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Medical Studies 1 > Resp Week 5 > Flashcards

Resp Week 5 Flashcards

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USMLE® Step 1 flashcards
1
Q

what are 7 components of alveoli

A

type 1 alveolar cells

type 2 alveolar cells

fibroblasts

capillaries

pericytes

macrophages

immune cells

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2
Q

describe type 1 pneumocytes

A

primary function is gas exchange involving diffusion of CO2 and O2 across an alveolar membrane

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3
Q

describe type 2 pneumocytes

A

primary function is to reduce surface tension by producing surfactant, thus increasing compliance

they also prevent mvmt of fluid into alveolus and activates immune system

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4
Q

in relation to Law of LaPlace, describe the function of surfactant

A

pressure is inversely proportional to radius meaning that a smaller object is more likely to collapse under pressure, meaning every time alveolar size decreases during expiration, the lung would collapse

surfactant decreases surface tension as the alveolar size decreases, thus preventing it from collapsing

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5
Q

what are 3 molecules that compose surfactant

A

phospholipids

neutral lipids

surfactant proteins

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6
Q

describe the development of the foetal lung

A

starts w laryngotracheal groove, caudal of the 4th pharyngeal pouch

then, endoderm lining the groove will become pulmonary endothelium and all glands of resp tract

then, muscles and CT originate from surrounding mesenchyme (mesodermal)

then, cilia present at wk 10

then, mucosal glands present at wk 12

then, lung has enough surfactant to support lung function by wk 35

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7
Q

describe alveolar macrophages of the alveolar-capillary unit

A

reside in mucous layer

these are responsible for clearance of apoptotic cells and cellular debris

serve an immune function as they are responsible for phagocytosis of foreign substances

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8
Q

describe fibroblasts of the alveolar-capillary unit

A

generates and synthesises ‘fibres’ which are a component of the lung interstitial

attracted to sites of injury when detected by type 2 pneumocytes, allowing for the alveolus to be sealed off for repair

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9
Q

describe how fibrosis can occur in the lungs

A

injury e.g smoking > type 2 pneumocytes release cytokines > fibroblasts migrate to area of injury > fibroblasts lay down collagen to repair > increased epithelial cell damage > impaired re-epithelialisation > fibrosis

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10
Q

describe the pulmonary circulation

A

transport of low O2 blood to lungs via pulmonary arteries

gas exchange at level of capillaries

transport of high O2 blood to heart via pulmonary veins

P. arteries have thinner walls than systemic circ. arteries

P. arteries and P. veins are not located next to each other (P.A travel w airways while P.V and lymphatics travel in septa b/w lobuli)

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11
Q

describe hypoxic pulmonary vasoconstriction

A

in contrast to systemic arterioles, which dilate in response to hypoxia, pulmonary pre-capillary arterioles constrict in response to alveolar hypoxia

this diverts blood to better ventilated areas of the lung, hence perfusion and ventilation are synchronised

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12
Q

describe bronchial circulation

A

Vasa Privata - private vessels that supply the lung parenchyma e.g smooth muscle, CT, cartilage etc

bronchial arteries originate from thoracic aorta and 3rd right intercostal artery

in 1/3 of instances, bronchial veins drain into the azygos vein and hemi-azygos or intercostal veins

in 2/3 of instances blood from the peripheral bronchial arteries drains into the pulmonary veins

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13
Q

what 3 main muscles are involved in respiration

A

diaphragm

external intercostals

internal intercostals

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14
Q

what is the role of the diaphragm in respiration

A

contracts/relaxes to expand/reduce thoracic cavity

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15
Q

what is the role of external intercostals in respiration

A

contracts to elevate ribs during inspiration

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16
Q

what is the role of internal intercostals in respiration

A

contracts to pull ribs down during expiration

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17
Q

describe the lymph drainage of the lungs

A

lung lymph > inferior and superior tracheobronchial lymph nodes > paratracheal lymph nodes > broncomediastinal trunks > right lymphatic duct

