10. COPD Flashcards

1
Q

What is COPD

A

non-reversible, long term deterioration in air flow through the lungs caused by damage to the lung tissue

almost always a result of smoking

causes an obstruction to the flow of air through the airways making it difficult to ventilate the lungs and making them prone to infection

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2
Q

how is COPD different to asthma

A

the obstruction is not significantly reversible with bronchodilators such as salbutamol

does not change markedly over several months

asthma has reversible airway obstruction (ie by more than 15%)

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3
Q

COPD clinically is a triad of which 3 things traditionally

A

emphysema
chronic bronchitis
small airway fibrosis

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4
Q

History:

what are the risk factors for COPD

A

tobacco smoking
indoor air pollution (ask about asbestos)
alpha-1 antitrypsin deficiency (leads to increased destruction of alveolar structures resulting in early onset emphysema)

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5
Q

History:

what is the usual presenting complaint in COPD

A

progressive dyspnoea and chronic productive cough

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6
Q

History:

what would your typical stereotypical patient present with

A

Suspect COPD in a long term smoker presenting with chronic shortness of breath, cough, sputum production, wheeze and recurrent respiratory infections, particularly in winter.

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7
Q

History:

name symptoms of COPD

A

dyspnoea: initially exertion but can progress to resting dypneoa
chronic productive cough: usually colourless but may be green during LRTIs
recurrent LRTIs
fatigue
headache (due to Co2 retention)
wheeze
impact of symptoms on daily life and occupation
previous exacerbations or hosptialisation

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8
Q

History:

what things would be significant in the patients PMH in relation to dyspnoea

A
anxiety and depression 
cardiovascular disease 
lung or liver disease 
osteoporosis 
asthma
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9
Q

History:

what major thing in the patents FH would you ask in particular

A

if they have had any lung or liver disease but consider underlying causes such as alpha-1-antitrypsin deficiency

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10
Q

why could liver disease cause symptoms of dyspnoea

A

Ascites elevates the diaphragms and causes basilar atelectasis, which contributes to dyspnea and mild hypoxia

also

AAT, the alpha-1 protein, is mainly produced by the liver. The main function of AAT is to protect the lungs from inflammation caused by infection and inhaled irritants such as tobacco smoke.

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11
Q

what medication in particular could cause a patient to have a dry cough

A

ACEi

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12
Q

Examination:

name some examination findings

A
tachypnoea 
wheeze onausculation 
pursed lips breathing 
barrel chest
tar staining of fingers 
central cyanosis (if hypoxic or polycythhaemic) 
palpable liver edge 
cor pulmonate signs - signs of RHF such as peripheral oedema, hepatomegaly and raised JVP 
CO2 retention flap
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13
Q

why would a patient have tachypnoea

A

due to increased neural respiratory drive to breathe

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14
Q

why would a patient have a wheeze on auscultation

A

due to inflammatory airway oedema and mucus obstructing the airway

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15
Q

why would a patient have pursed lips breathing

A

to increased airway resistance and therefore reduce expiratory flow limitation (and could have use of accessory muscles as well)

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16
Q

why would a patient have a palpable liver edge

A

due to hyper expansion so the liver is pushed down

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17
Q

name some signs of RHF

A

peripheral odema, hepatomegaly and raised JVP

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18
Q

name the important differential diagnosis for dyspnoea and a productive cough

A
Asthma 
bronchiectasis 
congestive heart failure 
lung cancer 
tuberculosis 
PE 
angina 
anemia
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19
Q

what features differentiate asthma from COPD

A

asthma has;
diurnal variation in symptoms and peak flow
history of atopy
eosinophilia (blood and sputum)
lung function test would show bronchodilator reversibility

*note that COPD and asthma can co-exist

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20
Q

what features differentiate bronchiectasis from COPD

A

expect larger volumes of sputum
more frequent lower respiratory tract infections often starting in childhood
high resolution chest CT would show bronchial dilation

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21
Q

what features differentiate congestive heart failure from COPD

A
orthopnoea 
paroxysmal nocturnal dyspnoea
history of cardiovascular disease 
final basal inspiratory crepitations 
elevated BNP in bloods 
echocardiogram would show reduced ejection fraction
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22
Q

what features differentiate lung cancer from COPD

A

weight loss
haemoptysis
chest X-ray and bronchoscopy would show the presence of tumour

