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ESA 3 > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

What does the kinetic theory of gases state?

A

That gases are particles moving around a space, that generate pressure by colliding with the walls of that space. Increased frequency and strength of those collisions, increases the pressure

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2
Q

What does Boyle’s law state?

A

That at a constant temperature, pressure is inversely proportional to volume

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3
Q

What does Charles’ law state?

A

Pressure is directly proportional to absolute temperature

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4
Q

What is the universal gas law?

A

Allows calculation of how volume will change as temperature and pressure change
Vol. x pressure = gas constant x temp (K)

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5
Q

What is partial pressure?

A

The fractional pressure of a gas in a maxture, normally at the same proportion as the fraction of volume of the gas in a mixture

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6
Q

What is vapour pressure?

A

The partial pressure that’s exerted by water molecules evaporating out and gas molecules dissolving into water

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7
Q

What is saturated vapour pressure?

A

Partial pressure when the rate of water molecules evaporating and gas molecules dissolving at the same time, is equal

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8
Q

What is meant by tension of a gas?

A

How readily the gas will leave a liquid

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9
Q

What is the mean pressure of pulmonary arteries, veins and capillaries?

A

Arteries - 12-15 mmHg
Capillaries 9-12 mmHg
Veins 5 mmHg

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10
Q

What is the optimal perfusion/ventilation ratio?

A

0.8

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11
Q

How can chronic hypoxic vasoconstriction lead to heart failure?

A

Increased vascular resistance from pulmonary vessels increases the afterload for the right ventricle - right ventricle failure

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12
Q

What is the distinguishing feature between components of the upper and lower respiratory tract

A

Lower respiratory tract components lie within the thorax

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13
Q

What are the components of the lower respiratory tract?

A

Trachea, bronchi (main, lobar, segmental, sub-segmental) bronchioles (main, terminal, respiratory), alveolar ducts and alveoli

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14
Q

What components of the respiratory system make up the conducting portion?

A

Nasal cavity, pharynx, larynx, trachea, primary bronchi, secondary bronchi, bronchioles and terminal bronchioles

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15
Q

Which components of the respiratory system make up the extra-pulmonary portion

A 
nasal cavity
pharynx
larynx 
trachea
primary bronchi
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16
Q

What are the functions of the nose?

A 
Smell
Respiration
Filtration of dust
Humidification of inspired air
Elimination of secretions from paranasal sinuses and lacrimal ducts
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17
Q

Where are conchae found?

A

Lateral walls of nasal cavity, hanging inferomedially

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18
Q

What is the purpose of conchae?

A

To provide increased surface area for heat exchange

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19
Q

What bones are the conchae formed by?

A

Inferior concha by the Inferior Concha bone

Middle and superioe conchae by the medial processes of the ethmoid bone

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20
Q

What lies superoposterior to the superior concha?

A

The Sphenoethmoidal recess which receives opening of ethmoid sinus

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21
Q

Where do the paranasal sinuses drain into?

A

Frontal - middle nasal meatus
Ethmoid - Middle and superior meatus
Maxillary - middle nasal meatus
Sphenoid - superior meatus via sphenoethmoidal recess

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22
Q

Where does the pharynx extend from and to?

A

From cranial base to inferior cricoid cartilage anteriorly and inferior C6 vertebra posteriorly

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23
Q

What are the different portions of the pharynx and where do they run from and to?

A

Nasopharynx - from Cranial base to soft palate
Oropharynx - from soft palate to superior border of epiglottis
Laryngopharynx - from superior epiglottis to inferior cricoid cartilage

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24
Q

What are the borders of the larynx?

A

From laryngeal inlet to inferior border of cricoid cartilage

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25
Q

How does the middle ear connect to the respiratory system?

A

Anteromedially through the Eustachian tube to the nasopharynx

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26
Q

What is the purpose of venous plexuses in the non-olfactory regions of the nasal cavity?

A

Swell every 20-30 minutes so that airflow alternates side to side to prevent overdrying

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27
Q

What are olfactory cells?

A

Bipolar neurones with one dendrite that extends to epithelial surface to form a swelling with non-motile cilia extending from it. Internal dendrites join up to make an olfactory nerve

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28
Q

What epithelia lines vocal cords?

