respiratory Flashcards

1
Q

upper respiratory tract includes

A

-nose and nasal cavity
-pharynx
-larynx

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2
Q

lower respiratory tract includes

A

-trachea [windpipe]
-bronchial tubes
-alveoli

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3
Q

nose and nasal cavity structure

A

-external nose constructed from bone and hyaline cartilage, is lined with a mucus membrane
-divided internally by nasal septum, two openings known as external nares or nostrils
-olfactory receptors are located in olfactory epithelium in roof of nose/nasal cavity

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4
Q

nose and nasal cavity functions

A

-warms air
-prevents dehydration
-covered with mucus membrane and traps particles
-cilia propel particles towards the pharynx where they can be swallowed

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5
Q

pharynx

A

-posterior to the nasal cavity and extends to larynx
-three regions - nasopharynx, oropharynx, laryngopharynx
-contains openings of the auditory tubes [aka pharyngotympanic tubes or eustachian tubes], linked to middle ear and equalises air pressure
-constructed of skeletal muscle [circular and longitudinal], lined with mucus membrane
-contains tonsils [palatine and lingual], patches of lymphatic tissues similar to lymph nodes, plays a role in immunity, subject to inflammation [tonsilitis], especially common in children/young adults

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6
Q

larynx

A

-connects pharynx with trachea
-constructed from 9 sections of cartilage
-contains vocal fold for speech
-also contains epiglottis

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7
Q

epiglottis

A

-in the larynx
-leaf shaped elastic cartilage
-closes off the glottis
-prevents food/fluid from entering trachea during swallowing

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8
Q

trachea

A

-tubular windpipe extending from the larynx to the two primary bronchial tubes
-4 layers : mucosa, submucosa, hyaline cartilage, adventitia

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9
Q

trachea mucosa

A

-inner most layer
-pseudostratified ciliated epithelium
-mucus traps particles and is propelled by the cilia to be swallowed

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10
Q

trachea submucosa

A

-mostly areolar [loose] connective tissue
-contains mucus secreting glands and their ducts

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11
Q

trachea hyaline cartilage

A

-16-20 incomplete cartilage rings
-open portion faces posteriorly towards the oesophagus - ends connected by trachealis muscle

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12
Q

trachea adventitia

A

-connective tissue outer layer

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13
Q

bronchial tubes structure

A

-trachea divides into 2 primary bronchi
-each primary bronchus feeds air into and out of either the left or right lung
-lined with pseudostratified ciliated epithelia
-also has incomplete cartilage rings
-lower internal ridge where the right and left
bronchi originate is known as the carina [very sensitive and triggers cough reflex]

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14
Q

bronchial tubes divisions

A

-primary bronchi divide into secondary or lobar bronchi [each secondary bronchus feeds a single lobe of the lung]
-these further divide into tertiary or segmental bronchi
-more divisions into smaller bronchioles
-smallest bronchioles known as terminal bronchi
-branching of bronchial tubes known as bronchial tree

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15
Q

epithelium changes to bronchial tubes

A

-primary, secondary and tertiary bronchi [pseudostratified ciliated columnar epithelium with goblet (mucus
secreting) cells]
-large bronchioles [simple ciliated with some goblet cells]
-smaller bronchioles [simple ciliated with few goblet cells]
-terminal bronchioles [simple cuboidal]

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16
Q

cartilage and smooth muscle changes to bronchial tubes

A

-as bronchial tubes get smaller, plates of cartilage replace incomplete rings
-smooth muscle content increases as cartilage decreases [smooth muscle present in spiral brands, helps keep bronchial tubes open]
-influenced by catecholamine [epinephrine and norepinephrine relaxes this muscle and causes
bronchodilation]
-muscle spasms may close off bronchial tubes [occurs during an asthma attack]

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17
Q

lungs

A

-paired organs that sit inside thoracic cavity
-left/right lung reside in separate double walled structures called pleural membranes [parietal pleura live the inside of thoracic cavity, visceral pleura cover the lungs]
-small space between these layers known as pleural cavity [contains lubricating fluid to allow smooth inflation and deflation of the lungs]

