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Sandra phase 1 > Respiratory physiology > Flashcards

Respiratory physiology Flashcards

1
Q

Surface tension issues

A
  • Causes collapsing of alveoli
  • Creates unequal ventilation
  • If alveoli collapse it pulls water into alveoli that are collapsing, resulting pulmonary oedema
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2
Q

Surfactant composition

A

90% phospholipid

10% protein

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3
Q

Explain phospholipids, what is their composition?

A

2 dipalmitoyl tails- hydrophobic

1 phosphatidylcholine head- hydrophilic

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4
Q

Proteins that make up surfactant

A

Albumin
IgA
Apoproteins: SpA, SpB, SpC, SpD

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5
Q

What is the name of CO2 when its bound to certain amino acids in the haemoglobin

A

Carbaminohaemoglobin (20%)

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6
Q

Deoxyhaemoglobin is said to be in the

A

T state

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7
Q

What is deoxygenated oxygen bound to?

A

Little 02
A lot of CO2
H+
2,3BPG (Helps stabilise deoxy HB)

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8
Q

Describe affinity for deoxy Hb

A

low O2 affinity
high CO2 affinity
high H+ affinity
stabilised by 2,3BPG

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9
Q

What is the chloride shift?

A

HCO3- is coming into/out of red blood cells, and Cl- is coming out/in

It depends if it’s inspired/expired respiration

Necessary so there isn’t a build-up of charge in red blood cell

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10
Q

How is carbonic acid made in red blood cells?

A

Due to chloride shift HCO3- is entering red blood cells. The oxygen bound Hb doesn’t want the H+protons and therefore the positive and negative charged ions attract and form carbonic acid.

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11
Q

What happens to the carbonic acid in the red blood cells during expired respiration?

A

It dissociates into H20 + CO2.

CO2 then diffuses out of blood cells -> capillary-> alveoli

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12
Q

Carbaminohaemoglobin what happens when O2 binds to Haemoglobin

A

Diffuses out into alveoli (High CO2 conc -> Low CO2 conc)

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13
Q

Where is carbonic anhydrase found? What is the effect of this on expired respiration

A

Red blood cells
This means that red blood cells would produce more CO2 which is leaving the cell and diffusing to alveoli in comparison to the blood plasma which is doing it at a much slower rate due to the absence of this enzyme

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14
Q

What is the Haldane effect?

A

red blood cell has:
Low affinity for CO2, H+, temp and 2,3 BGP
High affinity for O2
decrease in O2 disassociation

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15
Q

What structures contribute to the respiratory pump during normal quiet breathing?

A

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

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16
Q

What structures make up the conducting airways?

A

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

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17
Q

What is the function of the conducting airways?

A

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

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18
Q

What is respiratory epithelium?

A

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

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19
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 (the combined cross-sectional area is the least, which increases resistance).

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20
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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21
Q

Briefly describe quiet inspiration.

A

Inspiration is an active process.

  1. The external intercostal muscles and diaphragm contract (By phrenic nerve and intercostal nerves).
  2. The volume of the thoracic cavity increases
  3. Decrease in PPUL and PIP
  4. Increase in Tp Decrease in TTP + TRP
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22
Q

What is the ‘pump handle’ representing?

A

The movement of the sternum. In inspiration, the sternum moves anteriorly and superiorly increasing thoracic cavity volume

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

This happens when the external intercostals contract

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23
Q

What muscles are involved in forced inspiration

A

Scalene
Sternocleidomastoid
Pectoralis minor in some cases

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24
Q

Briefly describe expiration

A

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

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25
Q

What is quiet expiration dependent on?

A

Elasticity of lungs

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26
Q

What muscles are involved during forced expiration

A

Internal intercostals

Abdominal wall muscles:
External & Internal oblique
Transversus Abdominis
Recta abdominis

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27
Q

What is V/Q mismatch?

A

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

This is due to the fact that alveoli higher up would have better ventilation but worse perfusion due to gravity working against it and vice versa for alveoli near the bottom of the lung. This means that V and Q can never be fully equal

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28
Q

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

A

High ventilation low perfusion. Dead space

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29
Q

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

A

Pulmonary embolism.

