COPD Flashcards
Whats the pathophysiology of CoPD?
Chronic bronchitis:
1. Airway narrowing-> airflow limitation
2. Result of hypetrophy
3. And hyperplasia of muscus (goblet) cells of bronchial tree
4 bronchial wall inflammatio
5. Mucosal oedema.
Epithelial cell layer may ulcerate and when healed- squamous epithelium may replace the columnar (squamous metaplasia).
Inflamatory changes-
Lead to ciliary dysfunction, increased goblet size and number –> Xs mucus secretion + retention. Resp for decreased airflow, hypersecretion, chronic cough.
Both cases- changes are progressive and usually not reversible.
Empysema-
1. Dilatation and 2. Destruction of lung tissue distal to terminal bronchioles (alveoli).
3. Changes lead to loss of elastic recoil (normally keeps airways open during expiration.
↪️ assc w/ airflow limitation and air trapping.
Pink buffers- not cyanosed.- not perfused well.
Final outcome of inflammatory responses- elastin breakdown and subsequent loss of alveolar integrity.
Blue bloaters- chronic bronchitis - cyanosed+ barrel chest. (Gasp for air)
Usually they have both.
Chronic inflammation - affects central airways, peripheral airways, lung parenchyma and alveoili + pulmonary vasculature.
Narrowing + remodelling of airways, imcreased number of goblet cells, enlargment of mucus secreting glands in airways, and finally,
Subsequent vascular bed changes to leading to pulmonary HTN.
Activated macrophages, neutrophils and leukocytes are the core cells in these processes.
‼️Asthma- eosinophils. COPD- occasional acute exacerbation.
Whats the aetiology of COPD?
Smoking- activates macrophages and airway epithelia- release neutrophil chemotactic factors - IL8 + leukotriene B4. Neutrophils + macrophages release ptoteases that break down connective tissue in lung parenchyma –> emphysema + stimulate mucus hypersecretion.
Proteases are normally inhibited by a1- antitrypsin but in COPD- balance tipped in proteolysis.
In contrast to asthma- broncial wall infiltrate is predominally CD8+ (cytotoxic )T cells.
A1- antitryprsin deficiency- rare cause of early-onset emphysema.
Smoking-
Inflamatory response, cilia dupysfunction, oxidative injury.
Oxidative stress and imbalance of proteinases and antiproteinases.
Air pollution and occupational exposure.
What are some clinical features of COPD?
Cough
Production of sputum
Wheeze
Breathlessness, following many years of smokers cough.
Frequent infective exacerbations- purulent sputum.
O/E-
Severe- breatlessness at rest w/ prolonged expiration + use of accessory muscles (scalenes + sternocleidomastoid) , chest expansion poor, + hyperinflated lungs.
Pink buffers- breathlessness ! Not cyanosed.
Blue bloaters- hypoventilate - cyanosed, oedematous, features of CO2 retention (flapping tremor of outstreched hands, warm peripheries, bounding pulse, confusion in severe cases. )
How would u investigate COPD??
Hx, SOB, sputum production, physical examination, confirmation of airflow limitation with LFTs.
LFTs- spirometry
⬇️ FEV1 ⬇️ FEV1/FVC ratio
FBC- anaemia? ⬇️ eosinophils, ⬆️ neutrophils (polycythaemia)
CXR- pneumonia?
What are some complications?
Resp F 1+2
Cor pulmonale
(pulmonary resistance is increased due to destruction of pulmonary vascular bed and pulmonary vasoconstriction caused by hypoxia and acidosis. Ecentually,mincreased resistance leads to RH strain, and right ventrucular failure.
What are some other causes of exacerbations?
Result of pneumothorax(CXR) , HF( echo) PE( CTPA) and these must be excluded.
Prognosis- initial post bronchodilator FEv1- only 10% of pts with FEv
What the characteristics of COPD?
Irriversible airflow obstruction/limitation, prograssive (gradual onset) assc w/ persistent inflammatory response of lungs.
Developed- smoking
Umberal term- airway obstr- 1. Chronic bronchotos 2. Empysema.
Symptomatic after middle age.
If before-
Early onset emphysema -a1- antitrypsin deficiency.
