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Y1 - LSS - Respiratory System > 19. Respiratory System Practicals > Flashcards

19. Respiratory System Practicals Flashcards

1
Q

Outline the principal muscles associated with inspiration and expiration

A

The inspiratory muscles include:

o The diaphragm

o The accessory muscles

The accessory muscles include:

o External intercostals (infero-medial direction)

o Scalene

o Sternocleidomastoid (SCM)

The expiratory muscles include:

o Internal intercostals (infero-lateral direction)

o The internal and external oblique

o Rectus abdominis

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2
Q

Outline the additional non-respiratory actions of the principal respiratory muscles

A

Accessory muscles control air movement during other behaviours such as speech, laughter, coughing, sneezing, and vomiting

The diaphragm is an essential muscle in childbirth and is also used when vomiting

The rectus abdominis is used during laughing and coughing

The sternocleidomastoid is involved in movement of the head

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3
Q

Outline how contraction of inspiratory muscles causes the chest wall to expand and the lungs to enlarge

A

The diaphragm contracts and is pulled downwards, increasing the super-inferior dimensions of the thorax

The external intercostals contract, pulling the ribs up and out, increasing the antero-posterior dimensions of the thorax

The increased volume decreases the pressure, causing a pressure gradient; air rushes into the lungs, filling them

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4
Q

Outline how contraction of expiratory muscles causes the chest wall to contract and the lungs to reduce in size

A

The internal intercostal muscles, along with the oblique muscles and rectus abdominis causes the ribs to be pulled in and down decreasing the antero-posterior dimensions of the thorax

The diaphragm relaxes and is pushed upwards, decreasing the supero-inferior dimensions of the thorax

A pressure gradient is generated and so air is pushed out

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5
Q

Outline how these muscles will be differentially activated during different breathing states

A

The diaphragm alone is used in quiet breathing

The external intercostals are used on increased demand

The scalene, sternocleidomastoid and accessory expiratory muscles only are used in exercise or during high demand

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6
Q

Describe how to measure the respiratory volumes and capacities of the lung

A

Lung volumes are measured by spirometry

Height and weight of the subject are recorded first, followed by a minute of breathing at rest

The subject then breathes from the spirometer wearing a nose clip for 30 seconds; after a few normal breaths, a maximum inspiration and a slow maximum respiration are measured

This should ideally be repeated in different postures

The spirometer cannot be used to measure the residual volume (RV), and therefore cannot measure either
the functional residual capacity (FRC) or the total lung capacity (TLC)

These values must be obtained by the inert gas dilution technique:

o A tracer gas (helium) is used, which mixes with the air in the lungs but does not diffuse out; the volume is then determined by the amount that this gas is diluted as it mixes with the air in the lungs

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7
Q

Define Tidal Volume

A

Tidal Volume (VT)

The volume of air inspired in a single spontaneous breath

= ~500ml

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8
Q

Define Inspiratory Reserve Volume

A

Inspiratory Reserve Volume (IRV)

The additional volume that could be maximally inspired after a tidal volume inspiration

= ~3100ml

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9
Q

Define Expiratory Reserve Volume

A

Expiratory Reserve Volume (ERV)

The additional volume that could be maximally expired after a tidal volume expiration

= ~1200ml

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10
Q

Define Vital Capacity

A

Vital Capacity (VC)

The volume of air that is possible to maximally exhale following a maximal inspiration

= IRV + VT + ERV

= ~4800ml

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11
Q

Define Inspiratory Capacity

A

Inspiratory Capacity (IC)

The volume of air that it is possible to inspire at the end of a normal quiet expiration

= VT + ERV

= 3600ml

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12
Q

Define Residual Volume

A

Residual Volume (RV)

The volume of air remaining within the lungs and airways at the end of a normal quiet expiration

= ~1200ml

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13
Q

Define Functional Residual Capacity

A

Functional Residual Capacity (FRV)

The volume of air contained within the lungs and airways at the end of a tidal volume expiration; this is the equilibrium volume at which elastic recoil exactly balances the chest wall forces

= RV + ERV

= ~2400ml

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14
Q

Define Total Lung Capacity

A

Total Lung Capacity (TLC)

The volume of air contained within the lungs and airways at the end of a maximal inspiration

= RV + ERV + VT +IRV

= ~6000ml

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15
Q

Which individualised factors may influence the value of lung volume/capacities?

