COPD Flashcards
COPD is both a __________ and ____________ disease
restrictive and obstructive disease
Airway diseases are ___________
obstructive
Lung diseases are ___________
restrictive
COPD constitutes the following diseases/disorders…
chronic bronchitis
emphysema
COPD refers to a group of lung diseases that causes difficulty with breathing
In what ways does asthma differ from COPD ?
(biochemically?)
(later slide can be used)
reversibility with SABA
reversibility reflected with a reduction of eosinophils
List some symptoms of COPD
exertional breathlessness
chronic cough (reductive cough)
regular sputum production due to inflamed bronchi
frequent winter bronchitis
wheeze (can be occasional)
List some symptoms of COPD
exertional breathlessness
chronic cough (reductive cough)
regular sputum production due to inflamed bronchi
frequent winter bronchitis
wheeze (can be occasional)
Wheezing is a result of …
constriction of the airways
constriction of the bronchi
COPD has no clinical features of asthma. True or false
True
?? Inspirational/expirational wheezing
What are the characteristic of COPD presentation?
chronic symptoms- persistent and non-episodic symptoms
smoking
non- atopic (atopy is a predisposition to autoimmune responses to antigens; eczema, asthma, hayfever)
daily productive cough (mucous production due to bronchitis)
progressive breathlessness
Frequent infective exarcebations
chronic bronchitis- leads to wheezing
Emphysema- breathless sounds
What occurs in emphysema?
destruction of the alveoli/ air sacs
What assessments are required for COPD?
assess symptoms
assess the degree of flow limitation using spirometry (how much air goes in and out of the lungs)
assess the risk of exarcebations
assess comorbidities (heart disease, heart failure)
(assess effects on daily living)
How is COPD diagnosed?
there is no single diagnostic test
diagnosis of COPD relies on clinical judgement
clinical judgement of medical history, physical examination and spirometry to measure airway obstruction
Briefly outline the pathway for a COPD diagnosis
- consider COPD diagnosis based on patient history
- perform spirometry
- if no doubt- diagnose and start treatment
- reassess diagnosis in response to treatment
- consider COPD diagnosis based on patient history
- perform spirometry, if unlikely
-if still in doubt consider additional pointers - provisional diagnosis, start empirical treatment
- reassess diagnosis in view of response to treatment
How can you determine if a patient has a high risk COPD? (note: not high risk of)
use history of exarcebations and spirometry
high risk COPD; associated symptoms are worse; even worse lung function
What are indicators of high risk COPD?
two exarcebations or more withing the last yeaer
FEV1 < 50% of the predicted value
What is the most significant risk factor for COPD?
smoking
What are the hallmarks of COPD?
mucociliary damage (damage to lining of the bronchi)
inflammation (inflammation of bronchi)
tissue damage (alveoli and bronchi damage due to proteases)
What are the characteristics of COPD?
exarcebations
reduced lung function (FEV1 <50% of predicted value)
What are the symptoms of COPD?
breathlessness
worsening quality of life
What type of epithelium is the bronchi lined with ?
respiratory epithelium
pseudocolumnar epithelium whose function os to produce mucous
[cilia then sift the mucous into stomach (pH) or mouth (cough)]
the mucous sits on to of the respiratory epithelium that lines the bronchi
What is the consequence of the destruction of functional cilia?
stagnant mucous - increases the risk of infection; non moving fluid always increases the chance of infection (e.g. urine)
Give examples of agents that can cause damage to the cilia?
