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Phase 1 mine > Respiratory > Flashcards

Respiratory Flashcards

1
Q

what is the average minute volume

A

5 L of air per minute

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2
Q

what is the transpulmonary pressure (Ptp)

A

difference in pressure between the inside and outside of the lung = alveolar pressure - intrapleural pressure

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3
Q

what is intrapleural pressure (Pip)

A

pressure in the pleural space aka intrathoracic pressure

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4
Q

what is the alveolar pressure (Palv)

A

air pressure in pulmonary alveoli

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5
Q

what initiates inspiration

A

neurally induced contraction of diaphragm and ext intercostal muscles

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6
Q

how do ext intercostal muscles increase thoracic volume

A

activation of motor neurons cause contraction = upwards and outwards movement of ribs

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7
Q

what occurs as the thorax expands

A
  1. intrapleural pressure lowers
  2. transpulmonary pressure becomes more positive
  3. results in lung expansion as Ptp is becoming greater than elastic recoil exerted by lungs
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8
Q

why does air enter the lungs in inspiration

A

alveolar pressure becomes negative = inward airflow

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9
Q

at the end of inspiration why is there no airflow

A

alveolar pressure = atmospheric pressure

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10
Q

what initiates expiration

A

motor neurones to diaphragm and ext intercostal muscles stop firing = relax

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11
Q

why do the lungs passively collapse

A

relaxation causes intrapleural pressure to increase

+ decrease transpulmonary pressure = elastic recoil stronger so lungs collapse

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12
Q

how is air expelled from alveoli

A

reducing lungs = alveoli compressed = increase alveolar pressure = exceeds atmospheric pressure so air flows outward

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13
Q

what type of process is expiration at rest

A

passive

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14
Q

what is required during exercise

A

forced expiration

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15
Q

what occurs in forced expiration

A
  1. internal intercostals + abdo muscles also contract = increase intra-abdominal pressure
  2. ribs move down and in = force diaphragm further into thorax = decrease thoracic volume
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16
Q

what provides the greatest airways resistance

A

trachea bc smallest surface area

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17
Q

what is dead space

A

volume of air not contributing to ventilation = 175mls in total

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18
Q

what is the total combined area for gas exchange

A

40-100m squared

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19
Q

what are the 7 layers for gas exchange

A
  1. alveolar tissue
  2. tissue interstitium
  3. capillary endothelium
  4. plasma layer
  5. red cell membrane
  6. red cell cytoplasm
  7. Hb binding
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20
Q

what is ventilation-perfusion matching

A

to be most efficient = proportion of alveolar airflow and capillary blood flow to an area of the lung should be equal

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21
Q

what is the effect of V-P mismatch

A

pO2 will decrease and pCO2 will increase in systemic-arterial blood because not enough ventilation for perfusion

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22
Q

why is naturally some V-P mismatch

A

gravitational effects = increase filling of blood vessels at bottom of lung

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23
Q

what is hypoxic vasoconstriction

A

blood is diverted to better ventilated parts of the lung = unique to pulmonary vessels

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24
Q

what are 2 responses to V-P mismatch

A

hypoxic vasoconstriction and local bronchoconstriction

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25
Q

where does the control of breathing come from

A

medulla oblongata

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26
Q

what do the neurons of the dorsal respiratory group do

A
  1. fire during inspiration
  2. lead to contraction of inspiratory muscles
  3. lungs fill at constant rate
  4. end of inspiration = rapid decrease in excitation of inspiratory muscles
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27
Q

where is the respiratory rhythm generator located

A

in the pre-Botzinger complex of neurons in the upper part of the ventral respiratory group

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28
Q

what is the respiratory rhythm generator

A

pacemaker cells/neural network that set the basal respiratory rate

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29
Q

what is found in the pons

A

pneumotaxic centre

apneustic centre

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30
Q

what is the role of the pneumotaxic centre

A

inhibits apneustic centre
promotes expiration
can switch off inspiratory neurons to prevent hyperinflation

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31
Q

what is the role of the apneustic centre

A

stimulates the dorsal respiratory group

increases intensity of inhalation

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32
Q

what do the neurons of the ventral respiratory group do

A
  1. stimulated by DRG
  2. involved in inspiration and expiration
  3. stimulate accessory muscles of expiration
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33
Q

what do the mechano/chemoreceptors in the larynx do

A

inhibit central controller - medullary respiratory centre

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34
Q

what do the receptors in the pharynx do

A

receptors activated by swallowing to stop respiratory activity and protect against aspiration