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18
Q

what are 3 types of lymphatic vessels in the lungs

A

pleural (in CT of visceral pleura)

interlobular (in the interlobular septa)

intralobular

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19
Q

what is a cough

A

protective reflex to prevent irritants reaching smaller airways

involves forced expiration against a closed glottis

can be due to URTI, COPD, pertussis, GORD

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20
Q

outline the cough reflex pathway

A

irritant enters resp tract, contacting resp epithelium

then, innervation of vagal sensory fibres in the pharynx, trachea and bronchi

then, sensory fibres end in nucleus of the solitary tract (NTS) in brainstem

then, central cough generator (CCG) motor neurons

then, ventral resp group (VRG) motor neurons

then, innervation of resp muscles

then, forceful expiration against a closed glottis ie cough

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21
Q

what 2 fibres belong to the vagus nerve involved in the cough reflex

A

A8 fibres

C fibres

these are functional nociceptors and mechanoreceptors, which have cell bodies in the jugular and nodose ganglia of vagus nerve

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22
Q

the central cough generator stimulates the diaphragm via what

A

motor neurons C3-C5

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23
Q

the central cough generator stimulates the intercostal muscles via what

A

motor neurons T1-T11

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24
Q

the central cough generator stimulates the intrinsic laryngeal muscles via what

A

vagus nerve

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25
Q

the central cough generator stimulates the abdominal muscles via what

A

motor neurons T6-T12

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26
Q

describe the pathophysiology behind cough and sputum production

A

exposure to irritants > irritation of bronchial lining > inflammation of bronchial epithelium > goblet cells in bronchial epithelium become hyperactive > increased mucus production

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27
Q

what 4 causes of sputum

A

resp infections

GORD

bronchitis

allergies

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28
Q

how do resp infections cause sputum

A

pathogens > inflammation > increased mucus production

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29
Q

how does GORD cause sputum

A

stomach acid reach airways > irritation > inflammation > increased mucus production

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30
Q

how does bronchitis cause sputum

A

long term irritation > chronic inflammation of bronchial tubes > excessive mucus production

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31
Q

how do allergies cause sputum

A

allergens > immune response > inflammation + increased mucus production

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32
Q

what are the 4 components of respiration

A

pulmonary ventilation

diffusion

gas transport

gas exchange

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33
Q

describe air flow

A

high to low pressure

increase lung volume > negative alveolar pressure (relative to atmospheric pressure) > air inflow

relaxation of diaphragm and elastic recoil of lungs > positive alveolar pressure > air outflow

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34
Q

what is the formula for compliance

A

C = change in volume / change in pressure

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35
Q

what two factors determine compliance

A

elastic forces of lung

elastic forces caused by surface tension

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36
Q

what is tidal volume

A

total volume of air inhaled and exhaled per breath

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37
Q

what is inspiratory reserve volume

A

additional air that can be forcibly inhaled

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38
Q

what is expiratory reserve volume

A

additional air that can be forcibly exhaled

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39
Q

what is residual volume

A

air remaining in lungs after maximal exhalation

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40
Q

what is functional residual capacity

A

volume of air remaining in lungs after a normal exhalation

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41
Q

what is vital capacity

A

max amount of air that can be exhaled after a maximal inhalation

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42
Q

describe how pressure, volume, flow and resistance are related

A

volume = flow x resistance

in a given pressure difference, airflow is inversely related to resistance, meaning that a higher resistance results in lower airflow

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43
Q

describe changes in pressure during a normal breathing cycle

A

pleural pressure becomes more negative during inspiration, which causes alveolar pressure to drop below atmospheric pressure, resulting in airflow into lungs

as lungs expand, lung volume increases and the negative pleural pressure reaches its peak

at end of inspiration, alveolar pressure equals atmospheric pressure, stopping airflow

in expiration, pleural pressure becomes less negative, causing alveolar pressure to rise above atmospheric pressure leading to air outflow

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44
Q

define work of breathing

A

energy expenditure required to overcome the resistance and compliance of respiratory system during ventilation

involves respiratory muscles generating force to create necessary pressure gradients for inhalation and exhalation

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45
Q

what is transmural pressure

A

pressure difference across a structure’s wall, determining its distension or collapse

in case of lungs, it is critical for maintaining airway patency and integrity of alveolar structures

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46
Q

what is transpulmonary pressure

A

pressure difference b/w alveolar and pleural pressures, maintaining lung expansion

