophil - 70%

154
Q

Name two types of granules that are found in neutrophils

A

Primary granules and secondary granules

155
Q

What do primary granules contain?

A

• Myeloperoxidase (enzyme used to carry out anti-microbial activity)
• Elastase - enzyme that breaks down elastin in lungs - enables neutrophil to migrate
through lung to get to pathogen
• Cathepsins & defensins (anti-bacterial proteins)

156
Q

What do secondary receptors contain?

A

• Receptors
• Lysozyme - enzyme that breaks down bacterial cell walls
• Collagenase - enzyme that breaks down collagen, allows neutrophils to penetrate
hard to reach collagenised areas

157
Q

Describe six phases/functions of the Neutrophil

A

1) identifying threats using receptors
2) activation - switched of normally as can be dangerous
3) Adhesion - tethered to the endothelial cells of blood vessels via selectins
4) migration - neutrophils squeeze and migrate through the endothelial wall, follow a chemotactic gradient
5) phagocytosis
6) bacterial killing - hydrolytic enzymes in lysosomes

158
Q

What are the outcomes of chronic inflammation?

A

Tissue destruction, fibrosis, necrosis, chronic inflammation.

159
Q

Which results in inflammation, necrosis or apoptosis?

A

Necrosis.

160
Q

What is the difference between necrosis and apoptosis?

A

Apoptosis - controlled cell death, packaged and then phagocytosed
- necrosis is uncontrolled- cells swell - lysis - ROS and enzymes released - causes damage and inflammation

161
Q

Host defence: What is innate immunity?

A

Immunity that doesn’t require prior exposure. It usually involves phagocytosis and inflammation.

162
Q

What is adaptive immunity?

A

An antigen-specific immune response.

163
Q

What are the functions of lymphocytes?

A

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

164
Q

Name five different types of antibody

A
  • IgG
  • IgA
  • IgM
  • IgE
  • IgD
165
Q

Which antibodies are made to things we are allergic to?

A

IgA, IgD, IgE

166
Q

Which is the most abundant antibody

A

IgG

167
Q

which antibody is made at the beginning of infections?

A

IgM

168
Q

What is the function of helper T cells?

A

they secrete cytokines to attract macrophages and neutrophils etc.

169
Q

What is hypersensitivity?

A

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

170
Q

Hypersensitivity: What is the mechanism of a type 1 reaction?

A

Antigens interact with IgE bound to mast cells. Histamine is released. This can cause hay fever, asthma, acute anaphylaxis etc. (Antihistamines are often given as treatment).

171
Q

What can cause a type 1 hypersensitivity reaction?

A

Pollen, cat hair, peanuts (allergies).

172
Q

What can cause a type 2 hypersensitivity reaction?

A

Transplant rejection, transfusion mismatch.

173
Q

What is the mechanism of a type 2 reaction?

A
  • when antibodies IgM or IgG bind to the cell surface associated antigens
  • ## tissue injury
174
Q

What can cause a type 3 hypersensitivity reaction?

A

Fungal.

175
Q

What is the mechanism of a type 3 reaction?

A
  • IgG binds to soluble antigen
  • forms a circulating immune complex
  • immune complex is deposited in the skin and organs
  • causes immune response and leads to tissue damage
  • Farmer’s lung and pigeon fanciers lung
176
Q

What can cause a type 4 hypersensitivity reaction?

A

TB.

177
Q

What is the mechanism of a type 4 reaction?

A
  • Independent of antibodies
  • mediated by T-helper cells
  • pronounced secretion of cytokines from T helper cells activated by antigen
  • takes several days so called delayed hypersensitivity
178
Q

What is the Gell and Coombs classification?

A

It describes 4 types of hypersensitivity reaction.

179
Q

What structures contribute to the respiratory pump?

A

Bones (ribs and sternum), muscles (diaphragm and intercostals), pleura, nerves.

180
Q

What structures make up the conducting airways?

A

Nose, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles.

181
Q

What changes are seen in an ageing lung?

A

Decreased compliance, muscle strength, elastic recoil, immune function. Decreased response to hypoxia and hypercapnia. Impaired gaseous exchange.

182
Q

What happens to the FEV1 and FVC in an elderly person?

A

They both decrease and the residual volume increases.

183
Q

Which alveoli are preferentially ventilated and perfused?

A

Those at the base of the lungs.

184
Q

What 2 equations can be used to work out TLC?

A
  1. TLC = VC + RV.

2. TLC = TV + FRC + IRV.

185
Q

Why do you see decreased elastic recoil in an ageing lung?

A

The elastin degenerates and ruptures.

186
Q

Why do you see a decreased response to hypoxia and hypercapnia in an ageing lung?

A

The lung is more vulnerable and has a decreased awareness meaning these changes aren’t detected till late on.

187
Q

Why do you see the impaired gaseous exchange in an ageing lung?

A

The SA for gaseous exchange decreases and there is increased V/Q mismatch.

188
Q

Why does the residual volume increase in an ageing lung?

A

The chest wall changes shape. There is increased calcification and stiffness.

189
Q

What is the epithelium of the vocal cords?

A

Stratified squamous non-keratinising.

190
Q

What vertebral level does the larynx extend to?