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35
Q

name 3 myelinated pulmonary receptors

A

slowly adapting stretch (SASR)
rapidly adapting stretch (RASR)
irritant

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36
Q

name a non-myelinated pulmonary receptor

A

C fibres J receptors

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37
Q

what are SASR’s

A
  1. activated by lung distension
  2. high activity inhibits further inspiration = begin expiration
  3. if inflation maintained then slowly adapt to low frequency firing
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38
Q

what are RASR’s

A
  1. activated by lung distention
  2. produce brief burst of activity at onset of stimulus
  3. high activity causes bronchoconstriction
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39
Q

where are C fibres J receptors found

A

in capillary walls/interstitium

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40
Q

where are SASR’s found

A

in airway smooth muscle

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41
Q

where are RASR’s found

A

between airway epithelial cells

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42
Q

what are C fibres J receptors

A
  1. stimulated by increase in interstitial fluid

2. results in rapid, shallow breathing/bronchoconstriction

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43
Q

when might C fibres J receptors be stimulated

A

during vascular congestion = occlusion of pulmonary vessel/left ventricular heart failure/strenuous activity

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44
Q

what is the effect of neural input from j receptors

A

gives rise to sensations of pressure in chest = feels like breathing is difficult

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45
Q

where are the peripheral chemoreceptors found

A

bifurcation of common carotid arteries and arch of aorta = carotid bodies and aortic bodies

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46
Q

what are peripheral chemoreceptors stimulated by

A

decrease pO2 and increase H+ conc

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47
Q

where are type 2 cells found and what do they do

A

located on carotid sinus

release stored neurotransmitters on detection of hypoxia = stimulate carotid sinus nerve

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48
Q

what is the predominant peripheral chemoreceptor involved in control of respiration

A

carotid body input

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49
Q

when do peripheral chemoreceptors fire

A

only when pO2 is below 90%

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50
Q

what are the 3 effects of peripheral chemoreceptor stimulation

A
  1. increase resp rate and tidal volume
  2. direct blood flow towards kidneys and brain
  3. increase CO to maintain blood flow
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51
Q

where are the central chemoreceptors located

A

in the medulla

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52
Q

what do central chemoreceptors detect

A

changes in arterial pCO2 = more sensitive

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53
Q

what are the effects of central chemoreceptors

A

increase pCO2 = increase ventilation

decrease pCO2 = decrease ventilation

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54
Q

how are pCO2 changes detected by central chemoreceptors

A
  1. higher CO2 in blood = higher H+ but H+ impermeable to BBB
  2. CO2 diffuse to CSF
  3. react with CSF H2O = increase H+
  4. H+ detected by medulla chemoreceptors
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55
Q

what is alveolar recruitment

A

opening of collapsed alveoli

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56
Q

what is hypoxia

A

oxygen deficiency at tissue level

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57
Q

paCO2

A

arterial CO2

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58
Q

PACO2

A

alveolar CO2

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59
Q

PaO2

A

arterial O2

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60
Q

PAO2

A

alveolar O2

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61
Q

PIO2

A

pressure of inspired O2

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62
Q

VA

A

alveolar ventilation

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63
Q

VCO2

A

CO2 production

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64
Q

where does Hb dissociate with O2

A

in areas of low pO2 = metabolically active tissue

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65
Q

effect of high temperature on oxygen dissociation curve

A

shift to right = Hb has less affinity for O2

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66
Q

effect of low pH on oxygen dissociation curve

A

shift to right = Hb has less affinity for O2

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67
Q

effect of carbon monoxide

A

22x affinity for Hb than O2 = shifts curve to the left = decreases unloading of O2 from Hb to tissues

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68
Q

3 ways CO2 carried in blood

A
  1. bound to Hb as carbaminohaemoglobin = 23%
  2. plasma dissolved = 10%
  3. as HCO3- = 65%
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69
Q

acid base dissociation equation

A

CO2 + H2O = H2CO3 = HCO3- + H+

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70
Q

does deoxy or oxyhaemobglobin have a higher affinity for H+

A

deoxyhaemoglobin

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71
Q

what is Dalton’s law

A

total pressure = sum of partial pressures

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72
Q

what is Boyle’s law

A

pressure of a fixed amount of gas in a container is inversely proportional to containers volume P1V1 = P2V2