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47
Q

describe the pressure volume loop in relation to lung compliance

A

in a compliant lung, P-V loop demonstrates steep slope, indicating that a small increase in pressure leads to a significant increase in lung volume

in a less compliant lung, slope is flatter meaning more pressure is required to achieve the same volume change

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48
Q

what are 3 factors that affect airflow resistance

A

airway resistance

pulmonary resistance

chest wall resistance

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49
Q

describe airway resistance in terms of airflow resistance

A

resistance encountered by air moving through airways, influenced by airway diameter and the smooth muscle tone in bronchi and bronchioles

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50
Q

describe pulmonary resistance in terms of airflow resistance

A

the overall resistance to airflow within the lungs, incorporating airway resistance, lung tissue elasticity, and the viscoelastic properties of lung parenchyma

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51
Q

describe chest wall resistance in terms of airflow resistance

A

the resistance from the chest wall and diaphragm during breathing, influenced by muscle tone, rib cage stiffness, and the compliance of the thoracic cavity

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52
Q

describe the role of surface tension in the elastic recoil of the lung

A

contributes to the forces that drive lung deflation

cohesive forces b/w water molecules at air-liquid interface in the alveoli create an inward pull, which helps the lungs return to their resting state after expansion

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53
Q

describe regional differences in blood flow of lungs

A

when standing, lower parts of lung blood blow is higher than apex

lung subdivided into 3 zones (zone 1 = apex, zone 2 = middle, zone 3 = base)

zone 1 = lack of blood flow as alveolar pressure is higher than pressure in pulmonary arteries and veins

zone 2 = blood flow occurs in systole but not diastole as arterial pressure and venous pressure is higher than pressure in alveoli

zone 3 = constant supply of blood flow as arterial pressure is higher than pressure in veins and alveoli

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54
Q

describe pulmonary vascular resistance

A

larger at too small lung volumes bc large vessels are not held open by the stretch of filled alveoli

larger at too large lung volumes bc small vessels are compressed by stretch of filled alveoli

55
Q

describe the relationship b/w exercise and pulmonary vascular resistance

A

during exercise, pulmonary vascular pressure remains constant bc increased blood flow results in decreased pulmonary resistance, to compensate

this is caused by distension of pulmonary capillaries and recruitment of previously collapsed or narrowed capillaries

56
Q

what are the mechanisms by which PVR is modulated

A

vasoconstriction to increase PVR

vasodilation to decrease PVR

proliferation of smooth muscle cells to increase PVR

antiproliferation of smooth muscle cells to decrease PVR

57
Q

what are 5 factors affecting PVR and what effect do they have

A

endothelin-1 = increases PVR

histamine = increases PVR

catecholamines = increases PVR

NO = decreases PVR

adenosine = decreases PVR

58
Q

what are 3 factors influencing O2 dissociation

A

increased H+

increased temp

increased CO2

59
Q

what is the bohr effect

A

increased H+ and CO2 promotes offloading of O2 in the peripheral tissues (where PCO2 is high) and promotes O2 loading in the lungs (where PCO2 is low)

60
Q

what causes a left shift on the O2-Hb dissociation curve

A

demonstrates an increased affinity for O2 therefore:

decreased PCO2

decreased H+

decreased temp

61
Q

what causes a right shift on the O2-Hb dissociation curve

A

demonstrates a decreased affinity for O2 therefore:

increased PCO2

increased H+

increased temp

62
Q

what is the PO2 at the arterial end of capillaries

A

95mmHg

63
Q

what is the PO2 in the interstitial cells

A

45mmHg

64
Q

what is the PO2 in the intracellular solutions

A

23mmHg

65
Q

what is PO2 in the venous end of capillaries

A

45mmHg

66
Q

what is the PCO2 in the arterial end of capillaries

A

40mmHg

67
Q

what is the PCO2 in the interstitial cells

A

45mmHg

68
Q

what is the PCO2 in the intracellular solutions

A

46mmHg

69
Q

what is PCO2 in the venous end of capillaries

A

45mmHg

70
Q

by what 3 mechanisms does CO2 transport occur

A

dissolved state (5-10%)

bicarbonate ion (70%)

carbaminohaemoglobin (20-25%)

71
Q

describe the haldane effect

A

greater binding of O2 with haemoglobin increases the release (offloading) of CO2, thus CO2 release is promoted when venous blood is arterialised

