Lower respiratory tract diseases - COPD Flashcards
what does COPD stand for?
chronic OBSTRUCTIVE pulmonary disease
what is COPD?
= airflow limitation that is not fully reversible
- airflow limitation is progressive & associated with an abnormal inflammatory response of the lungs to noxious particles or gases
what causes COPD?
long term exposure to toxic particles or gases
= SMOKING
is COPD referring to one singular condition or is it an overarching diagnosis?
it is an OVERARCHING DIAGNOSIS, brining together a variety of clinical syndromes associated with airflow limitation and destruction of lung parenchyma
what is the most consistent pathological finding in COPD?
- increased numbers of mucus-secreting goblet cells in bronchial mucosa
what happens to the bronchi & lumen in more advanced cases of COPD?
- bronchi becomes inflamed
- pus is seen in the lumen
what is seen microscopically to the walls of the bronchi and bronchioles?
- walls of bronchi & bronchioles are infiltrated with acute & chronic INFLAMMATORY CELLS; e.g. lymphoid follicles
what follows inflammation?
IMPORTANT
- scarring and thickening of the walls which narrows the airways
explain the balance between proteases and antiproteases?
- noxious particles increase the number of proteinases
- these are normally neutralised by anti-proteinase
- but this increase in proteinase upsets the protienase-antiprotienase balance allowing proteinases to digest the lung tissue
- effectively causing emphysema
what are the 3 main features of COPD?
1) hypersecretion of mucus
2) small airway obstruction
3) alveolar destruction
what are the 2 diseases that comprise COPD?
1) chronic bronchitis
2) emphysema
what is emphysema?
abnormal permanent ENLARGEMENT OF AIR SPACES, accompanied by DESTRUCTION of their WALLS & without obvious fibrosis
what is enlargement of the air spaces trough to be a secondary cause of?
small airway inflammation and destruction
how is emphysema classified?
- classified according to the site of damage;
1) CENTRI-ACINAR emphysema
2) PAN-ACINAR emphysema
3) IRREGULAR emphysema
where is the centri-acinar emphysema located?
- usually involves the upper part of the lungs
- changes spreading outwards, starting from the bronchioles
what is centri-acinar emphysema associated with?
substation airflow limitation
where is pan-acinar emphysema located?
- usually seen in lower part of the lungs
- alveoli are completely destroyed
in what people is pan-acinar seen in?
people with alpha 1 ant-itrypsin deficiency
what is pan-acinar associated with?
- severe airflow limitation
- Va/Q mismatch
what does emphysema result in?
- expiratory airflow limitation
- air trapping
- impaired gas exchange
- Va/Q mismatch
how do people with COPD cope with respiratory infections?
- they cope badly
- the infections are often the cause of an exacerbation of COPD
symptoms of COPD
- productive chronic cough, white or clear sputum
- wheeze
- breathlessness
(could be as severe as breathless after getting dressed) - colds settle on the chest
systemic effects;
- hypertension
- osteoporosis
- depression
- decreased muscle mass with general weakness
who is most likely to get COPD?
- mainly diagnosed in middle aged-elderly
- smokers of many years
are symptoms of COPD chronic or acute?
chronic
what is an exacerbation
= an acute change in a patients baseline dyspnoea, cough and/or sputum
what causes an exacerbation of COPD?
- changes in weather, e.g. cold or damp
- viral upper resp tract infection
- viral of bacterial bronchitis
what are signs of mild COPD?
- there are few signs
- just quiet wheezes throughout the chest
what are signs of severe COPD?
- tachypnoeic (rapid breathing)
- prolonged expiration
- accessory muscles of respiration are used
- chest expansion is poor
- lungs hyperinflated
- pursing on the lips on expiration
what are later stages of COPD associated with?
How could this respiratory failure be treated?
respiratory failure
- PaO2 < 8kPa
OR
- PaCO2 > 7kPa
- removal of retained secretions (cough up secretions)
- respiratory support (non-invasive ventilatory techniques)
- respiratory stimulants (e.g. doxapram)
- corticosteroids, antibiotici and bronchodilators can be used
what is pulmonary hypertension?
HIGH blood pressure
what causes pulmonary hypertension?
- chronic alveolar hypoxia and hypercapnia
- leads to constriction of pulmonary arterioles
how is COPD usually diagnosed?
