CVR 4: Respiratory Flashcards

1
Q

What two areas of the brain not in the medulla oblongata are involved in the control of breathing?

A

Pneumotaxic and apneustic centres in the pons.

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2
Q

How many different areas of the brain are involved in controlling breathing?

A

Four

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3
Q

What areas of the brain not in the pons are involved in the control of breathing?

A

Dorsal respiratory group and ventral respiratory group, both in the medulla oblongata.

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4
Q

Which area of the medulla oblongata is predominantly active during inspiration?

A

The dorsal respiratory group (DRG).

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5
Q

What is the central pattern generator?

A

A neural network in the dorsal and ventral respiratory groups in the medulla oblongata, provides background ventilatory drive.

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6
Q

Concentration of which gas predominantly influences breathing?

A

CO2

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7
Q

Where are the central chemoreceptors and what do they monitor in regards to breathing?

A

In the brainstem.
CO2 passes across blood/brain barrier, leading to increase in hydrogen ions in CSF (bicarbonate buffer system).
Hydrogen ion concentration is monitored by chemoreceptors in the brainstem.

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8
Q

Where are the peripheral chemoreceptors for respiration and what do they measure?

A

Carotid bodies and aortic arch.
Measure PaCO2 predominantly, but also measure PaO2 and pH.

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9
Q

If PaO2 decreases, what happens to minute ventilation?

A

Increases.

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10
Q

In hypoxia, does a given PaCO2 level trigger higher or lower minute ventilation?

A

Higher.

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11
Q

What are the three types of mechanoreceptors in the lungs that send afferent information to the respiratory control centres via the vagus nerve?

A

Stretch, irritant, and J receptors (juxtapulmonary capillary)

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12
Q

Where are the receptors, activated by swallowing, which prevent respiratory activity during swallowing?

A

The pharynx.

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13
Q

Why can x-rays be dangerous?

A

They are a form of ionising radiation, which can damage tissue, cells, and DNA (mutagen).

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14
Q

What colour are more dense structures on an x-ray? Give an example.

A

White. E.g. bones.

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15
Q

On a chest x-ray, why is the diaphragm higher on the right?

A

Due to the presence of the liver.

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16
Q

What anatomical landmark on a chest x-ray can be used to assess symmetry?

A

The clavicles.

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17
Q

Why aren’t the anterior aspects of the ribs easily visible on a chest x-ray?

A

They are cartilaginous.

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18
Q

Which view is most ideal for a chest x-ray and why; AP (anterior-posterior) or PA (posterior-anterior)?

A

PA (posterior-anterior); patient facing the detector, standing up.
This is because there will be a crisper image and accurate size of the heart than in AP view, and the scapulae can be protracted.

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19
Q

Which causes more ionising radiation for a patient, chest x-ray or abdominal x-ray?

A

Abdominal x-ray.

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20
Q

Where should you look to check for cyanosis?

A

Under the tongue at glossal artery.

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21
Q

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

A

Both = hypoxaemia (low PaO2)
Type 1 = hypocapnia/normal PaCO2
Type 2 = hypercapnia (high PaCO2)

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22
Q

What causes Type 1 respiratory failure?

A

Many different causes, including infectious, congenital, and neoplasmic causes.

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23
Q

What causes Type 2 respiratory failure?

A

Lack of respiratory drive, excess workload, and bellows failure. Under-ventilation leading to hypercapnia. For example, in COPD.

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24
Q

Why might someone with anaemia not be cyanotic when severely hypoxic?

A

Cyanosis is caused by large amount of deoxygenated haemoglobin. Anaemic patient might not have enough haemoglobin to be cyanotic.

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25
Q

Why might it be dangerous to give too much oxygen to a patient with COPD?

A

In chronic hypercapnia, such as in COPD, chemoreceptors thought to reset. Breathing is no longer driven by increase in PaCO2 and instead driven by decrease in PaO2.
If give supplementary O2 and raise PaO2, the patient might lose their ventilatory drive and hypoventilate.

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26
Q

What is respiratory failure?

A

Failure of gas exchange; inability to maintain normal blood gases.

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27
Q

At the level of what rib is the optimal VQ ratio seen?

A

Rib 3

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28
Q

What does PaCO2 depend on?

A

A constant (K), the production of CO2 (VCO2), and alveolar ventilation (VA).

PaCO2 = K x VCO2 / VA

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29
Q

The total lung capacity is found by adding what two lung volumes?

A

Residual volume and vital capacity.

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30
Q

What are the four stages of lung development?

A

Embryonic
Pseudoglandular
Cannalicular
Alveolar

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31
Q

When is the alveolar stage of lung development?