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18
Q

alveoli

A

-clusters of inter-connected hollow spheres extend from an alveolar duct that is contiguous with each respiratory bronchus
-each alveolus is covered in pulmonary cap [for gas exchange]
-also covered in elastic fibres [stretch during inspiration, recoil to aid exhalation]
-macrophages are present on inner surface [no cilia or mucus for self cleaning]

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19
Q

respiratory zone of the lung

A

-when each terminal bronchus give rise to multiple respiratory bronchioles this is the start of respiratory zone
-also includes alveolar ducts [controls flow of air to alveoli], alveolar sacs and alveoli

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19
Q

conducting zone of the lung

A

-terminal bronchioles represent the end of conducting zone
-structures that carry air into and out of the lung

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20
Q

structure of alveoli

A

-constructed using simple squamous epithelial cells [known as type 1 cells]
-contains type 2 cells [septal cells], small cuboidal cells with microvilli, these secrete alveolar fluid [surfactant to reduce surface tension]
-alveolar wall and cap wall form respiratory membrane [gases must diffuse across this, very thin 0.5um to aid speed of diffusion]

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21
Q

pulmonary ventilation

A

-movement of air into and out of lungs is dependant on different air pressures [atmospheric air pressure and pressure inside our lungs]
-air movement follows Boyles law

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22
Q

Boyles law

A

-pressure is inversely proportional to volume
-if volume of a gas is increased, pressure reduces
-respiratory muscles make our lungs into a type of pump [if we increase volume air pressure reduces]

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23
Q

Boyles law and pulmonary ventilation

A

-intrapulmonary or alveolar pressure [to inflate lungs with external air, we must reduce air pressure within]
-to achieve this we increase lung volume
-once alveolar air pressure is lower than atmospheric pressure, air flows into our lungs
-to exhale we must increase alveolar air pressure by reducing the
lung volume
-air is expelled from our lungs once alveolar air pressure is greater than atmospheric air pressure

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24
Q

muscles of inhalation

A

-diaphragm [dome shaped muscle forms the lower section of thoracic cavity, flattens around 1cm during quiet breathing can flatten up to 10cm during strenuous breathing
-contraction contributes around 75% inhaled air]

-external intercostals [raise and widen the rib cage, contribute around 25% inhaled air]

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25
Q

three different air pressures

A

-atmospheric air pressure
-alveolar air pressure
-intrapleural air pressure [pressure inside pleural cavity]
-all pressures are in mmHg [millimetres of mercury]

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26
Q

alveolar surface tension

A

-affects pulmonary ventilation
-water molecules bound by hydrogen bonds, a stronger attraction to each other than to gas molecules in the air
-this surface tension pulls alveoli slightly inwards [reduces their volume]
-must be overcome to expand the volume of each alveolus, surfactant secreted by type 2 cells help reduce this.

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27
Q

lung compliance

A

-affects pulmonary ventilation
-describes the ease of lung expansion [caused by the difference between intrapleural and alveolar pressures]
-high compliance = easy to expand per unit changer of pressure
-low compliance = difficult to expand per unit change of pressure

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28
Q

low compliance may be caused by

A

-scarring of alveoli usually caused by diseases such as TB
-increased fluid in lung tissue [pulmonary oedema]
-deficiency of surfactant [increased surface tension]

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29
Q

airway resistance

A

-affects pulmonary ventilation
-resistance caused by walls of bronchial tubes
-normally dilated during inhalation and constrict a little during exhalation
-modulated by ANS
-any narrowing of obstruction to airways increase resistance
-seen in asthma and chronic bronchitis

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30
Q

respiratory rates

A

-adults average around 12 breaths/min, moving around 500ml of air per breath
-adaptable to the demands of oxygen by the body
-volume of air can increase by 50x during peak exercise over resting values [volume increases per breath, number of breaths/min increase]

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31
Q

total lung volume can be divided into

A

-residual volume
-tidal volume
-inspiratory reserve volume
-expiratory reserve volume

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32
Q

residual volume

A

-not all air expelled from lungs
-volume of air remaining in lungs after forced expiration

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33
Q

tidal volume

A

-resting volume of air inhaled and exhaled
-represents air moved in one breath

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34
Q

inspiratory reserve volume

A

-achieved during deep inhalation
-excess volume inhaled beyond the normal tidal volume

