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Phase 1 Medicine COPY > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What structures contribute to the respiratory pump?

A

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

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2
Q

What structures make up the conducting airways?

A

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

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3
Q

What is the function of the conducting airways?

A

To filter, warm, humidify and conduct air to the lungs.

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4
Q

What is respiratory epithelium?

A

Pseudo-stratified, columnar, ciliated, interspersed with goblet cells.

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5
Q

Where is the resistance greatest in the airway?

A

In the trachea - the trachea is longer (length adds resistance) and there is only one of it (branching decreases resistance).

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6
Q

What equation can be used to demonstrate resistance of an airway?

A

Poiseuille’s law: R = 8ƞl / πr^4.

ƞ = viscosity, l = length

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7
Q

Briefly describe inspiration.

A

Inspiration is an active process. The external intercostal muscles and diaphragm contract. The volume of the thoracic cavity increases and you get a negative intra-thoracic pressure; air is drawn in.

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8
Q

What is the ‘pump handle’ representing?

A

The movement of the sternum. In inspiration the sternum moves anteriorly and superiorly.

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9
Q

What is the ‘bucket handle’ representing?

A

The movement of the rib cage. In inspiration the rib cage moves upwards and outwards.

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10
Q

Briefly describe expiration.

A

Expiration is usually passive. The ribs move down and in, the diaphragm relaxes. The intra-thoracic volume decreases and the pressure increases. Air is forced out.

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11
Q

Which muscles are involved in active expiration?

A

The internal intercostals; these muscles contract pulling the ribcage inwards and downwards.

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12
Q

What is V/Q mismatch?

A

When the perfusion of blood in capillaries isn’t matching the ventilation of the alveoli.

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13
Q

What is it called when you have a high V/Q ratio?

A

Dead space. Lots of ventilation but no perfusion.

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14
Q

What is a cause of a high V/Q ratio (dead space)?

A

Pulmonary embolism.

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15
Q

What is it called when you have a low V/Q ratio?

A

Shunt. Lots of perfusion but no ventilation.

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16
Q

What is a cause of a low V/Q ratio (shunt)?

A

Pulmonary oedema.

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17
Q

What is perfusion of pulmonary capillaries dependent on?

A
  1. Pulmonary artery pressure.
  2. Pulmonary venous pressure.
  3. Alveolar pressure.
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18
Q

Does the apex of the lung have a high or a low V/Q? Why?

A

High - effect of gravity, far more perfusion at the base of the lung.

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19
Q

What are the 7 layers for gas exchange?

A
  1. Alveolar epithelium.
  2. Interstitial fluid.
  3. Capillary endothelium.
  4. Plasma layer.
  5. RBC membrane.
  6. RBC cytoplasm.
  7. Hb binding sites.
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20
Q

Name 4 causes of hypoxia.

A
  1. Hypoventilation.
  2. V/Q mismatch.
  3. Diffusion abnormality.
  4. Reduced PiO2.
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21
Q

Name 4 causes of hypercapnia.

A
  1. Increased dead space ventilation; rapid, shallow breathing.
  2. V/Q mismatch.
  3. Increased CO2 production.
  4. Reduced minute ventilation.
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22
Q

What is the alveolar gas equation?

A

PAO2 = PiO2 - (PaCO2/R)

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23
Q

What is Dalton’s law?

A

In a mixture of non reacting gases Ptotal = Pa + Pb. (P total is the sum of the pressures of individual gases).

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24
Q

What is Boyle’s law?

A

Pressure and Volume are inversely proportional:

P1V1 = P2V2.

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25
Q

What is 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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26
Q

What is the acid/base dissociation equation?

A

CO2 + H2O = H2CO3 = HCO3- + H+

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27
Q

What enzyme catalyses the formation of bicarbonate and hydrogen ions from CO2 and H2O?

A

Carbonic anhydrase.

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28
Q

What is the henderson hasselbalch equation?

A

pH = pKa + log (A-)/(HA)

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29
Q

What is Laplace’s law?