A

At 25 weeks until term.

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32
Q

Which stage of lung development occurs at 16-25 weeks?

A

Cannalicular

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33
Q

When is the pseudoglandular stage of lung development?

A

5-17 weeks

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34
Q

By what week in lung development do the lung buds enlarge to form right and left main bronchi?

A

5th week

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35
Q

What happens during the pseudoglandular stage of lung development?

A

Different cells/structures start to develop e.g. mucous glands.
Angiogenesis; however, pulmonary vessels will be constricted due to hypoxic environment (lungs full of fluid).

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36
Q

In lung development, when do the respiratory bronchioles and alveolar ducts develop?

A

16-25 weeks (Cannalicular stage)

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37
Q

In what stage of lung development do the alveolar sacs and type 1/2 pneumocytes develop?

A

Alveolar stage, 25 weeks until term.

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38
Q

When do the lungs finish developing?

A

3-5 years old.

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39
Q

Why is pulmonary vasoconstriction important in the foetus?

A

Oxygenated blood comes from the placenta into right side of the heart.
Pulmonary vasoconstriction increases pressure in right side of the heart, so blood preferentially flows through foramen ovale. Any remaining flows through ductus arteriosus.

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40
Q

What two vessels are joined by the ductus venosus? What organ does this cause a proportion of blood to bypass?

A

The umbilical vein and the inferior vena cava. Bypassing the liver.

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41
Q

Which carries oxygenated blood from the placenta to the foetus, the umbilical artery or the umbilical vein?

A

The umbilical vein.

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42
Q

How does the ductus arteriosus close after birth?

A

The muscular wall contracts, mediated by bradykinin.

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43
Q

How is the foramen ovale closed after birth?

A

In the first breath, lungs are oxygenated which causes pulmonary vessels to dilate. This drops the pressure in the right side of the heart. Foramen ovale closes as pressure in left side of the heart becomes higher than the right.

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44
Q

In Laplace’s law, what is the pressure in a sphere (e.g. alveoli) proportional to?

A

Surface tension and radius.

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45
Q

Why do premature babies, who haven’t developed surfactant yet, struggle to inflate their lungs?

A

Surfactant reduces surface tension of alveoli, reducing the pressure needed to overcome to inflate alveoli.

46
Q

Patients with chronic obstructive pulmonary disease (COPD) can develop pulmonary hypertension.

What heart failure is most likely to complicate severe pulmonary hypertension?

A

Right heart failure.

Severe pulmonary hypertension means the right ventricle has to work harder to pump blood through the pulmonary artery. Ultimately the right ventricle is unable to generate sufficient pressure and therefore starts to fail.

47
Q

The end diastolic volume (EDV) in the average healthy person’s left ventricle is 120mls.

If we assume normal ventricular function, what would you expect the end systolic volume (ESV) to be?

A

50ml

48
Q

The maintenance of blood pressure is an important homeostatic function of the cardiovascular system.

Describe the relationships of blood pressure (BP) & systemic vascular resistance (SVR) with the parasympathetic nervous system.

A

Trick question!

There is no parasympathetic innervation of blood vessels.

49
Q

Cardiac arrythmias can complicate a myocardial infarction.

Which artery most frequently supplies the Atrioventricular Node (AVN)?

A

The right coronary artery.

50
Q

What are the three types of host defences in the respiratory system?

A

Intrinsic, innate defence, and adaptive immunity.

51
Q

What type of host defence involves non-immune mechanisms?

A

Intrinsic defence.

52
Q

Give an examples of chemical epithelial barriers which are secreted from the epithelium and play a role in the respiratory tract host defence.

A

Anti-fungal/microbial peptides.
Anti-viral proteins.

53
Q

Does the alveolar epithelium have a role other than gas exchange?

A

Yes! Also has a host defence function; can be triggered to produce certain defence proteins when a pathogen is present.

54
Q

Mucus and cilia in the respiratory epithelium are an important host defence mechanism. Why?

A

Mucus and cilia together form the mucociliary escalator (AKA mucociliary clearance); wafting pathogens and particles up out of the respiratory tract.

55
Q

What is airway mucus and what is it made of?

A

A viscoelastic gel containing water, carbohydrates, proteins, and lipids.
Secretory product of goblet cells and submucosal glands.

56
Q

Why is mucus important in the respiratory tract?

A

Protects the epithelium from foreign material/pathogens and reduces fluid loss (prevents peri-cellular liquid from evaporating).

57
Q

What reflexes are an important part of non-immune host defence mechanisms?

A

Sneezing and coughing.

