COPD Flashcards
Causes
smoking environmental pollution alpha-1 trypsin deficiency occupation Chronic asthma passive/maternal smoking
investigation
Spirometry:
FEV1/FVC <70%
PEFR
Lung function tests:
-increased RV and TV due to trapped air from respiration
CO exchange tests
-decreased TLCO and KLO which are indications of the measure of gas exchange
Chest Radiogram : HYPER-INFLATED CHEST
-flattened diaphragm
-increased anterior-posterior diameter
-bullae
Blood count: increased WBC
BMI
Minimal response to treatment- ICS and SABA
Blood gases show reduced Pa02/ increased PaCo2
Sputum sample to look for bacteria/pathogens
signs
Cyanosis Accessory muscle used Breathing through pursued lips Reduced chest expansion Hyperinflated chest- BARREL CHEST prolonged expiration Tachypnea hyper resonance on percussion
symptoms
SOB- gradual onset with little exercise or at rest
cough- with little sputum production
Wheeze
Prolonged expiration: increases pressure in the lungs- prevents them from collapsing
Peripheral oedema
Cor pulmonale- due to Right heart hypertension
recurrent chest infection
weight loss
muscle mass loss
anxiety/depression
differences with asthma
over 35 year olds
no eczema
no nocturnal symptoms
sputum production
Non-pharmalogical treatment
- nutritional assessment
- psycological assessment
- smoking cessation
- flu vaccination
- pulmonary rehabilitation
Definition
Airflow obstruction in which most of the damage is irreversible though some can be improved by means of a bronchodilator
-Characterised by hyperinflation (emphysema) and airway obstruction (chronic bronchitis)
How does smoking lead to COPD
- contains reactive 02 free radicals- triggers an inflammatory response- inhibits the production of anti-proteases- increases proteases/elastase
- contains nicotine- triggers the production of neutrophils- increases elastase/protease
- inhibits the repair process/synthesis of elastin
- proteases are involved in the breakdown of debris and proteins
- leads to tissue damage- in alveoli= emphysema
consequences of smoking on FEV1 and COPD
20% of smokers develop COPD
Chances of developing COPD depends on pack years- if pack years is 20 high chance of COPD
In COPD patients non-smokers FEV1 falls at a rate of 30ml/year
In COPD patients who are smokers- FEV1 falls at a rate of 50-80ml/year
How does COPD develop?
Due to emphysema and/or chronic bronchitis
- thickening of airways
- build up of mucus in the lumen
- loss of elasticity- alveolar damage in particular loss of alveolar attachments
How does COPD present morphologically in large and small vessels?
In large vessels:
-proliferation of goblet cells- hyperplasia
-proliferation of mucous cells- hyperplasia
In small vessels:
-goblet cells present
-lots of inflammation and fibrosis
Alpha-1 anti-tripsin deficiency
Mutation: PiZZ
Normally: neutralises proteases released by neutrophils
How to treat acute COPD?
In order: 1 -Nebulised bronchodilator -IV Aminophylline -IV salbutamol 2 offer PREDNISOLONE- 40mg steroid for 5-7 DAYS 3 -antibiotics if sign of infection (macrolide, tetracycline or amino penicillin) 4 -Diuretic if oedema 5 consider hospital admission if very unwell -ventilate/intubate
When to give long term 02 ?
When Pa02< 7.3Kpa When Pa02 between 7.3 and 8 Kpa and -pulmonary hypertension -nocturnal hypoxia -Peripheral oedema
Pharmalogical treatment
-SABA If FEV<50% -ICS/LAMA -LAMA if FEV>50% 1 -LABA -LAMA 2- LABA +. ICS
IN worst case:
-ICS+ LABA +LAMA