A

T5

191
Q

Why does constriction of bronchioles cause significant increase in airway resistance and can cause an expiratory wheeze such as seen in asthma?

A

Bronchioles have no cartilage, only smooth muscle. This means they are more likely to constrict and increase airway resistance.

192
Q

Which respiratory tract structures are lined with smooth muscle and contain no cartilage?

A

Bronchioles.

193
Q

Anaphylaxis is caused by the cross-linking of an immunoglobulin on the surface of an inflammatory cell, resulting in the release of a potent chemical mediator. State the class of the immunoglobulin, the name of the cell and the name of the chemical mediator.

A
  • Immunoglobulin: IgE.
  • Cell: Mast cell.
  • Chemical mediator: Histamine.
194
Q

What are broncho-pulmonary segments?

A

Discrete functional and anatomical units of the lung. Each segment is supplied by a specific segmental/tertiary bronchus.

195
Q

How many bronchopulmonary segments are there in the right lung and left lung?

A

Right: 10
Left: 8

196
Q

What suppresses alveolar macrophage activation in a healthy lung?

A

Respiratory epithelium.

197
Q

Why is the lung at increased risk of inflammation?

A
  1. Huge area in contact with the external environment.

2. The lung contains the majority of our WBC’s at any one time.

198
Q

Name 3 types of T cells.

A
  1. Cytotoxic T cells.
  2. Helper T cells.
  3. Memory T cells.
199
Q

What is the function of cytotoxic T cells?

A

They track down infected cells.

200
Q

What is the function of helper T cells?

A

they secrete cytokines to attract macrophages and neutrophils etc.

201
Q

What comprises a respiratory acinus?

A

Respiratory bronchiole, alveolar duct and alveolus.

202
Q

What part of the respiratory tract lies behind the sternal angle?

A

The tracheal bifurcation.

203
Q

Give an example of restrictive lung disease?

A

Pulmonary fibrosis.

204
Q

Give an example of obstructive lung disease?

A

Chronic bronchitis, emphysema, COPD

205
Q

What is the affect of pulmonary fibrosis on the following: FEV1, FVC, PEF, TLC and DLCO?

A
  • FEV1 = reduced significantly.
  • FVC = reduced significantly.
  • PEF = Typically not variable.
  • TLC = reduced.
  • DLCO = reduced.
206
Q

What is the affect of emphysema on the following: FEV1, FVC, PEF, TLC and DLCO?

A
  • FEV1 = reduced.
  • FVC = normal or slightly reduced.
  • PEF = typically not variable.
  • TLC = increased (hyperinflation).
  • DLCO = reduced.
207
Q

What is the affect of asthma on the following: FEV1, FVC, PEF, TLC and DLCO?

A
  • FEV1 = normal or slightly reduced.
  • FVC = normal.
  • PEF = variable, diurnal fluctuation.
  • TLC = increased.
  • DLCO = normal.
208
Q

What is DLCO?

A

Uptake of CO in ml at standard temperature and pressure.

209
Q

What is the respiratory diverticulum an out-pouching of?

A

The foregut.

210
Q

What is the respiratory tract derived from?

A
  • anterior outpouching of Foregut
  • Endoderm - epithelial lining of trachea, larynx, bronchi and alveoli
  • mesoderm - splanchnic mesoderm gives rise to cartilage, muscle, connective tissue and visceral pleura
211
Q

When do the lung buds form?

A

4th week

212
Q

What is the respiratory diverticulum?

A

ventral outgrowth of the foregut endoderm

213
Q

What does the lung bud form from?

A

The respiratory diverticulum - an out-pouching of the fore gut endoderm

214
Q

What does the respiratory diverticulum go on to form?

A

lung buds

215
Q

What are the 5 stages of respiratory tract development called? What happens in these stages?

A
  1. Embryonic (0-5 weeks): lung buds enlarge, trachea develop
  2. Pseudoglandular (5-16 weeks): branching of trachea to form terminal bronchioles and angiogenesis occurs
  3. Canalicular (16-26 weeks): Respiratory bronchioles form and primitive alveoli form - 1/6 adult number
  4. Saccular (26w-birth): Terminal sacs form, type 1 and 2 pneumocytes develop and surfactant produced
  5. Alveolar (8 months to childhood): Alveoli mature, more alveoli and respiratory bronchioles
216
Q

Describe the first breath.

A
  1. Fluid is removed from the lungs.
  2. Adrenaline increases surfactant release.
  3. Air is inhaled.
  4. O2 VASODILATES pulmonary vessels.
  5. Umbilical arteries and ductus arteriosus constricts becoming medial umbilical ligaments and ligamentum arteriosum Foramen ovale closes.
217
Q

Embryology: When is surfactant produced?

A
  • 34 weeks gestation

- Massive increase 2 weeks prior to birth

218
Q

Premature babies may have surfactant deficiency. What are the consequences of this?

A
  1. Respiratory distress syndrome.
  2. Non-compliant lungs.
  3. Unequal aeration.
  4. Reduced lung volume.
219
Q

At birth what happens to the pulmonary artery pressure and the aortic pressure and what does this result in?

A
  • Pulmonary artery goes down exponentially
  • Aortic pressure increases
  • Lung pressure decrease systemic increased
  • blood moves into lungs via diffusion to be oxygenated

Phase 1 Med (7 decks)

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