58
Q

Name the four afferent nerves involved in the cough reflex.

A

Trigeminal, glossopharyngeal, superior laryngeal, vagus.

59
Q

What two efferent nerves are involved in the cough reflex?

A

Recurrent laryngeal and spinal nerves.

60
Q

Where are the sensory neurons which trigger the sneeze relfex?

A

In the nasal cavity.

61
Q

Do motor neurons for sneeze or cough reflex trigger more effectors?

A

Sneeze.

62
Q

Name the steps involved in respiratory epithelium repair/regeneration following insult/injury.

A

Spreading and de-differentiation (stop being cuboidal and ciliated).
Cell migration.
Cell proliferation (from basal cells).
Re-differentiation (become ciliated epithelial cells again).

63
Q

What feature of respiratory epithelium allows it to effect a complete repair?

A

Functional plasticity; they can change their phenotype.

64
Q

What airway abnormality are most chronic pulmonary diseases associated with?

A

Respiratory epithelial abnormalities.

65
Q

What potentially fatal issue can extreme failure of mucociliary clearance cause?

A

Mucus plugs; can cause obstruction when proteins in mucus polymerise to form large plugs.

66
Q

Is asthma hereditary?

A

Not necessarily, very complex, does run in families but there is no direct Mendelian inheritance of asthma.

67
Q

What is the most common lethal autosomal recessive genetic disorder in Caucasians?

A

Cystic fibrosis

68
Q

Which chromosome and where on this chromosome is the variant which causes cystic fibrosis?

A

Long arm of chromosome 7

69
Q

What causes cystic fibrosis?

A

Defect in code for CFTR (cystic fibrosis transmembrane regulator), causing abnormal transport of chloride ions across membrane, leading to build up of mucus.

70
Q

Approximately how common is cystic fibrosis?

A

1 in 2500 live births (1 in 25 people carry recessive gene).

71
Q

What is measured in newborns to screen for cystic fibrosis?

A

Trypsin.

72
Q

How many classes of abnormality of cystic fibrosis genotypes are there, and which is the most common?

A

6 classes. Most common is class II (delta F508 mutation).

73
Q

What is alpha-1 antitrypsin deficiency (A1ATD)?

A

Autosomal recessive/co-dominant genetic disorder, unable to produce enough antitrypsin so trypsin (serum protease) destroys lung tissue. Causes emphysema and bronchiectasis.

74
Q

Name 3 examples of interstitial disease with a genetic component.

A

LAM, neurofibromatosis, Gaucher disease.

75
Q

Name 4 common work exposures that cause asthma.

A

Latex, paints, shellfish, flour, isocyanate paint sprays.

76
Q

What are pneumoconioses and how are they categorised?

A

Dust related lung diseases.
Fibrogenic or non-fibrogenic.

77
Q

Give 2 examples of fibrogenic pneumoconioses.

A

Asbestosis and silicosis.

78
Q

What receptors do asthma drug treatments agonise/antagonise to promote bronchodilation?

A

Agonise beta 2 receptors (sympathetic) e.g. salbutamol.

Antagonise muscarinic receptors (parasympathetic) e.g. ipratropium.

79
Q

Which hypersensitivity reaction is typified by; IgE mediated, normally immediate and is seen in anaphylaxis, asthma, hay fever?

A

Type I

80
Q

Which hypersensitivity reaction is typified by; deposition of immune complexes, normally a 7-21 days time course, seen in hypersensitivity pneumonitis?

A

Type III

81
Q

Which hypersensitivity reaction is typified by; cytotoxic, antibodies bound to cell antigen, normally onset is hours to days, seen in transfusion reactions and Goodpasture syndrom (Anti GBM disease)?

A

Type II

82
Q

Which hypersensitivity reaction is typified by; T-cell mediated, normally onset of days to weeks/months, seen in tuberculosis and Stevens-Johnson syndrome.

A

Type IV

83
Q

In type I hypersensitivity reactions, what two types of mediators are released by antigen of allergen binding with IgE?

A

Soluble immediate mediators e.g. histamine, and granule delayed mediators e.g. proteases.

84
Q

True or false: Type II hypersensitivity reaction is an underlying mechanism for several autoimmune disorders.

A

True!

85
Q

What causes Type II hypersensitivity reactions?

A

Antibodies react with antigenic determinants on the host cell membrane (usually IgG or IgM). This can trigger different cell processes including complement activation.

86
Q

What symptoms can Anti Glomerular Basement Membrane Disease (anti GBM) cause and why?

