Respiratory System Flashcards

1
Q

What is the respiratory system involved in?

A
  • Gas exchange
  • Speech
  • Smell
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2
Q

What are the two functional parts of the respiratory system?

A
  • Conducting portion

- Respiratory portion

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3
Q

What does the Conducting portion of the respiratory system do?

A
  • Transports air

- Conditions air (warms and moistens)

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4
Q

What does the Respiratory portion of the respiratory system do?

A
  • Thin, moist, delicate membrane

- Site of gaseous exchange

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5
Q

What are the 4 paranasal sinuses?

A
  • Frontal sinuses
  • Ethmoidal cells
  • Maxillary sinuses
  • Sphenoidal sinus
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6
Q

What is the purpose of the 4 paranasal sinuses?

A

Warm, moisten and filter air

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7
Q

Why does air need to be conditioned?

A
  • Warmed for efficient gas exchange
  • Moistened to not damage delicate membranes
  • Filtered from pathogens
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8
Q

Anatomically, what does the conducting portion cover?

A

Nasal cavity to Terminal Bronchi

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9
Q

What are the subdivisions of the thoracic cavity?

A
  • Mediastinum

- Pulmonary cavities

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10
Q

What are the anatomical differences between the right and the left lung?

A

Right: 3 lobes, short, broad and larger
Left: 2 lobes, tall and narrow

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11
Q

What are the 3 lobes of the right lung?

A
  • Superior
  • Inferior
  • Med
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12
Q

What are the subdivisions of bronchi?

A
  • Right and Left main/primary Bronchus
  • Lobar Bronchi
  • Segmental bronchi of middle lobe
  • Terminal bronchi
  • Respiratory bronchioles
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13
Q

What are the alveolar sacks surrounded by?

A

Capillary beds that Receive deoxygenated blood via pulmonary arteries and Send oxygenated blood via pulmonary veins

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14
Q

What is an artery?

A

Carries blood away from the heart (oxygenated)

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15
Q

What is a vein?

A

Carries blood to the heart (deoxygenated)

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16
Q

How is the respiratory system divided anatomically?

A
  • Upper respiratory tract (Nasal cavity to pharynx to larynx)
  • Lower respiratory tract (Trachea to bronchi to lungs)
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17
Q

What is an URT infection?

A

Common cold

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18
Q

What is a LRT infection?

A

Pneumonia

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19
Q

What are the functions of the thoracic cage?

A

Protection and respiratory movements

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20
Q

Which ribs are ‘floating’ and why?

A

11 and 12 aren’t connected to the sternum

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21
Q

What is breathing?

A

The mechanism in which fresh atmospheric air passes to alveoli and stale air leaves alveoli

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22
Q

What are the 3 planes of movement in breathing?

A
  • Vertical
  • Antero-posterior
  • Transverse
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23
Q

What is the function of the diaphragm?

A
  • Closes off thoracic outlet
  • Separates thorax from abdomen
  • Plays major role in breathing
  • Apertures allow passage of structures (vessels, nerves, oesophagus) to and from abdomen.
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24
Q

Which nerves keep the diaphragm alive?

A

Phrenic nerves - C3, 4 and 5

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25
Q

What are the 3 thin muscle layers within each intercostal space?

A
  • External intercostal
  • Internal intercostal
  • Innermost intercostal
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26
Q

What else is found in each intercostal space?

A
  • Intercostal nerve
  • Intercostal artery
  • Intercostal vein
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27
Q

What are the pleura?

A

Each lung is surrounded by a membranous sac that encloses the lung and forms the pleural
cavity. There are two pleural cavities either side of the heart in the thorax.

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28
Q

What is the pleural cavity and it’s purpose?

A

It contains a thin film of fluid which a) helps the lungs to slide and b) creates
surface tension between the parietal and visceral (lung) layers to aid inspiration.

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29
Q

What are the two types of pleura?

A
  • Visceral

- Parietal

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30
Q

What are the 4 divisions of the parietal pleura?

A
  • Cervical
  • Costal
  • Diaphragmatic
  • Mediastinal
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31
Q

Why is it important to divide the parietal pleura into sections?

A

Different parts of the parietal pleura
receive sensory innervation from
different nerves (pain the patient reports may be in site or nerve origin)

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32
Q

What is ventilation?

A

The process of moving gases in (inspiration) and out (expiration) of the lungs

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33
Q

Whats breathing (V2)?