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30
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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31
Q

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

A

Pulmonary oedema.

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32
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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33
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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34
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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35
Q

Name 4 causes of hypoxia.

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

DR. HV

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36
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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37
Q

What is the alveolar gas equation?

A

PAO2 = PiO2 - (PaCO2/R)

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38
Q

Daltons 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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39
Q

What is Boyle’s law?

A

Pressure and Volume are inversely proportional:

P1V1 = P2V2.

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40
Q

What is Henry’s law?

A

The solubility of a gas is proportional to the partial pressure of the gas when it’s in equilibrium. S1/P1 = S2/P2.

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41
Q

What is the acid/base dissociation equation?

A

CO2 + H2O = H2CO3 = HCO3- + H+

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42
Q

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

A

Carbonic anhydrase.

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43
Q

What is the henderson hasselbalch equation?

A

pH = pKa + log [A-]/[HA]

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44
Q

What is Laplace’s law?

A

P = 2T/R.

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45
Q

Where is surfactant produced?

A

Lamellar bodies of type 2 pneumonocytes in the alveoli

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46
Q

When is surfactant produced?

A

It starts being produced from 24 weeks gestation and production increases rapidly around week 34 week. The increase production of surfactant is due to cortisol which is secreted by mother.

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47
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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48
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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49
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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50
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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51
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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52
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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53
Q

Where are SASR (slow adapting stretch receptors) located?

A

Found in smooth muscle around airways.

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54
Q

What activates SASR?

A

Lung distension.

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55
Q

How do SASR respond to activation?

A

They inhibit inspiration and so promote expiration.

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56
Q

Where are RASR (rapidly adapting stretch receptors) located?

A

Between airway epithelial cells.

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57
Q

What activates RASR?

A

Lung distension and irritants.

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58
Q

How do RASR respond to activation?

A

Bronchoconstriction.

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59
Q

What activates C fibres J receptors?

A

Increased interstitial fluid volume.

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60
Q

How do C fibres J receptors respond to activation?

A

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

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61
Q

Where are central chemoreceptors located?

A

Medulla oblangata.

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62
Q

What stimulates central chemoreceptors?

A

An increase in H+ concentration in the ECF.

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63
Q

Where are peripheral chemoreceptors located?

A

Carotid and aortic bodies.

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64
Q

What stimulates peripheral chemoreceptors?

A

increase PaCO2.
Decrease in O2
Change in pH due to metabolic acids

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65
Q

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

A

O2 is a bigger drive once it drops below 60mmHg otherwise its CO2

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66
Q

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

A

BOHR EFFECT. An increase in temperature and a decrease in pH.

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67
Q

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

A

Hb affinity decreases

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68
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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69
Q

What is a cause of respiratory acidosis?

A

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

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70
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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71
Q

What can cause respiratory alkalosis?

A

Hyperventilation in response to hypoxia.

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72
Q

What is the renal compensation mechanism for respiratory alkalosis?

A

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

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73
Q

What is a cause of metabolic acidosis?

A

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

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74
Q

What is the respiratory compensation mechanism for metabolic acidosis?

A

Chemoreceptors stimulated, enhancing respiration, PaCO2 decreases.

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75
Q

What is the respiratory compensation mechanism for metabolic alkalosis?

A

Chemoreceptors are inhibited, reduced respiration, PaCO2 increases.

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76
Q

What is the cause of metabolic alkalosis?

A

-

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77
Q

What is the cause of metabolic alkalosis?

A

FAST!

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78
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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79
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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80
Q

What is forced vital capacity?

A

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

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81
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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82
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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83
Q

How can you work out total lung capacity?

A

Add vital capacity to residual volume.

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84
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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85
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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86
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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87
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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88
Q

What is hypersensitivity?

A

The undesirable reaction produced by the immune system.

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89
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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90
Q

What is the parasympathetic neurotransmitter in the lungs?

A

Acetylcholine.

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91
Q

What is the sympathetic neurotransmitter in the lungs?

A

Noradrenaline.

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92
Q

What is the effect of Ach on the pulmonary vessels?

A

Bronchoconstriction and vasodilation.

