Week 1/2 - D - COPD - Symptoms/risk factors, mechanism, diagnosis, treatment (pharmacology), acute management Flashcards

1
Q

In a sentence, try and define COPD?

A

COPD is a common progressive disorder characterized by airflow obstruction that in some patients is partially reversible and is associated with frequent respiraotry infections

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2
Q

What are the presenting symptoms of COPD?

A

A chronic productive cough, dyspnoea and wheeze Usually in an elderly smoker

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3
Q

What are the risk factors for COPD?

A

CIgarette smoking is the most important risk factor (and passive smoking) Exposure to noxious (harmful/poisonous) particles - air pollution or occupational exposure Genetic predisposition Age >35

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4
Q

Describe the mechanism of how smoking / other pollutants lead to the damage seen in the lung in COPD? Try and name the neutrophil chemotactic factors released

A

Cigarette smoking and other pollutants stimulate macrophages which release neutrophil chemotactic factors such as IL-8 and leukotriene B4 The neutrophils and macrophages then release proteases that cause damage to the lungs (will ask about the damage caused on the next flashcard)

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5
Q

What damage do the proteases released by the neutrophils and macrophages cause to the lungs? (try and separate into chronci bronchitis and empyhsema symptoms - not spearated nowadays)

A

Neutrophils and macrophages release proteases that: Emphsyema - break down connective tissue in the lungs leading to distension and damage to the alveoli Chronic bronchitis - stimulate mucus hypersecretion and inflammation of the bronchiis/bronchioles (productive cough)

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6
Q

In COPD there appears to be an imbalance between proteases and antiproteases (either an increase in proteases, or a deficiency of antiproteases) which lead to inflammatory changes in the airways including damage of the respiratory mucosa. What is the anti-protease that can be deficient and therefore cause a genetic predispotion to COPD? Patients usually present younger

A

Alpha-1-antrypsin is a protease inhibitor - a genetic deficiency of this may lead to increase protease causing damage to the lungs

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7
Q

Symptoms of COPD - A chronic productive cough, dyspnoea and wheeze Usually in an elderly smoker On examination of a patient, what are the signs that match COPD?

A

COPD * Patient usually tachypnoiec using accessory muscles of respiration * There is hyperinflation of the lungs - due to destroyed alveolar walls, loss of elastic recoil * Hyperesonant percussion * Quiet breath sounds on auscultation

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8
Q

What are the 1st investigations carried out when trying to diagnose a patient with COPD? (do not need to state why or what is expected to be seen just yet)

A

Spirometry is carried out Post-bronchodilator spirometry Chest x-ray FBC BMI

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9
Q

* Spirometry is carried out * Post-bronchodilator spirometry * Chest x-ray * FBC * BMI When are the three times spirometry is carried out when assessing a COPD patient? What is the expected result if positive?

A

Perform spirometry: at diagnosis to reconsider the diagnosis, for people who show an exceptionally good response to treatment to monitor disease progression. FEV1/FVC <0.7 is a positive result

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10
Q

For most people, routine spirometric reversibility testing is not necessary as part of the diagnostic process or to plan initial therapy with bronchodilators or corticosteroids. * In asthma, BDR needs to be FEV1 improvement .200ml or 12-15% increase What BDR would indicate the patient did not have COPD?

A

COPD patients usually show a poor bronchodilatory response (measuring FEV1 post-bronchodilation with salbutamol or terbutaline) A change in FEV1 >400ml however would make the COPD diagnosis be reconsidered

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11
Q

* Spirometry is carried out * Post-bronchodilator spirometry * Chest x-ray * FBC * BMI Why are chest xray and FBC carried out?

A

CXR is carried out to exclude other pathologies - would show hyperinflation of the lungs FBC is carried out to identify anaemia (of chronic disease) and potential secondary polycythaemia

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12
Q

Why would secondary polycthaemia occur in COPD?

A

Secondary polycythemia most often develops as a response to chronic hypoxemia, which triggers increased production of erythropoietin by the kidneys - cause an increased in number of red blood cells

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13
Q

If the person is not a current smoker, their spirometry is normal and they have no symptoms or signs of respiratory disease, what should be considered?