A

The bodily function that leads to ventilation of the lungs. Also known as (external) respiration

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34
Q

What are the two classifications of diseases affecting ventilation?

A
  • Obstructive conditions (tubes aren’t as effective in conducting gases)
  • Restrictive conditions (loss of elasticity in the lungs or chest wall)
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35
Q

What are examples of obstructive conditions?

A

Asthma, chronic obstructive pulmonary disease, lung cancer

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36
Q

What are examples of restrictive conditions?

A

Intrinsic - pulmonary fibrosis

Extrinsic - pneumothorax, disorders of the thoracic skeleton

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37
Q

What moves during quiet breathing?

A

-diaphragm -external intercostals stabilise ribcage

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38
Q

What moves during increased effort breathing?

A
  • diaphragm
  • external intercostals lift & expand ribcage
  • accessory muscles
  • neck muscles
  • shoulder girdle muscles
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39
Q

Which nerves supply intercostals?

A

segmental thoracic nerves

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40
Q

What can spinal cord injury lead to?

A

ventilatory muscle paralysis

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41
Q

What is the effect of the thoracic cage expanding on the intrapleural space?

A

It exerts an increasing negative pressure on it

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42
Q

How is the volume of air moving in and out of the lungs during ventilation measured?

A

Spirometer

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43
Q

What are the 4 lung volumes?

A
  • Tidal volume
  • Inspiratory reserve volume
  • Expiratory reserve volume
  • Residual volume
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44
Q

What is the tidal volume?

A

Volume of air moved in or out of the lungs during normal breathing

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45
Q

What are the typical values of tidal volume?

A

At rest: 6-7 ml/Kg

Exercise: 15 ml/Kg

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46
Q

What is the Inspiratory reserve volume?

A

After a normal expiration, take as deep a breath in as possible

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47
Q

What is the Expiratory reserve volume?

A

After a normal inspiration, breath out as deeply as possible

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48
Q

What is the Residual volume?

A

Even after a maximal expiration, a volume of air remains in the lungs.

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49
Q

What is the cause of residual volume?

A

The rigid nature of the thorax and the pleural attachments of the lungs to the chest wall that prevent complete emptying of the lungs

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50
Q

Which lung volume cannot be measured by spirometry?

A

Residual volume

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51
Q

What is the total lung capacity?

A

TV + IRV + ERV + RV

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52
Q

What is the vital capacity?

A

TV + IRV + ERV

After a maximal inspiration make a maximal expiration

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53
Q

What is the functional residual capacity?

A

ERV + RV

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54
Q

What is a vitalograph spirometer used to measure?

A
  • the forced vital capacity (FVC)

- the forced expiratory volume in 1 second (FEV1)

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55
Q

What is a peak flow meter used to measure?

A

The peak expiratory flow rate (PEFR)

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56
Q

What is used to distinguish between obstructive and restrictive conditions?

A

FEV1/FVC ratio

reversibility of airflow limitation

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57
Q

What are the uses of PEFR?

A
  • Convenient way of measuring airway obstruction
  • Not as good as spirometry for airway limitation
  • Patients can use it to monitor COPD or asthma at hoem
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58
Q

When are the measurements of FEV1 and PEFR made?

A

Before and after inhalation

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59
Q

Is airway constriction in asthma reversible?

A

Yes. FEV1 and PEFR would be restored to normal after Salbutamol

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60
Q

Is airway constriction in COPD reversible?

A

No.
(or nearly irreversible
<15%, or <200 mL/s, improvement in FEV1 and PEFR after salbutamol)

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61
Q

What is the relationship between intrathoracic pressure and lung volume during tidal breathing?

A

Hysteresis

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62
Q

What is hysteresis?

A

the phenomenon in which the value of a physical property lags behind changes in the effect causing it

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63
Q

Why does hysteresis occur in the lungs?

A

because of the elastic nature of the tissues

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64
Q

What is compliance?

A

the change in lung volume per unit change in intrathoracic pressure

C = ΔV / ΔP

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65
Q

How is compliance measured?

A
  • Spirometry for volume

- Oesophageal balloon for pressure

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66
Q

What is the recoil pressure if the lungs?

A

Pressure driving the lung to collapse. Difference between alveolar pressure and intrapleural pressure.

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67
Q

What is the recoil pressure of the chest wall?

A

Intrapleural pressure – barometric pressure

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68
Q

What is the Functional Residual Capacity?