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73
Q

what is Henry’s law

A

at equilibrium the pp of gas molecules in liquid and gaseous phases must be identical

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74
Q

what is the alveolar gas equation

A

PAO2 = PiO2 - PaCO2/R

where R is the resp exchange ratio

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75
Q

what is the respiratory exchange ratio

A

ratio between amount of CO2 produced in metabolism and O2 used

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76
Q

pressure =

A

flow x resistance

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77
Q

what is the Law of Laplace

A

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

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78
Q

what is lung compliance

A

Cl = change in lung volume caused by given change in transpulmonary pressure = greater Cl = more readily the lungs expand

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79
Q

what is the significance of type 2 pneumocytes in the alveoli

A

produce surfactant = reduced cohesive forces between water molecules = lowers surface tension = increase lung compliance

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80
Q

what is the significance of surface tension in the alveoli

A

= attractive forces between water molecules = resists stretching = lungs require energy to overcome these forces

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81
Q

what is the henderson hasselbach equation

A

pH = 6.1 + log10 ( [HCO3-]/[0.03 * PCO2] )

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82
Q

what causes respiratory acidosis

A

hypoventilation = inadequate ventilation of alveoli = CO2 cannot be excreted adequately = pCO2 increase = H+ increase in blood

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83
Q

what causes respiratory alkalosis

A

hyperventilation = decrease arterial pCO2 = decrease H+ conc

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84
Q

how is acid base balance restored

A

alter respiratory rate = change pCO2

urinary system change reabsorption/production of HCO3- or H+

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85
Q

4 causes of hypoxia

A
  1. hypoventilation
  2. diffusion impairment
  3. shunting
  4. ventilation/perfusion mismatch
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86
Q

what occurs in diffusion impairment

A

thickening of alveolar membranes or decrease in SA = PaO2 and PAO2 cannot equilibrate

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87
Q

what occurs in shunting

A

anatomical abnormality
= mixed venous blood bypass ventilated alveoli
= mixed venous blood perfuses unventilated alveoli

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88
Q

what is hypercapnia

A

CO2 retention and increased PaCO2

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89
Q

what causes hypercapnia

A

hypoventilation

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90
Q

what occurs in type 1 respiratory failure

A

pO2 is low
pCO2 is low or normal
hypoxia

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91
Q

what can cause type 1 respiratory failure

A

pulmonary embolism

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92
Q

what occurs in type 2 respiratory failure

A

pO2 is low
pCO2 is high
hypercapnia

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93
Q

what causes type 2 respiratory failure

A

hypoventilation

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94
Q

what is inspiratory reserve volume IRV

A

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

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95
Q

what is expiratory reserve volume ERV

A

amount if air in excess tidal expiration that can be exhaled with maximum effort

96
Q

what is residual volume RV

A

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

97
Q

what is vital capacity VC

A

amount if air that can be exhaled with maximum effort after maximum inspiration = ERV + TD + IRV

98
Q

why do we test vital capacity

A

used to assess strength of thoracic muscles + pulmonary function

99
Q

what is functional residual capacity FRC

A

amount of air remaining in lungs after normal tidal expiration = RV + ERV

100
Q

what is inspiration capacity IC

A

maximum amount of air that can be inhaled after normal tidal expiration = TV + IRV

101
Q

what is total lung capacity TLC

A

maximum amount of air the lungs can contain = RV + VC

102
Q

what is tidal volume TV

A

amount of air inhaled or exhaled in one breath = 500ml per breath

103
Q

what is FEV1

A

forced expiratory volume in 1 second

approx 80% in 1 sec

104
Q

what is forced vital capacity FVC

A

total amount of air forcibly expired

105
Q

describe a flow volume curve

A

shows forced expiration = flow is greatest at start of expiration and declines linearly with volume

