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Radiography 1 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

what are the functions of the respiratory system

A

gas exchange –> oxygen into body, CO2 out
acid base balance –> Ph. 7.35 - 7.45
Thermoregulation
sound production
anatomical substrate for sense of smell
respiratory surface protection from dehydration, temp changes, invading pathogens

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2
Q

what affects acid base balance

A

Co2 increase = blood is more acidic, can lead to acidosis

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3
Q

what is the goal of breathing regarding compliance

A

minimise resistance, maximise compliance

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4
Q

what affects the work of breathing

A
  • resistance to airflow through respiratory tract
  • compliance of lungs (how easy it is to inflate)
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5
Q

what is pulmonary fibrosis

A

damage, thickening & scarring of alveoli, that causes stiffening of the lungs and makes breathing more difficult

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6
Q

what is bmr

A

basal metabolic rate, measures oxygen consumption under mental and physical conditions. can be used to evaluate thyroid function

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7
Q

what are the muscles of inspiration

A

external intercostals, diaphragm,

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8
Q

what is the path of air when breathing in

A

air from nose or mouth
pharynx –> splits into esophagus & trachea
larynx –> above trachea
2 primary bronchi
23 bronchial subdivisions
bronchioles (div. 12-23)
alveolar ducts
alveoli

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9
Q

diff between bronchi and bronchioles

A

bronchus has cartilage, bronchiole has muscle for diameter adjustment (resistance)

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10
Q

what is the anatomical dead space

A

oxygen in conducting portion of airways that can’t be used e.g. diffusion only occurs in alveoli & respiratory bronchioles

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11
Q

example of increasing anatomical dead space

A

going snorkelling, you naturally start breathing deeper

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12
Q

function of nose

A

clean warm & humidify air

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13
Q

what happens when air enters the nose

A

external nares provide particle filtration

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14
Q

what is on the lateral surfaces of the nasal cavity

A

3 pairs of bony ridges on either side called conchae

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15
Q

what is the function of conchae

A

slow down air flow & incr. turbulence so the air has time to warm up and humidify because they have mucosa and are highly vascularised e.g. compare nose breathing to throat breathing

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16
Q

what forms the medial wall of the nose

A

nasal septum

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17
Q

what forms the floor of the nose

A

maxilla (hard pal.) & palatine bone

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18
Q

what forms the roof of the nose

A

nasal, frontal, ethmoid & sphenoid bones

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19
Q

what forms the inferior part of the nasal septum

A

vomer bone

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20
Q

where are the meatus

A

spaces under the conchae

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21
Q

difference between ethmoidal sinuses and others

A

they are like lots of small air pockets below the frontal sinuses & between the eyes

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22
Q

where do sinuses drain

A

meatus - superior, middle, inferior

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23
Q

function of paranasal sinuses

A

don’t really know
lighten the skull
resonate voice
mucus secretions

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24
Q

pathology of sinuses

A

sinusitis, more common in maxillary because drainage requires movement upwards

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25
Q

what is the pharynx

A

wide muscular tube to conduct air, food, drink from base to CV6

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26
Q

what are the parts of the pharynx

A

nasopharynx - chonanae (co-annie) to soft palate
oropharynx - soft palate to epiglottis
laryngopharynx - epiglottis - larynx/oesophagus

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27
Q

what is larynx

A

guardian of air passage (air comes from laryngopharynx) and passes air to trachea
important in vocalisation

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28
Q

how is the larynx protected

A

3 large unpaired cartilage:
- epiglottis, moves prevents food from going to larynx and sends it to oesophagus
- thyroid cartilage - adam’s apple
- cricoid cartilage - ring at bottom superior to trachea
3 small paired cartilage:
- positioning vocal folds
- arytenoid cartilage, corniculate, cuneiform

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29
Q

what is the trachea

A

long tube that provides air from larynx to bronchi. it has C shaped hyaline cartilage rings

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30
Q

why are the hyaline cartilage in the trachea shaped the way they are

A

allows oesophagus to expand to transport large boluses of food e.g. it encroaches when there are big lumps

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31
Q

name of secondary bronchi

A

lobar

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32
Q

location of primary bronchi

A

outside lung

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33
Q

how many bronchopulmonary segments in each lung?

A

10 in right, 8-10 in left

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34
Q

which lung is smaller

A

left

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35
Q

what is unique about bronchopulmonary segments during surgery

A

they are self-contained, so can be completely removed because they have their own blood supply e.g. to remove a tumor

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36
Q

what are the pleurae

A

lining of connective tissue that covers & protects the lung, reduces friction, as well as ventilates it

parietal = stuck to chest wall

visceral = stuck to the lungs

extends from clavicle & 1st rib & 7th, 10th, 12tth ribs

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37
Q

where is the apex of the lung

A

root of neck above the 1st rib

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38
Q

what are the 4 types of pneumothorax

A

primary: absence of underlying condition
traumatic: gunshot, stab, biopsy - rips parietal pleura
secondary: underlying lung disease
tension: flap of tissue