A

the relaxation point of the respiratory system when chest wall & lung recoil pressures are equal but opposite (equilibrium)

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69
Q

Which diseases are associated with reduced compliance?

A
  • Circumferential burn
  • Pulmonary fibrosis
  • Kyphoscoliosis
  • Emphysema
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70
Q

What is surfactant produced by?

A

type II alveolar cells

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71
Q

What does surfactant consist of?

A

90% phospholipid, 10% protein

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72
Q

What does surfactant do?

A

Acts as a detergent to reduce alveolar surface tension

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73
Q

How does the surfactant reduce alveolar surface tension?

A
  • Increases pulmonary compliance
  • Prevents atelectasis
  • Aids alveolar recruitment
  • Minimises alveolar fluid
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74
Q

What illness is surfactant deficient in?

A

Infant respiratory distress syndrome (premature babies do not produce enough)

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75
Q

What is Pulmonary Fibrosis?

A

Pulmonary fibrosis is a condition in which the lung tissue becomes thickened, stiff and scarred over a period of time, becomes less elastic.

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76
Q

What is Kyphoscoliosis?

A

A deformity of the spine characterized by abnormal curvature of the vertebral column in two planes (coronal and sagittal). It is a combination of kyphosis and scoliosis

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77
Q

What is a Circumferential burn?

A

A burn that goes all the way round the body. The scar tissue is inelastic and restricts the expansion of the chest.

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78
Q

What is emphysema?

A

Type of COPD. It means destruction of the lung. In emphysema, the breathing tubes are narrowed and the air sacs are damaged.

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79
Q

What can cause alveoli in dependent lung regions to be poorly ventilated?

A

When the closing capacity exceeds the functional residual capacity

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80
Q

What is the law of Laplace in relation to the lungs?

A

According to the law of Laplace, the alveolar surface tension for a particular alveolar radius must be opposed by an appropriate transmural pressure.

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81
Q

How does the body stop smaller alveoli from collapsing and emptying into larger alveoli?

A

By producing surfactant which reduces the surface tension of the alveoli.

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82
Q

What happens to surfactant as alveolar volume increases?

A

It becomes more dispersed - and each alveolus produces the same amount of surfactant.

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83
Q

How is turbulent flow different from laminar flow?

A
  • Increased flow
  • Reduced calibre
  • Branching
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84
Q

Is laminar flow more efficient than turbulent flow?

A

Yes. Work increases by the power of 2 in turbulent

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85
Q

What percentage of your energy expenditure is the work of breathing in health at rest?

A

2-5% of energy expenditure

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86
Q

What percentage of your energy expenditure is the work of breathing at maximal hyperventilation?

A

30% of energy expenditure

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87
Q

What is your energy expenditure in restrictive conditions?

A

Work is minimised with rapid small volume breaths

88
Q

What is your energy expenditure in obstructive conditions?

A

Work is minimised with large volume slow breaths

89
Q

Where are breath sounds generated (stethoscope)?

A

Large airways. Breath sounds heard over the lungs are attenuated by the distal airways.

90
Q

What is the pressure gradient?

A

The difference in partial pressures of the respective gases in the alveolus and the blood

91
Q

What is the partial pressure of a gas in a mixture?

A

The pressure that it would exert if it was the only gas in the container

92
Q

Equation of partial pressure?

A

tot. pressure x fractional conc.

93
Q

Why is the pp of O2 in the alveoli lower than in room air?

A
  • Inspired air is humidified in the upper airway
  • In the alveoli oxygen is taken up while carbon dioxide is added
  • The body consumes more O2 molecules than it produces CO2 molecules (typically 1.25x)
94
Q

What is the pp of water vapour?

A

6.3kPa

95
Q

What is the pp of alveolar O2?

A

13.7kPa (considering pp of CO2)

96
Q

What is shunting of the blood?

A

Venous blood enters the bloodstream without passing through functioning lung tissue. Shunting of blood may result from abnormal vascular communications or from blood flowing through unventilated portions of the lung

97
Q

What is the relationship between the pp of a gas in solution and it’s solubility?

A

Inversely proportional.

Low solubility - high partial pressure

98
Q

What is more soluble in water ()2 or CO2)?

A

CO2 is 24x more soluble in water

99
Q

How long does it take for O2 to equilibrate across alveoli?