A

Haemoptysis and renal failure.
Type II hypersensitivity reaction; autoimmune reaction where antibodies to subunit on GBM are developed. GBM is found in alveoli and kidneys.

87
Q

What is another name for hypersensitivity pneumonitis?

A

Extrinsic allergic alveolitis

88
Q

What is hypersensitivity pneumonitis?

A

Acutely; inflammation of alveoli within the lung caused by hypersensitivity to inhaled agents. Chronically causes scarring of alveoli.
Can be fibrotic/non-fibrotic.

89
Q

What hobby/job is a common cause of hypersensitivity pneumonitis?

A

Having/working with birds!
Bird fancier’s lung.

Could also mention; farmer’s lung from working with mouldy hay. Saxophone player’s lung from bacteria inside instrument. etc.

90
Q

Give an example of common type IV hypersensitivity reaction condition. What does this condition cause in the lung?

A

Sarcoidosis. Causes granulomas (clusters of immune cells, can cause lymph node enlargement).

91
Q

In diving, at each 10m increase of depth how much does the atmospheric pressure increase by?

A

1 atm (760mmHg)

92
Q

What is the atmospheric pressure at sea level?

A

1atm or 760mmHg.

93
Q

What equation based on Boyle’s Law helps to calculate lung volume at a given depth when diving?

A

P1V1=P2V2
Pressure at sea level (1atm) * volume of lungs at sea level =
pressure at depth (e.g. 150m deep, will be 16ata) * volume of lungs at that depth.

94
Q

Why is hyperventilating before free diving/breath holding underwater dangerous?

A

Can cause drowning through shallow water blackout, because hyperventilating reduces PaCO2 artificially, so by the time PaCO2 rises again to trigger urge to surface and breathe, PaO2 has already reached dangerous enough levels to cause cerebral hypoxia and blackout.

95
Q

Why can surfacing from a dive be fatal if you hold your breath when resurfacing?

A

Lung volume increases as depth decreases. This increases intra-thoracic pressure forcing air out of lungs into other spaces e.g pneumomediastinum, pneumothorax, pulmonary gas embolism.

96
Q

Why do divers use low FiO2 gas mixes?

A

Because of the equation
PiO2 = FiO2 x Pressure (atmospheric).

If atmospheric pressure increases, PiO2 will increase with same FiO2.

At sea level PiO2 = 0.21 x 1 = 0.21.

97
Q

What is the Lorrain Smith Effect?

A

Pulmonary oxygen toxicity, symptoms are cough, chest tightness/pain, SOB.
Occurs if PiO2 is > 0.5ata.

98
Q

What happens to minute ventilation at altitude and why?

A

Increases to compensate for lower FiO2.

99
Q

What spirometry measured values can be used to diagnose airway obstructive disease (e.g. COPD)?

A

FEV1/FVC.
Obstruction is diagnosed when value <0.7

100
Q

What spirometry measured value can be used to diagnose airway restrictive disease (e.g. asbestosis)?

A

FVC <80% of predicted.

101
Q

In asthma, will MEF (mid expiratory flow) be low, normal, or high?

A

MEF will be low. This causes “scalloped” shape in the flow volume curve in spirometry.

102
Q

In COPD, will TLco (transfer estimate test with carbon monoxide) be low, normal, or high?

A

Low if they have emphysema; reduced surface area of alveoli for gas exchange.

103
Q

When might dynamic hyperinflation in a patient with COPD be observed and why?

A

During increased minute volume e.g. during exercise.
Reduced elasticity in the lungs in COPD increases end expiratory volume due to less recoil, unable to return lung volume to normal and they end up breathing at top of lung volume capacity.

104
Q

What is orthopnoea?

A

Breathlessness on lying down.

105
Q

Which immunoglobulin (Ig) is primarily secreted in breast milk?

A

IgA

106
Q

Ignoring any relatively small contribution of inspired water vapour, what is the approximate partial pressure of inspired oxygen (PiO2) in KPa for a patient on 40% oxygen?

A

40KPa

107
Q

In pulmonary fibrosis such as asbestosis, the carbon monoxide transfer factor is typically low. What does this measure assess?

A

Interaction between the alveolus, capillary and haemoglobin.

108
Q

What arterial blood gas results is typical of chronic Type 2 Respiratory Failure? Include PaO2, PaCO2, and HCO3.

A

Low PaO2, high PaCO2, normal/high HCO3.

109
Q

Through what process does adrenaline cause bronchodilation?

A

Adrenaline binds to β 2 -receptors in the smooth muscle of the bronchioles causing their relaxation.

110
Q

Changes in which three substances stimulate the carotid chemoreceptors?

A

O2, CO2, H+ ions.