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23
Q

what features differentiate TB from COPD

A

drenching night sweats
weight loss
positive sputum culture and microscopy

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24
Q

what features differentiate anaemia from COPD

A

would present more with fatigue and palpitations

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25
during an acute exacerbation what differentials is it important to consider along COPD
``` pneumonia PE pneumothorax acute heart failure pleural effusion cardiac ischemia or arrhythmia lung cancer upper airway obstruction ```
26
Dyspnoea is graded using the medical research council (MRC) dyspnoea scale. What does grades 1-5 mean
grade 1- breathless on strenuous exercise grade 2- breathless on walking up a hill grade 3- breathless that slows walking on the flat grade 4- stop to catch their breath after walking 100m on the flat grade 5- unable to leave the house due to breathlessness
27
how is COPD diagnoses
through clinical presentation plus spirometry
28
what would spirometry show in someone with COPD
it would show an obstructive picture their FEV1 would be limited as being able to blow air out is limited by the damage to their airways causing airway obstruction. Therefore in COPD: FEV1/FVC ratio <0.7 (carried out 15-20 minutes after a SABA)
29
where post-bronchodilator FEV1/FVC ratio is less than 0.7, the severity of the airflow obstruction is graded in what way
Graded using the gold staging (global strategy for obstructive lung disease) according to reduction in FEV1 compared to appropriate reference value Stage 1, mild — FEV1 80% of predicted value or higher. Stage 2, moderate — FEV1 50–79% of predicted value. Stage 3, severe — FEV1 30–49% of predicted value. Stage 4, very severe — FEV1 less than 30% of predicted value or FEV1 less than 50% with respiratory failure.
30
describe the FEV1 and FVC in someone with COPD
the FEV1 is reduced a lot more significantly because there is obstruction of air escaping from the lungs FEV1/FVC ratio is reduced
31
what other investigations would you order along side spirometry
``` CXR FBC BMI sputum culuture ECG and echocardiogram CT thorax serum alpha-1 antitrypsin transfer factor for carbon monoxide (TLCO) ABG ```
32
why would you carry out FBC
to look for polycythaemia or anaemia | polycythaemia (raised haemoglobin) is a response to chronic hypoxia
33
on an ECG what typical signs would you see if someone had cor pulmonale
peaked P waves and right axis deviation
34
describe type 1 respiratory failure
type 1 is associated with damage to lung tissue which prevents adequate oxygenation of the blood low O2 with normal CO2 indicates serious underlying pathology with the lungs such as. infection, odema or shunt
35
describe type 2 respiratory failure
this is also known as ventilatory failure and is low oxygen with increased CO2 Reduced ventilatory effect can be a result of gas trapping , such as in severe COPD and severe asthma
36
how can the body try and compensate in type 2 respiratory failure
the body can try and use the bicarbonate buffering system and so the kidney are stimulated to reabsorb more bicarbonate
37
what are the clinical features of hypercapnia
``` dilated pupils bounding pulse hand flap myoclonus confusion drowsiness coma ```
38
What can you offer a patient in regards to stopping smoking
professional advice nicotine replacement anti-depressant (bupropion) nicotine receptor blocker (varenicline)
39
what medication works for symptom relief and what reduces the exacerbation frequency
inhaled bronchodilators - work for symptom relief LABA and corticosteroids reduce exacerbation frequency
40
what is the initial long term management for COPD
it is essential for people to stop smoking patients should also have the pneumococcal and annual flu vaccination step 1: short acting bronchodilator, either a SABA (salbutamol or terbutaline) or SAMA (ipratropium bromide)
41
if the patient is still limited by symptoms or having exacerbations whilst using a SABA or SAMA what is the step up in treatment if a) they have no asthmatic features b) if they have asthmatic features (such as previous diagnosis of asthma/atopy, increased blood eosinophils, diurnal variation of peak flow, variation of FEV1 over time)
a) LABA and LAMA | b) LABA and ICS
42
in what circumstance would you prescribe the patient LABA and LAMA and ICS
if they still have symptoms on dual therapy that impacts quality of life OR has 1 severe/2 moderate exacerbations a year
43
in severe cases of COPD what are some additional options for treatment
nebulisers (salbutamol and/or ipratropium) oral theophylline oral mucoltyic therapy to break down the sputum (eg carbocisteine)) long term prophylactic antibiotics (azithromycin) long term oxygen therapy at home
44
in what circumstances would home oxygen be considered
in Severe COPD that is causing problems such as chronic hypoxia, polycythemia, cyanosis or heart failure secondary to pulmonary hypertension (cor pulmonale)
45
``` Give examples of the following class of inhalers, their common drug company names and the colour of the inhaler: SABA ```
salbutamol (aka Ventolin, airomir) - blue MDI | terbutaline (bricanyl)- blue/white dry powder
46
``` Give examples of the following class of inhalers, their common drug company names and the colour of the inhaler: LABA ```
salmeterol (serevent) - green/blue MDI | formoterol (oxis)- dry powder
47
``` Give examples of the following class of inhalers, their common drug company names and the colour of the inhaler: SAMA ```
ipratropium bromide (atrovent) - clear with green lid MDI
48
``` Give examples of the following class of inhalers, their common drug company names and the colour of the inhaler: LAMA ```
tiotropium (Spiriva)
49
``` Give examples of the following class of inhalers, their common drug company names and the colour of the inhaler: inhaled corticosteroid ```
beclomethasone (becotide or clenil)- brown MDI Fluticasone (flixotide)- orange MDI budesonide (pulmicort)- dry powder
50
give an example of an oral and an IV corticosteroid
oral - prednisolone | IV- hydrocortisone
51
give an example of a mucolytic
carbocisteine
52
what is the generic name for some of the LABA&corticosteroid dual inhaler a) salmeterol & fluticasone b) formoterol & budesonide
a) seretide - purple MDI | b) Symbicort - white/red powder
53
what is the main genetic causation of COPD and describe this deficiency
alpha-1 antitrypsin deficiency people with this are more susceptible to damage from smoking major function is to protect lung tissue elastin from neutrophil elastase-mediated destruction
54
what environmental factors can cause COPD
tobacco smoke exposure cannabis other smokes mineral dust (eg coal, cadmium) - quite rare now
55
describe the pathological changes and how this relates to symptoms
``` goblet cell hyperplasia produces mucus - causes cough and sputum airway narrowing (partly through inflammatory repsone from toxins in tobacco smoke and also fibrosis/scarring) - causes breathlessness and wheeze alveolar destruction - causes breathlessness ``` there is a large presence of lymphocytes in the mucosa which mediate the tissue damage
56
how does the pathological changes in COPD lead to hypoxia and hypercapnia
there is airflow obstruction which leads to impaired gas exchange -progressive decline in lung function --> progressive dyspnoea and disability --> right ventricular failure --> exacerbations
57
what is the major complication of COPD
``` cor pulmonale exacerbations pneumonia pneumothorax peripheral neuropathy cachexia ```
58
how can COPD lead to cor pulmonale
hypoxia leads to pulmonary arterial vasoconstriction this leads to increases pulmonary artery pressure this leads to right ventricular hypertrophy this leads to right ventricular failure
59
what is the major cause of a COPD exacerbation
viral or bacterial infection | mostly due to rhino viruses (no treatment currently) and usually a H influenza
60
how does a COPD exacerbation present
acute worsening of symptoms such as cough, SOB, sputum production and wheeze usually trigged by a viral or bacterial infection
61
what is respiratory acidosis
this is where they are retaining CO2 (cant get rid of it) and so their blood has become acidotic
62
what parameter would be raised, suggesting they are chronically retaining CO2 and why is this the cases
raised bicarbonate as their kidneys have responded by producing more bicarbonate to balance the acidic CO2 and maintain a normal PH
63
what kind of oxygen mask can you use in a patient with COPD in order to manage their oxygen levels
a venturi mask as it can deliver a specific percentage concentration of oxygen
64
medical treatment of an exacerbation: | what is the typical treatment is the patient is well enough to remain at home
prednisolone 30mg once daily for 7-14 days regular Inhalers or home news antibiotics is there is evidence of infection
65
medication treatment of an exacerbation: | what is the typical treatment options if the patient is in hosptial
nebulise bronchodilators (eg salbutamol 5mg/4h and ipratropium 500mcg/6h steroids (eg 200mg hydrocortisone or 30-40mg oral prednisolone antibiotics is evidence of infection physiotherapy can help clear sputum
66
give some medical options in severe cases if the patient doesn't responding to first line treatment for exacerbation of COPD
IV aminophylline non-invasive ventilation (NIV) intubation and ventilation with admission to intensive care doxapram can be used as a respiratory stimulant where NIV or intubation is not appropriate
67
what is pulmonary rehabilitation
individually tailored, multidisciplinary care program for people with COPD which aims to optimize physical and psychological condition through exercise training, education, and nutritional, psychological, and behavioural interventions