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respiratory_week_1_20190518190149 Flashcards

1
Q

what are the 4 steps of external respiration

A

ventilation (gas exchange between atmosphere n alveoli)exchange between air in alveoli and blood coming into lungstransport in blood between tissues and lungsexchange between blood and tissues

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2
Q

boyle’s law

A

at any temperature the pressure exerted by gas varies inversely with volume of gas

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3
Q

what is the forces that link lungs to thorax

A

intra pleural fluid cohesivenessnegative intrapleural pressure - creates gradient

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4
Q

values of different pressures

A

atmospheric - 760mmHg/101pKaintra alveolar - 760mmHg/101pKa (less for air to flow)intrapleural - 756mmHg

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5
Q

what muscles are used in active process of inspiration and forceful inspiration

A

external intercostals lift ribs and move sternum accessory: sternocleidomastoid, scalenus and pectoral

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6
Q

why is the phrenic nerve important in inspiration and expiration and where is it located

A

passes motor information to diaphragm and receives sensory information from it cervical 3, 4 and 5

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7
Q

what causes the lungs to recoil in the passive process of expiration

A

elastic connective tissue and alveolar surface tension (attraction between water molecules produce force which resists lung stretching)

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8
Q

what are the muscles of active expiration (hyperventilation)

A

abdominal muscles and internal intercostals

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9
Q

what are signs of pneumothorax

A

shortness of breath, chest pain, hyper resonant percussion note and decreased/absent breath sounds

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10
Q

which forces keep alveoli open

A

transmural pressure gradient pulmonary surfactant (secreted by type II alveoli and lowers surface tension to prevent smaller alveoli collapsing)alveolar independence

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11
Q

What are the lung volumes and capacities?

A

SEE PICTURE ON DOCUMENT

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12
Q

what is the FEV1/FVC ratio

A

proportion of forced vital capacity that can be expired in first second normal is >70%

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13
Q

what is equation of airway resistance

A

F = ΔP/R

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14
Q

what does airway obstruction do to airway pressure

A

causes fall in airway pressure along airway downstream resulting in airway compression and rising pleural pressure

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15
Q

what causes decreased pulmonary compliance (greater change in pressure needed for change in volume - stiffer)

A

pulmonary fibrosis, pulmonary oedema, lung collapse, pneumonia, absence of surfactant

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16
Q

what causes increased pulmonary compliance

A

if elastic recoil of lungs is lost and age

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17
Q

what increases the work of breathing

A

decreased pulmonary compliance, increased airway resistance, decreased elastic recoil

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18
Q

what is anatomical dead space

A

inspired air which remains in airways where it is not available for gas exchange - makes it more advantageous to increase depth of breathing rather than rate

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19
Q

what is alveolar dead space

A

ventilated alveoli which are not adequately perfused with blood

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20
Q

what is physiological dead space

A

alveolar dead space + anatomical dead space

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21
Q

what is the effect of decreasing O2 on pulmonary and systemic arterioles

A

vasoconstriction of pulmonaryvasodilation of systemic

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22
Q

what is the partial pressure gradient and what is the equation

A

pressure exerted by one gas if it occupies full volumePaO2 = PiO2 (PaCO2/0.8)when calculating PiO2, water vapour must be accounted for

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23
Q

what does a big gradient between alveolar PO2 and arterial PO2 suggest

A

problem of gas exchange in lungs or a right to left shunt in heart

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24
Q

what is ficks law of diffusion

A

the amount of gas that moves across sheet of tissue is proportional to area of sheet but inversely proportional to thickness

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25
Q

what is henrys law

A

the amount of gas dissolved in a given type and volume of liquid (blood) at a constant temperature is proportional to partial pressure of the gas in equilibrium with liquid

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26
Q

what is the equation for the oxygen delivery index

A

DO2l = CaO2 x Cloxygen content of arterial blood x cardiac index

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27
Q

what is equation for oxygen content of arterial blood

A

1.34 x haemoglobin conc x %Hb saturated with O2

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28
Q

what does the steep part of lower sigmoid curve signify

A

peripheral tissues will get a lot of oxygen for a small drop in capillary PO2

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29
Q

what is the Bohr effect do to the sigmoid curve

A

shift to right due to increased release of O2 caused by: increase PCO2, increase H+, increase temp, increase 2,3-BPG

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30
Q

what is special about HbF

A

2 alpha and 2 gamma structure so interacts less with 2,3BPG so higher affinity for O2

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31
Q

how much CO2 transported in solution and how is this done

A

10% - done by Henrys Law

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32
Q

how much CO2 transported as carbonate and how is this done

A

60% - formed in blood by CO2 + H2O ⇌ H2CO2 ⇌ H+ + HCO3- enzyme is carbonic anhydrase which occurs in RBC