A

0.25 seconds, CO2 takes less time

100
Q

What problems are caused by thickening of the alveolar-capillary membrane?

A

Diffusing capacity (O2) is reduced, eg. in left heart disease

101
Q

What is ARDS?

A

Acute Respiratory Distress Syndrome - a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. Symptoms include shortness of breath, rapid breathing, and bluish skin coloration.

102
Q

What is alveolar consolidation?

A

A region of (normally compressible) lung tissue that has filled with liquid instead of air

103
Q

What is a pulmonary edema?

A

A condition caused by excess fluid in the lungs. This fluid collects in the numerous air sacs in the lungs, making it difficult to breathe. In most cases, heart problems cause pulmonary edema

104
Q

What is an atelectasis?

A

Collapse or closure of a lung resulting in reduced or absent gas exchange

105
Q

What are the clinical features of disordered breathing?

A
  • snoring
  • daytime somnolence
  • associated with obesity and hypertension
106
Q

What are some examples of sleep disordered breathing?

A
  • Snoring (25% of people)

- Sleep apnoea (10%)

107
Q

What is sleep apnoea?

A

Breathing stops for 10+ seconds during sleep

108
Q

What are the treatments for sleep disordered breathing?

A
  • Weight loss

- CPAP (Continuous positive airway pressure)

109
Q

What cells produce airway lining fluid?

A

Ciliated epithelial cells and Goblet cells

110
Q

What type of Ciliated epithelial cells are found in the nose and pharynx?

A

Pseudostratified

111
Q

What type of Ciliated epithelial cells are found in the trachea and bronchi?

A

Columnar

112
Q

What type of Ciliated epithelial cells are found in the bronchioles?

A

Cuboidal

113
Q

What does the airway release mucin in response to?

A
  • airway irritation
  • tobacco smoke
  • infection
114
Q

What are the cillia inhibited by?

A
  • tobacco smoke
  • inhaled anaesthetics
  • air pollution
  • infections
115
Q

How does the airway lining fluid aid airway defense?

A
  • Muco-ciliary escalator

- Expectoration

116
Q

What are the clinical features of Cystic Fibrosis?

A
  • Autosomal recessive inheritance
  • Abnormal CF transmembrane regulator protein
  • Progressive lung infection and destruction
  • Affects all systems with epithelial surfaces
117
Q

Where are very large (>8μm) particles deposited?

A

Nose and Pharynx by inertial impaction

118
Q

Where are large (3-8μm) particles deposited?

A

Large airways by inertial impaction

119
Q

Where are small (0.5-3μm) particles deposited?

A

Bronchioles by sedimentation

120
Q

Where are very small (<0.5μm) particles deposited?

A

They are exhaled! by diffusion

121
Q

Why are the side effects of inhalers caused?

A
  • Particle size anywhere from 1-35μm
  • Small particles to bronchioles (beneficial)
  • Large particles to pharynx (side effects)
122
Q

What are the non-immunological systems of pulmonary defense?

A
  • Physical barrier and removal
  • Chemical inactivation (lysozome, protease enzymes eg. elastase, antimicrobial peptides)
  • Alveolar macrophages
123
Q

What is the humoral defence of the lungs?

A
  • lgA (nose and large airways)
  • lgG (small aitways)
  • lgE (allergic disease)
124
Q

What does inhaling carbon monoxide cause?

A

Decreased oxygen carriage

125
Q

What does inhaling nitrogen oxides cause?

A

Airway irritation and asthma

126
Q

What does inhaling ozone cause?

A

Airway irritation and cough

127
Q

What does inhaling particulate matter cause?

A

Lung and systemic inflammatory responce

128
Q

What is the relationship of amount of gas in solution to it’s temperature?

A

Proportional. More dissolves at a LOW temperature.

129
Q

How do we calculate oxygan saturation?

A

HbO2/HHb + HbO2

130
Q

How do we calculate volume of oxygen?

A

SO2 x [Hb] x 1.39 (Hüfner constant)

131
Q

What is the molecular basis of O2 binding?

A
  • O2 binding site to haem is in a crevice
  • In R ‘relaxed’ form O2 can access binding site
  • In T ‘tense’ form O2 is pushed out
132
Q

What causes thalassaemia?

A

Absent globin chain, so other globin chains are used, often unsurvivable.

133
Q

What causes sickle cell disease?

A

Defective globin chain - single amino acid substitution on the Beta globin chain.

134
Q

What causes methaemoglobin?