A

Stratified squamous non-keratinised

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29
Q

What is contained in each vocal cord?

A

Skeletal vocalis muscle

Vocal ligaments - large bundle of elastic fibres

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30
Q

What is the purpose of vocal cords in the respiratory system?

A

To help prevent foreign objects from reaching the lungs. They also close to build up pressure for the coughing reflex

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31
Q

What do clara cells secrete?

A

Surfactant lipoprotein and protein CC16

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32
Q

How is Protein CC16 useful clinically?

A

Used as marker.
High levels mean there’s been leakage across blood-air barrier
Low levels mean there’s lung damage

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33
Q

What type of cells are type 2 pneumocytes?

A

Simple cuboidal that secrete surfactant

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34
Q

What is a terminal bronchiole?

A

Bronchiole with now alveolar openings

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35
Q

What is an alveolar sac?

A

Composite air space, onto which many alveoli can open

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36
Q

What are the borders of the thoracic cage?

A 
Anterior - sternum and costal cartilages
Posterior - thoracic vertebrae
Laterally - ribs and intercostal spaces
Superiorly - thoracic inlet continuous with neck 
Inferiorly - diaphragm
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37
Q

What are the anterior articulations of the ribs?

A

Ribs 1-7 - sternum via costal cartilages
8-10 - costal cartilages
11,12 - end free in abdominal muscles

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38
Q

Which are the typical ribs?

A

Ribs 3-9

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39
Q

What do transverse costal facets of thoracic vertebra articulate with?

A

Articular facets of tubercle of ribs

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40
Q

What are the features that make the atypical ribs atypical

A

first - only 1 articular facet. Two transverse grooves separate by scalene tubercle, for passage of subclavian artery and vein
second - Rough area on superior surface - tuberosity of serratus anterior
10-12 - only 1 articular facet
11,12 - short with no neck or tubercle

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41
Q

What muscles are responsible for chest expansion in quiet respiration?

A 
External intercostals (30%) 
Diaphragm (70%)
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42
Q

Where are the openings of the diaphragm?

A

Entrance of vena cava at level of T8
Entrance of oesophagus at level of T10
Aortic hiatus at level of T12

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43
Q

What are the three sections of the diaphragm and where do they derive from?

A

Costal from internal surfaces of ribs 7 to 12
Sternal from posterior aspect of xiphoid process
Lumbar from L1-L3 and medial and lateral arcuate ligaments

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44
Q

Where do the intercostal vessels run?

A

Along inferior border in intercostal groove in order of vein, artery and nerve

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45
Q

Where do the intercostal veins drain into?

A

Anterior veins drain into internal thoracic then subclavian.

Right and left posterior drain into azygous and hemizygous veins respectively, then superior vena cava

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46
Q

What kind of lobes does each lung have?

A

Right has superior middle and inferior, formed by horizontal and oblique fissures.
Left has superior and inferior, formed by oblique fissure

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47
Q

Where does the trachea start and end?

A

Starts at inferior cricoid cartilage. Ends at level of sternal angle

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48
Q

How many pulmonary artery and veins are there?

A

1 artery per lung and 2 veins per lung

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49
Q

Where do bronchial arteries arise from?

A

2 on the left come directly from thoracic aorta

1 on the right comes from thoracic aorta via the 3rd intercostal artery

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50
Q

What do the bronchial veins drain?

A

Superficial drain visceral pleura and bronchi in hilum in azygous and accessory hemiazygous veins
Deep drain all the other bronchi into main pulmonary vein

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51
Q

What muscles are involved in quiet respiration?

A

External intercostals and diaphragm for quiet inspiration

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52
Q

What muscles are involved in forced inspiration?

A

Diaphragm, scalene, pectoralis major, sternocleidomastoid, serratus anterior, external intercostals

53
Q

What muscles are involved in forced expiration?

A

Abdominal muscles, internal intercostals, innermost intercostals

54
Q

What does alveolar gas have to diffuse through during exchange?

A 
Alveolar epithelial cell
Interstitial fluid
Capillary endothelial cell
Plasma
RBC membrane
55
Q

Why is oxygen exchange affected more than carbon dioxide in problems affecting diffusion?