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33
Q

how much CO2 transported as carbamino compounds and how is this done

A

30% - formed by combination of CO2 with terminal amine groups in blood proteins (e.g. globulin of haemoglobin to give carbamino-haemoglobin) reduced Hb can bind more CO2 than HbO2

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34
Q

what is the Haldane effect

A

removal of O2 from Hb increases ability to pick up CO2 and H+ O2 shifts CO2 dissociation curve (upwards diagnonal straight line) to right

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35
Q

parasympathetic stimulation of post-ganglionic cholinergic fibres

A

bronchial contraction mediated by M3 ACh receptors on ASM cells which increases mucus secretion by M3 on gland/globlet cells

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36
Q

parasympathetic stimulation of non-cholinergic fibres

A

vascular relaxation mediated by nitric oxide and VIP

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37
Q

sympathetic stimulation response

A

bronchial smooth muscle relaxation via B2-adrenoceptors on ASM activated by adrenaline &vascular contraction mediated by a1-adrenoceptors on vascular smooth muscle cells

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38
Q

what is the mechanism of contraction of smooth muscle

A

phosphorylation of regulatory myosin light chain (MLC) in presence of intracellular Ca2+ and ATP

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39
Q

what is the mechanism of relaxation of smooth muscle

A

dephosphorylation of MLC by myosin phosphatase which has constitutive activity

40
Q

how does extracellular signals, such as adrenaline, regulate MLC and myosin phosphatase

A

adrenaline stimulations phosphorylation and inhibition of MLC as well as phosphorylation and stimulation of myosin phosphatase - relaxation of bronchial smooth muscle

41
Q

what are the steps of the development of chronic asthma

A

1) increased mass of smooth muscle2) accumulation of interstitial fluid 3) increased secretion of mucus4) epithelial damage - exposes sensory nerve endings5) sub epithelial fibrosis

42
Q

what is thought to be the cause of asthma

A

immune imbalance between TH1 and TH2 lymphocytes - detailed steps on document

43
Q

what are the three different kinds of short acting agonists (SABA)

A

salbutamol, albuterol and terbutaline

44
Q

when are SABAs used

A

first line treatment for mind, intermittent asthma - relievers

45
Q

what is the mechanism of SABAs

A

stimulate B2 adrenoceptors to increase mucus clearance and decrease mediator release from mast cellsside effects - tachycardia, cardiac dysrhythmia and hypokalaemia

46
Q

what are the three different kinds of long acting agonists (LABA)

A

salmeterol (slow to act), formoterol and isoprenaline

47
Q

when are LABAs used

A

in addition to glucocorticoidsused for persistent asthma patients or patients with chronic obstructive pulmonary diseasework up to 12 hours

48
Q

what are the mechanism of LABA

A

same as SABA just longer acting

49
Q

what are the two different kinds of CysLT1 bronchodilators

A

montelukast, zarfirlukast

50
Q

when are CysLT1 bronchodilators used

A

in combination with others e.g. corticosteroidseffective against antigen induced (allergies) and exercised induced bronchospasm (2nd line treatment)

51
Q

what is the mechanism of CysLT1 bronchodilators

A

antagonists - act competitively with CysLT1 receptor since CysLTs (LTC4, LTD4 and LTE4) cause smooth muscle contraction, mucus secretion and oedema

52
Q

what are the five different kinds of muscarinic antagonists (anticholinergics)

A

ipratropium (short acting and non selective)tiotropium, glycopyronium, umeclidinium and aclidinium (long active and selective)

53
Q

when are muscarinic antagonists used

A

high therapeutic ratio so used in COPD on own or LAMA/LABA dual (LAMA prevents contraction)

54
Q

what is the mechanism of muscarinic antagonists

A

block post junctional M3 receptors in response to AChblock of M3 desirable but not M1/M2 because release of ACh can actually be increased by auto receptor antagonism

55
Q

what are the two different types of bronchodilators / anti-inflammatory Xanthines

A

theophylline (oral maintenance) and aminophylline (IV acute attacks) found in coffee

56
Q

when are Xanthines used

A

used to treat asthma and COPD - in combination with b2-adrenoceptor agonists and glucocorticoids

57
Q

what is the mechanism of Xanthines

A

non selective phosphodiesterase inhibitor which increases cAMP (second messengers that relax smooth muscle and exert anti-inflammatory effect)adverse effects involving CNS, CVS, GI and kidneys due to interactions involving CYP450s

58
Q

what are the four different kinds of glucocorticoids

A

beclometasone (chronic asthma), budesonide, fluticasone and prednisolone (severe or rapid deteriorating asthma)

59
Q

when are glucocorticoids used

A

2nd line additives,regulates inflammatory and immunological responseineffective in relieving bronchospasm but do treat/prevent asthmaused as ICS/LABA combo in COPD - benefit to patients who develop severe exacerbationssometimes unresponsive in COPD due to chronic tobacco smoke