A

P = 2T/R.

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30
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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31
Q

Where is surfactant produced?

A

It is produced by type 2 pneumocytes in the alveoli.

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32
Q

When is surfactant produced?

A

It starts being produced from 34 weeks gestation and production increases rapidly 2 weeks before birth.

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33
Q

List 4 functions of surfactant.

A
  1. Prevents alveoli collapse.
  2. Allows homogenous aeration.
  3. Reduces surface tension.
  4. Maintains functional residual capacity.
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34
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.
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35
Q

How can you treat surfactant deficiency?

A

Ensure the patient is warm and is receiving O2 and fluids. Begin surfactant replacement.

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36
Q

Briefly describe the controller-effector-sensor loop.

A

The sensor detects a change (hypoxia), sends signals along the afferent pathway to the controller. The controller then sends signals along the efferent pathway to the effector. The effector responds.

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37
Q

What does the pneumotaxic area do and where is it located?

A

It switches off inspiratory neurones and so allows expiration. It is located in the upper pons.

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38
Q

What does the apneustic centre do and where is it located?

A

It inhibits expiration by activation inspiratory neurones. It is located in the lower pons.

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39
Q

Where are SASR (slow adapting stretch receptors) located?

A

Found in smooth muscle around airways.

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40
Q

What activates SASR?

A

Lung distension.

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41
Q

How do SASR respond to activation?

A

They inhibit inspiration and so promote expiration.

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42
Q

Where are RASR (rapidly adapting stretch receptors) located?

A

Between airway epithelial cells.

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43
Q

What activates RASR?

A

Lung distension and irritants.

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44
Q

How do RASR respond to activation?

A

Bronchoconstriction.

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45
Q

What activates C fibres J receptors?

A

Increased interstitial fluid volume.

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46
Q

How do C fibres J receptors respond to activation?

A

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

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47
Q

Where are central chemoreceptors located?

A

Medulla oblangata.

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48
Q

What stimulates central chemoreceptors?

A

An increase in H+ concentration in the ECF.

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49
Q

Where are peripheral chemoreceptors located?

A

Carotid and aortic bodies.

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50
Q

What stimulates peripheral chemoreceptors?

A

A decrease in PaCO2.

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51
Q

What is the respiratory drive more senstitive 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.

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52
Q

Oxygen dissociation curve: what causes the curve to shift to the right?

A

An increase in temperature and a decrease in pH.

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53
Q

Oxygen dissociation curve: what does it mean when the curve shifts to the right?

A

There is increased O2 unloading. Hb’s affinity for oxygen has decreased.

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54
Q

Oxygen dissociation curve: what causes the curve to shift to the left?

A

A decrease in temperature and an increase in pH.

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55
Q

What is a cause of respiratory acidosis?

A

Inadequate ventilation; could be due to obstruction e.g. COPD.

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56
Q

What is the renal compensation mechanism for respiratory acidosis?

A

Increased ammonia formation. H+ secretion increases and there is increased HCO3- reabsorption.

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57
Q

What can cause respiratory alkalosis?

A

Hyperventilation in response to hypoxia.

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58
Q

What is the renal compensation mechanism for respiratory alkalosis?

A

H+ secretion decreases; more H+ is retained. HCO3- secretion.

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59
Q

What is a cause of metabolic acidosis?

A

Renal failure; loss of HCO3-, excess H+ production.

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60
Q

What is the respiratory compensation mechanism for metabolic acidosis?

A

Chemoreceptors stimulated, enhancing respiration, PaCO2 decreases.

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61
Q

What is the respiratory compensation mechanism for metabolic alkalosis?

A

Chemoreceptors are inhibited, reduced respiration, PaCO2 increases.

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62
Q

What is a cause of metabolic alkalosis?

A

Vomiting; loss of H+.

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63
Q

Is respiratory compensation fast or slow?

A

FAST!

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64
Q

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

A

Hypoxemia.

Causes: V/Q mismatch due to alveolar hypoventilation, high altitude, shunt, diffusion problem.

