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respiratory physiology Flashcards

1
Q

what innervates the smooth muscle of the airways to cause bronchoconstriction?

A
  • branches of the vagus nerve

- parasympathetic

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2
Q

where does the vagus nerve terminate?

A
  • parasympathetic ganglia in airway wall

- short post-ganglionic cholinergic fibres reach smooth muscle

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3
Q

what neurotransmitter does bronchoconstriction occur via?

A

ACh

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4
Q

what receptors does ACh act upon to cause bronchoconstriction?

A

muscarinic M3 receptors on muscle cells

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5
Q

what division of the nervous system causes bronchodilation?

A

sympathetic

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6
Q

what is the path of the nerve fibres that cause bronchodilation?

A
  • originate from spinal cord
  • terminate in ganglia near spinal cord
  • long post-ganglionic fibre goes directly to blood vessels
    and some smooth muscle cells
  • acts on adrenergic receptors (alpha and beta)
  • releases noradrenaline
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7
Q

what does activation of beta-2 receptors cause?

A
  • on airway smooth muscle

- causes muscle relaxation- activates adenylate cyclase which produces cyclic AMP

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8
Q

why is the sympathetic effect on airway tone weak compared to parasympathetic?

A

fewer sympathetic nerve fibres penetrate the lung parenchyma

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9
Q

what drugs can be used to treat bronchoconstriction?

A
  • anti-muscarinics

- LAMAs

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10
Q

what drugs can be used to reduce bronchodilation?

A
  • SABAs

LABAs

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11
Q

what are the key features of muscarinic receptors?

A
  • use G proteins as a signalling mechanism

- found on all effector cells stimulated by postganglionic cholinergic neurons of PNS/ SNS

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12
Q

what are key features of nicotinic receptors?

A
  • lignand-gated ion channels
  • found in autonomic ganglia of PNS and SNS
  • present at neuromuscular junctions in skeletal muscle
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13
Q

what does vasodilation lead to?

A

exudation of plasma- including antibodies

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14
Q

where is acute inflammation initiated?

A
  • tissues containing specialist macrophages

- e.g. kupffer cells and alveolar macrophages

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15
Q

what do specialist macrophages respond to?

A
  • PAMPs (pathogen- associated molecular patterns)

- DAMPs (damage- associated molecular patterns)

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16
Q

how do we recognise pathogens we have never seen before?

A

pathogen recognition receptors (PRRs)

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17
Q

what are the functions of alveolar macrophages?

A
  • microbial killing
  • co-ordination of inflammatory response via cytokine production
  • link to adaptive immune responses
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18
Q

what suppresses alveolar macrophages?

A

respiratory epithelium

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19
Q

what are neutrophils formed from?

A

myeloid cells

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20
Q

what are the functions of neutrophils?

A
  • identify threat- via receptors
  • activation of pathways
  • adhesion via integrins
  • chemotaxis- move along concentration gradients
  • phagocytosis
  • bacterial killing
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21
Q

what is the function of Clara cells?

A

secrete lipoproteins- prevents luminal adhesion

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22
Q

what secretes surfactant?

A

type 2 pneumocytes

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23
Q

what are the functions of surfactant?

A
  • reduces alveolar surface tension
  • prevent collapse of alveoli during expiration
  • facilitates expansion during inspiration
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24
Q

what is the composition of mucus?

A

lyoszymes, immunoglobulins, glycoproteins, water, dead leukocytes, inorganic salts

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25
Q

what are the 2 types of adaptive immunity?

A
  • humoral- B lymphocytes produce antibodies

- cell- mediated- T lymphocytes are activated

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26
Q

what is immune tolerance?

A

state of unresponsiveness of the immune system to substances or tissue that have the capacity to elicit an immune response (e.g. self-antigens, pregnancy or cancer)

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27
Q

what are the 2 types of tolerance?

A
  • central- auto reactive clones are deleted by thymic epithelial cells
  • peripheral- auto reactive clones escaping central tolerance are suppressed by T suppressor cells
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28
Q

what does the apneustic centre do?

A

stimulates dorsal and ventral respiratory group

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29
Q

what does the pneumotaxic centre do?

A

sends inhibitory signals to the dorsal respiratory group- allows respiratory rate to be controlled

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30
Q

what does the dorsal respiratory group do?

A

controls the rhythm of breathing- triggers inspiratory impulses in external intercostals

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31
Q

what does the ventral respiratory group do?

A

activated in times of stress/ exercise when forced expiration is required- controls the accessory muscles

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32
Q

what is an SASR?

A
  • mechanoreceptor
  • slow adapting stretch receptor
  • found in smooth muscle of airway
  • inhibits further inspiration
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33
Q

what is an RASR?