72
Q

describe fick’s law of diffusion

A

rate of gas transfer is proportional to the product of diffusing capacity across a membrane and the pressure gradient

73
Q

what is diffusing capacity

A

net rate of gas transfer for a partial pressure gradient of 1mmHg

74
Q

what four categories affect diffusing capacity

A

diffusion coefficient of gas

changes in effective SA of gas exchange membrane

changes in physical properties of membrane

changes in uptake of gases by RBC

75
Q

what 3 things influence membrane surface area in terms of diffusing capacity

A

body size (height)

lung volume

ventilation/perfusion

76
Q

what 3 things influence physical properties of membrane in terms of diffusing capacity

A

pulmonary congestion

interstitial oedema

membrane thickening

77
Q

what 2 things influence changes in uptake of gas by RBC in terms of diffusing capacity

A

Hb concentration

capillary transit time

78
Q

what are 2 types of V/Q mismatching

A

intrapulmonary shunt (V/Q = 0)

alveolar dead space (V/Q = infinity)

79
Q

describe intrapulmonary shunt in terms of V/Q

A

occurs when there is perfusion without ventilation

blood passes through the lungs without being oxygenated, e.g in conditions like atelecstasis (collapsed alveoli)

80
Q

describe alveolar dead space in terms of V/Q

A

occurs when there is ventilation without perfusion

air reaches the alveoli but no blood flow is available for gas exchange, e.g in pulmonary embolism

81
Q

what are 4 regional ventilation factors that influence V/Q

A

gravity (pleural pressure gradient)

anatomical expansion (bases of lung are larger)

lung compliance (bases are more compliant)

breathing pattern (changes alveolar recruitment)

82
Q

what are 4 regional perfusion factors that influence V/Q

A

gravity (hydrostatic gradient)

hypoxic pulmonary vasoconstriction (redirection)

pulmonary vascular structure (branching)

lung volume (changes ventilation volumes)

83
Q

what is the function of the control of alveolar ventilation

A

PaCO2 and PaO2 are tightly regulated in order to enable efficient oxygenation and gas exchange in the pulmonary circulation

84
Q

how is control of ventilation achieved

A

via neurogenic regulation

it is mediated by the respiratory centre in the medulla oblongata

85
Q

describe the respiratory control centre

A

contains 3 main respiratory groups:

dorsal respiratory group

ventral respiratory group

pontine respiratory group

86
Q

describe the function of the dorsal respiratory group

A

inspiratory neurons responsible for timing of the respiratory cycle (inspiration)

87
Q

describe the function of the ventral respiratory group

A

neurons that influence both inspiration and expiration

88
Q

describe the function of the pontine respiratory group

A

includes the pneumotaxic centre, responsible for limiting the depth of breathing, and apneustic centre, to delay the inspiratory off-switch

89
Q

what are the 3 predominate receptor types in the lung

A

slowly adapting stretch receptors (SASR)

rapidly adapting stretch receptors (RASR)

vagal C-fibre nociceptors

90
Q

what is the function of slowly adapting stretch receptors

A

predominately in the airways, acts as a lung volume sensor

91
Q

what is the function of rapidly adapting stretch receptors

A

located in superficial mucosa, stimulated by changes in TV, RR, and lung compliance

92
Q

what is the function of Vagal C-fibre nociceptors

A

free nerve endings found in bronchi and pulmonary capillaries, stimulated by oxidative stress, inflammation, or inhaled irritants

93
Q

describe the role of central chemoreceptors in the chemical control of respiration

A

CO2 passes the BBB

then, increase in PCO2 within CSF

then, CO2 forms carbonic acid, which dissociates to form a bicarbonate ion and hydrogen ion

then, pH decreases (peripheral H+ ions do not permeate the BBB)

then, transmission of this message to medullary respiratory neurons

then, change in pulmonary ventilation

94
Q

describe role of peripheral chemoreceptors in the chemical control of respiration