Increased airway resistance. Due to:
Decreased elastic recoil,
Fibrotic changes in lung parenchyma + luminal obstruction of airways by secretions.
Expiratory flow limitation promotes hyperinflation. + destruction to lung parenchyma- predispose COPD pts to hypoxia during exercise.
Progressive hypoxia–> vascular smooth muscle thickening w/ subsequent pulm HTN (late development- poor prognosis).
How would you manage COPD?
MDT- GP, resp nurse, resp physicians, physiotherapy, occupational therapy, dietetics, pallative care in emd stage COPD.
Cessation of smoking- nicotine replacement- transdermal patch, gum, inhaler, bupropion tablets.
Step 1. SABA and anticholinergics (ipatropium bromide) (inhalers or nebulizers) - spacer better
Step2. LABA (salmeterol, formoterol) mostly or LAMA - tiotropium, . If >2 exacerbations per year. NOT steroids.
Step 3. Steroids- combined LABA + steroid inhaler. Inhaled beclometasone in all who FEV1 2 exacerbations per year.
O2 therapy only for those who stopped smoking. And have PaO2 90%.
If sputum purulent give antibiotics- amoxicillin 500mg, 3x day 1week.
Yellow–> green sputum–> exacerbation, give mucolutics: oral carboasteine.
Offer oral prednisolone 30mg 7-14 days.
Give rescue packs - amoxicilline and prednisolone to keepmat home- educated on how to use.
Pulmonary rehab-
Offer to all pts with COPD esp recent hospitalisation for an exacerbation + those who consider themselves functionally disable.
Not suitable for ppl who cannot walk, have unstable angina or had MI.
Assesment of reversibility made with 2week course of prednisolone 30mg with measurment of LFTs before and after trx period. If FEV1 improvment >15% decrease dose and then put on inhaled steroids.
What do u use if penicilline allergic?
If penicillne allergy- erythromycin( diarrhoea) so use clarithromycin.
How do u prevent infx in COPD patients?
Prevention of infx-
Acute exacerbations commonly due to bacterial or viral infx. Should receive pneumococcal vaccine and annual influenza vaccination.
What are some additional tx for COPD?
Venesection of polycythaemia,
diuretics for oedema, exercise training to improve sens of well being and breathlessness
Calorie Dietary supplements to increase BMI.
What happens in an acute exacerbation of COPD?
Prone.
Diagnosed with 1.increased breathlessness, 2.wheeze, 3.Production of increased volume of purulent sputum.
Major compl- resp failure.
Commonest- B or V infx (Haemophilus influenza)
Mild- at home- resp teams- can visit up to 4x a day.
How would u manage an cute exacerbation of COPD who is admitted?
1.O2- 88-92%
Depend on hypoxaemia to maintain resp drive so O2 by Venturi mask (fixed-performance mask) low conc 24%_ not precipitating worsening yoercapnia and resp acidosis.
If ABGs do not show hypoventilation, CO2 retention and worsening acidosis O2 increases (28 then 35%)
2.
Bronchodilators - salbutamol and ipatropium bromide - air given nebuliser- + oral or IV coricosteroids. (30mg prednisolone)
3. Antibiotics - cefaclor, co-amoxiclav if hx of more purulent sputum or CXR changes. Cough sputum- culture–> narrow spec.
4.
Pts with life threatening resp F- require ventilatory assistance- bilevel positive airway pressure. (BiPAP) failing to respond in initial bronchodilators.
- Resp stimulant ; doxapram by slow iv infusion- helpsmshort term to arouse oatient to stimulate coughing with clearance of secretions.
RARE.
Airflow obstruction in COPD: what happens?
Remodeling !
⬆️ resistance of small conducting airways(not so elastic)
⬆️ compliance of lung due to emphysema.
What happens to the airways?
Disruption of epithelial bartier
- Poor mucociliary clearance
- Infiltration of airway walls by inflamatory cells.
- Deposition of connective tissue in airways
- Repair leads to remodelinh, rhickened airway walls, reduced diameter, + restricts the normal increase in diameter when inflating the lungs.
Broncioles: lose their shape, clogged w/ mucus.