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65
Q

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

A

Hypoxemia and hypercapnia.

Causes: inadequate alveolar ventilation due to reduced breathing effort, decreased SA, neuromuscular problems.

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66
Q

What is forced vital capacity?

A

Volume of air that can be forcibly exhaled after maximum inhalation.

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67
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.

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68
Q

How 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.

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69
Q

How can you work out total lung capacity?

A

Add vital capacity to residual volume.

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70
Q

What is tidal volume?

A

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

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71
Q

What changes are seen in an aging lung?

A

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

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72
Q

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

A

They both decrease and the residual volume increases.

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73
Q

What effect does hypoxia have on pulmonary vessels?

A

It vasoconstricts the vessels and so redirects blood to O2 rich alveoli.

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74
Q

What is hypersensitivity?

A

Undesirable reaction produced by the immune system.

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75
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 hayfever, asthma, acute anaphylaxis etc. (Antihistamines are often given as treatment).

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76
Q

What is the parasympathetic neurotransmitter in the lungs?

A

Acetylcholine.

77
Q

What is the sympathetic neurotransmitter in the lungs?

A

Noradrenaline.

78
Q

What is the effect of Ach on the pulmonary vessels?

A

Bronchoconstriction and vasodilation.

79
Q

What is the effect of noradrenaline on the pulmonary vessels?

A

Bronchodilation and vasoconstriction.

80
Q

Name 2 receptors for Ach.

A

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

81
Q

Host defense: What is innate immunity?

A

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

82
Q

Briefly describe the mechanism of inflammation.

A

Vasodilation results in exudation of plasma. Neutrophils and monocytes migrate into tissues.

83
Q

What are alveolar macrophages derived from?

A

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

84
Q

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

A

Moistens and protects airways.

Functions as a barrier to pathogens and foreign matter.

85
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.

86
Q

What is coughing?

A

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

87
Q

What does the lung bud form from?

A

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

88
Q

What is the septum called that seperates the lung bud from the oesophagus in the embryo?

A

Tracheoesophageal septum.

89
Q

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

A
  1. Embryonic (0-5 weeks): lungs and trachea develop.
  2. Pseudoglandular (5-16 weeks): branching of trachea.
  3. Canalicular (16-26 weeks): Respiratory bronchioles form.
  4. Saccular (26w-birth): Terminal sacs form.
  5. Alveolar (8 months to childhood): Alveoli mature.
90
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. Foramen ovale closes.
91
Q

Define anatomical dead space.

A

The volume of air taken in during a breath that does not enter the alveoli.

92
Q

Define physiological dead space.

A

The volume of air that is taken in during a breath that does not take part in gas exchange.

93
Q

What it total lung capacity equal to?

A

TLC = VC + RV.

94
Q

Where is the basic neural machinery for the generation of the respiratory rhythm located?

A

In the lower medulla.

95
Q

True or False: the intercostals are the main muscles of respiration.

A

False - the diaphragm is the main muscle of respiration.

96
Q

Which alveoli are preferentially ventilated and perfused?

A

Those at the base of the lungs.

97
Q

Why can hypoxia cause respiratory alkalosis?

A

Hypoxia leads to hyperventilation as the person tries to inhale more O2. This means you lose a lot of CO2 resulting in alkalosis.

98
Q

Define total lung capacity.

A

The vital capacity plus the residual volume. It is the maximum amount the lungs can hold.

99
Q

Define residual volume (RV).

A

The volume of air remaining in the lungs after a maximal exhalation.

100
Q

Define functional residual capacity (FRC).

A

The volume of air remaining in the lungs after a tidal volume exhalation.

101
Q

Define tidal volume (TV).

A

The volume of air moved in and out of the lungs during a normal breath.

102
Q

Define FEV1.

A

The volume of air that can be forcibly exhaled in 1 second.

103
Q

What 2 equations can be used to work out TLC?

A
  1. TLC = VC + RV.

2. TLC = TV + FRC + IRV.

104
Q

Define forced vital capacity (FVC).