A

As CO2 is more soluble than oxygen so it diffuses 21 times as fast as oxygen so oxygen diffusion is limiting, not carbon dioxide so oxygen exchange is affected first

56
Q

What are the partial pressures of oxygen and carbon dioxide in alveolar gas?

A

oxygen - 13.3 kPa

Carbon dioxide - 5.3 kPa

57
Q

How is atmospheric air related to air exchanged with blood?

A

Brought close to alveolar gas by ventilation where increase in volume of respiratory and terminal bronchioles in inspiration decreases pressure, so air is brought downwards through airways. Then, atmospheric air exchanges with alveolar gas through diffusion in terminal and respiratory bronchioles

58
Q

What is residual volume?

A

Volume left in the lungs at maximal expiration

59
Q

What is vital capacity?

A

The biggest breath that can be taken from maximal expiration to maximal inspiration

60
Q

What is the functional residual capacity?

A

The volume left in the lungs at resting expiratory level

61
Q

What is the inspiratory capacity?

A

The biggest breath that can be taken from resting expiratory level

62
Q

What is serial dead space?

A

aka anatomical dead space.
It’s the volume of the airways that aren’t involved in gas exchange.
Measured by nitrogen washout test

63
Q

What is physiological dead space?

A

All the dead space of lungs. Calculated by adding serial dead space and alveolar dead space (aka distributive dead space)
Avleolar DS is the volume of lungs that are adapted to take part in gas exchange but don’t either due to damage or poor blood supply.
Physiological dead space can be determined by measuring dilution of alveolar air by dead space air by measuring pCO2

64
Q

How is alveolar ventilation rate calculated?

A

Pulmonary ventilation rate (tidal volume x resp rate) MINUS dead space ventilation rate (dead space volume x resp rate)

65
Q

How is compliance measured?

A

Volume change per unit of pressure change

66
Q

How is specific compliance measured?

A

Volume change per unit pressure change/starting volume of lungs

67
Q

How does surfactant help keep small alveoli intact?

A

Normally, laplace’s law is applied and so alveoli with larger radius have lower pressure than small alveoli, therefore if interconnected, air will flow from high pressure to low pressure and small alveoli will collapse into large alveoli.
However, with surfactant, as surface area increases, its effects lessen so surface tension is higher so pressure in large alveoli remains high

68
Q

What does laplace’s law state?

A

Pressure = (2 x surface tension)/Radius

69
Q

What is poiseulle’s law?

A

Resistance = pressure/rate of flow

Resistance = (8 x air viscosity x tube length)/ pi x (radius)^4

70
Q

What is FVC?

A

Forced vital capacity - volume that can be expired from full lungs

71
Q

What is FEV1?

A

Forced Expiratory Volume in 1 second - volume expired in first second of expiration, from full lungs

72
Q

What is a restrictive deficit?

A

Where lungs are hard to fill that may be due to stiffness or reduced inspiratory effort (muscle weakness, deformity) but still easy to empty. Gives a reduced FVC but FEV1 is more than 70% of FVC as proportionally, lungs can empty normally

73
Q

What is an obstructive deficit?

A

When small airways are overly narrowed in expiration so it’s hard to force air out through them. Gives a low FEV1 but normal FVC

74
Q

How do flow volume loops work?

A

Plot Flow rate against either volume expired or volume of lungs.
Use vitalograph trace of volume against flow rate.
Flow rapidly increases as there’s low resistance initially in expiration then as airways narrow and resistance increases, Volume expired increases but flow rate decreases until flow rate = 0 and volume of lungs = residual volume/ volume expired = total lung capacity
Total volume expired = vital capacity

75
Q

How does the helium dilution test work?

A

After normal expiration, where patient’s lungs are at FRC, patient’s connected to a system with know concentration of helium and known volume of gas. Patient then breathes normally until an equilibrium is reached and the new concentration of helium in container is calculated. As amount = C x V and amount has to have stayed constant as helium is inert and system is closed, orignal C x V = New C x V in whole system. This V2 is equal to original volume + FRC. As all other 3 variables are know, V2 can then be calculated and from that FRC can be calculated.
Residual volume can then be found as Residual volume = FRC - Expiratory Reserve Volume, that’s found by spirometry

76
Q

How does the transfer factor test work?