H. influenzae
smoking (noxious agent)
Briefly outline the disease process in COPD
cigarette smoke
alveolar macrophage releases neutrophil chemotactic factors, cytokines (IL-8), mediators (LTB4), oxygen radicals
acute inflammatory cells are attracted to the site (alveoli)
neutrophil releases proteases
Proteases are involved in the destruction of the alveolar wall (emphysema)
Proteases leads to mucous hypersecretion (chronic bronchitis)
this all leads to progressive airflow limitation
(protease inhibitors not enough to inhibit the action of protease and minimise collateral damage to tissue)
There is a ____________ imbalance in emphysema
protease (less anti-protease/protease inhibitor to minimise the effects)
There is also often a genetic predisposititon to not having enough anti-proteases and thus increasing the risk of developing emphysema
this therefore increases the ri
What is the consequence of the destruction of emphysema?
impaired gas exchange
there is less available tissue to exchange CO2 and O2
What are the hallmarks of chronic bronchitis?
chronic neutrophilic inflammation
mucous hypersecretion (due to damaged lining)
smooth muscle spasm and hypertrophy (bronchospasms; common symptom with asthma)
partially reversible
What are the hallmarks of emphysema?
alveolar destruction
impaired gas exchange
loss of bronchial support
irreversible
Briefly outline the chronic cascade in COPD
progressive fixed airflow obstruction
impaired alveolar gas exchange
respiratory failure - decrease in PaO2, increase in PaCO2
pulmonary hypertension
right ventricular hypertrophy/failure (cor pulmonale)
death
What is the consequence of an increased PaCO2?
acidosis; change/decline in pH; enzymes are affected by this; cell metabolism is affected by this
What is cor pulmonale? Why does it occur in COPD patients?
this is an abnormal enlargement of the right hand side of the heart as a result of diseases of the lungs or pulmonary vessels
occurs in COPD patients because more effort is required to pump blood lung that has all this scar tissue/damage
According the COPD treatment algorithm, how should patients at risk of COPD (cough sputum) be treated?
avoidance of risk factors/influenza vaccine
According the COPD treatment algorithm, how should patients with mild COPD (FVC<70, FEV >80% of predicted or no symptoms) be treated?
SABA (Short acting beta agonist)
According the COPD treatment algorithm, how should patients with moderate IIA COPD(FEV1/FVC <70%, 50% FEV, <80% predicted, +/- symptoms) be treated?
Regular (1 or more) bronchodilators
rehabilitation
According the COPD treatment algorithm, how should patients with moderate IIB COPD(FEV1/FVC <70%, =30% FEV, <80% predicted, +/- symptoms) be treated?
inhaled corticosteroids if it is a lung function response (alveoli)
According the COPD treatment algorithm, how should patients with severe COPD(FEV1/FVC <70%, FEV, <30% predicted, presence of respiratory failure or right heart
failure) be treated?
inhaled corticosteroids if lung function response or if repeated exarcebations
treatment of complications, surgery, LTOT
LTOT-long term oxygen therapy
Treatment of COPD is dependent…
the GOLD stage
GOLD 1 - mild: FEV1 ≥80% predicted.
GOLD 2 - moderate: 50% ≤ FEV1 <80% predicted.
GOLD 3 - severe: 30% ≤ FEV1 <50% predicted.
What are the non-pharmacological treatment options for management of COPD ?
smoking cessation +/- nicotine/bupoprion
immunisation- influenza/pneumococcal
physical activity
oxygen - domiciliary
venesection
lung volume reduction surgery
What are the pharmacological treatment options for management of COPD?
SAMA/LAMA- ipatropium/tiotropium
SABA/LABA- salbutamol/salmeterol
LAMA-LABA- glycopyrronium/indacaterol
LABA-ICS- salmeterol/fluticasone
PDE4I- roflumilast
Mucolytic - carbocisteine (break down mucous)
SAMA- short acting muscarinic antagonist
LAMA- long acting muscarinic antagonist
SABA- short acting beta agonist
LABA- long acting beta agonist
ICS- inhaled corticosteroids
Fluticasone, a novel steroid, is much stronger than beclamethasone. True or false
true
What is the long term side effect of taking synthetic steroids?
adrenal insufficiency
stops natural production of adrenal hormones (catecholamines, aldosterone)
What pharmacological interventions are used for the treatment of stable COPD?
broncodilators
beta agonist inhaler - salbutamol and terbutaline.