A

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

105
Q

Define expiratory reserve volume (ERV).

A

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

106
Q

Define inspiratory reserve volume (IRV).

A

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

107
Q

What is lung compliance?

A

A measure of the lung’s ability to stretch and expand. Compliance = ∆V/∆P.

108
Q

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

A

The elastin degenerates and ruptures.

109
Q

Why do you see decreased muscle strength in an ageing lung?

A

There is a decrease in type 1, fatigue resistant fibres. And muscle mass also decreases.

110
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.

111
Q

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

A

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

112
Q

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

A

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

113
Q

Why does the residual volume increase in an ageing lung?

A

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

114
Q

What is the main cell involved in acute inflammation?

A

Neutrophils.

115
Q

What can the pneumotaxic area override?

A

The apneustic area.

116
Q

Name 4 non-immune host defense mechanisms.

A
  1. Mucus.
  2. Muco-cilliary escalator.
  3. Epithelium.
  4. Cough.
117
Q

What layer of the tri-laminar disc is the respiratory tract derived from?

A

The endoderm.

118
Q

What is the respiratory diverticulum an out-pouching of?

A

The foregut.

119
Q

What does the respiratory diverticulum go on to form?

A

The lung buds.

120
Q

Give 2 ways that oxygen is carried around the body?

A
  1. Bound to Hb.

2. Dissolved in blood.

121
Q

What is Hb affinity for O2?

A

How readily Hb acquires and releases O2 at respiring tissues.

122
Q

Does the umbilical vein carry oxygenated blood or deoxygenated?

A

Oxygenated (umbilical artery carries deoxygenated).

123
Q

What is the importance of the ductus venosus in foetal circulation?

A

It is used to bypass the liver. Oxygenated blood from the umbilical vein can go straight to the IVC and not through the liver.

124
Q

Define vital capacity.

A

The maximum volume of air that can be exhaled after a maximal inhalation.

125
Q

What is the normal tidal volume in an adult?

A

500ml.

126
Q

What cell type lines most of the surface of an alveoli?

A

Type 1 pneumocytes.

Type 2 are more numerous but type 1 are squamous and so are responsible for more of the SA.

127
Q

What is the thickness of the air-blood barrier in nm?

A

200-800 nm.

128
Q

What is the epithelium of the vocal cords?

A

Stratified squamous non-keratinising.

129
Q

What is the base, apex and roof of the maxillary sinus formed from?

A

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

130
Q

Which sinus is a labyrinth of air cells?

A

The ethmoid.

131
Q

What vertebral level does the larynx extend to?

A

T5.

132
Q

True or False: alveolar macrophages release interleukins.

A

True - this is important in the coordination of an immune response.

133
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.

134
Q

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

A

Bronchioles.

135
Q

Define peak expiratory flow (PEF).

A

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

136
Q

Define airway obstruction.

A

Impediment to inspiratory and expiratory air flow.

137
Q

Define airway restriction.

A

When the lungs are restricted from full expansion.

138
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.
139
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.

140
Q

How many broncho-pulmonary segments are there in the right lung?

A

10.

141
Q

How many broncho-pulmonary segments are there in the left lung?

A

8.

142
Q

What effect does hypoxia have on systemic vessels?

A

Vasodilation.

143
Q

How do we recognise pathogens we have nerve seen before?

A

Pattern recognition receptors - PRRs.

144
Q

What are the causative agents of acute inflammation?

A

Pathogens, damaged tissue.

145
Q

What are the causative agents of chronic inflammation?

A

Persistent acute inflammation, persistent foreign bodies, autoimmune reactions.

146
Q

What are main cells involved in acute inflammation?

A

Neutrophils! Also eosinophils and basophils.

147
Q

What are main cells involved in chronic inflammation?

A

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

148
Q

What are the primary mediators in acute inflammation?

A

Vasoactive amines.

149
Q

What are the primary mediators in chronic inflammation?

A

Cytokines, growth factors, ROS etc.