35
Q

expiratory reserve volume

A

-achieved during deep expiration
-excess volume exhaled beyond normal tidal volume

36
Q

lung capacities

A

combinations of different lung volumes
[often used to determine lung function]
-inspiratory capacity
-functional residual capacity

37
Q

inspiratory capacity

A

-inspiratory reserve volume + tidal volume
-maximum volume of air inhaled from normal expiratory level

38
Q

functional residual capacity

A

-expiratory reserve volume + residual volume
-volume of air remaining in lungs after normal expiration

39
Q

vital capacity

A

-inspiratory reserve volume + tidal volume + expiratory reserve volume
-maximum volume of air that can be inhaled/exhaled

40
Q

total lung capacity

A

-vital capacity + residual volume

41
Q

respiratory centre

A

-two clusters of neurons responsible for breathing
-medullary respiration centre in medulla oblongata
-pontine respiratory group in pons

42
Q

atmospheric air pressure

A

-atmospheric pressure at sea level is 760mmHg
-at around 5,500m air pressure is half that at sea level [380mmHg]

43
Q

atmospheric air gases

A

-N2 78.6%
-O2 20.9%
-Ar 0.093%
-CO2 0.04%
-H2O and others 0.367%

44
Q

air partial pressure and Daltons law

A

-calculate individual contribution to the total air pressure by a single gas
-total air pressure is the sum of partial pressures of all gases in a mixture [Daltons law]
-can calculate partial pressure if total air pressure and percentages of gases is known

45
Q

atmospheric air partial pressures at see level

A

-PN2 597.4mmHg
-PO2 158.8mmHg
-PAr 0.7mmHg
-PCO2 0.3mmHg
-PH2O 2.8mmHg
-total 760mmHg

46
Q

oxygen and carbon dioxide partial pressure

A

-O2 = 20.9% of atmospheric air
-partial pressure = 159mmHg
-CO2 = 0.04% of atmospheric air
-partial pressure = 0.3mmHg

47
Q

partial pressure of CO2 and O2 in alveoli/pulmonary cap

A

-diffusion reliant on conc. gradients
-partial pressure of oxygen must be higher in alveoli compared to blood in pulmonary cap. [this ensures oxygen diffuses into blood]
-partial pressure of carbon dioxide must be higher in pulmonary capillary blood compared to alveoli [ensures carbon dioxide diffuses out of blood and into lungs]

48
Q

henrys law

A

-when gas is in contact with a liquid, the dissolved gas is proportional to its partial pressure and solubility
-a high partial pressure and solubility will increase amount of gas dissolved in solution
-principles of Henrys law are dependant on a gas’s solubility
-O2 has poor solubility in water due to nonpolar nature
-CO2 is 24 times more soluble [combines with H2O to form H2CO3

49
Q

partial pressures in respiratory system

A

-atmospheric air
-PO2=159mmHg
-PCO2=0.3mmHg
-alveolar air
-PO2-104mmHg
-PCO2=40mmHg
-differences due to small tidal volume, O2 constantly diffusing into blood, CO2 high is residual and expiratory reserve volumes

50
Q

pulmonary capillary blood - oxygen poor, oxygen rich and tissue cell

A

-oxygen poor
-PO2 = 40mmHg
-PCO2 = 45mmHg
-oxygen rich
-PO2 = 100mmHg
-PCO2 = 40mmHg
-tissue cell
-PO2 = 40mmHg
-PCO2 = 45mmHg

51
Q

oxygen transport

A

-oxygen has poor solubility in water [only 1.5% dissolves in plasma]
-98.5% binds to haemoglobin in RBCs
-each haemoglobin molecule contains four haem units -each one binds one O2 molecule
-when O2 is bound to haemoglobin it is known as oxyhaemoglobin

52
Q

haemoglobin dynamics

A

-O2 binding to haemoglobin is easily reversable
-oxyhaemoglobin is fully saturated
-oxyhaemoglobin saturation is dependant of PO2