A

located in aortic arch and carotid body to detect levels of PO2 (mainly), PCO2 and H+

receptors in aortic arch transmit message to medullary respiratory neurons via vagus nerve, and receptors in carotid body transmit message via glossopharyngeal nerve

this then leads to a change in pulmonary ventilation

95
Q

describe J-receptors

A

located near pulmonary capillaries

respond to capillary pressure changes

stimulation leads to tachypnea

96
Q

describe chest wall reflexes

A

activated by receptors in chest muscles, joints and skin

prevent overinflation or sudden deflation of the lung

e.g hering-breuer reflex and deflation reflex

97
Q

describe lung reflexes

A

activated by irritant and stretch receptors in lung tissue

detect harmful particles and chemicals

activate coughing and bronchoconstriction

assist in maintaining overall TV

98
Q

outline the hering-breuer reflex

A

inflated lung

then, activation of stretch receptors

then, impulse generated

then, inhibition of inspiratory centre

then, expiration reduces lung inflation

99
Q

outline the deflation reflex

A

extreme lung deflation (eg pneumothorax)

then, activation of compression receptors

then, impulse generated

then, stimulation of inspiratory centre

then, rapid forced inspiration attempts to restore lung volume

100
Q

describe the respiratory regulation of acid-base balance

A

homeostatic regulation of pH in extracellular fluid

an increase in PCO2 leads to decreased pH, stimulating central chemoreceptors to increase ventilation

respiratory acidosis is caused by hypoventilation, which leads to increased PCO2 and decreased pH

respiratory alkalosis is caused by hyperventilation, which leads to decreased PCO2 and increased pH

101
Q

outline the process of exercise hyperpnea

A

aerobic exercise

leads to, metabolic acidosis and mechanical stress on muscles

leads to , detection by central and peripheral chemoreceptors and detection by muscle proprioceptors, respectively

leads to, initiation of respiratory control centre

leads to, hyperventilation

leads to, expulsion of CO2 which restores homeostasis

102
Q

what are pulmonary function tests

A

measurement of various aspects of pulmonary functions e.g lung mechanics, volumes, flows, pressures, pre-op function etc

103
Q

what are 3 examples of pulmonary function tests

A

spirometry

single breath diffusing capacity of carbon monoxide

subdivisions of lung volume

104
Q

what does spirometry measure

A

how much and how fast air can be inhaled and exhaled to and from lungs

105
Q

what are two devices used for spirometry

A

volume displacing devices or flow sensing devices

for volume displacing, blow > displacement is measure and thus flow is calculated

flow sensing, measure flow and integrate that flow to measure volume

106
Q

describe the spirometry procedure

A

adult patient seated and children patient stand > nose clipped and lips sealed around mouthpiece > instructed to fill lung completely then blast air out until empty > then inhale as fast as possible when empty > repeat 3-8 times > give bronchodilator > repeat experiment 20 mins after bronchodilation

107
Q

what are 5 PFT parameters

A

forced expiratory volume (FEV1)

forced vital capacity (FVC)

peak expiratory flow (PEF)

mid forced expiratory flow (FEF25-75%)

forced expiratory time (FET)

108
Q

define FEV1

A

maximum amount of air that can be expelled in one second

109
Q

define FVC

A

maximum amount of air that can be expired in one breath

110
Q

define PEF

A

fastest speed at which air can be expired

111
Q

define FEF25-75%

A

average flow rate between 25 and 75% of FVC

112
Q

define FET

A

time take for FVC to be completely expired

113
Q

describe obstructive ventilatory defects

A

causes airflow limitations, thus it is difficult to empty lungs

results in reduced airway calibre and reduced elastic recoil

decreased FEV1, decreased or same FVC, and decreased FEV1/FVC ratio

114
Q

describe restrictive ventilatory defects

A

issues with compliance of lungs causes reduced lung volumes

results in difficulty to fully expand lungs

decreased or same FEV1, decreased FVC, increased or same FEV1/FVC ratio

115
Q

what are 4 examples of obstructive ventilatory defects

A

asthma

chronic bronchitis

emphysema

foreign bodies

116
Q

what are 4 examples of restrictive ventilatory defects

A

congestion

pleural effusion

kyphoscoliosis

fibrosis

117
Q

describe the significance of bronchodilator response in the obstructive pattern

A

typically, 200ug salbutamol (bronchodilator) is given post spirometry to create a comparison

a 10% of baseline value in FEV1 or FVC indicates reversibility of obstructive defect

particularly important in case of conditions such as asthma that are reversible in nature

