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Year 3 > Week Three - Case One > Flashcards

Week Three - Case One Flashcards

1
Q

what is COPD characterised by

A

airflow obstruction, most commonly a result of a combination of chronic bronchitis and emphysema

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2
Q

what is bronchitis

A

cough and sputum production on most days for at least 3 months during the last two years

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3
Q

what is emphysema

A

enlarged airspaces distal to the terminal bronchioles with destruction of the alveolar walls

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4
Q

what is different between asthma and COPD

A

there is little to no reversibility of the obstruction

the airflow limitation is usually progressive and is associated with an abnormal inflammatory response of lung tissues to certain particles

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5
Q

COPD is the ‘…..’ leading cause of death worldwide

A

COPD is the fourth leading cause of death worldwide

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6
Q

what is the FEV1;FVC ratio in COPD

A

<70%

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7
Q

how many people in the UK have COPD

A

1.5 million

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8
Q

when is COPD unlikely to develop

A

with a smoking history less than 10 pack years

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9
Q

what percentage of smokers will develop COPD

A

10-20%

up to 50% of those with a >20 pack year smoking history will get COPD

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10
Q

what are the other causes of COPD

A

Coal mining

Exposure to air pollution – particularly from indoor fires and cooking in the developing world

Genetic, i.e. α1 –antitrypsin deficiency causes emphysema

Low socioeconomic status and low birth weight are predisposing factors
Low birth weight is associated with reduce maximum lung capacity in adulthood

Asthma and COPD may also co-exist

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11
Q

what are the symptoms of COPD

A

Breathlessness (dyspnoea)
Cough – may or may not be productive (of sputum)
Regular exacerbations

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12
Q

what is the reduced cricosternal distance

A

<3cm

this is the distance between the cricoid cartilage and the sternal angle - this is reduced due to hyperinflation - thus the thorax is raised in relation to the cricoid cartilage

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13
Q

what are the signs of COPD

A

tachypnoea

use of accessory muscles in respiration

hyperinflation

reduced cricosternal distance

reduced chest expansion

resonant chest sounds

quiet breath sounds

wheeze

stridor

cyanosis

cor pulmonale

prolonged expiration

pursed lip breathing

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14
Q

where would there be quiet breath sounds

A

over areas of emphysematous bullae

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15
Q

what is wheeze

A

an abnormal high pitched or low pitched breath sound heard on expiration.

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16
Q

what does polyphonic wheeze mean

A

it is made up of many different notes, and thus this shows it is caused by many abnormal airways

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17
Q

what is wheeze normally caused by

A

abnormally narrowed airways

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18
Q

what is a monophonic wheeze indicative of

A

a single airway obstruction, and this is most likely to be a cancerh

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19
Q

what is stridor

A

the name for a sound heard on inspiration

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20
Q

what is stridor typically caused by

A

upper airway obstruction - such as croup

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21
Q

what is prolonged expiration due to

A

because their FEV1 is low, they have to have prolonged expiration to allow for adequate respiration

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22
Q

what is pursed lip breathing

A

it creates a smaller opening through which air can exit the respiratory system, keeps the pressure in the airways higher.

stops smaller airways from collapsing, and thus creates a larger surface area for gas transfer

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23
Q

what does pursed-lip breathing reduce

A

dyspnoea

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24
Q

what is the dynamic closure point in COPD

A

in COPD some of the airways will collapse at a point proximal to many of the alveoli

occurs due to the destruction of elastin tissue

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25
Q

what helps the VQ mismatch

A

pursed lip breathing

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26
Q

what does COPD lead to

A

gas trapping

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27
Q

what does gas trapping lead to

A

leads to an increase in dead space and leads to hyperinflation

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28
Q

what are the three lung function tests performed (spirometry)

A

FVC<80% predicted

FEV1/FVC<0.7, OR <LLN (lower limit of normal)

Increased residual volume

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29
Q

what will a CXR show

A

Possibly hyperinflation, but often normal
Flat hemi-diaphragms
Large central pulmonary arteries
Decreased peripheral vascular markings
Bullae
Cylindrical heart

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30
Q

what will an ECG show

A

right atrial and ventricular hypertrophy suggestive of cor pulmonate, leading to large p waves on ECG

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31
Q

what will an ABG show

A

often normal, but in advanced disease, there may be:
Decreased PaO2
Increased PaCO2

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32
Q

what kind of anaemia would show on a FBC

A

normocytic normochromic anaemia of chronic disease

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33
Q

what else would you test for in COPD

A

alpha-1 antritrypsin

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34
Q

what is required to confirm a diagnosis of COPD

A

spirometry is required to conform diagnosis. the official diagnostic cut off is fev1/fvc ratio <0.7

in patients over 65 and under 45, the ratio may not be as reliable and specialist spirometry may be required to clarify the diagnosis in borderline cases

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35
Q

when should you consider COPD as the diagnosis

A

Patients >35 with symptoms of breathlessness and cough and / or sputum production
All smokers and ex-smokers >35

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36
Q

what result suggests asthma or mixed COPD/asthma

A

an FEV1 increase of greater than 400mls

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37
Q

what is the mild COPD FEV% predicted

A

60-80%

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38
Q

what are the symptoms of mild COPD

A

Variable
Typically few symptoms
Breathlessness on moderate exertion
No effects on ADLs
May be cough and sputum production

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39
Q

what is the moderate COPD FEV % predicted value

A

40-60%

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40
Q

what are the symptoms of moderate COPD

A

Breathlessness when walking on flat ground
Exacerbations
Some limitation of ADLs

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41
Q

what is the severe COPD FEV % predicted value

A

<40%

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42
Q

what are the symptoms of severe COPD

A

SOB on minimal exertion
Daily activities severely limited
Frequent and severe exacerbations

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43
Q

what is the difference in asthma and COPD diurnal variation in FEV1

A

there is no diurnal variation in FEV1 in COPD as opposed to asthma

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44
Q

what kind of infiltrate is seen in COPD and asthma

A

in COPD, there is neutrophil infiltrate

in asthma, there is eosinophil infiltrate

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45
Q

how Is COPD mediated

A

via CD8

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46
Q

how is asthma mediated

A

via CD4

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47
Q

what is the hyper secretion of mucus due to

A

marked hypertrophy of mucus-secreting glands and hyperplasia of goblet cells. reduces lumen size and increasing distances for gas diffusion

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48
Q

what are the other pathologic markings seen in COPD

A

Abnormal dilation of air spaces with destruction of alveolar walls

Inflammation and scarring, reducing size of lumen of airways and reducing lung elasticity

Initially small airways are affected and this initial inflammation is reversible, whereas in later stages larger airways become affected and the process is no longer reversible

Epithelial layer becomes ulcerated and squamous epithelium may be replaced by columnar cells, resulting in increased gas diffusion distance

49
Q

what is chronic bronchitis defined as

A

cough and sputum production on most days for at least 3 months during the last two years

50
Q

what is seen in chronic bronchitis

A

An enlargement in mucus secreting glands (hypertrophy)
An increased number of goblet cells (hyperplasia)

51
Q

what is the main cell involved in the inflammation reaction

A

neutrophil, is asthma the main inflammatory cell is the eosinophil

52
Q

how does the FEV1 decrease

A

After events of inflammation, there will be scarring and fibrosis of the tissue. This thickens the walls of the airway, and thus reduces the size of the lumen (thus decreasing the amount of air you can get into and out of the lungs quickly (FEV1),and also increasing the distance that gasses have to travel in order to diffuse properly.

53
Q

when does the COPD process become irreversible

A

when the larger airways become affected

54
Q

what are the squamous epithelium replaced by

A

columnar cells

55
Q

what is emphysema

A

causes enlarged airspaces distal to the terminal bronchioles, with destruction to the elastin alveolar walls causing decreased elastic recoil

56
Q

what are the three main pathological effects in COPD

A

Loss of elasticity of the alveoli

Inflammation and scarring – reducing the size of the lumen, as well as reducing elasticity

Mucus hypersecretion – reducing the size of the lumen and increasing the distance gasses have to diffuse.

57
Q

what is alpha1 antitrypsin

A

is an enzyme that destroys other enzymes

58
Q

what exactly does alpha1 antitrypsin do

A

It destroys several proteases, including trypsin, elastases and collagenases. In the deficiency, these enzymes aren’t destroyed, and they are allow to happily eat away at the lung tissue, leading to COPD.
The condition is genetic, and is autosomal dominant. You need to be homozygous to have clinical effects, and about 1/5000 people are. 1/10 are carriers of the gene.
The deficiency accounts for about 2% of cases of emphysema in the UK.

59
Q

what are the proteinases that act in the lung often released by and what does this mean for smokers

A

The proteinases that act in the lung are often released by inflammatory cells, such as macrophages. Thus, in smoking, there are more of these around, and the effect becomes exaggerated. This also explains the mechanism of emphysema in a normal individual who smokes.

60
Q

what does pink puffers refer to

A

used to refer to patients who have a near normal PaO2, and a normal or low PaCO2 (due to hyperventilation). They ‘puff’ to increase their alveolar ventilation – and by doing so they are able to keep their blood gas values normal. These patients generally have emphysema or at least a higher degree of emphysema than bronchitis. These are likely to enter type I respiratory failure.

61
Q

what are blue bloaters

A

used to refer to patients who have decreased alveolar ventilation. They have a low PaO2 and a high PaCO2. They are cyanosed but not breathless (because their respiratory centre has become sensitised). They rely on hypoxic drive to maintain adequate ventilation. They often go on to develop cor pulmonale. These patients are more likely to be type II respiratory failure. ‘Bloater’ – due to cor pulmonale.

62
Q

what is an exacerbation of COPD defined as

A

a change in patients baseline symptoms such as;
- worsening SOB
- increase cough
- increase sputum

63
Q

who are exacerbations most common in

A

History of previous regular exacerbations
History of GORD / reflux
More severe disease (low FEV1)

64
Q

what are frequent exacerbation associated with

A

a increased rate of decline of respiratory function as measured by FEV1

65
Q

what are the indications for hospital admission during an acute exacerbation of COPD

A

Sats <92%
Not responsive to outpatient management
Inability to eat or sleep to due breathlessness
Very low exercise tolerance (e.g. <10m)
Confusion (may be due to hypercapnia)
Unable to cope at home
Co-morbidities suggestive of likely poor outcome

66
Q

what is given when O2 stats are less than 88% and what should O2 stats be maintained at for patients with COPD

A

Oxygen therapy – if sats are <88% – beware of CO2 retention
Give controlled O2 therapy to maintain sats at 88-92%

67
Q

what should you do if PaCo2 has risen >1.5pKa

A

consider using a non-invasive ventilation i.e CPAP

68
Q

what is PaCo2 dependent on

A

ventilation i.e the volume of air inhaled and exhaledwh

69
Q

what is PaO2 dependent on

A

alveolar gas transfer (oxygenation) and the percentage of oxygen inhaled

70
Q

what els should be given to control or manage the exacerbation

A

Give salbutamol (e.g. 4-8 puffs (400-800mcg) via spacer, or nebulised 2.5-5mg in solution), and ipratropium (e.g. 4 puffs (80mcg) or nebulised 0.5mg)

71
Q

what steroids are given

A

typically 50mg prednisolone OD for 5 days
Tapering is not required after short courses such as these

72
Q

what are the two most common causes of bacterial exacerbations

A

Streptococcus pneumoniae – this is a Gram-positive diplococcus.

Haemophilus influenzae – this is a Gram-negative coccobascillus.

73
Q

what is the first line treatment for bacterial infection

A

amoxicillin 500mg tds for 7 days

Second and third line options might include doxycycline (100mg PO for 5-7 days) co-amoxiclav and ciprofloxacin (if penicillin allergy)

74
Q

what is the usual dosage for long term oxygen therapy

A

give 2L via nasal prongs for at least 15 hours per day

75
Q

what are the only two things that can prolong the life expectancy in COPD

A

smoking cessation and LTOT

76
Q

what are the goals of pharmacological management in COPD

A

To reduce the rate of exacerbations
To provide symptomatic relief

77
Q

example of a SABA

A

salbutamol – 200μg every 4-6 hours

78
Q

example of a LABA

A

salmeterol

79
Q

example of a SAMA

A

. ipratropium – 40μg 4x a day

80
Q

example of a LAMA

A

tiotropium

81
Q

examples of ICS

A

beclomethasone, fluticasone

82
Q

what is step one in inhaler treatments - typically used for mild disease

A

Step 1 – SABA or SAMA – short acting drugs that are bronchodilators – Typically corresponds with mild disease

83
Q

what is step 2

A

Add LABA or LAMA – for longer acting bronchodilation – typically corresponds with moderate disease
Some studies have shown that LAMAs – particularly tiotropium – are more effective than LABAs
About a 35% reduction in risk of hospital admission compared to LABAs

84
Q

what should you not use with LAMA

A

a SAMA

85
Q

what is step 3

A

Add ICS – a single inhaler combined LABA/LAMA/ICS may be appropriate – typically corresponds with severe disease

86
Q

what are the benefits of inhalers

A

Bronchodilators relieve breathlessness
Inhaled steroids reduce the frequency and severity of exacerbations. However, high doses have been associated with an increased risk of pneumonia

87
Q

what is the brand name for salbutamol

A

Ventolin

88
Q

what is the brand name of tiotropium

A

Spiriva

89
Q

what is reduced when you give LTOT

A

the pulmonary arterial pressure

90
Q

what are the indications for LTOT

A

PaO2 <7.3kPa
PaO2 <8kPa, and patient also has polycythaemia, hypoxaemia, peripheral oedema or pulmonary hypertension

Patients should be asses for LTOT when they have:
FEV1 30-49% predicated
Cyanosis
Sats <92% when well on pulse oximetry

91
Q

what is type two respiratory failure a result of

A

alveolar hypoventilation

92
Q

how do you treat type II respiratory failure

A

Give controlled oxygen therapy, starting at 24% O2
Recheck the ABG after 20 minutes – if the PaCO2 is steady or lower, then you can increase the O2 to 28%.

If the PaCO2 has risen >1.5kPa– then consider giving a respiratory stimulant such as doxapram (1.5-4mg/min IV) or assisted ventilation.

You can also see CO2 retention as physical signs – the patient will become drowsy and confused
If this fails consider intubation / ventilation

93
Q

what is cor pulmonale

A

right sided heart failure, as a result of pulmonary hypertension

94
Q

what are the obstructive lung diseases

A

COPD
asthma
bronchiectasis
CF

95
Q

what are the characteristics of OLD

A

‘Obstructive pattern’ on PFT’s – see below
Disease mechanisms affect the bronchi and bronchioles, usually in a diffuse pattern across the whole lung

96
Q

what is the obstructive pattern lung disease

A

Reduced FEV1 (<80% of normal)

Reduced FEV1:FVC ratio
(<70%)

Often normal or slightly increased FVC

Total lung capacity is increased – but this is mainly due to an increased residual capacity due to hyperexpansion

Reduced peak flow

97
Q

what are examples of restrictive lung disease

A

pulmonary fibrosis
sarcoidosis
obesity

98
Q

what is RLD caused by

A

disease in the interstitium of the lung – and this is usually an increase in the amount of tissue in the interstitium of the lung.

99
Q

what is the restrictive pattern in lung disease

A

Reduced FVC
Reduced FEV1
Normal FEV1:FVC ratio
Normal PEFR

100
Q

what are the main causes of restrictive lung disease

A

fibrosis of the lung

Asbestosis

Radiation fibrosis

Drugs – common ones include amiodarone (anti-arrhythmic) and methotrexate (anti-folate and anti-metabolite drug – used in cancer and auto-immune diseases)

Rheumatoid arthritis

ARDS – acute respiratory distress syndrome
this is an acute onset syndrome, which present with shortness of breath, bilateral infiltrates on the CXR and may occur within 48 hours of an acute illness

101
Q

look up and learn the MRC dysnponea scale

A
102
Q

what is the type of cancer developed from asbestos exposure

A

at risk of asbestosis and mesothelioma. Asbestos exposure also increases the risk of lung cancer, in particular adenocarcinoma.

103
Q

what can exposure to birds cause

A

hypersensitivity pneumonitis

104
Q

is chronic productive cough common in COPD or asthma

A

in COPD

105
Q

is night time waking with SOB/wheeze common in COPD or asthma

A

asthma

106
Q

what are the hallmark symptoms of COPD

A

shortness of breath
chronic cough
sputum production

107
Q

what is the genetic predisposition to COPD

A

alpha-1 antitrypsin

108
Q

what is the only intervention that will slow disease progression in COPD

A

Quitting smoking is the only intervention that will stop the accelerated lung function decline seen in smokers, and revert the individual to the gradual rate of lung function decline that occurs with increasing age.

109
Q

what is the steps that result in cor pulmonate

A
  1. hypoxia
  2. pulmonary artery vasoconstriction
  3. increased pulmonary artery pressure
  4. right ventricular hypertrophy
  5. right ventricular failure
110
Q

what are the three treatments used for COPD that are not used for asthma

A

LAMA
theophylline
carbocisteine

111
Q

what is magnesium used for

A

Magnesium is a bronchodilator typically used for treating acute exacerbations of asthma, and rarely used in acute exacerbations of COPD.

112
Q

what are brand names for LABAs

A

oxis

serevent

113
Q

what are brand names for LAMAs

A

Spiriva

seebri

114
Q

what are brand names for LABA+ICS

A

fostair (formoterol and beclomethasone)

seretide (salmeterol and fluticasone)

Symbicort (formoterol and buydesonide)

115
Q

what are the triple therapy inhaler brand names (LABA+LAMA+ICS)

A

Trelegy Ellipta (fluticasone + umeclidinium + vilanterol)

Trimbow (beclomethasone + glycopyrronium + formoterol)

116
Q

what is type one respiratory failure defined by

A

a PaO2 of less than 8kPa. It indicates a serious underlying pathology with the lungs such as infection, oedema or a shunt.

117
Q

what is type II respiratory failure defined by

A

when PaCO2 is more than 7kPa. Reduced ventilatory effort can be a result of gas trapping, such as in COPD and severe asthma, due to chest wall deformities, muscle weakness or central causes of respiratory depression.

118
Q

what are the correct management steps for acute exacerbation of COPD

A
  • reduce the flow of oxygen, aiming for target saturations of 88-92%
  • give back-to-back nebulisers (salbutamol and ipratropium)
  • give oral steroid and antibiotics
  • recheck arterial blood gas after one hour
119
Q
A

Year 3 (63 decks)

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