150
Q

What are the outcomes of chronic inflammation?

A

Tissue destruction, fibrosis, necrosis, chronic inflammation.

151
Q

What are the outcomes of acute inflammation?

A

Resolution.

152
Q

What suppresses alveolar macrophage activation in a healthy lung?

A

Respiratory epithelium.

153
Q

Which results in inflammation, necrosis or apoptosis?

A

Necrosis.

154
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.

155
Q

What is the function of mucus?

A

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

156
Q

What mechanism moves airway mucus up into the throat?

A

Muco-ciliary escalator.

157
Q

What is mucus composed of?

A

Water, carbohydrates, lipids and proteins.

158
Q

Name 4 non-immune host defence mechanisms.

A
  1. Epithelial barrier.
  2. Mucus.
  3. Muco-ciliary escalator.
  4. Coughing.
159
Q

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

A

Recurrent laryngeal and spinal nerves.

160
Q

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

A

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

161
Q

What is adaptive immunity?

A

An antigen-specific immune response.

162
Q

What is the function of B cells?

A

Antibody production.

163
Q

Name 3 types of T cells.

A
  1. Cytotoxic T cells.
  2. Helper T cells.
  3. Memory T cells.
164
Q

What is the function of cytotoxic T cells?

A

They track down infected cells.

165
Q

What is the function of helper T cells?

A

they secrete cytokines to attract macrophages and neutrophils etc.

166
Q

What can cause a type 1 hypersensitivity reaction?

A

Pollen, cat hair, peanuts (allergies).

167
Q

What can cause a type 2 hypersensitivity reaction?

A

Transplant rejection, transfusion mismatch.

168
Q

What can cause a type 3 hypersensitivity reaction?

A

Fungal.

169
Q

What can cause a type 4 hypersensitivity reaction?

A

TB.

170
Q

What are the functions of lymphocytes?

A

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

171
Q

What is the Gell and Coombs classification?

A

It describes 4 types of hypersensitivity reaction.

172
Q

Describe the mechanism and give examples of a type 1 hypersensitivity reaction.

A
  • Mechanism: immunological memory to something causing an allergic response. IgE antibodies bind to mast cells -> histamine release.
  • Anaphylaxis, hayfever etc. Can be caused by pollen, allergens.
173
Q

Describe the mechanism and give examples of a type 2 hypersensitivity reaction.

A
  • Mechanism: immunoglobulins bound to surface antigens.

- Transfusion mismatch or transplant rejection.

174
Q

Describe the mechanism and give examples of a type 3 hypersensitivity reaction.

A
  • Mechanism: immune complexes, activation of complement.

- Fungi and pigeon droppings etc. (pigeon fancier’s lung).

175
Q

Describe the mechanism and give examples of a type 4 hypersensitivity reaction.

A
  • Mechanism: T cell mediated.

- Reactions to TB.

176
Q

What comprises a respiratory acinus?

A

Respiratory bronchiole, alveolar duct and alveolus.

177
Q

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

A

The tracheal bifurcation.

178
Q

Give an example of a restrictive lung disease?

A

Pulmonary fibrosis.

179
Q

Give an example of an obstructive lung disease?

A

Chronic bronchitis and emphysema.

180
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.
181
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.
182
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.
183
Q

What is DLCO?

A

Uptake of CO in ml at standard temperature and pressure.

184
Q

Define inspiratory capacity (IC).

A

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

185
Q

What are the 6 stages of neutrophil action?

A
  1. Identify threat.
  2. Activation.
  3. Adhesion.
  4. Migration.
  5. Phagocytosis.
  6. Bacterial killing.
186
Q

What is the consequence of mucus plugs in the lungs?

A

Airway obstruction which can ultimately lead to death.

187
Q

What is the equation for trans-pulmonary pressure?

A

Transpulmonary pressure = alveolar pressure - pleural pressure. (TPP is always positive).

188
Q

What layer of the trilaminar disc is pleura derived from?

A

Mesoderm.

Phase 1 Medicine COPY (10 decks)

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