- usually clinical, based on history of breathless & sputum production in a CHRONIC SMOKER.
if a patient has the symptoms of COPD but isn’t a smoker, what is the explanation most likely to be?
asthma
UNLESS, there is a family history of alpha 1 antitrypsin deficiency
what is alpha 1 antitrypsin?
= a proteinase inhibitor produced in the liver
- secreted into the blood and diffuses into the lungs
- it inhibits proteinases that are capable of destroying alveolar wall connective tissue
what happens if there is an alpha 1 deficiency?
the alpha 1 anti-trypsin accumulates in the liver, leading to low levels in the lungs
- so the proteinase isn’t being inhibited
- therefore it can destroy the alveolar walls & connective tissue
- leading to symptoms of COPD
how can the diagnosis of COPD be confirmed?
what would lung function pattern be?
by spirometry results that show IRREVERSIBLE AIRFLOW OBSTRUCTION
- PEFR reduced
- reduced FEV1
- reduced FVC
- FEV1/FVC ratio REDUCED
- FEV1 response to B2 agonists < 15%
in patients with COPD, what sit the FEV1 usually?
< 80%
- if the FEV1 is > or equal to 80%, a diagnosis of COPD is only made if there are respiratory signs of COPD
what is the ratio of FEV1/FVC that would show COPD?
< 70%
What would a chest X-ray show in a patient with COPD?
- relatively normal
- overinflation of lungs
- low, flattened diaphragm
- presence of large bullae
- blood vessels may be pruned
- large proximal vessels & relatively little blood visible in peripheral lung fields
what is the single most useful measure to help manage COPD?
tell them to stop smoking
give 3 examples of bronchodilators?
1) B-adrenoceptor agonists
2) theophylline
3) anti-muscarinic drugs
give an example of short acting B-adrenoceptor agonists (SABA)?
what do short acting B-adrenoceptor agonists do?
- e.g. salbutamol
- feel less breathless after inhaling one
in more severe COPD, what sort of b-adreneoceptor should be used?
= a LABA
= long acting beta-2 adrenoceptor agonists
give 3 examples of a LABA?
1) formoterol
- 12microgram powder inhaler, twice daily
2) salmeterol
- 50micrograms twice daily
or
3) indacaterol
- 150 to 130 mcirograms once daily
what do theophylline do?
- they are of little benefit in COPD
- but they may help control symptoms of dysponae & wheeze
what do anti-muscarinic drugs do?
they give more prolonged & greater bronchodilator
give examples of 2 long acting agents?
1) tiotropium (18micrograms daily)
2) aclidinium (375micrograms daily)
what are the drugs tiotropium and aclidnium preferred over?
they are prefered over ipratropium or oxitropium
what is tiotropiums effect?
- improves quality of life but doesn’t effect decline of FEV1
what drugs could be given to reduce sputum viscosity and reduce the number of exacerbations?
= ANTI-MUCOLYTIC AGENTS
e.g. carbocisteine 2.25g daily
when should corticosteroids be used?
- in symptomatic patients with moderate/severe COPD
what corticosteroid drug should always initially be given?
PREDNISOLONE, 30mg
- with measurements of lung function before and after the treatment period
if there is evidence of substantial improvement in airflow limitation (FEV1 increase of > 15%), what change should be made to the drugs?
- prednisolone should be discontinued
- replaced by INHALED CORTICOSTEROID (beclometasone, 40micrograms twice daily)
what effect do combinations of corticosteroids and B2 agonists have?
- protect against lung function decline
- don’t improve overall mortality
when should antibiotics be given?
- promptly in an exacerbation
- should always be given in acute episodes
why should they be given during exacerbations and acute episodes?
= prevent hospital admissions & further lung damage
what PaO2 value should long term oxygen therapy be offered to?
patients with PaO2 < 7.3 kPa (when breathing air)
what medical conditions allows long term oxygen therapy to given to people with a PaO2 of 7.3-8kPa?
people with;
- pulmonary hypertension
- secondary polycythaemia
- nocturnal hyperaemia
- peripheral oedema
- evidence of pulmonary hypertension
what value might the PaO2 drop to in patients with COPD during the night?
2.5kPa
= profound nocturnal hypoxaemia
what is pulmonary rehabilitation and how can it help patients with COPD?
= exercise training that. can modestly increase exercise capacity
- diminished sense of breathlessness
- improved general wellbeing
what other measures can be done for people with COPD?
1) regular vaccines
2) alpha 1 anti-trypsin replacement
- (weekly or monthly infusions)
3) surgery
- lung transplantaion
- surgical bullectomy