106
Q

what does a low FVC indicate

A

airway constriction

107
Q

what is the FEV1/FVC ratio

A

proportion of FVC exhaled in the 1st second = FEV1/FVC

108
Q

what is airway obstruction indicated by

A

low FEV1/FVC ratio = below 0.7 but normal FVC

109
Q

what is airway restriction indicated by

A

FEV1/FVC ratio high (normal) or lower than 80% but FVC is low

110
Q

what are the characteristics of pulmonary circulatory vessels

A

thin walls
minor muscularisation
no need for redistrobution

111
Q

what are the characteristics of systemic circulatory vessels

A

thick walls
signification muscularisation
redistribution is required

112
Q

what has higher pressures, systemic or pulmonary circulation

113
Q

conditions for vasoconstriction/vasodilation in pulmonary vs systemic vessels

A 
pulmonary = if lack of o2 then vasoconstriction occur to divert away from poor ventilation 
systemic = if lack of o2 then vasodilation to increase blood flow and therefore o2 to that area
114
Q

name 2 structural and functional changes to the lung with ageing

A
  1. delayed response to hypoxia/hypercapnia = vulnerable to vent failure
  2. FEV1 and FVC decrease = may indicate obstructive and so may mask respiratory symptoms/disease
115
Q

how is gas exchange impaired in the ageing lung (7)

A
  1. costal catilages stiffer
  2. respiratory muscle mass decrease
  3. reduction in type 2a muscle fibres = fast-fatigue resistant ones = more tired when breathing
  4. denervation of muscle fibres = less contraction
  5. loss of elastic recoil
  6. V-P mismatch increase
  7. reduced alveolar SA and lung blood flow
116
Q

what are the effects on the immune system of the lung with ageing (3)

A
  1. fewer glandular epithelial cells = less protective mucus
  2. decrease sputum clearance
  3. less effective mucociliary system
117
Q

when is IgE made

A

in response to things were allergic to

118
Q

who tf are gell and coombs

A

they classified hypersensitivity into 4 types

119
Q

type 1 gell and coombs

A

IgE = causes an acute immediate allergic reaction

e.g. acute anaphylaxis/hayfever

120
Q

type 2 gell and coombs

A

IgG bound to cell surface antigens = fairly quick attacks bodies own cells
e.g. transfusion reactions /autoimmune disease

121
Q

type 3 gell and coombs

A

immune complexes deposited causing local inflammation = IgG

e.g. post streptococcal/SLE/ farmer’s lung

122
Q

type 4 gell and coombs

A

T cell mediated delayed type hypersensitivity (DTH) = granulation tissues
e.g. TB/contact dermatitis

123
Q

what is an allergen

A

an antigen that causes an allergic reaction

124
Q

what is atopy

A

an inherited exaggerated IgE response to antigens

125
Q

what occurs in initial exposure to antigens

A

some antibody synthesis and production of B memory cells

126
Q

what occurs on exposure to allergen in type 1 reactions

A
  1. allergens are presented by B cells
  2. this activates t helper cells = help produce IgE antibodies + trigger mast cells
  3. mast cells secrete inflammatory mediators = initiate local inflammatory response
127
Q

what are the inflammatory mediators in type 1 reactions

A

histamine and chemokines

128
Q

what are the effects of histamine in acute inflammation

A 
bronchoconstriction = difficulty breathing
vasodilation = swelling
129
Q

how does vasodilation lead to signs of acute allergic reaction

A

more blood flow = redness

greater permeability = fluid moves out of cells = swelling

130
Q

what causes anaphylaxis and what are the symptoms

A

mast cells secrete large amount of mediators = enter circulation
leads to severe hypotension, vasodilation, bronchoconstricion + mucus hypersecretion

131
Q

what neurotransmitter is associated with parasympathetic nerves supplying the airways

A

acetylcholine

132
Q

what is the intrinsic tone of the airways governed by

A

parasympathetic NS

133
Q

what type of receptor does acetylcholine interact with

A

muscarinic = M3 cholinergic receptors

134
Q

what does an increase in parasympathetic activation of the airways lead to

A

= too much Ach = bronchoconstriction

135
Q

what neurotransmitter is associated with sympathetic nerves supplying

A

noradrenaline NAd

136
Q

what part of the airways are innervated by parasympathetic

A

vasculature, glands, airways in lungs via vagus

137
Q

what part of the airways are innervated by the sympathetic

A

does not directly innervate airways

= vasculature and glands

138
Q

what is the effect of sympathetic activation

A

cause NAd to be released to adrenal glands = release adrenaline = binds to beta-2-adrenoreceptors on airway muscles = broncodilation