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93
Q

What is the effect of noradrenaline on the pulmonary vessels?

A

Bronchodilation and vasoconstriction

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94
Q

Name 2 receptors for Ach.

A

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

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95
Q

Host defense: What is innate immunity?

A

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

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96
Q

Briefly describe the mechanism of inflammation.

A

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

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97
Q

What are alveolar macrophages derived from?

A

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

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98
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.

99
Q

What is the mucociliary 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.

100
Q

What is coughing?

A

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

101
Q

What does the lung bud form from?

A

The respiratory diverticulum - an out-pouching of the foregut.

102
Q

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

A

Tracheoesophageal septum.

103
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.
104
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.
105
Q

Define anatomical dead space.

A

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

106
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.

107
Q

What it total lung capacity equal to?

A

TLC = VC + RV.

108
Q

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

A

In the lower medulla.

109
Q

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

A

False - the diaphragm is the main muscle of respiration.

110
Q

Which alveoli are preferentially ventilated and perfused?

A

Those at the base of the lungs.

111
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.

112
Q

Define total lung capacity.

A

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

113
Q

Define residual volume (RV).

A

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

114
Q

Define functional residual capacity (FRC).

A

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

115
Q

Define tidal volume (TV).

A

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

116
Q

Define FEV1.

A

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

117
Q

What 2 equations can be used to work out TLC?

A
  1. TLC = VC + RV.

2. TLC = TV + FRC + IRV.

118
Q

Define forced vital capacity (FVC).

A

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

119
Q

Define expiratory reserve volume (ERV).

A

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

120
Q

Define inspiratory reserve volume (IRV).

A

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

121
Q

What is lung compliance?

A

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

122
Q

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

A

The elastin degenerates and ruptures.

123
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.

124
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.

125
Q

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

A

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

126
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.

127
Q

Why does the residual volume increase in an ageing lung?

A

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

128
Q

What is the main cell involved in acute inflammation?

A

Neutrophils.

129
Q

What can the pneumotaxic area override?

A

The apneustic area.

130
Q

Name 4 non-immune host defense mechanisms.

A
  1. Mucus.
  2. Muco-cilliary escalator.
  3. Epithelium.
  4. Cough
131
Q

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

A

The endoderm.

132
Q

What is the respiratory diverticulum an out-pouching of?

A

The foregut.

133
Q

What does the respiratory diverticulum go on to form?

A

The lung buds.

134
Q

Give 2 ways that oxygen is carried around the body?

A
  1. Bound to Hb.

2. Dissolved in blood.

135
Q

What is Hb affinity for O2?

A

How readily Hb acquires and releases O2 at respiring tissues.

136
Q

Does the umbilical vein carry oxygenated blood or deoxygenated?

A

Oxygenated (umbilical artery carries deoxygenated).

137
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.

138
Q

Define vital capacity.

A

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

139
Q

What is the normal tidal volume in an adult?

140
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.`

141
Q

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

A

200-800 nm.

142
Q

What is the epithelium of the vocal cords?

A

Stratified squamous non-keratinising.`

143
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.

144
Q

Which sinus is a labyrinth of air cells?

A

The ethmoid.`

145
Q

What vertebral level does the larynx extend to?

146
Q

True or False: alveolar macrophages release interleukins.

A

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

147
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.

148
Q

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

A

Bronchioles.

149
Q

Define peak expiratory flow (PEF).

A

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

150
Q

Define airway obstruction.

A

Impediment to inspiratory and expiratory air flow.

151
Q

Define airway restriction.

A

When the lungs are restricted from full expansion.

152
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.
153
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.

154
Q

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

155
Q

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

156
Q

What effect does hypoxia have on systemic vessels?

A

Vasodilation.

157
Q

How do we recognise pathogens we have nerve seen before?

A

Pattern recognition receptors - PRRs.

158
Q

What are the causative agents of acute inflammation?

A

Pathogens, damaged tissue.

159
Q

What are the causative agents of chronic inflammation?

A

Persistent acute inflammation, persistent foreign bodies, autoimmune reactions.

160
Q

What are main cells involved in acute inflammation?

A

Neutrophils! Also eosinophils and basophils.