53
Q

other factors affecting oxyhaemoglobin saturation

A

-acidity -binding decreases with acidity [Bohr effect], H+ increase causes oxygen to dissociate from haemoglobin [this effect is advantageous in tissues with a high H+ conc. as it increases oxygen unloading]
-carbon dioxide partial pressure -increased PCO2 decreases O2 binding, CO2 binds to haemoglobin forming carbaminohaemoglobin
-temperature -increased heat reduces oxygen binding to haemoglobin

54
Q

carbon dioxide transport

A

-transport in the blood three ways
-bicarb ions -HCO3- [accounts for around 70% of CO2 transport, present in plasma and produced by carbonic anhydrase, reaction reverse in pulmonary cap. CO2 exhaled]
-carbamino compounds [23% of CO2 transport, haemoglobin is predominate protein in blood, CO2 binds to it, promoted by high PCO2]
-dissolved CO2 [dissolved in plasma 7%]

55
Q

alveolar ventilation

A

-during inhalation not all alveoli are ventilated equally, alveoli at the apex/top of lungs receive the least amount of air [50% difference]
-the weight of fluid in plural cavity is greatest at the base of lung, this increases the intrapleural pressure.
-alveoli here are less expanded and have higher compliance, therefore they can be filled with more air

56
Q

difference in perfusion

A

-perfusion greater at the base of the lung, gravity results in more blood flowing in lower sections of the lungs
-use of ratio of ventilation to perfusion to determine how equally matched they are. V/Q [ventilation/perfusion]

57
Q

V/Q ratio

A

-V/Q in middle of the lung =1 [ventilation matches perfusion]
-V/Q in base of lung =0.3 [greater perfusion]
=V/Q in apex of lung =2.1 [greater ventilation]

58
Q

pulmonary vs systemic perfusion

A

-systemic circuit is high pressure system, vascular resistance regulates blood flow
-pulmonary circuit is a low pressure system, parallel pathways for blood flow, low vascular resistance -1/10th systemic

59
Q

low alveolar oxygen content

A

-pulmonary vasoconstriction
-limits blood flow to these alveoli
-blood shunted to alveoli with higher oxygen content
-bronchioles dilate to flow more air to increase oxygen delivery

60
Q

high alveolar carbon dioxide content

A

-bronchioles dilate to flow more air to increase carbon dioxide and oxygen diffusion

61
Q

disorders affecting alveola ventilation

A

-ventilation also depends on resistance of conduction airways
-some diseases that affect pulmonary ventilation
-restrictive pulmonary disorders
-obstructive pulmonary disorders
-masses [tumours or scar tissue]

62
Q

restrictive pulmonary disorders

A

-pulmonary fibrosis
-pulmonary oedema

63
Q

obstructive pulmonary disorders

A

-asthma
-chronic bronchitis
-emphysema

64
Q

pulmonary fibrosis

A

-scarring of lung tissue [normal tissue replaced by fibrotic tissue]
-reduces lung compliance
-inhibits oxygen diffusion
-often caused by autoimmune disorders
-causes also include TB, asbestosis and silicosis

65
Q

pulmonary oedema

A

-most commonly caused by heart problems
-congestive heart failure [left ventricle/left AV valve dysfunction. blood backs up on left side of heart as it cannot be pumped effectively into systematic circuit. increased pressure in pulmonary blood vessels forces fluid out, fluid collects in alveoli]
-hypertensive crisis [increased afterload inhibits left ventricular stroke volume]
-pulmonary cap membrane damage [makes caps more permeable to fluids, can be causes by infection such as pneumonia, also irritants such as toxic gases from industrial welding, sulphur dioxide and chlorine gas]

66
Q

asthma

A

-associated with chronic inflammation of bronchial tubes
-characterised by bronchospasms, increased mucus secretion and airway obstruction
-caused by genetic and environmental factors
-environmental factors include [allergens, pollutants, drugs including aspirin, sulphates used as preservatives in wine, beer, etc]

67
Q

chronic bronchitis

A

-is an inflammatory condition
-results in excess thick mucus secretion, loss of ciliary function, increased risk of infection

68
Q

emphysema

A

-causes loss of alveolar walls
-results in large air spaces that remain full of air after exhalation, this prevents new, oxygen rich air from entering lungs

69
Q

air flow through conducting airways

A

-airflow follows similar principles to blood flow, pressure difference drives flow, resistance from airway walls
-10% reduction is airway radius = 52% increase in resistance, 35% decrease in airflow