60
Q

what is the mechanism of glucocorticoids

A

decrease formation of TH2 and causes apoptosis, prevent production of IgE, reduce number of cells and decrease Fcs expression, prevent allergen-induced influx into lung also recruit HDACs to switch off transcription of genes encoding inflammatory proteins

61
Q

what is the one type of cromones

A

sodium cromogilcate

62
Q

when is cromones used

A

second line drugs used prophylactically (to prevent) in treatment of allergic asthma in children reduces both phases of asthma attack but late phase requires frequent dosing inhaled steroid

63
Q

what is the mechanism of cromones

A

mast cell stabiliser and includes weak anti-inflammatory effect

64
Q

what is the two types of monoclonal antibody treatment

A

omalizumab and mepolizumab

65
Q

when is monoclonal antibody treatment used

A

for patients with severe, persistent allergic asthma requires IV administration

66
Q

what is the mechanism of monoclonal antibody treatment

A

omalizumab - directed against IgE - inhibits binding to IgE which inhibits TH2 response and associated mediator releaseMepolizumab - directed against IL-5 - blocks TH2 and used for severe refractors eosinophilia asthma (>4%)

67
Q

what is the one type of PDE4 inhibitor

A

rofumilast

68
Q

when is PDE4 inhibitor used

A

suppresses inflammation and emphysema in COPD oral treatment for severe COPD accompanied by chronic bronchitis

69
Q

what is the mechanism of PDE4 inhibitor

A

PDE4 is prominent PDE expressed in neutrophils, T cells and macrophages to inhibition has inhibitory effects on inflammatory and immune cells

70
Q

what is the components of triple inhalers that have recently been approved for moderate/severe COPD (not asthma or bronchospasm)

A

fluticasone, umeclidinum and vilanterol

71
Q

how much oxygen given in acute asthma

A

at least 60% O2intubated ventilation if falling PaO2 continues

72
Q

minimal symptoms and few exacerbations

A

SAMA/SABA

73
Q

more symptoms and few exacerbations

A

LABA/LAMA

74
Q

all range of symptoms with frequent exacerbations

A

ICS/LABA/LAMA (increased eosinophilia)or LABA/LAMA

75
Q

acute COPD exacerbation treatment

A

nebuliser high dose salbutamol and ipratropium or oral prednisolone24-28% O2 titrated against PaO2/PaCO2

76
Q

when is the only time COPD patient intubated

A

if reversible e.g. pneumonia

77
Q

what happens at C6 vertebrate

A

larynx becomes trachea (palpated at jugular notch) and pharynx becomes oesophagus

78
Q

the isthmus of the thyroid gland is anterior to what?

A

tracheal cartilages 2-4

79
Q

what arteries supplies chest wall

A

bilateral posterior intercostal arteries

80
Q

where is phrenic nerve found

A

in neck on anterior surface of scalenus anterior muscle and in thorax descending over lateral aspects of heart

81
Q

what is lung lobe

A

area of lung that each of lobar bronchi supply with air (right has 3 - upper, middle, lower)

82
Q

what is bronchopulmonary segment

A

area of lung lobe that each one of segmental bronchi supply with air (each lung has 10)

83
Q

which muscles are between ribs and intercostal spaces

A

external intercostals internal intercostals innermost intercostals

84
Q

what is the nerve supply of intercostal spaces

A

anterior rams of spinal nerve

85
Q

what is the posterior blood supply of intercostal spaces

A

thoracic aorta and azygous vein

86
Q

what is anterior blood supply of intercostal spaces

A

internal thoracic artery and internal thoracic vein

87
Q

why is the right dome of diaphragm usually more superior

A

presence of liver

88
Q

what does the muscular part of diaphragm attach to

A

sternum, lower 6 ribs & costal cartilage and L1-L3 inferiorly

89
Q

what is the costodiaphragmatic recess and where is it located

A

most dependent part of the pleural cavity (inferior when upright) located between diaphragmatic parietal pleura and costal parietal pleura

90
Q

what is the most inferior region laterally of pleural cavity

A

costophrenic angle

91
Q

what causes blunting of angles and fluid level seen on CXR

A

abdominal fluid in pleural cavity draining into recess

92
Q

where is lung apex auscultated

A

superior to medial 1/3rd of clavicle

93
Q

where is middle lobe auscultated

A

between ribs 4 and 6 in mid-clavicular and mix auxiliary lines

94
Q

where is lung base found

A

T11

95
Q

where is sternal angle located

A

rib 2

96
Q

where is horizontal fissure located

A

rib 4

97
Q

where is oblique fissure located

A

rib 6 anteriorly rising to T3 vertebral level posteriorly

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