A

Defective Fe atom (Fe3+ rather than Fe2+), drug induced, metHb doesn’t carry oxygen.

135
Q

What causes CO Hb?

A

Wrong ligand, smoking/house fires, CO blocks O2 binding site.

136
Q

What is a buffer?

A

a buffer is a solution that can minimise changes in the free H+ concentration
and therefore in pH

137
Q

How do we calculate pH?

A

pH= - log10 [H+]

138
Q

What is a normal blood pH range?

A

pH 7.35 - 7.45

139
Q

What 3 different forms is CO2 carried in in the blood?

A
  • Dissolved in the blood (temp dependent, 3ml per dl)
  • Carbamino compounds (bound to R-NH2 groups on proteins, 4ml per dl)
  • As carbonic acid/bicarbonate (45ml per dl of blood)
140
Q

What catalyses the slow reaction of buffering of CO2 in the blood?

A

Carbolic hydrase

141
Q

What is the Hamburger shift?

A

The chloride shift refers to the exchange of bicarbonate (HCO3−) and chloride (Cl−) across the membrane of red blood cells

142
Q

What is the Haldane effect?

A

Ability of deoxygenated blood to carry more CO2 than oxygenated blood

143
Q

How is H+ excreted?

A

In urine, controlled by pH in a slow response

144
Q

What can cause respiratory alkalosis?

A

Hyperventilation

145
Q

What can cause metabolic alkalosis?

A
  • Vomiting

- Abuse of antacid remedies

146
Q

What can cause respiratory acidosis?

A

Ventilatory failure

147
Q

What can cause metabolic acidosis?

A
  • Renal failure
  • Diabetic ketoacidosis
  • Shock
148
Q

What does the upper respiratory tract consist of?

A

The conducting portion:

  • Nasal cavities
  • Nasopharynx
  • Oropharynx
149
Q

What does the lower respiratory tract consist of?

A

-Larynx
-Trachea
-Bronchi
-Bronchioles
-Terminal bronchioles
Then the respiratory portion:
-Respiratory bronchioles
-Alveolar ducts
-Alveolar sacs
-Alveoli

150
Q

What are the lungs developed from?

A

Endoderm

151
Q

What are the connective tissues of the lungs developed from?

A

Mesoderm

152
Q

Where does the lung bud first form?

A

The ventral wall of the foregut

153
Q

What is the gut tube divided into?

A
  • Foregut
  • Midgut
  • Hindgut
154
Q

When does the lung bud appear?

A

Day 22

155
Q

How does the lung bud develop?

A
  • Grows ventrocaudally
  • Tracheoesophageal ridges separate the respiratory diverticulum from the foregut (except laryngeal inlet)
  • Dorsally oesophagus
  • Ventrally trachea and lung bud which has now divided to form two lung buds
156
Q

What is a fistula?

A

An abnormal channel or passageway connecting one internal organ to another, or to the outside surface of the body

157
Q

How many live births do fistulas occur in?

A

1 in 3000 to 4500 live births

158
Q

Why does a Tracheoesophageal fistula occur?

A

Incomplete division of foregut into oesophageal and respiratory portions

159
Q

In what % of cases is a Tracheoesophageal Fistula associated with oesophageal atresia?

A

85-90%

160
Q

What is a oesophageal atresia?

A

A congenital medical condition that affects the alimentary tract. It causes the esophagus to end in a blind-ended pouch rather than connecting normally to the stomach.

161
Q

What is a fistula between the trachea and oesophagus sometimes called?

A

H-type tracheoesophageal fistula

162
Q

What are the signs of a H-type tracheoesophageal fistula?

A
  • Abdomen rapidly distends as stomach fills with air.
  • MIlk enters respiratory system
  • Some stomach contents (acid/enzymes) will enter the respiratory system
163
Q

What other congenital abnormalities are TOF’s associated with?

A
V-Vertebral defects
A-Anal Atresia
(C)-Cardiac defects
T-Tracheo-oesophageal fistulas
E-Esophageal atresia
R-Renal abnormalities
(L)-Limb defects
164
Q

What are the acronyms for congenital diseases?

A

VACTERL

VATER

165
Q

When does further differentiation result in formation of the main bronchi/secondary bronchi?

A

Week 5

166
Q

When do the tertiary bronchi develop?

A

Week 6

167
Q

How many bronchopulmanory segments are found on each side at 6 weeks?

