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Flashcards in COPD + OSA Deck (28):

Definition of COPD

Airway obstruction that is not fully reversible


Elements of COPD?

Obstruction occurs as a result of noxious stimuli like cigarette smoke causing damage to the alveolar septa and causing hypersecretion of mucous
It includes elements of both chronic bronchitis and emphysema


Pathophysiology? Brief summary

1. Smoke = noxious agent --> inflammation (proteinase-antiproteinase imbalance)
2. Causes small airway disease and parenchymal destruction
3. Loss of elastic recoil and airways collapse --> obstruction.

Breakdown in alveoli and destruction of pulmonary capillary bed --> this leads to increased pulmonary vascular pressures.

Proteinase-antiproteinase imbalance = excess production of elastinase from neutrophils outweighs alpha anti 1 proteinase and this leads to alveolar wall breakdown.


What is an acute exacerbation?

change in dyspnoea baseline, cough or sputum that are not day to day fluctuations


What criteria do we use for acute exacerbations?

Anthonisen criteria:
1. Increased dyspnoea
2. Increased sputum production
3. Sputum becomes discoloured


What can cause an acute exacerbation?

Infection, anxiety, heart failure, systemic infection etc.


What is pulmonary rehabilitation? who runs it? what are its two main components?

Program/course that runs over 6-8 weeks, that aims to reduce exacerbations and hospital admissions. 2 parts= education and improving fitness. Supervised by physiotherapists


treatment/management of COPD?

1. B2 agonists (bronchodilation)
2. Anticholinergics (bronchodilate almost as well as B2 agonists) --> tiotropium
3. Inhaled corticosteroids (not a lot of role to play in COPD long term, but it does reduce acute exacerbations in very severe COPD patients)
4. Combination therapy= seretide and symbicort
Make sure that the patient is up to date with influenza + pneumoccocal vaccinations


why do we see pursed lip breathing in a COPD patient?

In COPD, the airways are destructed by noxious stimuli like smoke leading to enlarged diffuse alveolar spaces (emphysema). During inspiration the airways and alveoli inflate with air, and during normal expiration, there is passive recoil, however the airways do not close. In emphysema, the airways close during expiration, and so some pressure is needed to keep it open. Hence patients will purse their lips during expiration


what scale do we use for diagnosing OSA?

Epworth sleepiness scale + overnight pulse oximetry


if CPAP does not work for OSA, then what can we give?

Modafinal, a CNS stimulant drug


what would you expect to see in an ABG of a patient with COPD and OSA?

high CO2 and HCO3-. Body compensates over time to accept a higher level of CO2


what might we see in the FBE for someone with long term COPD?

secondary polycythaemia due to hypoxaemia


how might we manage acute exacerbation of COPD in hospital?

1. Bronchodilator via nebuliser (salbutamol, ipratropium, terbutaline)
2. Corticosteroids (prednisolone or hydrocortisone)
3. Oxygen
4. Antibiotics


how many levels of severity are there for COPD?

4 stages; categorised by FEV1


what is the relationship between COPD and pneumothorax?

pneumothorax may occur if a bullous ruptures (emphysema)


how would we deal with nocturnal hypoxaemia for COPD patients?

Bipap machine


why might we be wary of giving O2 to a COPD patient?

Possibility that they may be a CO2 retainer. This is when inadequate removal of CO2 leads to a chronic hypercapneic state. When oxygen is delivered, there may be further suppression of respiratory drive and exacerbation of VQ mismatch, making the whole problem worse. However the chance of the COPD patient is a CO2 retainer is very low


If the patient is young, or has not been exposed to cigarette smoke, and has COPD- what would you consider?

alpha 1 antitrypsin deficiency


what are some characteristics of a COPD CO2 retainer seen at the end of the bedside?

Pink puffers- hypercapnia leads to cutaneous vasodilation which results in warm hands/peripheral. Also appears to be quite flushed in the cheeks


what is something you want to do in ED before administering oxygen to a COPD patient?

arterial blood gases


for paediatric OSA- what is the gold standard treatment?



what are some oral appliances to manage OSA?

mandibular advancement splint


what is central sleep apnoea?

apnoeas caused by reduction in respiratory drive


main cause of central sleep apnoea?

cardiac failure


causes of hypoventilation?

1. reduced respiratory centre
2. neuromuscular disease
3. chest wall deformity
4. Obesity
5. increased ventilation


what causes acute COPD exacerbations?

heart failure + arrhythmias


what is the pathophys of OSA?

sleep--> upper airway closes--> snores--> low o2, and Co2 rises--> increased respiratory effort--> arousal--> upper airways dilates--> falls asleep again--> daytime somnolence + compensated hypercapnia