A

Patient makes full expiration then rapid full inspiration containing air mixture containing a very small fraction of Carbon monoxide. Breath is held for 10 seconds then concentration of CO is taken mid-exhalation. The difference in levels of CO then gives rate of transfer of CO in ml/min/kPa so diffusion capacity of lungs is calculated as diffusion capactiy is the only limiting factor due to CO’s extremely high capacity to Hb

77
Q

What is the solubility coefficient of oxygen?

A

0.01mmol/L/kPa at 37degrees

78
Q

What diseases can give a low transfer factor result?

A

Diseases which destroy alveolar membrane eg emphysema

Diseases which increase length of blood-gas barrier eg interstitial lung disease or pulmonary oedema

79
Q

What effect do pCO2 and HCO3- conc have on pH?

A

High HCO3- moves reaction between HCO3- and H+ in direction of CO2 formation so there’s less H+ so pH rises
High pCO2 pushes reaction in direction of HCO3- formation so there’s more H+ so pH falls

80
Q

When are carbamino compounds formed?

A

When CO2 reacts with protein part of haemoglobin

81
Q

What is the henderson hasselbach equation?

A

pH= 6.1 + Log( HCO3-conc/ (pCO2 x 0.23) )

82
Q

What are the normal pCO2 and CO2 content in arterial and venous blood?

A

Arterial - pCO2 = 5.3 kPa and content = 21.31 mmol/l

Venous - pCO2 = 6.0 kPa and content = 23.21 mmol/l

83
Q

What percentage of transported CO2 is transported in its various forms?

A

Dissolved CO2 - 8%
Carbamino compund - 12%
as HCO3- - 80%

84
Q

How does hyperventilation affect pH?

A

Lowers pCO2. sing Henderson Hesselbach equation, lower pCO2 increases pH.

85
Q

What are the general effects of hypoxia?

A

Causes Hypercapnia so respiratory acidosis and pH can fall below 7. This means that enzymes can become lethally denatured

86
Q

How is calcium concentration affected by hyperventilation?

A

Hyperventilation causes respiratory alkalosis. Calcium is only soluble in acid so in a higher pH, it can’t stay in the blood. This makes nerves hyper excitable so can cause tetany

87
Q

What is compensated respiratory acidosis?

A

Acidosis persists so kidneys respond by decreasing secretion of HCO3- to try and increase pH

88
Q

What is compensated metabolic acidosis?

A

Acidosis persists so body compensates by increasing ventilation to reduce pCO2 and restore CO2:HCO3- to normal

89
Q

What detects falls in inspired pO2?

A

Peripheral chemoreceptors in aortic and carotid bodies. Only stimulated by large changes and so they increase respiratory rate and tidal volume and heart rate and divert blood to brain and kidneys

90
Q

What are changes in pCO2 detected by?

A

Peripheral chemoreceptors but these are insensitive.
Central chemoreceptors in medulla. These rapidly alter ventilation and react to changes in the pH of the cerebrospinal fluid

91
Q

What controls the HCO3- conc. of the CSF?

A

Choroid plexus cells which alter HCO3- levels in persisting changes and so can reset ‘normal’ HCO3- level

92
Q

What is the difference between type 1 and 2 respiratory failure?

A

Type 2 has low levels of oxygen and high CO2 but type 1 has low oxygen and normal/low CO2

93
Q

What are the 5 factors needed to maintain arterial pO2 in the normal range?

A 
pO2 in inspired air
Alveolar ventilation
Normal alveolar capillary membrane
Ventilation perfusion matching
All of right ventricular output passes through gas exchanging alveoli
94
Q

What can cause low pO2 in inspired air?

A

Normally in people living at high altitudes so everything else is normal

95
Q

What can cause hypoventilation?

A

Neuromuscular problems such as respiratory depression in opiate overdose, muscle weakness or head injury.
Chest wall problems such as kyphosis, scoliosis, morbid obesity, trauma, pneumothorax
DDifficulty ventilating lungs due to airway obstruction, COPD, severe asthma or severe fibrosis

96
Q

What can cause an impairment in gas diffusion?