A

10 right

8 left

168
Q

When does the branching continue to form terminal bronchioles?

A

Week 16

169
Q

When are the respiratory bronchioles developed by?

A

Week 26

170
Q

When do the first alveoli develop?

A

Week 36

171
Q

What forms the visceral mesoderm?

A
  • Cartilage
  • Smooth muscle
  • Connective tissue
  • Capillaries
172
Q

What does the visceral mesoderm form?

A

Visceral Pleura

173
Q

What does the parietal mesoderm form?

A

Parietal pleura

174
Q

What is pulmonary agenesis?

A
  • Complete absence of bronchi and vasculature
  • Can be unilateral or bilateral
  • Bilateral agenesis is incompatible with life
175
Q

Why does pulmonary agenesis occur?

A

Occurs when lung bud fails to split

176
Q

What is the clinical presentation of pulmonary agenesis?

A
  • Child usually develops respiratory distress
  • Remaining lung is compromised, usually by a lower respiratory tract infection.
  • 60% have other congenital anomalies including cardiac lesions, diaphragmatic hernias, and skeletal anomalies
  • Agenesis of the right lung is associated with a higher frequency of anomalies
  • May present with cyanosis
177
Q

What does left agenesis look like on X-ray/endoscopy?

A

X-ray: enlarged right lung, deviation of heart and trachea

Endoscopy: absent left bronchus

178
Q

What is pulmonary hypoplasia?

A
  • All components are present, but incompletely developed
  • Severity of hypoplasia determines the degree of respiratory compromise
  • May be found in association with congenital diaphragmatic hernia (CDH)
179
Q

What is branching morphogenesis?

A
  • Supernumerary lobes or segments

- Little functional sugnificance

180
Q

What are some examples of abnormal lung development?

A
  • Pulmonary hypoplasia
  • Branching morphogenesis
  • Pulmonary agenesis
181
Q

What 4 periods is the maturation of the lungs divided into?

A
  1. Pseudoglandular
  2. Canalicular
  3. Saccular/Terminal sac
  4. Alveolar
182
Q

What weeks does the pseudoglandular period span?

A

5-17 weeks

183
Q

What occurs during the pseudoglandular period?

A

Branching of the respiratory tree has occurred to form terminal bronchioles. Respiration NOT possible, fetus could not survive.

184
Q

What weeks does the canalicular period span?

A

16-25 weeks

185
Q

What occurs during the canalicular period?

A
  • Terminal bronchioles give rise to respiratory bronchioles, which give rise to alveolar ducts
  • Mesodermal tissue becomes highly vascularised
  • Respiration is possible towards end of period as some terminal sacs have developed at the ends of the respiratory bronchioles (and remember highly vascularised)
  • Low chance of fetal survival
186
Q

What occurs during the canalicular period?

A
  • Terminal bronchioles give rise to respiratory bronchioles, which give rise to alveolar ducts
  • Mesodermal tissue becomes highly vascularised
  • Respiration is possible towards end of period as some terminal sacs have developed at the ends of the respiratory bronchioles (and remember highly vascularised)
  • Low chance of fetal survival
187
Q

What occurs during the terminal sack period?

A
  • Further terminal sacs (primitive alveoli) develop
  • Epithelium thins and capillaries come into ‘contact’ with epithelium
  • Blood-air barrier formed
  • Surfactant forms a film over the internal walls of terminal sacs.
  • Decreases surface tension thus facilitating inflation
  • Fetus born at 24 weeks can survive but may suffer Respiratory Distress Syndrome
188
Q

What occurs during the terminal sack period?

A
  • Further terminal sacs (primitive alveoli) develop
  • Epithelium thins and capillaries come into ‘contact’ with epithelium
  • Blood-air barrier formed
  • Surfactant forms a film over the internal walls of terminal sacs.
  • Decreases surface tension thus facilitating inflation
  • Fetus born at 24 weeks can survive but may suffer Respiratory Distress Syndrome
189
Q

When does the alveolar period occur?

A

36 weeks to 8 years

190
Q

What occurs during the alveolar period?

A
  • Development of the lungs after birth is due mainly to an increase in the number of respiratory bronchioles and alveoli
  • 95% of mature alveoli do not develop until after birth
191
Q

What occurs to the respiratory system DURING birth?