A
  • rapid adapting stretch receptor
  • found between airway epithelial cells
  • activated by lung distention and irritants
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34
Q

what are C-fibres?

A
  • located in small airways, blood vessels and interstitial tissues between pulmonary capillaries and alveolar walls
  • unmyelinated sensory nerve fibres
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35
Q

what are J-fibres?

A
  • found in lung parenchyma
  • activated by increased interstitial fluid
  • cause increased respiratory rate- results in decreased oxygenation
  • innervated by vagus fibres
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36
Q

what are central chemoreceptors?

A
  • present below ventral surface of medulla

- detect changes in pH of CSF

37
Q

what are peripheral chemoreceptors?

A
  • carotid bodies and aortic arch

- detect changes in arterial pH and concentration of co2

38
Q

what do the chemoreceptors do?

A

detect changes in concentration of CO2/ pH and send efferent impulses to respiratory centres

39
Q

what is the main respiratory drive?

A

PaCO2

40
Q

what is the main respiratory drive in type 2 respiratory failure?

A

PaO2- hypoxic drive

41
Q

what is alveolar recruitment?

A
  • vasodilation occurs- causes increased blood flow to alveoli
  • results in increased amount of O2 absorbed
  • stimulated by damage to lung or in times of stress/ exercise
42
Q

what is Daltons law?

A

total pressure exerted by a mixture of gases is equal to the sum of the pressures that would be exerted by each of the gases if it alone were present and occupied the same volume

43
Q

what is Boyles law?

A

pressure is inversely proportional to volume for a fixed mass of gas at a constant pressure

44
Q

what is Henrys law?

A

at a constant temperature, the amount of a given gas that dissolves in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid

45
Q

what is the alveolar gas equation?

A

PAO2= PiO2 - (PaCO2/ R)

46
Q

what is Laplaces law?

A

P= 2T/ R (P= transmural pressure, T= tension of walls, R= radius)

47
Q

what is the action of surfactant?

A
  • active phospholipid produced by type 2 pneumoyctes
  • eliminates surface tension
  • allows homogenous aeration
  • allows maintenance of functional residual capacity
48
Q

where is there a high V/Q ratio in a healthy patient?

A
  • apex

- due to gravity- less blood flow to apex- so perfusion is less

49
Q

what is the V/Q ratio used to assess?

A

amount of air that reaches alveoli compared to blood that reaches the alveoli

50
Q

what would a V/Q ratio higher than 1 indicate?

A

pulmonary embolism

51
Q

what would a V/Q ratio lower than 1 indicate?

A

a shunt- due to asthma or chronic bronchitis

52
Q

what are the layers from gas exchange? (from lung- blood)

A
  • surfactant layer
  • type 1 pneumocyte outer membrane
  • type 1 pneumocyte cytoplasm
  • type 1 pneumocyte outer membrane
  • basement membrane
  • vascular endothelial cell
  • erythrocyte cell membrane
53
Q

what are the 3 ways carbon dioxide can be transported?

A
  • dissolved in plasma
  • bound to haemoglobin- carbaminohaemoglobin
  • cytoplasm of red blood cell
54
Q

how does a low pH/ high concentration of arterial co2 affect the oxygen dissociation curve?

A
  • curve shifts right

- dissociates more readily at tissues

55
Q

how does high pH/ low concentration of CO2 affect the oxygen dissociation curve?

A
  • curve shifts left

- O2 dissociates less readily from tissues

56
Q

how does an increase in temperature affect the oxygen dissociation curve?

A
  • shifts to the right

- haemoglobin denatures, so O2 is released more readily

57
Q

what is the inspiratory reserve volume?

A

maximum additional volume of air that can be drawn in over a normal breath

58
Q

what is the expiratory reserve volume?

A

maximum volume of air that can be exhaled from the end respiratory position

59
Q

what is the inspiratory capacity?

A

amount of gas n the lungs after maximal inhalation

60
Q

what is the functional residual capacity?

A

volume in the lungs when breathing at rest

61
Q

what is vital capacity?

A

the greatest possible volume of air that can be expelled from the lungs after taking the deepest possible breath

62
Q

what is FEV1?

A

forced expiratory volume in 1 second (litres)

63
Q

what is FVC?

A

forced vital capacity (litres)

64
Q

what does a low FEV1/ FVC ratio indicate?

A

airway obstruction

65
Q

why does airway obstruction result in a low FEV1/ FVC ratio?

A
  • patients have a difficulty expelling air- results in a low FEV1
  • can maintain a near normal FVC
66
Q

what can a high FEV1/ FVC ratio indicate?

A

airways restriction

67
Q

why does airway restriction result in a high FEV1/ FVC ratio?

A
  • no difficulty expelling air- so a normal FEV1

- difficulty maintaining lung volume- reduced FVC

68
Q

what is the effect of hypoxia on pulmonary and systemic circulation?

A
  • pulmonary- vasoconstriction

- systemic- vasodilation

69
Q

what does alkalosis cause?

A

pulmonary vasodilation

70
Q

what is. respiratory acidosis?

A
  • increased PaCO2= decrease in pH and increase in HCO3-
  • renal compensation occurs- more bicarbonate ions reabsorbed
  • respiratory compensation- hyperventilation
71
Q

what is respiratory alkalosis?

A
  • decreased PaCO2= increased pH and decrease in HCO3-

- renal compensation- reduced absorption of HCO3-

72
Q

what are causes of hypoxia?

A
  • inadequate oxygenation of blood in lungs- extrinsic reasons (deficiency of O2 in atmosphere)
  • abnormal V/Q ratio
  • cardiac shunts
  • anaemia
  • inadequate O2 transport to tissues
73
Q

what are key features of Type 1 respiratory failure?

A
  • occurs due a V/Q mismatch caused by a shunt
  • patient will be hypoxic and have hypocapnia
  • caused by pneumothorax, asthma or pulmonary fibrosis
74
Q

what are key features of type 2 respiratory failure?

A
  • occurs secondary t reduced airflow w/ alveolar hyperventilation
  • patient will be hypoxic and have hypercapnia
  • caused by COPD, drug overdose or myasthenia gravis
75
Q

what are the causes of hypercapnia?

A
  • hypoventilation
  • lung disease
  • only occurs in association w/ hypoxia when.hypoxia is caused by hyperventilation or circulatory deficiency
76
Q

what are the main effects of ageing on the lung?

A
  • bones in chest become thinner and change shape- ribcage unable to expand as effectively
  • weakened inspiratory muscles
  • alveoli lose shape- breakdown of elastin
  • airways close up
  • nerves in airways become less sensitive= less coughing= increases susceptibility to infection
  • lungs less able to recover from exposure to harmful substances
77
Q

what is the type 1 Gell and Coombs classification?

A
  • IgE-immediate

- actue anaphylaxis, hay fever

78
Q

what is the type 2 Gell and Coombs classification?

A
  • IgG/IgM
  • bound to cell-surface antigens
  • antibody-mediated reaction
  • transfusion reactions, autoimmune disease
79
Q

what is the type 3 Gell and Coombs classification?

A
  • immune complexes
  • body attacks areas where complexes accumulate
  • systemic lupus, rheumatoid arthritis, farmers lung
80
Q

what is the type 4 Gell and Coombs classification?

A
  • T- cell mediated DTH (delayed-type hypersensitivity)

- tuberculosis, type 1 diabetes, inflammation of thyroid

81
Q

how is histamine released in type 1 reactions?

A
  • B cells stimulated to produce IgE antibodies
  • IgE antibodies bind to receptors on surface of mast cells
  • exposure results in mast cells covered in IgE antibodies degrading- releases histamine
82
Q

what does histamine cause?

A
  • vasodilation
  • increased vessel permeability
  • smooth muscle spasm
  • leukocyte extravasation
83
Q

what is the effect of diving on the lung?

A
  • diver inhales, pre-hyperventilation
  • gas compression occurs- holds breath whilst diving
  • PaO2, PaN2, PaCO2 rise
  • minimal N2 absorption
  • CO2 builds up- desire to breathe
  • returns to surface- PaO2, PaN2, PaCO2 fall
  • whilst under water diving reflex occurs- bradycardia, apnoea, peripheral vasoconstriction
84
Q

what can diving cause?

A
  • oxygen toxicity
  • decompression illness
  • inert gas narcosis
  • pulmonary barotrauma
85
Q

what is the effect of altitude on the lung?

A
  • less availability of gas
  • causes hypoxia, hyperventilation and tachycardia
  • alkalosis occurs- renal compensation occurs- reducing reabsorption of HCO3-
86
Q

what can high altitude cause?

A
  • mountain sickness

- cerebral and pulmonary oedema

87
Q

what are the 5 stages of respiratory embryology?

A
  • embryonic
  • psuedoglandular
  • canalicular
  • saccular
  • alveolar
88
Q

what happens during the first breath?

A
  • fluid squeezed out of lungs by birth process
  • adrenaline stress results in increased surfactant release
  • air inhaled
  • oxygen vasodilates pulmonary arteries
  • umbilical arteries constrict
  • ductus arterioles constricts

Nicks phase 1 flashcards (16 decks)

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