A

These volumes can be influenced by body weight, height, age and gender

There are charts that help predict these values

However, there will be inter-subject variability

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16
Q

Which lung volumes/capacities can be measured buy the use of a simple spirometer

A

The spirometer cannot be used to measure the residual volume (RV), and therefore cannot measure either the functional residual capacity (FRC) or the total lung capacity (TLC)

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17
Q

How are lung volumes/capacities that cannot be measured by a simple spirometer measured?

A

The inert gas dilution technique is used

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18
Q

How might the lung volumes/capacities change during exercise?

A

During exercise the ventilation rate is increased, so the tidal volume will be increased; the tidal volume is the main value that changes

ERV, IRV, FRC and the IC all change

The values of RV, TLC and VLC cannot be changed at all

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19
Q

State which lung volumes/capacities (including RV, FRC, VC, TLC) are changed from normal for:

(1) A severe chronic restrictive lung disorder
(2) A severe chronic obstructive pulmonary disorder,

And give reasons for these changes

A

Severe chronic obstructive disease:

  • VC would either be decreased or would remain constant; TLC could decrease based upon the VC changes
  • FRC would increase, as would RV
  • In an obstructive disease, the patient has hyper-inflated lungs from which it is difficult to expel air

Severe chronic restrictive disease:

  • RV would be unchanged, whilst a decrease in VC (and TLC by extension) would occur
  • FRC would be significantly reduced
  • In restrictive conditions, the patients cannot fill their lungs as they cannot expand them enough; this
    consequently lowers vital capacity greatly
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20
Q

Briefly describe two methods that can be used (indirectly) to evaluate airways resistance

A

Forced expiratory volume (FEV1) is measured using a vitalograph

Peak expiratory flow rate (PEFR) is measured using a peak flow meter

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21
Q

Define FVC and FEV1

A

Forced vital capacity (FVC): the maximum volume of air expired as forcefully and rapidly as possible following a maximum inspiration

Forced expiratory volume (FEV1): the volume of gas expired in the first one second of this manoeuvre

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22
Q

Explain why FEV1 may be reduced in both obstructive and restrictive lung disease

A

FEV1 may be reduced in both obstructive and restrictive lung disease:

o In restrictive disorders, there is a low compliance, so the vital capacity is much compromised

o Although vital capacity can be normal in obstructive disorders, airway narrowing results in a high resistance, which slows expiration

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23
Q

Explain the significance of the ratio FEV1/FVC and state an approximate normal value in a young healthy subject

A

The ratio FEV1/FVC is an estimate of airway resistance

The ratio should normally be around 1, as a healthy subject would be able to breathe out the air in his/her

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24
Q

Predict and explain the change (if any) in the ratio FEV1/FVC in obstructive lung disease

A

Vital capacity may be normal, but FEV1 is reduced due to airway resistance and so the ratio decreases

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25
Q

Predict and explain the change (if any) in the ratio FEV1/FVC in restrictive lung disease

A

Vital capacity is reduced dramatically, but airway resistance is normal, so both values decrease and the ratio stays the same

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26
Q

Explain why the Wright Peak Flow meter may be particularly useful for patients with asthma or COPD

A

It is small, inexpensive, and easy to use, which means that peak flow can be monitored at home

Patients can be educated to recognise when the values change to a degree that they should seek medical advice

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27
Q

State which values for FVC, FEV1, FEV1/FVC, and PEFR generally increase with increase in subject size as measured by the subject’s height

A

FVC, FEV1, FEV1/FVC ratio, and PEFR generally increase with increased subject size, as measured by height

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28
Q

State which values for FVC, FEV1, FEV1/FVC and PEFR generally decrease with age after peaking at about 20 years

A

FVC, FEV1, FEV1/FVC ratio, and PEFR generally decrease with age after peaking at 20

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29
Q

State which values for FVC, FEV1 and PEFR are lower in females than in males of the same age and height

A

FVC, FEV1, FEV1/FVC ratio, and PEFR are generally lower in females than in males of the same age and height

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30
Q

Which changes in structure and function may increase airway resistance

A

These changes in structure and function may increase airway resistance:

  • Bronchoconstriction:

o Smooth muscle contracts in the wall of the airways
o This is frequently the case in asthmatics

  • Physical blockage:

o An example is increased mucus secretion
o This leads to more viscous mucus, which is more difficult to remove and thus forms mucus plugs in airways

  • Loss of radial traction (outward pull)
  • Change to the airway wall structure:

o The lumen can narrow, which occurs frequently in asthmatics

  • Airway inflammation:

o This leads to swelling of tissue and a reduction in luminal diameter

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31
Q

Indicate what happens to arterial PO2, PCO2 and O2 saturation during breath holding

A

Arterial PO2 decreases

Arterial PCO2 increases

Consequently, oxygen saturation of the blood falls:

o There is less oxygen for the haemoglobin to carry

o Carbon dioxide now binds to the haemoglobin to be carried back to the lungs to be removed

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32
Q

Indicate what effect the following manoeuvres have on arterial PO2, PCO2 and O2 saturation

A

Over-breathing of room air:

  • Arterial PO2 increases
  • Arterial PCO2 decreases
  • O2 saturation remains constant

Normal:

  • Arterial PO2 increases greatly
  • pCO2 remains constant
  • O2 saturation rises slightly

Over-breathing of oxygen:

  • Arterial PO2 increases even more greatly
  • pCO2 goes down
  • O2 saturation rises slightly
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33
Q

Briefly explain why the changes in arterial pO2 and pCO2 during a breath-hold eventually lead to an inability to sustain the breath hold

A

Increased pCO2 and decreased pO2 stimulates the central and peripheral chemoreceptors, which instigate nervous impulses from the respiratory centre that overcome voluntary suppression by the apneustic centre:

o This forces the subject to stop holding his/her breath and take another breath of fresh air to bring oxygen levels back up and lower carbon dioxide levels

34
Q

Identify the relative importance of changes in arterial pO2 and pCO2 in determining how long a breath can be held following normal breathing (i.e. from normal blood gas levels) and comment on the main reason for this

A

Ventilation increases linearly with pCO2, but a marked fall in pO2 must occur before there is a noticeable rise in ventilation:

o This means that if the arterial pO2 falls significantly during breath-hold, the various responses will cause the ventilation rate to be increased and so the breath can no longer be held

35
Q

Explain why breath-holding time may alter if PO2 and PCO2 are changed immediately before a breath hold

A

If pCO2 is reduced immediately before breath hold, stimulation of the chemoreceptors will occur in the required degree at a later time, thereby allowing the breath to be held for longer

There is, however, little effect if the pO2 is changed before the breath hold

36
Q

Identify what factors other than PCO2 and PO2, may influence breath-holding time

A

Neural stimuli from the chest wall and lung receptors induce chest expansion and thus influence breath holding time

37
Q

Outline the factors which determine alveolar pO2 and pCO2

A

The factors that determine alveolar PO2 and PCO2 are:

o Composition of inspired air

o Alveolar ventilation

o Metabolic rate (O2 use and CO2 production)

38
Q

Define hypoventilation and hyperventilation

Distinguish between the latter and the raised level of ventilation (hyperpnoea) observed during exercise

A

Hypoventilation: breathing at an abnormally shallow and slow rate, resulting in increased pCO2

Hyperventilation: breathing at an abnormally rapid rate (at rest) leading to a decreased pCO2

Hyperpnoea: rapid ventilation appropriate for a metabolic acidotic state, as observed in exercise

39
Q

Understand the relationship between alveolar pO2 and pCO2 and end-pulmonary capillary pO2 and pCO2

Explain the consequences of this for systemic arterial pO2 and pCO2

A

Alveolar PO2 and PCO2 and end-pulmonary PO2 and PCO2 should be the same respectively due to the efficiency of the diffusion process

40
Q

Know how (if at all) a reduction in Hb concentration in the blood (anaemia) affects arterial pO2, pCO2 and oxygen content

Explain the effectiveness (or lack of it) of breathing an oxygen-enriched gas mixture in correcting any abnormalities associated with anaemia

A

A reduction of haemoglobin concentration in the blood, or anaemia, does not affect arterial pO2 or pCO2

However, anaemia drastically decreases oxygen content

Hyperventilation with oxygen-rich gas will improve pO2 will improve pO2, but since the haemoglobin present is already 97% saturation, it will not cause a significant rise in oxygen content

41
Q

Know how (if at all) a reduction in ventilation rate below normal (hypoventilation) affects arterial pO2, pCO2 and oxygen content

Explain the effectiveness (or lack of it) of breathing an oxygen-enriched gas mixture in correcting any abnormalities associated with hypoventilation

A

Hypoventilation causes a decrease in pO2 and oxygen content, and a rise in pCO2

Breathing an oxygen-enriched gas will improve pO2 and return oxygen content to normal, but will also reduce pCO2

42
Q

State the normal values for arterial pO2, pCO2, Hb saturation, and Hb concentration

A

pO2: 13.3 kPa

pCO2: 5.3 kPa

Hb saturation: 97%

Hb concentration: 15 g/dl

43
Q

Outline COPD

A

COPD can consist of three pathological conditions, bronchitis, emphysema and small airways disease, but people with COPD do not necessarily have all three conditions

44
Q

Which level of the respiratory tract is affected by bronchitis?

A

This affects the bronchi mainly and generally not the bronchioles

The bronchi here are cartilaginous as they are part of the large airway path compared to the non-
cartilaginous bronchioles which are part of the small airway

45
Q

Which level of the respiratory tract is affected by emphysema?

A

This mainly affects the respiratory bronchioles, especially of smokers

It leads to the loss of the connective tissue scaffold, basement membrane and normal cell organisation

There is also a loss of surface area and elastic recoil of alveoli, which compromises gas exchange

46
Q

Which level of the respiratory tract is affected by small airways disease

A

This affects the bronchioles and other non-cartilaginous regions of the airways

47
Q

Why does the assessment of Mr Jones include lung function testing?

[See http://www.icsmsu.com/exec/wp-content/uploads/2011/12/ABS-Respiratory_System.pdf Page 87]

A

Lung function tests measure FEV1, vital capacity, and so on to obtain a baseline level of measurements to measure against

These tests will be repeated after the trial and a comparison of the two results will be done

48
Q

Why does the assessment of Mr Jones include bronchoalveolar lavage?

[See http://www.icsmsu.com/exec/wp-content/uploads/2011/12/ABS-Respiratory_System.pdf Page 87]

A

An endoscope is passed through the respiratory tract and then into the lungs, in through the bronchioles and alveoli

The endoscope aspirates a sample of tissue and other material, much like in a biopsy; the sample is then analysed

The material aspirated is known as a peripheral wash and contains:

o Surfactant, found in the epithelia and produced by Type II cells

o Macrophages

o Neutrophils

The number of these inflammatory cells (neutrophils and macrophages) is analysed:

o In healthy lungs, there should be a ratio of 70% macrophages to 30% neutrophils

o In COPD, there is a ratio of 70% neutrophils to 30% macrophages

The purpose of the branchoalveolar lavage is to obtain a cell count of inflammatory cells

49
Q

Why does the assessment of Mr Jones include high resolution CT scanning?

[See http://www.icsmsu.com/exec/wp-content/uploads/2011/12/ABS-Respiratory_System.pdf Page 87]

A

High resolution CT scans offer a far more detailed scan than regular CT, allowing things to be seen on a micro scale

With bronchitis, the small airways would appear to be denser in number on the scan

With emphysema, there would be many holes in the small airways of the lungs

With COPD, the small airways would again seem to be denser

50
Q

Define bronchoalveolar lavage

A

Bronchoalveolar lavage is a medical procedure in which a bronchoscope is passed through the mouth or nose into the lungs and fluid is squirted into a small part of the lung and then collected for examination

It is typically performed to diagnose lung disease

51
Q

What happens to the structure of the lung during emphysema?

A

There are many holes in the small airways of the lungs, which are the result of an endogenous immune response

The macrophages and neutrophils contain proteases, which are released during the inflammatory phase of emphysema

These proteases break down the host tissue in order to help cell migration and break down any particulate matter deposited in the lungs

The neutrophils release many oxygen free radicals, which are very toxic:

o These reactive oxygen species are secreted to kill any infecting microbes

The macrophages also secrete many chemicals prior to the phagocytosis of the foreign or infecting microbe:

o Lysozymes within the macrophage complete the digestion of the microbe

However, if either the oxygen free radicals, lysozymes, or proteases leak out of the inflammatory cell, they cause irreversible damage to the host tissue:

o It is basically protease secretion overload that causes tissue destruction in emphysema

Emphysema is far more prevalent in smokers:

o This is due to a deficiency in the enzyme α-1-antitrypsin, which circulates in the blood and is able to mop up all the excess proteases

52
Q

Why do the small airways become obstructed?

A

Small airways are easily obstructed by particular matter and mucous

Smokers inhale cigarette smoke, which contains many harmful particles that obstruct their airways:

o This leads to the ‘smoker’s cough’, as coughing is the only way smokers can manage to remove some of these trapped particles

53
Q

Why do the small airways become stenosed?

A

The airway becomes damaged in some way, either due to the endogenous immune response or by cigarette smoke

As it is repaired, the airway narrows as new tissue grows to replace the old, damaged tissue

The scar tissue remains and narrows the airway

54
Q

What are the changes in epithelial cell profile and secretions during bronchitis?

A

Excess mucous is produced by the goblet cells as the number of goblet cells increases; at the same time, the number of ciliated cells decreases

Consequently the trapped particles cannot be removed by the cilia, as there are not enough of them, and they tend to beat in a disordered fashion

Coughing is the only way possible to attempt to clear the blocked airways, leading to the characteristic smoker’s cough

As the mucous traps particles, dirt, and foreign microbes, the inflammatory cell number also increases

In the peripheral lung, there are likely to be deposits of particle matter

In conducting lung airways, there are likely to be deposits of foreign infecting cells and so many neutrophils
will be found here

55
Q

Why would a protease inhibitor help treat COPD?

A

A protease inhibitor inhibits the action of the secreted proteases

It is only given to people who stop smoking completely as inhaled cigarette smoke will tend to inhibit protease inhibitors

56
Q

Why don’t endogenous inhibitors work in COPD?

A

An example of an endogenous inhibitor is a tissue inhibitor of metalloproteinases (TIMP)

Endogenous inhibitors do not work as there is proteolytic overload:

o Too many protease enzymes have been released into the lungs, causing damage

An endogenous inhibitor would not remove any of the protease already present

The oxidants in cigarette smoke also prevent endogenous inhibitors from working

57
Q

Why are dual inhibitors used in COPD

A

A dual inhibitor would be effective, as the protease inhibitor would inhibit the protease already present in the lungs and the endogenous inhibitor would act by preventing the release of more protease

There would be a synergistic effect in limiting the protease action

58
Q

What might cause problems with the efficacy of inhaled therapy and could this problem be solved?

A

The excess mucous present in the lungs would not allow inhaled therapy to be effective

Some of it would be coughed up in order to try and remove it, but not enough would be removed

The method of massaging the chest may also help to remove some of the mucous

Administration of mucolytic, which breaks down mucous, would be the only effective way of removing the excess mucous

59
Q

Would Mr. Jones feel better if he used a bronchodilator?

[See http://www.icsmsu.com/exec/wp-content/uploads/2011/12/ABS-Respiratory_System.pdf Page 89]

A

A bronchodilator would help, as it makes breathing easier:

o The airways would be dilated

However, if the airways are constricted due to reasons other than bronchoconstriction, the effectiveness of the bronchodilator would be lessened

60
Q

Outline Mr Jones post-treatment

[See http://www.icsmsu.com/exec/wp-content/uploads/2011/12/ABS-Respiratory_System.pdf Page 89]

A

The LFT should show improvement:

o FEV1 should increase

o VT should increase

Bronchoalveolar lavage should show a drop in inflammatory cell numbers

CT scan would not show a decrease in the number of holes in the lungs:

o Some may appear to have been healed, but this will not be functional tissue; rather, it is scar tissue

o If therapy was successful, there should not be any more holes in the lung walls than before the treatment

61
Q

Be able to identify the following structures/cells on a histological section, photomicrograph or electron micrograph of normal lung tissue:

Bronchiole; pulmonary artery; alveolar duct; alveolus; ciliated epithelial cell; goblet cell, clara cell, type 1 pneumocyte; type 2 pneumocyte; alveolar macrophage

A

[See http://www.icsmsu.com/exec/wp-content/uploads/2011/12/ABS-Respiratory_System.pdf Page 90]

[See Google Images]

62
Q

Define the difference between metaplasia and dysplasia and be able to differentiate between them in a histological section of lung tissue

A

Metaplasia: the reversible change in differentiation from one fully differentiated type to another

Dysplasia: an abnormal pattern of growth in which some of the histological features of malignancy are present

Hyperplasia: an increase in size of a tissue or organ resulting from an increase in the number of cell

Hypertrophy: an increase in size of a tissue or organ resulting from an increase in size of individual cells

63
Q

Define lobectomy and pneumonectomy

A

Lobectomy: removal of a lung lobe

Pneumonectomy: removal of a complete lung

64
Q

Describe what is meant by emphysema, pleural effusion, atelectasis and haemoptysis

A

Emphysema: destruction of the walls of the alveoli, producing abnormally large air spaces

Pleural effusion: accumulation of fluid in the pleural space, possible causing pleurisy

Atelectasis: incomplete expansion of the lung or portion of the lung due to airway obstruction, lung
compression or inadequate pulmonary surfactant

Haemoptysis: coughing up of blood

65
Q

Identify, with reference to the picture of the lung section, the macroscopic characteristics of emphysema

[See http://www.icsmsu.com/exec/wp-content/uploads/2011/12/ABS-Respiratory_System.pdf Page 91]

A

A: Normal lung

B: Emphysema

D: Normal lung

E: Emphysema

66
Q

Outline finger clubbing, hyperinflation, central cyanosis and tachypnoea, and state whether these are symptoms or signs

A

Signs:

  • Finger clubbing: increased nail bed sponginess, which leads to a loss of angle between the nail and the nail bed
  • Hyperinflation: increased volume and hyper-expansion of the thorax due to expiratory airflow limitation
  • Central cyanosis: a bluish tongue that indicates a low pO2 of around 7-8 kPa
  • Tachypnoea: an increase in respiratory rate to maintain pCO2 and pO2 within normal range
67
Q

Outline dyspnoea, cough, haemoptysis and chest pain, and state whether these are symptoms or signs

A

Symptoms:

  • Dyspnoea: shortness of breath or an unpleasant awareness of breathing
  • Cough: a rapid expiratory manoeuvre due to stimulation of irritant receptors in the respiratory tract membrane
  • Haemoptysis: the coughing up of blood from the nose, nasopharynx, vocal cords or lower respiratory tract
  • Chest pain: pain in the thorax, attributable to various causes:

o Pleural pain is due to infection, infarction, and connective tissue disease

o Mediastinal pain is due to a large pulmonary embolism or mediastinal lymphadenopathy

o Chest wall pain is due to rib fracture, nerve root pain, or costonchondritis, which is the inflammation of the junction between the bone and cartilage

68
Q

Outline lymphadenopathy

A

Lymphadenopathy or adenopathy is disease of the lymph nodes, in which they are abnormal in size, number, or consistency

Lymphadenopathy of an inflammatory type (the most common type) is lymphadenitis, producing swollen or enlarged lymph nodes

69
Q

When a patient states they are breathless, what simple assessment would you want to perform, and what physical sign would you be looking for?