161
Q

What are main cells involved in chronic inflammation?

A

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

162
Q

What are the primary mediators in acute inflammation?

A

Vasoactive amines.

163
Q

What are the primary mediators in chronic inflammation?

A

Cytokines, growth factors, ROS etc.

164
Q

What are the outcomes of chronic inflammation?

A

Tissue destruction, fibrosis, necrosis, chronic inflammation.

165
Q

What are the outcomes of acute inflammation?

A

Resolution.

166
Q

What suppresses alveolar macrophage activation in a healthy lung?

A

Respiratory epithelium.

167
Q

Which results in inflammation, necrosis or apoptosis?

168
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.

169
Q

What is the function of mucus?

A

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

170
Q

What mechanism moves airway mucus up into the throat?

A

Muco-ciliary escalator.

171
Q

What is mucus composed of?

A

Water, carbohydrates, lipids and proteins.

172
Q

Name 4 non-immune host defence mechanisms.

A
  1. Epithelial barrier.
  2. Mucus.
  3. Muco-ciliary escalator.
  4. Coughing.
173
Q

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

A

Recurrent laryngeal and spinal nerves.

174
Q

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

A

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

175
Q

What is adaptive immunity?

A

An antigen-specific immune response.

176
Q

What is the function of B cells?

A

Antibody production.

177
Q

Name 3 types of T cells.

A
  1. Cytotoxic T cells.
  2. Helper T cells.
  3. Memory T cells.
178
Q

What is the function of cytotoxic T cells?

A

They track down infected cells.

179
Q

What is the function of helper T cells?

A

they secrete cytokines to attract macrophages and neutrophils etc

180
Q

What can cause a type 1 hypersensitivity reaction?

A

Pollen, cat hair, peanuts (allergies).

181
Q

What can cause a type 2 hypersensitivity reaction?

A

Transplant rejection, transfusion mismatch.

182
Q

What can cause a type 3 hypersensitivity reaction?

183
Q

What can cause a type 4 hypersensitivity reaction?

184
Q

What are the functions of lymphocytes?

A

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

185
Q

What is the Gell and Coombs classification?

A

It describes 4 types of hypersensitivity reaction.

186
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.
187
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.

188
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).

189
Q

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

A
  • Mechanism: T cell mediated.

- Reactions to TB.

190
Q

What comprises a respiratory acinus?

A

Respiratory bronchiole, alveolar duct and alveolus.

191
Q

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

A

The tracheal bifurcation.

192
Q

Give an example of a restrictive lung disease?

A

Pulmonary fibrosis.

193
Q

Give an example of an obstructive lung disease?

A

Give an example of an obstructive lung disease?

194
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.
195
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.
196
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.
197
Q

What is DLCO?

A

Uptake of CO in ml at standard temperature and pressure.

198
Q

Define inspiratory capacity (IC).

A

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

199
Q

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

A
  1. Identify threat.
  2. Activation.
  3. Adhesion.
  4. Migration.
  5. Phagocytosis.
  6. Bacterial killing.
200
Q

What is the consequence of mucus plugs in the lungs?

A

What is the consequence of mucus plugs in the lungs?

201
Q

What is the equation for trans-pulmonary pressure?

A

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

202
Q

What layer of the trilaminar disc is pleura derived from?

203
Q

Define minute volume?

A

5 litres of air a minute moved by the respiratory pump

204
Q

Define Transpulmonary pressure (Ptp)?

A

difference in pressure between the inside and

outside of the lung (alveolar pressure - intrapleural pressure)

205
Q

Define Intrapleural pressure (Pip)?

A

the pressure in the pleural space, also known as

intrathoracic pressure

206
Q

Define Alveolar pressure (Palv)?

A

Air pressure in pulmonary alveoli

207
Q

What is the total combined area for gas exchange?

A

What is the total combined area for gas exchange?

208
Q

What is ventilation-perfusion matching?

A

To be most efficient, the correct proportion of alveolar airflow (ventilation) and capillary blood flow (perfusion) shows be available to each alveolus

209
Q

What is PaCO2?

A

Arterial CO2

210
Q

What is PACO2?

A

Alveolar CO2

211
Q

What is PaO2?