A

Increased path length, eg in pulmonary oedema
Structural changes such as fibrosis
Reduced availability for diffusion such as in emphysema

97
Q

What can cause a ventilation-perfusion mismatch?

A

Reduced ventilation to some alveoli such as in lobar pneumonia
Reduced perfusion of some alveoli such as in pulmonary embolism

98
Q

What kind of airflow obstruction is there in asthma?

A

Widespread
Variable
Reversible either spontaneously or with treatment

99
Q

What are the most common symptoms of asthma?

A

A high pitched, expiratory, polyphonic wheeze
A dry, nocturnal cough that’s exercise induced
Breathlessness on exertion
Chest tightness
Variable airflow obstruction

100
Q

What signs may be found on examination?

A

Hyperexpansion of chest
Indrawing of costal cartilages in children
Maybe be history or asthma/eczema
Hyperresonant on percussion

101
Q

What tests are done to help diagnose asthma?

A

Flow-volume loop - will show scalloping, reduced PEFR, reduced FEV1:FVC and >12% improvement on salbutamol.
Skin prick allergy testing for atopic asthma
Chest X-ray to rule out differential diagnooses

102
Q

What happens in the Immediate response phase of an asthma attack?

A

Macrophages present antigens to t lymphocytes which activates T cells, especially Th2, which release cytokines, attracting mast cells and eosinophils. Th2 cells also activate B cells which produce IgE antibodies.
IgE antibodies interact with the antigen, causing mast cell degranulation and release of mediators, including histamine and prostaglandins. This causes bronchoconstriction

103
Q

What happens in the late phase response of asthma?

A

There’s infoltration of full spectrum of inflammatory cells, causing airway inflammation. Eosinophils release leukotriene C4 which are toxic to epithelial cells so cause shedding.

104
Q

What causes reduction of airway calibre in asthma?

A

Mucosal oedema due to vascular leak
Thickening of bronchial wall due to inflammatory cell inflammation
Oversecretion of mucus
Shedded epithelia being incorporated into mucus, increasing thickness
Smooth muscle contraction

105
Q

What remodelling is found in poorly controlled asthma?

A

Hyperplasia of smooth muscle
Damage to epithelia
Thickening of basement membrane due to collagen deposition

106
Q

What drugs can precipitate an asthma attack?

A

Beta blockers

NSAIDs

107
Q

What steps are taken in management of asthma?

A

Education
Primary prevention - quit smoking, lose weight, avoid exposure to triggers
Pharmacological - Beta agonists eg salbutamol for in exacerbations
Corticosteroids as preventative anti-inflammatory

108
Q

What are the signs of a severe asthma attack?

A

Unable to complete sentences
Respiratory rate > 25 per min
Pulse >110bpm
PEFR <50% of predicted value

109
Q

What are the signs of a life threatening asthma attack?

A 
PEFR <33% of predicted
Silent chest (wheeze sound of improvement)
Cyanosis
Feeble respiratory rate
Bradycardia
hpotension
Exhaustion/confusion/coma
Normal/ high pCO2 with low pO2
Low pH
110
Q

What factors decrease reabsorption of pleural fluid?

A

Blockage of lymphatics

Increase in systemic venous pressure

111
Q

What are the most common symptoms and signs of interstitial lung disease?

A 
Dyspnoea (often progressive)
Dry cough
Exercise intolerance
Tachypnoea
Tachycardia
Respiratory crackles
Signs of right heart failure
112
Q

What treatments can cause Interstitial lung disease?

A 
Radiation
Methotrexate
Nitrofurantoin
Chemotherapy
Amiodarone
113
Q

What is cryptogenic fibrosing alveolitis?

A

Ideopathic interstitial lung disease.
Increase in number of activated neutrophils which attract neutrophils and eosinophils so immune response causes tissue damage and fibrosis. Common sign is finger and toe clubbing as well as normal ILD symptoms

114
Q

What is extrinsic allergic alveolitis?