A

Breathlessness can be tested during a shuttle walking test

Signs include tachypnoea:

o Tachypnoea is an appropriate involuntary response in which the respiratory rate is increased to maintain PO2 and PCO2

o Hyperventilation is instead a voluntary increase in the minute ventilation that results in a fall in arterial PCO2

Other signs include a sense of doom, wheezing, chest pain, cold, clammy skin and central cyanosis

70
Q

State what is meant by the term central cyanosis and briefly explain why it is assessed by looking at the tongue; also distinguish between central and peripheral cyanosis

A

Peripheral cyanosis:

  • Peripheral cyanosis can be indicated by a bluish colour of the hands
  • However, a bluish colour of the hands could also indicate poor peripheral circulation

Central cyanosis:

  • Central cyanosis is often due to a circulatory or ventilatory problem that leads to poor oxygenation of blood in the lungs
  • Assessment of the tongue colour is preferred
  • A bluish tongue indicates a low arterial PO2 of 7-8kPa
71
Q

Describe how hyperinflation is assessed (i) on physical examination (ii) from the results of lung function testing; also briefly explain why hyperinflation commonly accompanies COPD

A

Hyperinflation commonly accompanies COPD, as the predominant problem in COPD is expiratory flow limitation

Expiratory flow is limited, resulting in air trapping and therefore an increased volume of air in the lungs at the end of expiration

Signs present upon examination include:

o Prolonged expiratory phase
o Expanded, barrel-shaped chest
o Reduced overall movement of ribcage
o Apex beat of the heart not palpable
o Increased activity of the sternocleidomastoid

Results of the lung tests include increased TLC, RV, and FRC, as it is harder to breathe out

72
Q

Indicate the respiratory characteristics that can be assessed by palpation and percussion of the chest

A

Palpitation:

  • Reduced overall movement of the chest wall: Hyperinflation
  • Reduced local chest wall movement: Consolidation
  • Deviation of the trachea to: Collapse
  • Deviation of the trachea away: Tension pneumothorax

Percussion:

  • Note reduced: Lung collapse, effusion, or consolidation
  • Note increased: Pneumothorax
73
Q

Briefly describe what is meant by the terms ‘wheeze’ and ‘crackles’

Indicate what conditions are associated with these breath sounds

A

Wheeze:

  • Wheeze is a musical sound that reflects the airways narrowing
  • It can be caused by a generalised disease such as asthma, COPD, or pulmonary oedema, or by a localised
    factor such as a tumour or foreign bod

Crackle:

  • Crackle is the equalisation of the intra-luminal pressure of the collapsed small airways during inspiration
  • This occurs in Acute Respiratory Distress Syndrome (ARDS), pulmonary fibrosis, and bronchiectasis.
74
Q

Describe the physical characteristics of pitting oedema. Give one example of a respiratory disorder that could be associated with this

A

Pitting oedema is the accumulation of fluid within the connective tissue of the skin in a gravitational distribution

An indentation remains after gentle pressure is applied over a bony prominence

It may arise in conditions like COPD or pulmonary hypertension

75
Q

State which physical characteristics of sputum are indicative of respiratory pathology, briefly stating why

A

Colour

Consistency

Volume

Smell

76
Q

Outline the relevance of sputum colour with regards to respiratory pathology

A

Clear/White: COPD

Green: Chest infection

Blood-stained red: Pulmonary embolism

Blood-stained rusty red: Pneumonia

Blood-stained pink: Pulmonary oedema

77
Q

Outline the relevance of sputum consistency with regards to respiratory pathology

A

Mucoid: COPD

Thick: Cystic fibrosis

High volume of clear sputum: Asthma

78
Q

Outline the relevance of sputum volume with regards to respiratory pathology

A

Over 20ml per day: Bronchiectasis or Cystic fibrosis

79
Q

Outline the relevance of sputum smell with regards to respiratory pathology

A

Foul smelling: Anaerobic chest infection

80
Q

Outline bronchiectasis

A

Bronchiectasis is a disease in which there is permanent enlargement of parts of the airways of the lung

Symptoms typically include a chronic cough with mucus production

Other symptoms include shortness of breath, coughing up blood, and chest pain

Y1 - LSS - Respiratory System (19 decks)

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