139
Q

where are nicotinic receptors found

A

post-ganglionic neurons and neuromuscular junction

140
Q

what is the action of beta-adrenergic receptors in the lung

A

act via stimulatory G proteins = increase cyclic AMP in postsynaptic cell

141
Q

what is the action of cAMP

A

diffuses in the lung = decrease calcium coc = results in bronchodilation

142
Q

what do nicotinic receptors respond to

A

acetylcholine and nicotine

143
Q

what is the difference between nicotinic and muscarinic receptors

A 
nicotinic = acts as channel for +ve ion, usually Na+ = always excitatory
muscarinic = use G protein
144
Q

how does respiratory epithelium protect the airways

A
  • moistens and protects
  • acts as barrier
  • prevent infection/injury by mucociliary escalator
145
Q

name 3 secretions of the epithelium

A

antibodies
lysozyme
lactoferrin

146
Q

what does lactoferrin do

A

binds to iron to prevent bacteria from accessing iron it needs to function

147
Q

what does respiratory epithelium and upper GI tract secrete

148
Q

how does mucus defend

A

contains antibodies

very sticky - prevent particles from entering blood

149
Q

name 2 chemical barriers that respiratory epithelium produces

A

anti-fungal peptides

anti-microbial peptides

150
Q

what is a cough

A

explosive expiration to clear tracheobronchial tree of secretion/foreign material

151
Q

where are the receptors of the cough reflex found

A

larynx/trachea/bronchi

152
Q

what are the 2 processes by which a cough may be initiated

A

voluntarily or reflexively

153
Q

describe the mechanism of a cough

A
  1. receptors stimulate inspiratory neurons on medulla = deep inspiration
  2. epiglottis/vocal cords trap air in lung
  3. abdominal/internal intercostals contract forcefully = pressure in lungs rises
  4. positive intrathroacic pressure = narrowing of trachea
  5. vocal cords/epiglottis open wide suddenly = air expelled at 75-100mph
154
Q

why do the vocal cords/epiglottis open so suddenly in coughing

A

large pressure difference between airways and atmosphere + tracheal narrowing = rapid flow rates through trachea

155
Q

what is airway mucus

A

viscoelastic gel containing water, carbs, proteins

156
Q

where/what secretes mucus

A

goblet cells of airway surface epithelium

submucosal glands

157
Q

what is the role of mucus

A
  1. protects epithelium from foreign material + fluid loss

2. transported to from lower resp tract to pharynx by airflow + mucociliary clearance

158
Q

what is the role of the muco-ciliary escalator

A
  1. constantly brings mucus up airway by cilia beating in directional waves
  2. protects epithelium by physical contact
159
Q

what are type 1 pneumocytes

A

thin flat squamous cells lining 95% of alveolar surface

160
Q

what is the role of type 1 pneumocytes

A

involved in gas exchange

161
Q

what are type 2 pneumocytes

A

granular cuboidal cells of alveoli typically found at blood air barrier

162
Q

what are alveolar macrophages

A

roam freely within alveoli and phagocytose material/cell debris

163
Q

where do alveolar macrophages develop from

A

differentiate from monocytes in main blood stream

164
Q

what happens to macrophages that carry particulates (3)

A
  1. enter respiratory/terminal bronchioles
  2. adhere to ciliated mucus-coated epithelium = 1st step of muco-ciliary escalator
  3. carried up to trachea then cleared in mucus by coughing
165
Q

what is adaptive immunity

A

response to pathogen following initial exposure = slower response to specific microbes

166
Q

what are T cells

A

type of lymphocyte involved in cell-mediate immunity and direct killing of cells

167
Q

where are T cells made

A

in bone marrow but mature in the thymus

168
Q

what do cytotoxic T cells do

A

travel to target location
bind to target via antigens on target
directly kill target via secreted chemicals

169
Q

what do T helper cells do

A

assist in activation and function of B cells/ macrophages/cytotoxic T cells

170
Q

what is the role of antigen presenting cells

A

phagocytose foreign material
process and present antigen
activate lymphocytes

171
Q

what are the properties of the adaptive immune response (4)