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39
Q

what happens when a tension pneumothorax occurs

A

cardiac output decreases due to compression of the inferior vena cava. this will decrease venous return and can lead to edema & even cardiac arrest

additionally arterial bp drops, tachycardia can be auscultated & neck veins are distended

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40
Q

what is pneumothorax

A

pleural effusion/collapsed lung

negative pleural pressure is lost as a result of the seal of the pleural space being punctured

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41
Q

what are the 3 surfaces of the lungs

A

diaphragmatic surface (base) that sits on diaphragm
costal surface, largest surface, adjacent to ribs
mediastinal surface is in contact with midline/mediastinum

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42
Q

what separates the lung lobes

A

fissures - oblique & horizontal (only in right lung)

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43
Q

what is the parietal pleura

A

thin membrane lining chest wall

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44
Q

what is the visceral pleura

A

thin membrane lining lung. space between parietal & visceral pleura is called the pleural cavity containing intrapleural fluid

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45
Q

what is the purpose of pleural fluid

A
  1. reduces friction as lung moves relative to chest wall because friction can cause tissue damage & inflammation
  2. creates surface tension e.g. pleural fluid bond –> pleural linkage because the lung is trying to collapse and the chest wall is trying to expand
46
Q

what is pleural effusion

A

build-up of fluid when lungs secrete too much and don’t re-absorb. can accumulate due to poor heart pumping &/ inflammation and may cause pneumothorax

47
Q

what is pneumothorax

A

air in the thorax, pierces parietal visceral membrane, air gets in, breaks surface tension, lung collapses

48
Q

what does pneumothorax look like on an xray

A
49
Q

what does tension pneumothorax look like on a xray & what does it do

A

pushes heart to the right lung due to presence of air & can cause acute failure of heart. happens when the hole that allowed air into the pleural cavity has a flap that seals it during expiration (so air only gets in during inspiration) and increases the pressure that pushes the heart to the other side

50
Q

what is atelectasis

A

loss of lung volume secondary to alveolar collapse. not caused by leakage of air into space but rather:

  • obstruction of bronchi = obstructive
  • compressive = compression on lungs e.g. PE, tension pneumothorax
  • contraction = scarring of lungs
  • adhesive = lack of surfactant decreases surface tension
51
Q

what is traumatic/spontaneous pneumothorax

A

air comes from outside through chest wall or from lungs, both leading to collapse
mainly caused by COPD - chronic obstructive pulmonary disease

52
Q

what are the main types of COPD

A

Pulmonary emphysema & chronic bronchitis

53
Q

treatment for pneumothorax

A

chest drain

54
Q

what is the purpose of bronchiole constriction

A

to slow down air to either filter out particles (bushfire), or warm up air (cold weather)

55
Q

what pathology is hyperconstriction of bronchioles

A

asthma

56
Q

what is unique about the blood travelling to the alveoli

A

it is low in oxygen and gets oxygenated as it passes the alveoli via the pulmonary capillaries

57
Q

what factors determine the effectiveness of gas exchange/diffusion

A
  1. driving force/partial pressure gradient. oxygen will move from highly concentrated area to low concentrated area
  2. surface area (large area is provided by capillaries)
  3. a small distance for the gas to travel –> provided by thin respiratory membrane
58
Q

what is the purpose of pulmonary surfactant

A

secreted by type ii alveolar cells to facilititate compliance & expansion

Reduces the surface tension on the alveoli

59
Q

what are the types of alveolar cells

A

type I = respiratory membrane, together with capillary endothelium
type II = pulmonary surfactant

60
Q

what is the main cause of respiratory issues in premature babies and what is IRDS

A

lungs haven’t started making pulmonary surfactant yet so atelectasis is likely

IRDS = infant respiratory distress syndrome

61
Q

how is oxygen transported in the blood

A
  1. physically disolved in blood plasma
  2. bound to heme in haemoglobin molecules with red blood cells

haemoglobin transports more than plasma

62
Q

what is normal PO2

A

100mHg

63
Q

how much O2 can dissolve in 1L of blood at normal PO2

A

3mL = 15mL/min

64
Q

what type of O2 contributes to PO2

A

the O2 dissolved in blood plasma, not the O2 bound to heme in haemoglobin

65
Q

what are the pathologies of too much or too little haemoglobin

A

too little = anaemia
too much = polycythemia

66
Q

how do you determine saturation of oxygen in haemoglobin

A

amount of heme that are bound. 4 per molecule

67
Q

what is the main factor that determines the binding capacity of haemoglobin

A

PO2

68
Q

how much oxygen is consumed at rest and during exercise

A

at rest 250mL
exercising = more (the remainder of oxygen that has not been diffused to muscles like a reserve)

69
Q

what are the binding properties of haemoglobin

A
  • the curve is asymptotically shaped
  • at low PO2 levels it is hard for binding to occur
  • in the middle binding is easier
  • as PO2 gets really high, it is harder to bind again
  • look at graph
70
Q

how is PO2 measured

A

mm Hg

71
Q

what happens when PO2 falls

A

haemoglobin will release oxygen. when it’s bound it’s unavailable, but when released, it’ll move into blood plasma and be available to cells