A

Where inhalation of organic material triggers an allergic response in alveoli and bronchioles.
Can be acute with rapid progression where alveoli are infiltrated with inflammatory cells e.g. famer’s lung
Or chronic with granuloma formation and progressive fibrosis e.g. in bird fancier’s lung

115
Q

How is pulmonary sarcoidosis staged?

A

Using chest x ray.
0 - normal CXR
1 - signs of Bilateral Hilar Lymphadenopathy
2 - BHL + peripheral pulmonary infiltrates
3 - peripheral pulmonary infiltrates only
4 - Progressive fibrosis with bulla formation and pleural involvement

116
Q

What is paraneoplastic syndrome?

A

Symptoms/syndrome/disease caused by presence of cancer in the body but not due to local presence of cancer cells. Mediated by either immune response to tumour of by release of humoral components by tumour cells

117
Q

What are the different histological types of lung cancer?

A

Small cell carcinoma

Non-small cell carcinoma - squmous, adeno, large cell

118
Q

What does prognosis of lung cancer depend on?

A 
Stage
Cell type
comorbidities
Performance status of patient
Biochemical markers
119
Q

Explain the TNM staging of lung cancer

A

T = tumour size
T1 - Small and contained
T2 - larger, grown into main bronchus, visceral pleura or caused lobar collapse
T3 - Larger. Invading chest wall/ diaphragm/ pericardium. More than 1 nodule in same lung.
T4 - Nodules in more than one lobe of the same lung. Invading heart, major blood vessels, laryngeal nerve etc
N = regional lymph node involvement.
N0 - no lymph nodes involved
N1 - Most proximal lymph nodes affected
N2 - Lymph nodes of proximal mediastinum affected
N3 - Lymph nodes of distal mediastinum or supraclavicular nodes affected
M = Metastases
M0 - no distal cancer spread
M1 - Lung cancer cells in distal locations

120
Q

How do SCC and NSCC respond to treatment (cancer)

A

20 % of NSCC are operable and of those operated on, 50% survive 5 years. Radical radiotherapy may be used if tumour is operable but patient’s unfit for surgery.
SCC responds to combination therapy but 75% have metastases on presentation and death from cerbral metastases is common

121
Q

How do primary lung tumours present?

A

First with a cough that is ignored then depending on disease progression, may be dyspnoea, haemoptysis, monophonic wheeze, chest pain weight loss, lethargy and nerve compression

122
Q

What biopsy techniques are used for lung cancer?

A

Bronchoscopy
Surgical
needle

123
Q

How does TB present normally?

A 
Tiredness/malaise
Cough
Low grade or hectic fever
Weight loss and anorexia
Night sweats
if a pleural effusion then Dysponoea
Haemoptysis
Pallor
Palpable cervical lymph nodes
124
Q

How does miliary TB show up, radiologically?

A

With multiple little ‘seeds’

May also be microabscesses in liver and spleen

125
Q

How does a host respond to TB?

A

Macrophages carry out phagocytosis but can’t complete as lipids in cell wall of MTB prevent formation of phagolysosome.
Frustrated phagocytosis leads to formation of granulomas with caseating center, as well as stimulates more better equipped macrophages.
Neutrophils, chemokines and cytokines are released which cause inflammatory infiltrate into the lung. Macrophages present MTB to T lymphocytes and caseating centers are calcified but still contain the bacterium.

126
Q

What is Ghons’ focus?

A

Initial focus of TB infection. From here bacilli can drain into hilar lymph nodes (focus+nodes = primary focus)

127
Q

What happens in post primary TB?

A

MTB proliferates in caseating center, causing liquefaction so a cavity forms. Fibrous tissue forms to try and contain the lesion but normally isn’t successful. Caseous material can then spread into blood vessels or bronchial tree.
There is inflammatory exudate into alveoli and if MTB spreads into the pleura or if there’s a hypersensitivity reaction then there may be pleural effusion

128
Q

How is TB treated?

A

Multi-drug therapy to try and reduce drug resistance.
Initial phase lasting 2 months of isoniazide, rifampicin, ethambutal and pyrazinamide
Continuation phase of 4 months or 12 months if CNS involvement, of rifampicin and isoniazide

129
Q

In a respiratory history, how do you calculate pack-years?

A

Number of packs a day x number of years

ESA 3 (5 decks)

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