A
  1. specific
  2. self-tolerance
  3. pathogen elimination
  4. immunological memory
172
Q

what are B cells

A

type of lymphocyte

involved in antibody production

173
Q

how do B cells make antibodies

A

activated by T helper then differentiate into plasma cells = secrete antibodies

174
Q

where are B cells made

A

made and mature in bone marrow but stored in secondary lymphoid organs

175
Q

name the 5 types of antibodies

A 
IgA
IgD
IgE = allergens
IgG = most abundant
IgM
176
Q

how do T helper cells activate B cells (3)

A
  1. migrate to antigen site and undergo activation
  2. migrate to B cell activation site
  3. antigen presenting B cells make direct contact with antigen specific T cells via surface receptors + cytokine secretion = B cell activation
177
Q

how much is 1atm

A

10m of water

178
Q

boyles law with lungs at depth

A

P1V1 = P2V2

remember 1atm at the surface

179
Q

importance of henrys law with lungs at depth

A

= proportionally more gas dissolves in tissues at depth

so if ascend faster than rate of gas clearance = results in decompression illness

180
Q

what is the diving reflex with free diving

A

aponea = stop breathing
bradycardia
peripheral vasoconstriction

181
Q

what is FiO2

A

fraction of inspired O2 = never changes = 0.21

182
Q

explain why the PiO2 at sea level is 21KPa

A

Patm x Figas = 100kPa x 0.21 = 21KPa

183
Q

what is classed as extremely high altitude

A

18000 ft = 5400m

184
Q

pressure of arterial CO2 (PaCO2) is directly proportional to

A

1/alveolar ventilation

185
Q

what is the alveolar gas equation

A 
PAO2 = PiO2 - PaCO2/R
R = co2 produced - o2 consumed = 0.8 with normal diet
186
Q

arterial pressure of O2 (PaO2) =

A

PAO2 - (A-aDO2) = difference between arterial/alveolar O2

= 12.5 - 1 = 11.5KPa

187
Q

what is A-aD

A

arterial-alveolar difference

tends to be 1KPa

188
Q

normal PaO2 at sea level

A

10.5-13.5KPa

189
Q

normal PaCO2 at sea level

190
Q

effect of altitude on pressure

A

as altitude rises pressure decreases but not linearly
need to be 5000m to halve barometric pressure
FiO2 remain constant 0.21
PiO2 falls

191
Q

effect of altitude on lungs (3)

A
  1. hypoxia lead to hyperventilation results in increase minute ventilation/lower PaCO2
  2. initial alkalosis - compensated by renal bicarb excretion
  3. tachycardia
192
Q

name 2 high altitude illnesses

A

acute mountain sickness

high altitude pulmonary oedema

193
Q

where is the respiratory tract derived from

A

foregut endoderm and associated mesoderm

194
Q

what develops from the endoderm

A
  1. trachea epithelial lining
  2. larynx
  3. bronchi
  4. alveoli
195
Q

what develops from the splanchnic mesoderm

A
  1. cartilages
  2. muscle
  3. connective tissue
  4. visceral pleura
196
Q

what happens at 4th development

A

lung bud forms - initially as respiratory diverticulum from foregut endoderm

197
Q

what is the pseudogladular stage

A

5-16 weeks

branching of buds to form terminal bronchioles + angiogenesis

198
Q

what is the canalicular stage

A

16-26 weeks

each terminal bronchiole divides into respiratory bronchioles = divide into ducts

199
Q

what is the saccular stage

A

26 weeks - birth

terminal sacs and capillaries form = 1/6th the adult no. of alvoli at birth

200
Q

what is the alveolar stage

A

8months - childhood

alveoli mature/more resp bronchioles and alveoli

201
Q

what is the PaO2 in a foetus

202
Q

why is blood shunted in foetal heart

A

high vascular resistance in lungs = pressure higher in right side of heart = blood shunt to left through foramen ovale

203
Q

what is the effect of high oxygen on systemic circulation in a foetus

A

in hypoxia = vasodilation to allow more o2 to tissues so in high oxygen = vasoconstriction as not as much o2 required