72
Q

what are the implications of a 70-100 mmHg PO2

A
  • dissociation curve is flat here
  • O2 content of arterial blood is hardly affected
  • breathing pure oxygen
  • mild respiratory functions won’t affect..?
73
Q

what are the implications of a 10-50 mmHg PO2

A

the curve is very steep, so a small change in PO2 will result in a drastic release of O2 from the haemoglobin, making it available to diffuse from the pulmonary capillaries to the systemic capillaries (tissue)

74
Q

what is normal PO2 of venous blood

A

40 mmHg

75
Q

what is the utilisation coefficient

A

the capacity to provide more O2 to tissues e.g. when exercising

76
Q

what causes the PO2 dissociation curve to shift

A
  • right = Hb binding is now lower in high temp, high acidity, high PCO2 e.g. in increased metabolic activity
  • left = low PCO2, low temp, low acidity, Hb binds more O2
77
Q

what causes the PO2 dissociation curve to shift

A
  • right = Hb binding is now lower in high temp, high acidity, high PCO2 e.g. in increased metabolic activity
  • left = low PCO2, low temp, low acidity, Hb binds more O2 –> occurs more in pulmonary capillaries
78
Q

what is the most important muscle of inspiration

A

diaphragm, long thin large muscle to increase/dec thoracic volume

79
Q

what muscles work with diaphragm to change thoracic volume

A

intercostal

80
Q

what innervates the diaphragm

A

phrenic nerve

81
Q

what innervates the intercostal muscles

A

intercostal nerves

82
Q

what can further reduce intrapulmonary pressure

A

action of accessory muscles

83
Q

what is boyles gas law

A

increase in thoracic volume causes a decrease in intrapulmonary pressure. intrapulmonary pressure falls to a level below atmospheric pressure during inspiration

84
Q

what are the accessory muscles for inspiration

A

sternocleidomastoid and scalenus

85
Q

what happens in between inspiration and expiration

A

relaxation of inspiratory muscles

86
Q

what decreases the size of the chest cavity

A
  1. relaxation of diaphragm
  2. elastic recoil of alveoli
87
Q

look at xrays of inspiration & expiration

A
88
Q

which rib does the diaphragm sit at during inspiration & expiration

A

inspiration = border of 10th rib
expiration = 9th rib

89
Q

why does the heart look bigger in expiration

A

the capacity of the lungs decreases

90
Q

what is normal tidal breathing in mL

A

500 mL

91
Q

what is total lung capacity

A

5 700 mL for a male, 4 500 mL for a female

92
Q

what is the residual volume

A

1 200 mL

93
Q

what is FRC

A

functional residual capacity, where the lungs sit at rest. Capacity is about 2 200 mL

94
Q

what are the features of normal breathing

A
  • rhythmic
  • involuntary
  • occurs without conscious thought
  • can be controlled by hyper/hypoventilation but ultimately autonomic control takes over
95
Q

what unconsciously increases breathing rate

A

exercise or arousal

96
Q

what part of the brain initiates breathing

A

medullary respiratory centre

97
Q

what part of the brain regulates breathing

A

dorsolateral pons / respiratory centres

98
Q

where are the breathing centres of the brain

A

image

99
Q

where are the peripheral chemoreceptors

A

in the carotid body, a vascular organ on the wall of the carotid artery

100
Q

what receptors work when there is low PO2 and what do they do

A

peripheral chemoreceptors via IX cranial nerve

effects:
- increase rate & depth of ventilation
- increase sympathetic nerve activity to cardiovascular system = vasoconstriction
- blood flow to peripheral tissues decreases so it can be sent to brain & heart

101
Q

what receptors sense CO2 & what are their response

A

central chemoreceptors in medulla oblongata

they increase the rate & depth of breathing

102
Q

explain the physiology of CO2 stimulating chemoreceptors

A

increase in arterial blood CO2 = increased CO2 in medulla because high level of CO2 causes diffusion from capillaries to interstitial fluid. together they produce carbonic acid which stimulates the medullary chemoreceptors and increase rate and depth of breathing by activating dorsal & ventral respiratory groups

103
Q

what is pleural effusion

A

excess fluid in the pleural space

104
Q

what are the types of pleural effusion

A

transudative, exudative, lymphatic

105
Q

what is a transudative PE

A
106
Q

what is exudate PE

A

inflammation of pulmonary capillaries leading to fluid leaking into pleural space

caused by trauma, malignancy, infection, pneumonia

107
Q

what is lymphatic PE or chylothorax

A

lymphatic fluid accumulates because thoracic duct is obstructed

108
Q

what does PE look like on an xray

A

blurring as fluid settles into costophrenic angles

will look layered if patient is lying down

109
Q

what is hemothorax

A

blood in pleural space

110
Q

What is the characteristic of alveoli in pathologies like COPD and fibrosis

A

The elasticity

More elastic in copd

Less elastic in fibrosis

Radiography 1 (13 decks)

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