A

Alternative diagnose Alpha-1-antitrypsin deficiency

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14
Q

Untreated COPD and asthma are frequently distinguishable from Hx and exam in people presenting for the first time. Use longitudinal observation of people (with spirometry, peak flow or symptoms) to help differentiate COPD from asthma Are these symptoms asthma or COPD: * Smoker/ex smoker ; Symptoms under 35; Chronic productive couhg; Breathlessness; Night time waking with breathlessness and/or wheeze ; Significant diurnal or day-to-day variability of symptoms

A

https://s3.amazonaws.com/classconnection/403/flashcards/11907403/jpg/ppngjpgpngjpgpng-1713CA5751653019BED.jpg

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15
Q

Should the lung volumes be measured, what would happen to the lung volumes in COPD?

A

There would be an increase in Residual volume - minimal volume of air left in lung after maximal contraction Total lung capacity - hyperinflation of lungs due to alveolar wall destruction and loss of elastic recoil means more air Decrease in vital capacity - cannot exhale due to obstruction

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16
Q

What is step 1 in COPD management?

A

At every opportunity, advise and encourage every person with COPD who is still smoking (regardless of their age) to stop, and offer them help to do so. - smoking cessation Also give immunisations to influenza and pneumococcus

17
Q

What is one pack year and how is it calculated?

A

One pack year is defined a sa person who smokes 20 cigarettes a day, every day for one year Number of cigarettes smoked per day / 20 Then multiply by the number of years smoked (apparently 15 pack years

18
Q

What is the initial empirical treatment to relieve breathlessness and exercise limitation?

A

Offer patient a SABA or SAMA Short acting B2 adrenoreceptor agonist - salbutamol or terbutaline Short acting muscarinic antagonist - ipratroprium (non-selective)

19
Q

Human airways express M1, M2 and M3 muscarinic receptors at different locations Explain how they are active?

A

M1 muscarinic receptors -facilitate fast neurotransmission mediated by Ach M2 muscarinic receptors - act as inhibitory autoreceptors reducing release of ACh (blockade therefore increases release of ACh) M3 muscarinic receptor -ASM mediate contraction to ACh (also present on mucus-secreting cells evoking increased secretion)

20
Q

Why is their a functional desirability for LAMAs versus SAMAs (ipratropium)? LAMAs (tiotropium, glycopyrronium, aclidinium, umeclidinium) over ipratropium

A

Ipratropium non selectively blocks M1,2,3 receptors Block of M3 (and M1) is desirable, but block of M2 is not because release of ACh from parasympathetic post-ganglionic neurones is increased by inhibitory autoreceptor antagonism

21
Q

Stepping up from the SABA or SAMA Patients must have spirometry confirmed COPD and remain breathless or have exacerbations despite: * having used or been offered treatment for tobacco dependence if they smoke and * optimised non-pharmacological management and relevant vaccinations and * using a short-acting bronchodilator. How is the next step in therapy decided in COPD patients? What must COPD patients be aware of before taking steroids?

A

Patients are offered different treatment dependent on whether they have Asthmatic features / features suggesting steroid responsiveness Patients who take ICS should be aware of an increased risk of side effects (including pneumonia)

22
Q

What are Asthmatic features / features suggesting steroid responsiveness?

A

This includes * any previous, secure diagnosis of asthma or of atopy * higher blood eosinophil count >4%, * substantial variation in FEV1 over time (at least 400ml), * or substantial diurnal variation in peak expiratory flow (at least 20%)

23
Q

If a patient has Asthmatic features / features suggesting steroid responsiveness, what is the treatment? If a patient does not have Asthmatic features / features suggesting steroid responsiveness, what is the treatment?

A

Asthmatic features / features suggesting steroid responsiveness - prescribe LABA + ICS No Asthmatic features / features suggesting steroid responsiveness - prescribe LABA + LAMA

24
Q

In patients taking a LABA+ICS (features suggestive of asthma/steroid responsiveness), when is step up treatment offered and what is this?