A

Arterial O2

212
Q

What is PAO2?

A

Alveolar O2

213
Q

What is PIO2?

A

Pressure of Inspired Oxygen

214
Q

What is V̇A?

A

Alveolar ventilation

215
Q

What is V̇CO2?

A

CO2 production

216
Q

What is the equation for the reaction between 1 O2 and a haem unit?

A

O2 + Hb ⇄ HbO2

217
Q

What are the two forms of haemoglobin?

A

Hb (deoxyhaemoglobin) and HbO2 (oxyhaemoglobin)

218
Q

What is the relationship between partial pressure of arterial CO2 and alveolar ventilation?

A

The partial pressure of arterial CO2 is inversely related to alveolar ventilation: PaCO2 = kV̇CO2 / V̇A

219
Q

What is the equation for pressure?

A

Flow x resistance

220
Q

What is Lung Compliance?

A

the change in lung volume caused by a given change in transpulmonary pressure; the greater the lung compliance, the more readily the lungs are expanded

221
Q

What are the determinants of lung compliance?

A

Elasticity of lung tissues and surface tension of the air-water interfaces of the alveoli

222
Q

What is the bicarbonate buffer equation?

A

CO2 +H2O ⇄ H2CO3 ⇄ HCO3- + H+

223
Q

What are the four types of hypersensitivity?

A

Type 1- IgE

Type 2-(IgG bound to cell surface antigens/ IgM)

Type 3- Immune complexes, activation of complement/IgG

Type 4-Cell Mediated Delayed-Type Hypersensitivity (DTH)

224
Q

Does the lung have a function in the foetus?

225
Q

What respiratory tract structures come from endoderm?

A

epithelia lining of trachea, larynx, bronchi & alveoli

226
Q

epithelia lining of trachea, larynx, bronchi & alveoli

A

cartilages, muscle,connective tissue of tract & visceral pleura

227
Q

What are the different stages of lung development?

A

Pseudoglandular-5-16 weeks
Canalicular- 16-26 weeks

Terminal Sac- 26 weeks to birth(Type 1 and 2)
Alveolar- 8mo to childhood

228
Q

What happens in the pseudoglandular phase?

A

Branching to form terminal bronchioles

229
Q

What happens in the Alveolar Phase?

A

Alveoli mature, more respiratory bronchioles and alveoli

230
Q

What is hypoxia?

A

Inadequate O2 delivery to tissues

231
Q

What are symptoms of early stages of hypoxia?

A

Restlessness
Anxiety
Tachycardia
Tachypnoea ( accelerated respiration process)

232
Q

What are symptoms of late stages of hypoxia?

A

Bradycardia (HR<60BPM)
Extreme restlessness
Dyspnoea (shortness of breath)
Cyanosis (blue)

233
Q

Types of hypoxia

A
  1. Hypoxemic hypoxia
  2. Ischaemic (Stagnant) hypoxia
  3. Anaemic hypoxia
  4. Histotoxic hypoxia
234
Q

What is the pneumotaxic centre responsible for?

A

Fine tuning respiratory rate + depth

Transition from inspiration to expiration

235
Q

Central chemo receptor respond to?

A

Respond to changes in pH in response to changes PaCO2

236
Q

What does apneustic centre do?

A

Control inspiration

237
Q

What is one of the complexes that the Ventral Respiratory Group control?

A

Preboteinger complex-> Pacemaker neurons

238
Q

What branches of spinal cord innervate the diaphragm

A

C3-C5 (phrenic nerve)

239
Q

What branches of spinal cord innervate the external intercostals

A

T1-T11 (intercostal nerve)

240
Q

Regulation of Breathing: Factors Influencing Rate and Depth

A 
Central chemoreceptors
proprioceptors
peripheral chemoreceptors
SASR
Irritant receptors
Juxta capillary receptors
241
Q

Centres of CNS involved in breathing

A 
VRG
DRG
Apneustic centre (lower pons)
Pneumotaxic centre (upper pons)
Central chemoreceptos
242
Q

What is the p.p in the lungs of 02

243
Q

What is the p.p in the capillaries of 02

Sandra phase 1 (16 decks)

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