118
Q

what are subdivision of lung volumes

A

otherwise known as static lung volumes

volumes of gas in the lungs at a given time during the respiratory cycle

119
Q

outline the process of lung dilution

A

patient breathes in known quantity of helium-oxygen mixture, which contains a precise concentration of helium gas

then, inhaled helium mixes w gases present at lungs, eventually reaching equilibrium (ensures uniform distribution of helium within lung airspaces)

then, patient exhales mixture of helium and gases fro their lungs into a spirometer > measures concentration of helium in the exhaled breath

then, by comparing initial and exhaled concentrations of helium, the dilution of helium in the lungs is calculated. this info helps determine lung volume and other pulmonary parameters

120
Q

describe whole body plethysmography

A

patient seated in cabin w nose clipped and lips sealed > breathe normally to measure inhalation and exhalation

respiratory effort done against closed shutter as pressure in box, volume in box and change in pressure are known thus volume of lungs can be measured

enables measurement of reserve volume and total vital capacity, entities that cannot be measured w spirometry

121
Q

describe static lung compliance

A

changes in lung volume per unit of pressure in the absence of flow

122
Q

describe single breath diffusing capacity of carbon monoxide

A

aka transfer factor of carbon monoxide

reflects SA and diffusing properties of alveolar capillary membrane, volume of capillary blood Hb in contact w alveolar gas and rate of binding b/w Hb and carbon monoxide

123
Q

what causes reduced DLCO (diffusion capacity of lungs for CO)

A

less Hb available for CO binding

anemia

PE

emphysema

124
Q

what causes elevated DLCO (diffusion capacity of lungs for CO)

A

more Hb available for CO binding

polycythaemia

erythrocytosis

125
Q

outline how CAD can lead to dyspnea

A

stenosis/occlusion

leads to, myocardial ischemia

leads to, reduced oxygen to myocardium

leads to, damage to heart muscle

leads to, reduced Q

leads to, inadequate circulation of oxygenated blood

leads to, increased workload of breathing

leads to, dyspnea

126
Q

outline how cardiomyopathy can lead to dyspnea

A

heart muscle enlargement/stiffening

leads to, reduced Q

leads to, inadequate circulation of oxygenated blood

leads to, increase workload of breathing

leads to, dyspnea

127
Q

outline how valvular disease can lead to dyspnea

A

stenosis/regurgitation

leads to, increased pulmonary pressure putting strain on right heart

leads to, RV becoming weakened due to strain

leads to, inadequate circulation of oxygenated blood

leads to, increased workload of breathing

leads to, dyspnea

128
Q

outline how inflammation of the pericardium can lead to dyspnea

A

fluid build up

leads to, fluid-reduced contractility

leads to, reduced Q

leads to, inadequate circulation of oxygenated blood

leads to, increase workload of breathing

leads to, dyspnea

129
Q

outline how anaemia can lead to dyspnea

A

decreased RBC count

leads to, reduced Hb

leads to, reduced oxygen carrying capacity

leads to, insufficient oxygen delivery to tissues and cells

leads to, reduced oxygen availability at lungs

leads to, dyspnea

130
Q

outline how COPD can lead to dyspnea

A

inflammation leads to narrowed airways

leads to, obstructed flow of air in/out of lungs

leads to, reduced oxygen uptake

leads to, reduced oxygen availability at lungs

leads to, dyspnea

131
Q

outline how asthma can lead to dyspnea

A

bronchoconstriction

leads to, reduced airway diameter which reduced oxygen intake

leads to, increase workload of breathing

leads to, dyspnea

132
Q

outline how pneumonia can lead to dyspnea

A

inflammation and fluid buildup in the lungs

leads to, reduced gas exchange capacity

leads to, inadequate circulation of oxygenated blood

leads to, increase workload of breathing

leads to, dyspnea

133
Q

what is your approach to a patient with acute dyspnea

A

history (speed of onset of dyspnea, associated symptoms, what happened immediately before onset, other medical problems)

exam (vital signs [O2 sat], chest [wheezing, etc], heart, extremities [oedema, cyanosis], mental status)

investigations (ECG, CXR, CBE)

appropriate intervention

133
Q

what is your approach to a patient with chronic dyspnea

A

history

examination

investigations

assessment

management plan

reassessment

Medical Studies 1 (16 decks)

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