70
Q

modulators of airway diameter -smooth muscle

A

-smooth muscle in airways contains receptors to neurotransmitters and hormones

71
Q

modulators of airway diameter -muscarinic receptors

A

-muscarinic receptors bind acetylcholine and causes bronchoconstriction

72
Q

modulators of airway diameter -B adrenergic receptors

A

-B adrenergic receptors bind adrenaline, causing bronchodilation, also bind sympathomimetics [albuterol [salbutamol/Ventolin] and salmetrol, used by asthmatics to cause bronchodilation]

73
Q

effects of acidosis and alkalosis

A

-acidosis results in depression of CNS [caused by a loss of synaptic transmission, pH below 7 leads to disorientation, possible coma and death]
-alkalosis causes overexcitement of CNS and peripheral nervous system [nervousness, muscle spasms and convulsions and death]

74
Q

types of acidosis/alkalosis

A

-respiratory acidosis
-metabolic acidosis
-respiratory alkalosis
- metabolic alkalosis

75
Q

respiratory acidosis

A

-result of high CO2 conc. above 45mmHg, increased CO2 forms more H2CO3 = more H+, failure to maintain adequate alveolar ventilation and/or perfusion to remove CO2
-causes include -lung disease, damage to respiratory muscles or innervation, drugs that may reduce ventilation rate

76
Q

metabolic acidosis

A

-to much acid is produced by working cells, failure of kidneys to removed H+ from blood
-causes include -kidney disease, diabetic acidosis [ketoacidosis], lactic acidosis [ineffective oxidative metabolism], loss of bicarb ions due to severe diarrhea, poisoning [aspirin, methanol]

77
Q

respiratory alkalosis

A

-blood PCO2 below 35mmHg, results in an increase pH [decrease H2CO3 formation and subsequent H+ conc.]
-causes include hyperventilation -removal of to much CO2 by respiratory system

78
Q

metabolic alkalosis

A

-high systemic blood conc. of HCO3-, binds more H+ and reduces acidity
-causes include a high intake of alkaline drugs [sodium bicarb], extreme vomiting [loss of gastric acids [HCL]]

79
Q

regulation of pH

A

-three mechanisms
-buffering systems [quickest] [rapid but do not removal H+ from body]
-removal of carbon dioxide [minutes] [increasing pulmonary ventilation rate and depth to remove excess CO2]
-excretion of H+ by kidneys [slowest] [only mechanism that eliminates H+ from body]

80
Q

carbonic acid-bicarbonate buffering system

A

-primary buffering system
-H2CO3 -carbonic acid acts as a weak acid
-HCO3 -bicarb ion acts as weak base [kidneys can synthesis and resorb HCO3]
-can adjust both an excess or shortage of H+
-when there is a drop in pH [increased H+], bicarb ions are used to bind free H+, CO2 can then be removed during exhalation

81
Q

response to exercise -demands

A

-exercise places major demand on body [increased O2 consumption and CO2 production]
-to met these demands [pulmonary ventilation and perfusion are increased, vasodilation occurs in working muscles to increase blood flow, PO2 and PCO2 dive diffusion in both external/internal respiration]

82
Q

response to exercise -ventilation

A

-anticipation of exercise stimulates increased breathing rate and depth [driven by limbic system]
-breathing pattern then dependent on exercise intensity [via feedback from chemoreceptors measuring PO2, PCO2 and H+]

83
Q

response to exercise -perfusion

A

-increased pulmonary perfusion [cardiac output increases in both systemic and pulmonary circuits, same stroke volume in each ventricle]
-pulmonary perfusion rises
-increases the O2 diffusing capacity 3x [due to pulmonary cap being fully perfused]

84
Q

cardiac output during exercise

A

-increases heart rate, O2 consumption, stroke volume, cardiac output

85
Q

ageing affect on respiratory system

A

-negative
-elasticity lost from airways down to alveoli
-alveoli become baggy
-chest wall also becomes more rigid
-results in a loss of vital capacity of up to 35%
-loss of bronchial tube ciliary function and reduction in alveolar macrophages increase risk of infection and disease