A
  • Breathing movements start in utero and serve to remove amniotic fluid
  • Kicks starts muscles of respiration into action
  • At birth any remaining lung fluid rapidly reabsorbed by capillaries
  • At birth any remaining lung fluid rapidly reabsorbed by capillaries
  • Circulatory changes
192
Q

What would RDS present like in a birth at 23 weeks?

A
  • Laboured breathing, threatens infant with immediate asphyxiation
  • Increased rate of breathing
  • Mechanical ventilation needed
  • Damage to alveolar lining, fluid and serum proteins leak into alveolus
  • Continued injury may lead to detachment of alveolar lining
  • Chronic injury in preterm infants may cause bronchopulmonary dysplasia
193
Q

What is dysplasia?

A

Dysplasia means ‘abnormal formation’ so that a part/cell is abnormal

194
Q

What treatments are available for RDS?

A
  • Glucocorticoid treatment accelerates fetal lung development and surfactant production (given during pregnancy to mothers at higher risk of premature birth)
  • Surfactant therapy - natural or artificial surfactant
195
Q

What is perfusion?

A

Blood flow through any organ

196
Q

What is the effect of gravity on the alveoli?

A

Apical alveoli are about 4 times larger than basal alveoli in upright posture. Basal alveoli can expand more than apical alveoli. Basal regions of lungs have better ventilation than apical regions.

197
Q

Which vessels supply bronchial circulation?

A
  • Bronchial artery from thoracic aorta

- Bronchial vein to superior vena cava

198
Q

What are the blood vessels running through the lung parenchyma called?

A

Extra-alveolar vessels

199
Q

Where does gas exchange start in the lungs?

A

Beyond terminal bronchioles, blood vessels form capillary beds (starting with smaller arterioles)

200
Q

How many alveoli are there on average?

A

280 billion capillaries form a dense network in the walls of 300 million alveoli

201
Q

What are the effects of emphysema on gas exchange?

A
  • Widespread destruction and dilatation of distal airway
  • Regional destruction of vascular beds
  • Poor gas exchange and hypoxia
202
Q

What is hydrostatic pressure?

A

Force exerted by weight of a fluid (blood/ water) due to gravity

203
Q

What is the hydrostatic pressure across the lungs considered in relation to?

A

The position of the right ventricle

204
Q

What affects the diameter of the extra-alveolar vessels?

A

Lung volume

205
Q

What is zone 1 of the lungs?

A

Alveolar dead space:

  • Good ventilation but no perfusion
  • No gas exchange
  • Poor blood flow
  • Apices of the lungs, very small area in healthy people
  • P alveolar > P arterial > P venous
  • Blood flow determined by difference in P alveolar and P arterial
206
Q

What is zone 2 of the lungs?

A

Recruitment zone:

  • Lower down the lung than zone 1
  • Higher P arterial due to higher hydrostatic pressure
  • Recruitment of more alveolar unit especially in systole
  • P arterial > P alveolar > P venous
  • Blood flow determined by difference in P arterial and P alveolar
207
Q

What is zone 3 of the lungs?

A

-Lung bases
-Hydrostatic forces raise P arterial and P venous above
P alveolar
-P arterial > P venous > P alveolar
-Continuous blood flow
-Blood flow determined by difference in P arterial and P venous

208
Q

What is the physiological dead space?

A

Anatomic dead space + alveolar dead space

209
Q

What is the anatomic dead space?

A

Conducting airways; no gas exchange

210
Q

What is the alveolar dead space?

A

Unperfused or poorly perfused alveoli

211
Q

What is a pulmonary embolism?

A

A blockage of an artery in the lungs by a substance (blood clot) that has moved from elsewhere in the body through the bloodstream

212
Q

What are the signs and symptoms of a pulmonary embolism?

A
  • Shortness of breath
  • Chest pain particularly upon breathing in
  • Coughing up blood
  • Severe hypoxia
  • Enlarged alveolar dead space
  • May potentially lead to death
213
Q

What is a pulmonary shunt?

A

Occurs when the alveoli fill with fluid, causing parts of the lung to be unventilated although they are still perfused OR Deoxygenated blood reaching left side of the heart either bypassing lungs or failing to get oxygenated in the lungs

214
Q

What is pneumothorax?

A

Collapsed lung. Occurs when air leaks into the space between your lung and chest wall. This air pushes on the outside of your lung and makes it collapse.

215
Q

How is pneumothorax treated?

A
  • Immediate needle decompression

- Chest drain connected to an underwater sealed system