204
Q

what is the role of oxygen in pulmonary circulation of the foetus

A

in hypoxia = vasoconstriction

in high oxygen = vasodilation as allows more o2 to be picked up

205
Q

what occurs in the lungs at birth

A
  1. fluid in lungs is squeezed out by birth process
  2. adrenaline released due to stress = increases surfactant release
  3. air is inhaled
  4. oxygen vasodilates pulmonary arteries
206
Q

what occurs to the umbilical arteries and ductus arteriosus at birth

A

constrict to become the medial umbilical ligament and ligamentum arteriosum respectively

207
Q

how is blood moved to lungs at birth

A

pulmonary artery pressure goes down and aortic pressure goes up so blood moves into lungs via diffusion to be oxygenated

208
Q

when is surfactant produced in the foetus

A

from 34 weeks gestation

dramatic increase 2 weeks prior to birth

209
Q

what occurs in respiratory distress syndrome of the newborn

A

type 2 pneumocytes are too immature to function = low surfactant levels = decrease lung compliance = breathing causes exhaustion/lung collapse/death

210
Q

what is respiratory epithelium

A

pseudostratified ciliated columnar epithelial cells interspersed with goblet cells
lines tubular portions of respiratory tract

211
Q

what epithelium lines the nose

A

keratinising and non-keratinising squamous epithelium

respiratory epithelium

212
Q

what is olfactory epithelium

A

roof of nasal cavity/lateral walls = pseudostratified columnar epithelium of olfactory cells - serous glands of bowman lie below

213
Q

what are sustenacular cells

A

tall narrow in contact with basement membrane
have bulky cytoplasm near lumen = accumulates yellow/brown pigment
= support olfactory epithelium

214
Q

what epithelium lines the vocal cords

A

false folds = upper = respiratory
true folds = lower = stratified squamous
vestibule = between = respiratory

215
Q

vocal cords contain

A

elastic tissue = conus elasticus

voluntary skeletal muscle = vocalis muscle

216
Q

what colour do goblet cells stain with H&E stain

217
Q

what is a mucosa associated lymph tissue MALT

A

at connective tissue in bronchius = no capsule, intimately related to epithelium

218
Q

what epithelium lines the terminal/respiratory bronchioles

A

simple cuboidal epithelium sparsely ciliated + has spirally arranged smooth muscle and no cartilage

219
Q

where are clara cells found

A

in terminal bronchioles = secretory and synthetic so have large ribosomes/ER/granules

220
Q

type 1 pneumocytes appear

A

thin + 40% population

221
Q

type 2 pneumocytes appear

A

globular, round, dark staining nuclei

222
Q

what happens to fixed/septal macrophages

A

remain in interstitium between cells/tissue

223
Q

how to distinguish pulmonary vessels from systemic

A

pulmonary = longitudinally running elastic fibres in walls

  • well defined medial
  • well defined elastic tissue
224
Q

where will fibroblasts be found

A

in walls of alveoli = produce collagen type 3 (reticulin) and elastic tissue for recoil

225
Q

what is the structure of the visceral pleura

A 
flat mesothelial cells
loose fibrocollagenous tissue
irregular ext elastic layer
interstitial fibrocollagenous layer
irregular int elastic layer
226
Q

what type of response do central chemoreceptors provide

A

slow response

227
Q

what type of response fo peripheral chemoreceptors provide

A

rapid response

228
Q

what is a pulmonary embolism

A

blood clot prevent perfusion of lungs

229
Q

what is pneumonia

A

infection prevents ventilation of alveoli

230
Q

how does copd affect the body

A

less gas exchange SA

in expiration airway collapses = trap air in chest = buildup of CO2

231
Q

how does asthma affect the body

A

can expire CO2 faster than can receive O2
hypoxic because low O2 but normal CO2 = type 1 resp failure
long term become hypercapnic

232
Q

what is the term to describe malignant tumour in pleural membranes

A

mesothelioma

233
Q

what conditions lead to type 1 resp failure

A

pulmonary embolism

V/P mismatch

234
Q

what condition may lead to type 2 resp failur

A

opioid overdose

235
Q

what is PEF

A

peak expiratory flow = effort dependent

236
Q

what is FEF

A

forced expiratory volume

FEF25 = forced expiratory flow rate when 25% volume has been expelled

Phase 1 mine (12 decks)

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