Antimuscarinic inhalers e.g. ipatropium
What are the most common agents in blue inhalers?
salbutamol
terbutaline
The effects of long acting bronchodilator inhalers are similar to those of short acting bronchodilator inhalers. What is the difference?
each dose of long acting bronchodilator inhalers can last up to 12 hour
long acting bronchodilators include LAMA and LABA
When are long acting bronchodilator inhalers indicated?
if symptoms remain troublesome despite taking a short acting bronchodilator
Give an example of SABA
salbutamol
Give an example of a SAMA
ipatropium
Give an example of a LAMA
Tiotropium
Give examples of LABA
salmeterol
formoterol
indicaterol
What is the only long-acting antimuscarinic inhaler?
Tiotropium
Inhaled corticosteroids are only licensed in COPD in combination with…
LABA
long acting beta agonist e.g. salmeterol
What is the aim of ICS therapy in COPD?
inflammation plays a central role in COPD (inflammation of bronchi walls, inflammation induced secretion of proteases) therefore ICS is aimed and halting and reversing inflammation
What is the effect of ICS therapy on COPD?
decrease the rate of exarcebation
improve response to bronchodilators
decrease dyspnoea in stable COPD
Outline the treatment of acute COPD
nebulised high dose of salbutamol (SABA) and ipatropium (SAMA)
oral prednisolone
antibiotic (amoxycillin/doxycycline) if infection
24-28% O2 titrated against PaO2/PaCO2
Physio to aid sputum expectoration (to aid coughing)
Non invasive ventilation to allow higher FiO2 (CPAP)-continuous positive airway pressure
ITU intubated assisted ventilation only if reversible component (e.g. pneumonia)
What is the function of CPAP?
(continuous positive airway pressure)
prevents the collapse of the airways as it maintains the pressure in them
it is very difficult to inflate already collapsed airways
Outline the differences between asthma and COPD
Asthma:
non smokers
allergic
early/late onset
intermittent symptoms
non productive cough
non progressive
eosiniophilic inflammation
diurnal variability (varies during day)
good corticosteroid response
good bronchodilator response
preserved FVE and TLCO (total lung capacity(
normal gas exchange
COPD:
Smokers
non- allergic
late onset
chronic symptoms
productive cough
progressive decline
neutrophilic inflammation (release proteases)
no diurnal variability (does not vary during the day)
poor corticosteroid response
poor bronchodilator response
reduced FVC and TLCO
impaired gas exchange
What is a pink puffer? How can you identify them?
pin puffers work hard to maintain the partial pressure of O2
They tend to have barrell shaped, hyperinflated chests and breathe through pursed lips
Breathing through pursed lips allows them to create pressure preventing the collapse of their lungs
What are blue bloaters?
Blue bloaters are blue due to hypoxia and polycythaemia
Polycythaemia due to compensatory overproduction of RBCs which reduces production of other blood cells. Increases viscocity of the blood
blue bloaters are often obese and have oedema
They are dependent on their hypoxia for their respiratory drive. Lack of oxygen keeps the lungs working to keep up with oxygen demand
What is contraindicated management of blue bloater COPD patients ?
giving large amounts of oxygen
oxygen should be delivered at very gradual levels
Oxygen delivery will deprive then of their respiratory drive leading to significant hypercapnia (increased partial pressure of carbondioxide) and thus an acid-base imbalance
List problems to consider in COPD patients
risk of infection (stagnant mucous)
chronic lung disease- cor pulmonale and heart failure
cough, sputum and resistance to antibiotics
emphysema- difficulty breathing when lying flat!
heart failure
treatment and side effects
steroids- ICS especially fluticasone (MRONJ)
Oxygen- hypoxic drive/respiratory drive
What are some outpatient COPD considerations?
steroids
position of patient- do not lie emphysema patient flat; harder for them to breathe
halitosis - sweet smell of pseudomonas
pink puffers and blue bloaters
candidal infection (ICS)
COPD rarely occurs in isolation. True or false
What other smoking related diseases can be caused?
True
ischaemic heart disease
