10. COPD Flashcards
What is COPD
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
how is COPD different to asthma
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%)
COPD clinically is a triad of which 3 things traditionally
emphysema
chronic bronchitis
small airway fibrosis
History:
what are the risk factors for COPD
tobacco smoking
indoor air pollution (ask about asbestos)
alpha-1 antitrypsin deficiency (leads to increased destruction of alveolar structures resulting in early onset emphysema)
History:
what is the usual presenting complaint in COPD
progressive dyspnoea and chronic productive cough
History:
what would your typical stereotypical patient present with
Suspect COPD in a long term smoker presenting with chronic shortness of breath, cough, sputum production, wheeze and recurrent respiratory infections, particularly in winter.
History:
name symptoms of COPD
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
History:
what things would be significant in the patients PMH in relation to dyspnoea
anxiety and depression cardiovascular disease lung or liver disease osteoporosis asthma
History:
what major thing in the patents FH would you ask in particular
if they have had any lung or liver disease but consider underlying causes such as alpha-1-antitrypsin deficiency
why could liver disease cause symptoms of dyspnoea
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.
what medication in particular could cause a patient to have a dry cough
ACEi
Examination:
name some examination findings
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
why would a patient have tachypnoea
due to increased neural respiratory drive to breathe
why would a patient have a wheeze on auscultation
due to inflammatory airway oedema and mucus obstructing the airway
why would a patient have pursed lips breathing
to increased airway resistance and therefore reduce expiratory flow limitation (and could have use of accessory muscles as well)
why would a patient have a palpable liver edge
due to hyper expansion so the liver is pushed down
name some signs of RHF
peripheral odema, hepatomegaly and raised JVP
name the important differential diagnosis for dyspnoea and a productive cough
Asthma bronchiectasis congestive heart failure lung cancer tuberculosis PE angina anemia
what features differentiate asthma from COPD
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
what features differentiate bronchiectasis from COPD
expect larger volumes of sputum
more frequent lower respiratory tract infections often starting in childhood
high resolution chest CT would show bronchial dilation
what features differentiate congestive heart failure from COPD
orthopnoea paroxysmal nocturnal dyspnoea history of cardiovascular disease final basal inspiratory crepitations elevated BNP in bloods echocardiogram would show reduced ejection fraction
what features differentiate lung cancer from COPD
weight loss
haemoptysis
chest X-ray and bronchoscopy would show the presence of tumour
what features differentiate TB from COPD
drenching night sweats
weight loss
positive sputum culture and microscopy
what features differentiate anaemia from COPD
would present more with fatigue and palpitations
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
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
how is COPD diagnoses
through clinical presentation plus spirometry
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)
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.
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
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
why would you carry out FBC
to look for polycythaemia or anaemia
polycythaemia (raised haemoglobin) is a response to chronic hypoxia
on an ECG what typical signs would you see if someone had cor pulmonale
peaked P waves and right axis deviation
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
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
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
what are the clinical features of hypercapnia
dilated pupils bounding pulse hand flap myoclonus confusion drowsiness coma
What can you offer a patient in regards to stopping smoking
professional advice
nicotine replacement
anti-depressant (bupropion)
nicotine receptor blocker (varenicline)
what medication works for symptom relief and what reduces the exacerbation frequency
inhaled bronchodilators - work for symptom relief
LABA and corticosteroids reduce exacerbation frequency
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)
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
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
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
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)
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
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
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
Give examples of the following class of inhalers, their common drug company names and the colour of the inhaler: LAMA
tiotropium (Spiriva)
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
give an example of an oral and an IV corticosteroid
oral - prednisolone
IV- hydrocortisone
give an example of a mucolytic
carbocisteine
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
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
what environmental factors can cause COPD
tobacco smoke exposure
cannabis
other smokes
mineral dust (eg coal, cadmium) - quite rare now
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
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
what is the major complication of COPD
cor pulmonale exacerbations pneumonia pneumothorax peripheral neuropathy cachexia
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
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
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
what is respiratory acidosis
this is where they are retaining CO2 (cant get rid of it) and so their blood has become acidotic
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
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
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
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
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
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
