COPD

Question 1

Nice definitiion

Answer 1

Airflow obstruction, usually progressive, Not fully reversible and does not change markedly over several months. caused by smoking

Question 2

Two main componenets of COPD

Answer 2

Chronic bronchitis

Emphysema

Question 3

Chronic bronchitis

Answer 3

the production of sputum on most days for at least 3 months in at least 2 years (when other causes of chronic cough have been excluded)

Question 4

Emphysema

Answer 4

abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles

Question 5

Risk factors

Answer 5

Cigarette smoking
Environmental pollution, burning of biomass fuels, occupational dusts
Alpha 1 anti-trypsin deficiency

Question 6

Pathophysiology of COPD

Answer 6

• In chronic bronchitis, there is airway narrowing, and hence airflow limitation, as a result of hypertrophy and hyperplasia of mucus secreting glands (airways >4mm in diameter) of the broncial tree, bronchial wall inflammation and mucosal oedema
• The epithelial cell layer may ulcerate and when the ulcers heal, squamous epithelium may replace collumnar epithelium (squamous metaplasia)

Emphysema

• Emphysema is defined pathologically as dilation and destruction of the lung tissue distal to the terminal bronchioles.
• Emphysematous changes lead to loss of elastic recoil, which normally keeps airways open during expiration
• this is associated with expiratory airflow limitation and air trapping

Pathogenesis

• cigaette smoke causes mucous gland hypertrophy in larger airways
• leads to chronic inflammatory cell infiltrate (CD8 T lymphocytes, macrophages and neutrophils in the airways and walls of bronchi and bronchioles
• These cells release inflammaotry mediators (elastases, proteases, Il-1 and 8 and TNF-alpha)
• This attracts inflammatory cells (and further amplify the process), induce structural changes and breakdown connective tissue (protease-antiprotease imbalance) in the lung parenchyma result in emphysema
• Alpha-1 antitrypsin is a major protease inhibitor and is inactivated by cigarette smoking
• Infections (viral and bacterial) may play a role in maintaining inflammation.
• Cigarette smoke interferes with ciliary action of the respiratory epithelium.

Question 7

Small airway disease

Answer 7

• early process in the development of COPD
• airways 2 - 3 mm in diameter, “ bronchiolitis”
• goblet cell hyperplasia
• narrowing of the bronchioles due to mucus plugging, inflammation and fibrosis

Question 8

Centri-acinar

Answer 8

damage around respiratory bronchioles, upper lobes

Question 9

Pan-acinar

Answer 9

acini are uniformly enlarged from level of respiratory bronchiole to terminal blind alveoli. Lower zones, can get large bullae (associated with alpha 1 anti-trypsin deficiency)

Question 10

Paraseptal

Answer 10

distal portion of acinus affected, can form enlarged airspaces 0.5>2cm in diameter

Question 11

Irregular emphysema

Answer 11

acinus irregularly invovled

Question 12

Respiratory failure in COPD

Answer 12

V/Q mismatching in areas of emphysema and air trapping leads to hypoxaemia
Loss of diffusing surface area and loss of respiratory drive causes raised PaCO2

Question 13

Clinical features of COPD

Answer 13

Consider the diagnosis of COPD for people who are over 35, and smokers or ex-smokers, with any of

• exertional breathlessness
• chronic cough
• regular sputum production
• frequent winter ‘bronchitis’
• wheeze

Question 14

Spirometery results in COPD

Answer 14

Spirometry- Obstructive Pattern - i.e. FEV1/FVC ratio < 70 % (both reduced)

Severity defined by FEV1(compared to predicted)

Question 15

Investigations in COPD

Answer 15

Spirometery- see other card

CXR

• overinflation, low and flattened diaphragms, bullae, pruned blood vessels with large proximal vessels and relatively little blood visible in peripheral lungs

HRCT chest -

• if in doubt about diagnosis - look for emphysematous changes

Blood tests:

• FBC - polycythaemia (raised Hb and PCV) if has chronic hypoxaemia

Sputum cultures -

• Send for analysis in acute exacerbations
• Common pathogens - Strepococcus pneumoniae, Haemophilus influenzae

BMI

• Low BMI (<21) associated with poorer prognosis

ABG - see other slides (pink puffer, blue bloater)

ECG- If signs of cor pulmonale

Question 16

Pink puffer

Answer 16

• high respiratory drive, ↓PaO2, ↓PaCO2, desaturates on exercise, Type 1 Respiratory failure
• O/E - pursed lip breathing, use accessory muscles, wheeze, indrawing of intercostals, tachypnoea

Question 17

Blue bloater

Answer 17

• low respiratory drive, ↓PaO2, ↑PaCO2, right heart failure (oedema), Type 2 respiratory failure
• O/E - confusion, drowsiness, cyanosis, wheeze, hypoventilation, warm peripheries and bounding pulse, flapping tremor, peripheral oedema

Question 18

Scale to assess level of breathlessness in COPD

Answer 18

MRC Dyspnoea Scale - used to assess level of breathlessness in COPD

Grade 1: Dyspnoea on strenuous exercise.

Grade 2: Short of breath when hurrying or walking up a slight hill.

Grade 3: Walks slower then contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace

Grade 4: Stops for breath after walking about 100 meters or after a few minutes on level ground

Grade 5: Too breathless to leave the house, or breathless when dressing or undressing

Question 19

Management of stable COPD

Answer 19

Step 1

• