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Respiratory 1

Erin Dunn PHASE 1 MED English 197 cards

Respiratory 1

Cards in this deck (197)

  1. 1Describe the nose?Most superior portion of the respiratory tract
    - Warms inspired air (0.25 seconds of contact)
    - Humidifies air
    - Filters inspired air of pathogen using cilia to trap particulates
    - Defence function - cilia take inhaled particles backwards to be swallowed
  2. 2What are the nasal meatuses?Superior meatus: Has olfactory epithelium, olfactory nerve penetrates into superior meatus through pores in the cribform plate - sphenoid sinus drains here
    Middle meatus: more sinuses drain here (inc maxillary)
    Inferior meatus: nasolacrimal duct drain her e
    What are the nasal meatuses?
  3. 3What lines the nose?The anterior nose opens into the enlarged vestibule which is skin lined and has stiff hairs
    The surface area of the nose is doubled by turbinates
  4. 4Describe the paranasal sinuses?- Pneumatised areas of the frontal, maxillary, ethmoid and sphenoid bones
    - Arranged in pairs
    Describe the paranasal sinuses?
  5. 5Define: pneumatised?A bone that is hollow or contains many air cells
  6. 6Describe the frontal sinuses?- Within the frontal bone
    - Lie of the orbit
    - Innervataion: opthalamic division (V1) of the trigeminal nerve (CNV)
  7. 7Describe the maxillary sinuses?- Located within the body of the maxilla
    - Pyramidal in shape
    - Innervation: Maxillary division (V2) of the Trigeminal nerve (CNV)
    - Base: Lateral wall of the nose
    - Apex: Zygomatic process of the maxilla
    - Roof: follow of orbit
    - Floor: alveolar process
    Open into the MIDDLE MEATUS
  8. 8Describe the ethmoid sinuses?- Between the eyes
    - Labyrinth of air cells
    - Innervation: Opthalamic (V1) and Maxillary (V2) branches of the trigeminal nerve (CNV)
    - Open into middle meatus
  9. 9Describe the caverous sinuses?Contians caroitd artery, ocularmotor nerve (CNIII), trochlear (CNIV), trigeminal (CNV) and abductens (CNVI)
  10. 10Describe the sphenoid sinusMedial to the canervous sinus
    Inferior to optic canal, dura and pituarty gland
    Empties into the sphenoethomoidal recess, lateral to the attachment of the nasal septum
    - Innervation: Opthalmic (V1) branch of the trigeminal nerve (CNV)
  11. 11What is the pharynx?A fibromuscular tube which takes filtered air to the larynx
    Lined with squamous and columnar ciliated epithelium
    Extends from the base of the skull to C6
  12. 12What epithelium lines the pharynx?Nasopharynx = pseudostratified, cilitated columnar epithelium (same as nasal cavity)
    Oropharynx and laryngopharynx = Non keratinising squamous epithlium
  13. 13What is the valvular function of the larnyxPrevents liquid and food from entering the lungs
  14. 14Describe the structure of the larynx?- Rigid structure
    - Consists of 9 CARTILAGES
    (6) Paired = Cuneiform, Corniculate and Arytenoid
    (3) Unpaired = Epiglottis, thyroid and cricoid
  15. 15How are the vocal chords changed?The arytenoid cartilages rotate on the cricoid cartilage to change vocal chords
  16. 16What innervates the larynx?Vagus Nerve (CNX)
    Superior laryngeal and Recurrent laryngeal nerve
  17. 17What does the superior laryngeal nerve innervate?Divides into the internal (sensation) and external (motor)
    External innervated the cricothyroid muscle
  18. 18What does recurrent laryngeal nerve innervate?Provides motor innervation for ALL larynx muscles apart from the cricothyroid muscles
  19. 19Where does the left recurrent laryngeal nerve run?Runs laterally to the arch of the aorta, loops UNDER the aortic arch and ascends between the trachea and oesophagus
  20. 20Where does the right recurrent laryngeal nerve run?Loops underneath the right subclavian artery, then runs up the plane between the trachea and oesophagus
  21. 21What could a tumour/ulcer on or near the reccurent laryngeal nerve cause?Hoarse voice
  22. 22What is the main function of the lungs?Gaseous exchange
  23. 23What is the area of gas exchange PER lung20m2
    40 m2 for both lung s
  24. 24What is minute volume?The volume of air inhaled /exhaled in a minute
    Approx 5 litres
  25. 25What is cardiac output?Volume of blood pumped out by the heart a minute
    5 litres per minute
  26. 26Where is the trachea?Extends from the larynx to the carina
    C6 to T5
  27. 27Describe the trachea?Oval in cross section
    Semicircular hyaline cartilages (C shaped cartilages increase flexibility)
    Pseudo-stratified, ciliated, columnar epithelium
    Goblet cells
    Upper trachea is more mobile than distal trachea
  28. 28Describe the main bronchi?- Consist of left and right main bronchus
    - Sharp division at the carina
  29. 29Which bronchus is more vertically disposed and why?The RIGHT main bronchus is more vertically disposed
    Therefore more risk of trapping things and choking
    Related to the right pulmonary artery
    1.2 to 5cm
  30. 30Describe the left main bronchus?Comes off at more of an angle
    5cm
    Related to the aortic arch
  31. 31What do the lobar bronchi supply?Right: upper lobe, middle lobe and lower lobe THEREFORE 3 divisions
    Left: upper lobe and lower lobe
    THEREFORE 2 divisions
  32. 32How many segmental branches are there?Right = 10 branches
    Left = 8 branches
  33. 33What is the organisation of bronchi?Main bronchi
    Lobar bronchi
    Segmental bronchi
    Terminal bronchioles
    Respiratory bronchioles
    Alveolar ducts
    Alveoli
  34. 34Describe the alveoli?Type I pneumocytes
    Type 2 pneumocytes
    Alveolar macrophages
    Basement membrane
    Membrane is 1 micron thick
    Columnar ciliated epithlium
  35. 35What innervates the lung?The PULMONARY PLEXUS lies between each hilum, it receives innervation from both right and left vagus nerve
    AND T2 - T4 ganglia of the sympathetic trunk
  36. 36What innervates bronchodilation and bronchocontriction?Bronchodilation = sympathetic input from sympathetic trunk
    Bronchoconstriction = parasympathetic input from the vagus nerve
  37. 37Which lung is larger and why?Right lung is large that the left due to the the silhouette of the heart
  38. 38Describe the lung pleura?2 main layers of mesodermal origin one cell thick, both continuous with eachother at the lung root
    VISCERAL: applied to the lung surface - only has autonomic innervation
    PARIETAL: applied to the internal chest - has pain sensation via phrenic nerve
  39. 39Describe the blood supply of the lungs?Pulmonary and Bronchial circulations
    PULMONARY :
    The left and right pulmonary arteries run from the right ventricle
    BRONCHIAL :
    17 orders of branching
    Bronchus and pulmonary arteries run together via the bronchiovascular bundle
    Pulmonary veins run on their own
  40. 40What is transpulmonary pressure?Difference in pressure between the inside and outside of the lung
    Alveolar pressure - intrapleural pressure
  41. 41What is interpleural pressure?The pressure in the pleural space
    Also known as the inter thoracic pressure
  42. 42What is alveolar pressure?Air pressure in the pulmonary alveoli
  43. 43What initiates inspiration?A neurally induced contraction of the diaphragm and the external intercostal muscles located between the ribs
  44. 44What is the most important muscle during normal quiet breathing?The diaphragm
  45. 45What innervates the diaphragm?The phrenic nerve, which arises from C3, C4 and C5
  46. 46Describe inspiration?1. The diaphragm contracts causing its dome to move downwards thereby enlarging the thorax increasing its volume
    2. Simultaneously, the activation of the motor neurones in the intercostal nerves to the EXTERNAL intercostal muscles causes them to contract, up and out movement, further increasing in thoracic volume
    3. As the thorax expands, the intrapleural pressure is being lowered and the transpulmonary pressure is becoming more positive = resulting in lung expansion as TP is larger than elastic recoil
    4. The lung expansion results in alveolar pressure becoming negative
    5. Inwards airflow
    6. At the end of inspiration, the chest wallk is no longer expanding but yet to start passive recoil, glottis open so
    alveolar pressure = atmospheric pressure
    Since elastic recoil balanced by transpulmonary pressure
  47. 47Describe expiration? at rest1. At the end of inspiration, the motor neurones to the diaphragm and external intercostal muscles decrease their firing so that muscles can relax, diaphragm ASCENDS decreasing thoracic volume
    2. As they relax, the lungs and chest walls start to passively collapse due to to elastic recoil because muscle relaxation increases intrapleural pressure decreasing transpulmonary pressure so it is less than the elastic recoil
    3. As the lungs become smaller the air in the alveoli becomes temporarily compressed resulting in an increase in alveolar pressure resulting in outwards air flow
  48. 48Describe the characteristics of expiration at rest vs. forced?Expiration at rest is passive relying only on the relaxation of the external intercostal muscles and diaphragm and the elastic recoil of the lungs
    On certain occurs e.g. excercise the expiration of larger volumes of air is required and resulting in forced expiration which involves the contraction of the internal intercostal muscles
  49. 49Describe forced expiration?1. On top of the actions mentioned in expiration at rest, the internal intercostal muscles also contract as do the abdominals
    2. This results in the ribs moving downwards and inwards - actively decreasing thoracic volume, abdominal contraction increases intra-abdominal pressure more thereby forcing the relaxed diaphragm further up into the thorax
    3. Resulting in a greater volume of air being expelled
  50. 50Why is there the greatest resistance in the trachea?Because although bronchioles are small, when you add them all up they have a much GREATER surface area therefore providing much less resistance
  51. 51Define: Dead space?The volume of air not contributing to ventilation
    Anatomically theres around 150mls in the alveoli and 25mls in the lungs
    So 175 mls of dead space in total
  52. 52Where does gas exchange take place?Between the alveoli and capillaries
  53. 53What is bulk flow?Net movement down a concentration gradient due to the random motion of individual molecules
  54. 54What allows O2 and CO2 movement in the airways?Bulk flow
    This requires a large surface area with minimal distance for gases to move across as well as adequate perfusion of blood
  55. 55How many alveoli are there per lung?300 milllion
  56. 56How many capillaries per alveolus?1000
    An individual RBC may come into contact with multiple alveoli
  57. 57What are the 7 layers that gases must diffuse through? Alveoli to cappilaries?1. Alveolar epithelium
    2. Tissue interstitium
    3. Capillary endothelium
    4. Plasma layer
    5. Red cell membrane
    6. Red cell cytoplasm
    7. Haemoglobin binding
  58. 58Describe ventilation perfusion matching? V/QEach alveolus is capable of receiving CO2 from, and supplying oxygen to the pulmonary capillary blood
    To be most efficient, the correct proportion of alveolar airflow (ventilation) and capillary blood flow (perfusion) shows to be available
  59. 59Describe ventilation perfusion mismatch?The main effect of ventilation perfusion mismatching is that the partial pressure of oxygen is decreased in the systemic arterial blood
    In healthy people there is naturally some ventilation perfusion inequality
  60. 60Why is there naturally some V/Q mismatch in healthy people?Gravitational effects
    One effect of upright posture is increased filling of the blood vessels at the bottom of the lung due to gravity - contributing to the difference in blood flow distribution in the lung
    This explains why the PO2 is roughly 5mmHg higher than in arterial blood
  61. 61What are the extremes that can cause V/Q mismatch?1. The may be ventilated alveoli but no blood supply at all due to a blood clot
    2. There may be adequate blood flow through areas of lung but no ventilation due to a collapsed alveoli
  62. 62What else can cause V/Q mismatch?Disease, regional changes in lung compliance, airway resistance and vascular resistance
  63. 63What is a local homeostatic response to V/Q mismatch?- Hypoxic pulmonary constriction
    - Local bronchoconstriction
  64. 64Describe hypoxic pulmonary constriction?A decrease in ventilation within a group of alveoli and nearby blood vessels leads to vasoconstriction
    Diverting blood away from the poorly ventilated area
    This effect is unique to the pulmonary arterial vessels since in systemic circulation the opposite would occur
    Ensures that blood flows away from diseases areas and towards well ventilated
  65. 65Describe local bronchoconstriction?If there is a local decrease in blood flow within a lung region due to e.g. a small blood clot in a pulmonary arteriole
    The local decrease in blood flow will mean there is less systemic CO2 in the area, resulting in a decreased partial pressure of CO2
    This will cause bronchioconstriction to divert air to areas with better perfusion
  66. 66PaCO2?arterial CO2
  67. 67PACO2?Alveolar CO2
  68. 68PaO2arterial O2
  69. 69PAO2Alveolar O2
  70. 70PIO2Pressure of Inspired O2
  71. 71VA?Alveolar ventilation
  72. 72VCO2?CO2 Production
  73. 73Describe the structure of haemoglobin?- Four subunits bound together
    - Subunits consist of a haem and a polypeptide together
    - This means a single haemoglobin can bind to 4 oxygen molecules because each haem can have one oxygen
  74. 74What is the reaction between oxygen and haemoglobin?O2 + Hb ⇄ HbO2
    Thus haemoglobin can exist as deoxyhaemoglobin and oxyhaemoglobin
  75. 75Describe the oxygen dissociation curve?Sigmoid shaped because of the four haemoglobin subunits
    The reactions of the four subunits occurs sequentially with each combination facilitating the next one
  76. 76At what partial pressure of oxygen is the haemoglobin 90% saturated?60 mmHg
    From this point onwards a further increase in the partial pressure of oxygen produces only a small increase in oxygen binding
    The curve plateaus
  77. 77Why is the plateau important and higher O2 pressures?In situations such as high altitude with pulmonary disease, a moderate reduction in alveolar O2 partial pressure and thus arterial partial pressure
    O2 is decreased from the normal value of 100 to 60mmHg, total quantity of O2 carried by haemoglobin would only decrease by 10%
    The plateau provides and excellent safety factor so that even a significant limitation of lung function still allows almost normal oxygen saturation of haemoglobin
  78. 78What does an increase in temperature do to the oxygen dissociation curve?Shifts it RIGHT
    Haemoglobin has less affinity for oxygen
    Easier to get rid of CO2
    Temperature is increased because of the heat produced by tissue metabolism
  79. 79What happens to the oxygen dissociation when there is a decrease in pH or increased acidity?Shifts it RIGHT
    Haemoglobin has less affinity for oxygen
    pH is decreased because of the elevated CO2 partial pressure and the release of metabolically produced acids (lactic)
  80. 80How does carbon monoxide effect the oxygen dissociation curve?Carbon monoxide has a 200 times greater affinity for the oxygen binding sites on haemoglobin than O2
    For this reason, it reduces the amount of oxygen that combines with haemoglobin
    Shifts the curve LEFT
  81. 81Describe the relationship between arterial CO2 and alveolar ventilation?The partial pressure of arterial CO2 is inversely related to alveolar ventilation
    PaCO2 ⇄ kV̇ CO2 / V̇A
  82. 82What are the three ways that CO2 is carried in the blood?1. Bound to haemoglobin (23%)
    CO2 + Hb ⇄ HbCO2
    2. Plasma dissolved (10%)
    3. As bicarbonate/HCO3- (60-65%)
  83. 83How is CO2 carried as bicarbonate?How is CO2 carried as bicarbonate?
  84. 84What enzyme catalyses the formation of H2CO3?Carbonic anhydrase
  85. 85What happens to the carbonic acid as soon as it is formed in the RBC?It dissociates into HCO3- and H+ and then the HCO3- moves out of the RBC into the plasma via a transporter
    This transporter exchanges on HCO3- for at chloride ion to maintain electroneutrality within the erythrocyte and the plasma
  86. 86Why is venous blood only slightly more acidic than arterial blood?The H+ binds to deoxyhaemoglobin since deoxyhaemoglobin has a greater affinity for H+
    Only a small amount of H+ generated in the blood remains free
    This is why venous blood is only slightly more acidic than arterial blood
  87. 87What happens chemically as the venous blood enters the lungs?Deoxyhaemoglobin becomes converted to oxyhaemoglobin
    In that conversion, H+ is released and picked up in the tissues
    H+ reacts with HCO3- to form carbonic acid
    Broken down to CO2 and H2O by carbonic anhydrase and the CO2 is diffuses to the alveoli to be expired
  88. 88Why is there net diffusion of CO2 from blood to the alveoli?Because when blood reaches the longs the partial pressure of CO2 in the blood is higher than alveolar CO2 so there is a net diffusion
  89. 89What is the usual pH of blood>7.4
    7.35 - 7.45
  90. 90How is balance of pH maintained in the body?Balance is maintained by mechanisms that generate, buffer and eliminated acids and bases
    Most body acids and bases are weak
  91. 91What are the three main buffering systems of body fluid pH?1. Intra and extracellular buffers
    2. The lungs eliminating CO2
    3. Renal HCO3- absorption and H+ elimination
  92. 92Describe respiratory acidosis?When a person HYPOventilates, there is inadequate ventilation of the alveoli meaning that CO2 cannot be excreted and expired adequately
    The partial pressure of CO2 increases thereby resulting in more carbonic acid being produced and thus increased H+ concentration
  93. 93Describe respiratory alkalosis?When a person is HYPERventilating, this would decrease arterial partial CO2 pressure and thus H+ concentration resulting in respiratory alkalosis
  94. 94What is the Henderson-Hasselbalch equation?pH=6.1* + log10([HCO3-]/[0.03*PCO2])
    It is the dissociation constant for the bicarbonate buffer system
    0.03*PCO2 = estimate of H2CO3
    0.03 = the blood CO2 solubility co-efficient
  95. 95What is Dalton's Law?The pressure exerted by each gas in a mixture of gases is independent of the pressure exerted by the other gases
    This is because the gas molecules are so far apart that they do not affect each other
    Each gas in a mixture behaves as if there are no other gases presnt
    So the total pressure of the mixture is simple the sum of the individual pressures (pp) when are directly proportional to its concentration
  96. 96What Boyle's Law?The pressure of a fixed amount of gas in a container is inversely proportional to the containers volume
    P1V1 = P2V2
  97. 97What is Henry's Law?The amount of gas dissolved in a liquid is proportional to the partial pressure of that gas with which the liquid is in equilibrium with
    At equilibrium the partial pressures of the gas molecules and the liquid and gaseous phases must be identical
  98. 98What is the alveolar gas equation?PAO2 = PiO2 - PaCO2/R
    R - the respiratory exchange ratio which is the ratio between the amount of CO2 produced in the metabolism and oxygen used
  99. 99Describe the relationship between pressure, flow and resistance?Pressure = flow x resistance
  100. 100What is the law of Laplace?Describes the relationship between pressure (P), surface tension (T) and the radius of on an alveolus (r)
    P = 2T/r
  101. 101What is lung compliance? (Cl)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
  102. 102What are the determinants of lung compliance?- Stretchability of the lung tissues
    - Surface tension of the air water interface
  103. 103How does the stretchability of lung tissues determine lung compliance?A thickening and thus a loss in the stretchability of the lungs connective tissues results in a decreased lung compliance
  104. 104How does the surface tension from air water interfaces determine lung compliance?The surface of the alveolar cells are moist, thus alveoli are effectively air filled sacs lined with water
    At an air water interface the attractive forces between the water molecules known as surface tension, make the water lining like a stretch ballon
    Thus the expansion of the lungs requires energy to not only stretch the connective tissue but also to overcome the surface tension of the water layer lining the alveoli
  105. 105How is the surface tension of water overcome in the lungs?The type II pneumocytes in the alveoli produce a surfactant which markedly reduced the cohesive forces between the water molecules on the alveolar surface
    This surfactant lowers the surface tension which in turn increases the lung compliance making it easier to expand the lungs
  106. 106What would happen if these was no surfactant in the lungs?In pure water the surface tension is so great that eventually lung expansion wouls require exhausting muscular effort resulting in lung collapse
  107. 107When does the amount of surfactant decrease?When breaths as small and constant
    However a deep breath stretches the type II pneumocytes stimulating the secretion of surfactant
  108. 108What is Inspiratory Reserve Volume? IRVThe amount of air in excess tidal inspiration that can be inhaled with maximum effort
  109. 109What is Expiratory Reserve volume? ERVThe amount of air in excess tidal expiration that can be exhaled with maximum effort
  110. 110What is Residual Volume? RVThe amount of air remaining in the lungs after maximum expiration, keeps alveoli inflated between breaths and mixes with fresh are on inspiration
  111. 111What is vital capacity? VCThe amount of air that can be exhaled with maximum effort after maximum inspiration
    ERV + TV + IRV
    Used to asses the strength of the thoracic muscles as well as pulmonary function
  112. 112What is functional residual capacity? FRCThe amount of air remaining in the lungs after normal expiration
    RV + ERV
  113. 113What is Inspiration Capacity? ICThe maximum amount of air that can be inhaled after a normal tidal expiration
    TV + IRV
  114. 114What is the Total Lung Capacity? TCThe maximum amount of air that the lungs contain
    RV + VC
  115. 115What is Tidal Volume? TVThe amount of air inhaled or exhaled in one normal breath
    Usually around 500ml per breath
  116. 116What is FEV1?Forced Expiratory Volume in one second
    In which a person take a maximal inspiration and then exhales maximally as fast as possible
    The important value is the FRACTION of the total forced vital cap in one seocnd
  117. 117What fraction of vital capacity can be exhaled in one second in healthy individuals?80% of the vital capacity
  118. 118Describe the procedure measuring FEV1?1. Breath in total lung capacity
    2. Exhale as fast as possible in one second
    3. Volume produced is the forced vital capacity for 1 second
  119. 119Describe the FEV6 graph?Flow is greatest at the start of expiration however it declines linearly with volume
  120. 120What is FEF25?Flow at point when 25% of total volume to be exhaled has been exhaled
  121. 121When would an FEV1 be considered normal or low?If the result is 80% or greater than the predicted value then it is considered normal
    If the FEV1 is lower than 80% then it is low
  122. 122What is FVC, and what is a considered normal for FVC?Forced vital capacity
    80% of predicted vital capacity is considered normal
    Low FVC = airways restriction
  123. 123What are the indicators of airways restriction?If the ratio of FEV1/FVC is high i.e normal but the FVC is low
    This is airway restriction
  124. 124What are the indicators of airways obstruction?If the ratio of FEV1/FVC is below 0.7
    This is airway obstruction
  125. 125What is the diagnosis? Measured values FEV1 = 1.8 FVC = 3.3 Predicted values FEV1= 2.94 FVC 3.70Ratio of measured values = 1.8/3.3= 0.55 which is low
    Look at predicted values
    FEV1 1.8/2.94 = 61% low
    FVC 3.3/3.7 = 89% normal
    Low ratio, Low FEV, Normal FVC =
    AIRWAYS OBSTRUCTION
  126. 126What is the diagnosis? Measured values FEV1 = 1.1 FVC = 1.2 Predicted values FEV1= 3.6 FVC = 4.55FEV1/FVC ratio = 1.1/1.2 = 92% normal
    Look at predicted values
    FEV1 = 1.1/3.6 = 31%
    FVC = 1.2 / 4.55 = 26%
    Normal ratio, Low FEV1, Low FVC =
    AIRWAYS RESTRICTION
  127. 127How is inspiration initiated in the lungs?Inspiration is initiated by a burst of action potentials in the spinal motor neurons to inspiratory muscles like the diaphragm
    Vagus nerve arises from C3, C4 and C5 for the diaphragm
  128. 128Where does control of breathing reside?Control of breathing resides primarily in the neurons in the medulla oblongata, the same area of the brain that controls the major cardiovascular control centres
  129. 129What are the two main anatomical components of the medullary respiritory centre?Dorsal Respiratory Group: These primary fire during inspiration and have input to the spinal motor neurons that active respiratory muscles involved in inspiration
    Ventral Respiratory Group: Respiratory rhythm generator is located in the pre Botzinger complex of the neurons in the upper part of the VRG
  130. 130What does the Ventral respiratory group contain?Contains expiratory neurons that appear to be most important when large increases in ventilation are required e.g. during strenuous physical activity
  131. 131What is the respiratory rhythm generator composed of?Pacemaker cells and a neural network that acting together set the basal respiratory rate
    During quiet breathing the respiratory rhythm generator activates inspiratory neurons in the VRG that depolarise the inspiratory spinal motor neurons
  132. 132What does the apneustic centre do?An area of the lower pons called the apneustic centre is thought to be involved in fine tuning the output of the inspiratory neurones of the medulla by continuing to active the inspiratory neurone it inhibit expiration
  133. 133What can override the apneustic centre?The pneumotaxic centre
  134. 134What is the pneumotaxic centre?Regulates and on occasion can override the apneustic centre
    It is also known as the pontine respiratory group in the upper pons and it acts to smooth the transition between inspiratory and expiration
    It is also thought to be involved in switching off inspiratory neurons to prevent hyperinflation allowing expiration
  135. 135What are the receptors of the nose, nasopharynx and larynx?Chemo and mechanoreceptors
    Some appear to sense and monitor flow
    Stimulation of these receptors appear to inhibit the central controller i.e. medullary respiratory centre
  136. 136What are the receptors of the pharynx?Has receptors that appear to be activated by swallowing - respiratory activity stops during swallowing protecting against the risk of aspiration of food or liquid
  137. 137Describe Slowly Adapting Stretch Receptors? SASRsMyelinated
    Maintain a persistant or slowly decaying receptor potential during constant stimulus - imitating action potentials for the duration of the stimulus
    Found in airway smooth muscle and activated by lung distension
    High activity inhibits further inspiration and inhibits further inspiration thus beginning expiration
    If inflation is maiting they slowly adapt to low frequency firing
  138. 138Describe Rapid Adapting Stretch Receptors? RASRsMyelinated
    Generate a receptor potential and action potentials at the onset of a stimulus but very quickly cease responding
    Found between airway epithelial cells
    Activated by lung distension and irritants
    Produce a brief burst of activity and high activity causes bronchoconstriction
    Might be involved in the cough reflex
  139. 139Describe C fibres and J receptors?Non myelinated
    Found in either the capillary walls or the interstitium
    Stimulated by an increase in lung interstitial pressure causes by the collection of fluid in the interstitum
    Such an increase can occur during the vascular congestion cause by PE or left ventricular heart failure
    Activity results in rapid breathing, shallow breathing, bronchoconstriction, cardiovascular depression and a dry cough
    In addition, J receptors gives rise to the sensation of pressure in thickest and dyspnea
  140. 140What is the interstitum?Pulmonary interstitium is a collection of support tissues within the lung that includes the alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues.
  141. 141What are the pulmonary stretch receptors?Slowly adapting stretch receptors
    Rapidly adapting stretch receptors
    C fibres and J receptors
  142. 142What are the most important inputs for automatic control of ventilation at rest?Peripheral (arterial) chemoreceptors
    Central chemoreceptors
  143. 143Describe the locations of the peripheral chemoreceptors?Located high in the neck at the bifurcation of the common carotid arteries and in the thorax on the arch of the aorta
    Carotid = carotid bodies
    Aorta = aortic bodies
    In both locations they are quite close to but distinct from the arterial baroreceptors and are in intimate contact with the arterial blood
  144. 144Describe the function of the composition of the peripheral chemoreceptors?Composed of specialised receptor cells stimulated by:
    - decrease in PaO2
    - Decrease in pH (increase in H+)
    Type II cells are located here and on detection of hypoxia release stored neurotransmitters that stimulate the carotid sinus nerve
    These provide excitatory input to the medullary inspiratory neurons
  145. 145What is the predominant peripheral chemoreceptor?The carotid body input
  146. 146When are the peripheral chemoreceptors stimulated?They are not sensitive to small reductions in arterial partial O2 pressure, it is only when the partial pressure of O2 comes close to 60mmHg where haemoglobin is close to 90% saturated when the peripheral chemoreceptors really begin to dire
  147. 147Describe the effects of carbon monoxide on the peripheral chemoreceptors?CO does not effect the amount of O2 that can dissolve in the blood therefore does not alter the oxygen diffusion capacity of the lung, the arterial pressure is unaltered meaning that there is not increase peripheral chemoreceptor output
  148. 148Describe the location and action of the central chemorecepotr?Located in the medulla
    Provides excitatory synaptic input to the medullary inspiratory neurons
    Stimulated by a decrease in pH of the brains CSF however HOWEVER since blood brain barrier is readily impermeable to H+ this is poorly reflected
    However, CO2 diffuses readily into the CSF and blood partial CO2 pressure can influence CSF pH enabling central chemoreceptors to detect H+ changes
  149. 149What would a very small change in arterial PaCO2 result in?Very small increases in the arterial PaCO2 pressure causes a marked reflex in ventilation
    The reflex mechanisms controlling ventilation prevent small increases in arterial partial CO2 pressure to a much greater degree than they prevent equivalent decrease in arterial O2 pressure
  150. 150What is ventilatory drive sensitive to?Ventilatory drive is extremely sensitive to changes in arterial partial CO2 pressure of blood entering the brain
  151. 151What would happen if there is an increase in arterial CO2 pressure?If there is an increase in the PaCO2 then some of the extra CO2 will diffuse into the CSF and react with H2O resulting in more H+ ions enabling the central chemoreceptors to detect the pH change and increase ventilation by stimulation the medullary inspiratory neurons
  152. 152What accounts for most of the increased ventilation stimulation?Central chemoreceptors account for 70% of increase ventilation
  153. 153Describe hypoxia?Defined as a deficiency of oxygen at the tissue level
    The most common type of hypoxia is hypoxic hypoxia or hypoxemia which is where the PaO2 is reduced
  154. 154What are the most common causes of hypoxia?1. Hypoventilation
    2. Diffusion impairment
    3. Shunting
    4. Ventilation perfusion mismatch
  155. 155Describe hypoventilation?Results in an increased PaCO2
    Failure to ventilate the alveoli quickly
    Causes by muscular weakness, obesity, loss of respiratory drive (e.g. morphine)
  156. 156Describe diffusion impairment?Results from the thickening of the alveolar membranes or a decrease in their surface area
    Causes the blood PaO2 and the PAO2 to fail to equilibrate
    Caused by pulmonary oedema, anaemia, interstitial fibrosis
  157. 157Describe shunting?An anatomical abnormality of the cardiovascular system that causes mixed venous blood to bypass the ventilated alveoli passing rom the right side of the heart to the left side e.g. ventricular septal defect (VSD) - Eisenmenger's Syndrome
  158. 158Describe ventilation perfusion mismatch?Most common cause of hypoxemia
    Occurs in chronic obstructive pulmonary disorder and many other lung diseases
    Arterial partial CO2 pressure may by normal or increased depending on how much ventilation is reflexively stimulated
    Can be caused by a pulmonary embolism, asthma, pneumonia and pulmonary oedema
  159. 159What is hypercapnia?Carbon dioxide retention and increased arterial partial CO2 pressure
    Principally caused by hypoventilation
    Can sometimes be caused by ventilation perfusion mismatch depending on how much ventilation is reflexively stimulated
  160. 160Describe type 1 respiratory failure?pO2 is low
    pCO2 is low or normal
    1 change = low pO2 then normal/low pCO2
    Pulmonary embolism (type of V/Q mismatch) causes type 1
  161. 161Describe type 2 respiratory failure?pO2 is low
    pCO1 is high
    2 changes = low pO2 + high pCO2
    Hypoventilation causes type 2
  162. 162Describe the vascular physiology of the lungs?There are two circulations in the lungs: the pulmonary circulation and the bronchial circulation
    PULMONARY CIRCULATION:
    - Main circulation
    - From right ventricle
    - Receives 100% of cardiac output
    - Red cell transit time 5 seconds
    - Surfacea area for gas exchange 50 to 100 m2
    - 280bn capillaries and 300m alveoli
    BRONCHIAL CIRCULATION:
    - Receives 2% of bronchial circulation n
  163. 163Describe the differences in pulmonary v.s. systemic circulation?PULMONARY:
    - Vessel wall is thin
    - Minor muscularisation
    - No need for redistribution
    SYSTEMIC:
    - Vessel wall is thick
    - Significant muscularisation
    - Redistribution is required
    - MUCH higher pressure
  164. 164Describe the parasympathetic regulation of the airways?Neurotransmitter: Acetylcholine
    Innervates via: Vagus nerve
    Innervates: vasculature, glands and airways in lungs
    Intrinsic tone of the airways is governed by the parasympathetic system
    Ach interacts with muscarinic cholinergic receptors on the muscle to provide a general level of intrinsic muscle tone
  165. 165What type of nerve releases acetylcholine?Acetylcholine is released by both the sympathetic and parasympathetic but in the lungs, ACh is primary released by parasympathetic
  166. 166Describe the sympathetic regulation of the airways?Neurotransmitter: Noradrenaline
    Innervates via: sympathetic trunk
    Innervates: Vasculature and glands - does not directly influence the airways
  167. 167How does the sympathetic system indirectly influence the airways?Sympathetic activation causes NAd to be
    released to the adrenal glands and can
    result in the release of adrenaline (from
    adrenal medulla) which in turn binds to
    beta-2-adrenoreceptors on muscles of
    the airways and subsequently results in
    bronchoDILATION - thus this is the
    indirect effect of the sympathetic system
    on the airways
  168. 168What are the different types of receptors in the lungs?- Cholinergic receptors
    - Nicotinic receptors
    - Muscarinic receptors
    -Adrenergic receptors (alpha and beta)
  169. 169Describe cholinergic receptors ?- Neurons that release Ach are called cholinergic neurons
    - Neurons associated with Ach system degenerate in people with Alzheimers disease
  170. 170Describe nicotinic receptors?- Respond to Ach as well as nicotine
    - Stimulated by both sympathetic and parasympathetic but predominantly parasympathetic
    - Found in post ganglionic neurons and at neuromuscular junctions
    - Contains a ligand gated channel that is permeable to both Na+ and K+ ions but since Na_ has a larger electrochemical driving force the net effect of opening these channels is depolarisation
  171. 171Describe muscarinic receptors?- ACh receptors that form G coupled receptor complexes
    - Parasympathetic
    - Many types: M1,M2 M3, M4 and M5
    - M3 plays an important role in that airways
  172. 172Describe the action of the M3 receptor?1. ACh binds to M3 receptor
    2. Receptor couples with Gq protein
    3. Gq protein activates phospholipase C (PLC)
    4. Phospholipase C catalyses the breakdown of a plasma membrane phospholipid to a DAG and IP3
    5.DAG acts as a second messenger and actives a family of proteins known as protein kinase C (PKC)
    6. IP3 binds to the ligand gated Ca2+ receptors located on the endoplasmic reticulum in the bronchial cells which open when IP3 is bound to them, resulting in Ca2+ release stimulating BRONCHOCONSTRICTION
  173. 173What are the different types of adrenergic receptors?Neurons that release NAd are called adrenergic:
    Alpha = alpha 1 and alpha 2
    Beta = Beta -1 (heart) Beta-2 (lung) Beta-3 (adipose)
  174. 174How do the alpha receptors act?Alpha-1: Acts postsynaptically to either stimulate or inhibit the activity of different types of K+ channels
    Alpha-2: Acts presynaptically to inhibit noradrenaline release
  175. 175How to beta-2 receptors act?G Coupled Protein Receptor
    1. Ad or NAd binds to the receptor
    2. Receptor couples with Gs protein
    3. Gs protein activitates Gs protein
    4. Adenyl cyclase the catalyses the conversion of cytosolic ATP to cyclic 3'5'adenosine monophosphate or cAMP
    5. cAMP acts as a second messenger then diffuses in the lung resulting in a decrease in calcium concentration as well as other effect e.g. activating PKA resulting in BRONCHODILATION
  176. 176What do beta-2 receptors cause?Bronchodilation
  177. 177What are the types of receptor ligand?Agonist
    Antagonist
  178. 178Describe the action of an agonist receptor ligand?Agonist: a compount that binds to the receptor and activates it, demonstrating both affinity and efficacy
  179. 179Describe the action of an antagonist receptor ligand?Antagonist: a compount that blocks the effect of an agonist by competing with a chemical messenger for its binding site
    It does not active signalling normally thus blocking its action - it has affinity by zero efficacy
  180. 180How does affinity determine wither or not a ligand acts as an agonist or antagonist?Affinity is shown by BOTH agonists and antagonists
    Affinity is the degree to which a particular messenger binds to its receptor and is determined by the affinity of the receptor for the messenger
    A receptor with a high affinity will bind at lower concentrations than a receptor of low affinity
  181. 181How does efficacy determine weather or not a ligand acts as an agonist or antagonist?Describes how well a ligand activates a receptor
    High efficacy agonist: large change in receptor shape upon binding
    Low efficacy agonist: small change in receptor shape when binding
    Antagonist: No conformational change to receptor shape when binding
  182. 182What are some of the agonists for receptors?Muscarine binds to the muscarinic acetylcholine receptor
    Nicotine binds to the nicotinic acetylcholine receptor
  183. 183What are some of the antagonists for receptors?Atropine binds to muscarinic acetylcholine receptor
    Used to help people poisoned with marine
  184. 184How are symptoms in asthma and COPD alleviated?Asthma and COPD results in difficulty breathing due to inflammation
    To alleviate symptoms bronchodilators are given to increase bronchoconstriction
    Muscarinic antagonists are allow given to block bronchodilaton
  185. 185What beta agonists are used in asthma and COPD?Beta agonists increase bronchodilaton
    Short acting (around 4 hours): Salbutamol and terbutaline
    Long acting (around 12 hours): Salmeterol and formoterol
  186. 186What muscarinic antagonists are used in asthma and COPD?Muscarinic antagonists want to decrease bronchoconstriction
    Short acting (around 4 hours): Ipratropium
    Long acting (around 12 hours): Tiotropium
  187. 187Summarise the parasympathetic influence on the respiratory system?Neurotransmitter: Acetyl Choline
    Receptor: Muscarinic 3 (M3)
    Effect: Constriction
  188. 188Summarise the sympathetic influence on the respiratory system?Neurotransmitter: Noradrenaline, which acts on the adrenal glands to release adrenaline
    Receptor: Beta-2-adrenoreceptor
    Effect: Dilation
  189. 189What is epithelium?Tissues composed of cells that line the cavities and surfaces of structures throughout the body
    Lies on top of connective tissue - the two layers are separated by a basement membrane
  190. 190Describe the respiratory epithelium?Ciliated Pseudostratified Columnar Epithelium
    - Serves to moisten and protect the airways
    - Also function as a barrier to potential pathogens
    - Prevents tissue infection and tissue injury by action of the muscocilary escalator
  191. 191How do glands help defend lungs?The various skin glands, salivary glands and lacrimal glands secrete antimicrobial chemicals such as:
    Antibodies
    Lysozymes - destroys bacterial cell walls
    Lactoferrin - prevents bacteria obtaining iron
  192. 192What are the non immune host defence mechanisms?Epithelium (Respiratory)
    Surface defence mechanisms e.g. glands and mucous
    Physical defence mechanisms e.g. coughingand sneezing
  193. 193What are the surface defence mechanisms?Glands secreting antimicrobial chemicals
    Mucus
    Chemical barriers from respiratory epithelium including anti fungal and antimicrobial peptides
  194. 194Describe coughing?A cough is an explosive expiration that provides a normal protective mechanism for clearing the tracheobronchial tree of secretions and foreign material
    A cough may be initiated voluntarily or reflexively
  195. 195Describe the action of coughing?When the receptors are stimulated, the medullary inspiratory neurons reflexively cause a deep inspiration (2.5L)
    The epiglottis closes and the vocal chords shut tightly to entrap air within the lung
    Abdominal muscles contract forcefully pushing against the diaphragm
    Internal intercostal muscles also contract forcefully
    Pressure in the lungs rises to 100mmHg or more
    Markedly postive intrathoracic pressure causes narrowing of the trachea
    Vocal cords and epiglottis suddenly open widely
    The large differential pressure between airways and atmosphere coupled with tracheal narrowing expels air at velocities ranging from 75 to 100 mph
  196. 196Describe mucus?Airway mucous is a viscoelastic gel containing water, carbohydrate, proteins and lipids
    It is a secretory product of the goblet cells of the airway surface epithelium and submucosal glands
    Protects epithelium from foreign lateral and fluid loss
    Transported via mucociliary escalator that constantly moves mucus by cilia beating in directional waves
    Consists of a superficial gel later and a liquid (surfactant) layer that bathes cilia
  197. 197Describe epithelial injury?Infections caused by viruses often target specific epithelial cells whereas bacterial are less specific
    Following an injury to the airway epithelium, the epithelium can carry out a fully repair i.e it regenerates itself
    This is due to the fact that epithelium exhibits a level of functional plasticity and when this goes wrong it can result in pulmonary disease

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PHASE 1 MED (Cardiovascular and Respiratory ) Flashcards on Respiratory 1, created by Erin Dunn on 28/01/2019.
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