A

Step up treatment is offered if: * 1 severe exacerbation (requiring hospitilisation) or * 2 moderate exacerbations or * day to day symptoms affecting quality of life Prescribe LAMA + LABA + ICS

25
Q

In patients taking a LABA + LABA (features not suggestive of asthma/steroid responsiveness), when is step up treatment offered and what is this? (for this step up, one option is a 3 month steroid trial, what would make you continue the steroids after the trial)

A

For people with COPD who are taking LAMA+LABA, consider LAMA+LABA+ICS if: they have a severe exacerbation (requiring hospitalisation) or they have 2 moderate exacerbations within a year. For people with COPD who are taking LAMA+LABA and whose day-to-day symptoms adversely impact their quality of life: consider a trial of LAMA+LABA+ICS, lasting for 3 months only-continue if symptoms have improved

26
Q

State the COPD manageemnt from smoking cessation all the way to LAMA + LABA + ICS

A

https://s3.amazonaws.com/classconnection/403/flashcards/11907403/png/ppngjpgpngjpg-1713CE8F1470A34FFBA.png

27
Q

When may long term therapy with domiciliary O2 be considered?

A

Only to be considered when person has: Clinically stable non-smokers with PaO2 <7.3kPa despite maximal treatment or (dont remember this, too much - PaO2 above 7.3 and below 8.0 plus disease related to COPD) eg secondary polycythaemia, peripheral oedema, pulmonary hypertension

28
Q

When are long term oral steroids considered for COPD? When are mucolytics considered? name one

A

Long term oral steroids are not normally recommeneded. May require low dose of oral steroids to continue if patient cannot be withdrawn following an acute exacerbation Mucolytics eg carbocysteine- for people with a chronic productive cough of sputum - reduces sputum viscosity

29
Q

When is prophylactic antibitoic therapy used in COPD and what is the drug of choice?

A

Consider azithromycin (a macrolide) in people with COPD who: * Do not smoke * Have optimised pharmacological management * AND * Continue to have frequent (4 or more in a year) or prolonged exacerbations

30
Q

What is the inhaled corticosteroid pneumonia triad? - the three reasons that increase the likelihood of pneumonia in COPD patients

A

There is * corticosteroid immunosuppression * impaired muco-ciliary clearance * altered lung microbiome

31
Q

An exacerbation is a sustained worsening of the patient’s symptoms from their usual stable state which is beyond normal day-to-day variations, and is acute in onset. What are the commonly reported symptoms of a COPD exacerbation?

A

Commonly reported symptoms are worsening of breathlessness, cough, increased sputum production and change in sputum colour Sputum changes from normal mucoid/yellow to a green colour

32
Q

A general classification of the severity of an acute exacerbation - mild, moderate, severe Mild exacerbation, the person has an increased need for medication, which they can manage in their own normal environment What is the difference between moderate and severe exacerbation?

A

Moderate exacerbation requires treatment with systemic corticosteroids and/or antibiotics Severe exacerbation - there is a rapid deterioration in resp status and patient requires hospitalization

33
Q

What investigations are carried out in a COPD exacerbation?

A

Pulse oximetry ABG and CXR if patient is in hospital FBC, CRP, ECG if hospital also

34
Q

What is the treatment algorithm for acute exacerbation of COPD? WHen are antibiotics given?

A

ISOAP * Ipratropium and Salbutamol nebulised (bronchodilators and reduced mucus secretion) * Give O2 if sats

35
Q

What are the antibiotics of choice in an acute exacerbation of COPD?

A

Antibiotics in acute exacerbation of COPD 1st line - amoxicillin If pen allergic - usually doxcycline (can try clarithromycin)

36
Q

If the patient fails to respond to the acute treatment (ipratropium/salbutamol, oxygen, antibiotics, prednisolne) What can be considered?

A

Consider non-invasive ventilation Noninvasive positive-pressure ventilation (eg, pressure support or bilevel positive airway pressure ventilation by face mask) is an alternative to full mechanical ventilation. Noninvasive ventilation appears to decrease the need for intubation, reduce hospital stay, and reduce mortality in patients with severe exacerbations