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
2
Q
what is bronchitis
A
cough and sputum production on most days for at least 3 months during the last two years
3
Q
what is emphysema
A
enlarged airspaces distal to the terminal bronchioles with destruction of the alveolar walls
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
5
Q
COPD is the ‘…..’ leading cause of death worldwide
A
COPD is the fourth leading cause of death worldwide
6
Q
what is the FEV1;FVC ratio in COPD
A
<70%
7
Q
how many people in the UK have COPD
A
1.5 million
8
Q
when is COPD unlikely to develop
A
with a smoking history less than 10 pack years
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
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
11
Q
what are the symptoms of COPD
A
Breathlessness (dyspnoea)
Cough – may or may not be productive (of sputum)
Regular exacerbations
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
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
14
Q
where would there be quiet breath sounds
A
over areas of emphysematous bullae
15
Q
what is wheeze
A
an abnormal high pitched or low pitched breath sound heard on expiration.
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
17
Q
what is wheeze normally caused by
A
abnormally narrowed airways
18
Q
what is a monophonic wheeze indicative of
A
a single airway obstruction, and this is most likely to be a cancerh
19
Q
what is stridor
A
the name for a sound heard on inspiration
20
Q
what is stridor typically caused by
A
upper airway obstruction - such as croup
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
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
23
Q
what does pursed-lip breathing reduce
A
dyspnoea
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
25
what helps the VQ mismatch
pursed lip breathing
26
what does COPD lead to
gas trapping
27
what does gas trapping lead to
leads to an increase in dead space and leads to hyperinflation
28
what are the three lung function tests performed (spirometry)
FVC<80% predicted
FEV1/FVC<0.7, OR
29
what will a CXR show
Possibly hyperinflation, but often normal
Flat hemi-diaphragms
Large central pulmonary arteries
Decreased peripheral vascular markings
Bullae
Cylindrical heart
30
what will an ECG show
right atrial and ventricular hypertrophy suggestive of cor pulmonate, leading to large p waves on ECG
31
what will an ABG show
often normal, but in advanced disease, there may be:
Decreased PaO2
Increased PaCO2
32
what kind of anaemia would show on a FBC
normocytic normochromic anaemia of chronic disease
33
what else would you test for in COPD
alpha-1 antritrypsin
34
what is required to confirm a diagnosis of COPD
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
35
when should you consider COPD as the diagnosis
Patients >35 with symptoms of breathlessness and cough and / or sputum production
All smokers and ex-smokers >35
36
what result suggests asthma or mixed COPD/asthma
an FEV1 increase of greater than 400mls
37
what is the mild COPD FEV% predicted
60-80%
38
what are the symptoms of mild COPD
Variable
Typically few symptoms
Breathlessness on moderate exertion
No effects on ADLs
May be cough and sputum production
39
what is the moderate COPD FEV % predicted value
40-60%
40
what are the symptoms of moderate COPD
Breathlessness when walking on flat ground
Exacerbations
Some limitation of ADLs
41
what is the severe COPD FEV % predicted value
<40%
42
what are the symptoms of severe COPD
SOB on minimal exertion
Daily activities severely limited
Frequent and severe exacerbations
43
what is the difference in asthma and COPD diurnal variation in FEV1
there is no diurnal variation in FEV1 in COPD as opposed to asthma
44
what kind of infiltrate is seen in COPD and asthma
in COPD, there is neutrophil infiltrate
in asthma, there is eosinophil infiltrate
45
how Is COPD mediated
via CD8
46
how is asthma mediated
via CD4
47
what is the hyper secretion of mucus due to
marked hypertrophy of mucus-secreting glands and hyperplasia of goblet cells. reduces lumen size and increasing distances for gas diffusion
48
what are the other pathologic markings seen in COPD
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
what is chronic bronchitis defined as
cough and sputum production on most days for at least 3 months during the last two years
50
what is seen in chronic bronchitis
An enlargement in mucus secreting glands (hypertrophy)
An increased number of goblet cells (hyperplasia)
51
what is the main cell involved in the inflammation reaction
neutrophil, is asthma the main inflammatory cell is the eosinophil
52
how does the FEV1 decrease
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
when does the COPD process become irreversible
when the larger airways become affected
54
what are the squamous epithelium replaced by
columnar cells
55
what is emphysema
causes enlarged airspaces distal to the terminal bronchioles, with destruction to the elastin alveolar walls causing decreased elastic recoil
56
what are the three main pathological effects in COPD
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
what is alpha1 antitrypsin
is an enzyme that destroys other enzymes
58
what exactly does alpha1 antitrypsin do
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
what are the proteinases that act in the lung often released by and what does this mean for smokers
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
what does pink puffers refer to
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
what are blue bloaters
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
what is an exacerbation of COPD defined as
a change in patients baseline symptoms such as;
- worsening SOB
- increase cough
- increase sputum
63
who are exacerbations most common in
History of previous regular exacerbations
History of GORD / reflux
More severe disease (low FEV1)
64
what are frequent exacerbation associated with
a increased rate of decline of respiratory function as measured by FEV1
65
what are the indications for hospital admission during an acute exacerbation of COPD
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
what is given when O2 stats are less than 88% and what should O2 stats be maintained at for patients with COPD
Oxygen therapy – if sats are <88% – beware of CO2 retention
Give controlled O2 therapy to maintain sats at 88-92%
67
what should you do if PaCo2 has risen >1.5pKa
consider using a non-invasive ventilation i.e CPAP
68
what is PaCo2 dependent on
ventilation i.e the volume of air inhaled and exhaledwh
69
what is PaO2 dependent on
alveolar gas transfer (oxygenation) and the percentage of oxygen inhaled
70
what els should be given to control or manage the exacerbation
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
what steroids are given
typically 50mg prednisolone OD for 5 days
Tapering is not required after short courses such as these
72
what are the two most common causes of bacterial exacerbations
Streptococcus pneumoniae – this is a Gram-positive diplococcus.
Haemophilus influenzae – this is a Gram-negative coccobascillus.
73
what is the first line treatment for bacterial infection
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
what is the usual dosage for long term oxygen therapy
give 2L via nasal prongs for at least 15 hours per day
75
what are the only two things that can prolong the life expectancy in COPD
smoking cessation and LTOT
76
what are the goals of pharmacological management in COPD
To reduce the rate of exacerbations
To provide symptomatic relief
77
example of a SABA
salbutamol – 200μg every 4-6 hours
78
example of a LABA
salmeterol
79
example of a SAMA
. ipratropium – 40μg 4x a day
80
example of a LAMA
tiotropium
81
examples of ICS
beclomethasone, fluticasone
82
what is step one in inhaler treatments - typically used for mild disease
Step 1 – SABA or SAMA – short acting drugs that are bronchodilators – Typically corresponds with mild disease
83
what is step 2
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
what should you not use with LAMA
a SAMA
85
what is step 3
Add ICS – a single inhaler combined LABA/LAMA/ICS may be appropriate – typically corresponds with severe disease
86
what are the benefits of inhalers
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
what is the brand name for salbutamol
Ventolin
88
what is the brand name of tiotropium
Spiriva
89
what is reduced when you give LTOT
the pulmonary arterial pressure
90
what are the indications for LTOT
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
what is type two respiratory failure a result of
alveolar hypoventilation
92
how do you treat type II respiratory failure
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
what is cor pulmonale
right sided heart failure, as a result of pulmonary hypertension
94
what are the obstructive lung diseases
COPD
asthma
bronchiectasis
CF
95
what are the characteristics of OLD
‘Obstructive pattern’ on PFT’s – see below
Disease mechanisms affect the bronchi and bronchioles, usually in a diffuse pattern across the whole lung
96
what is the obstructive pattern lung disease
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
what are examples of restrictive lung disease
pulmonary fibrosis
sarcoidosis
obesity
98
what is RLD caused by
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
what is the restrictive pattern in lung disease
Reduced FVC
Reduced FEV1
Normal FEV1:FVC ratio
Normal PEFR
100
what are the main causes of restrictive lung disease
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
look up and learn the MRC dysnponea scale
102
what is the type of cancer developed from asbestos exposure
at risk of asbestosis and mesothelioma. Asbestos exposure also increases the risk of lung cancer, in particular adenocarcinoma.
103
what can exposure to birds cause
hypersensitivity pneumonitis
104
is chronic productive cough common in COPD or asthma
in COPD
105
is night time waking with SOB/wheeze common in COPD or asthma
asthma
106
what are the hallmark symptoms of COPD
shortness of breath
chronic cough
sputum production
107
what is the genetic predisposition to COPD
alpha-1 antitrypsin
108
what is the only intervention that will slow disease progression in COPD
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
what is the steps that result in cor pulmonate
1. hypoxia
2. pulmonary artery vasoconstriction
3. increased pulmonary artery pressure
4. right ventricular hypertrophy
5. right ventricular failure
110
what are the three treatments used for COPD that are not used for asthma
LAMA
theophylline
carbocisteine
111
what is magnesium used for
Magnesium is a bronchodilator typically used for treating acute exacerbations of asthma, and rarely used in acute exacerbations of COPD.
112
what are brand names for LABAs
oxis
serevent
113
what are brand names for LAMAs
Spiriva
seebri
114
what are brand names for LABA+ICS
fostair (formoterol and beclomethasone)
seretide (salmeterol and fluticasone)
Symbicort (formoterol and buydesonide)
115
what are the triple therapy inhaler brand names (LABA+LAMA+ICS)
Trelegy Ellipta (fluticasone + umeclidinium + vilanterol)
Trimbow (beclomethasone + glycopyrronium + formoterol)
116
what is type one respiratory failure defined by
a PaO2 of less than 8kPa. It indicates a serious underlying pathology with the lungs such as infection, oedema or a shunt.
117
what is type II respiratory failure defined by
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
what are the correct management steps for acute exacerbation of COPD
- 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
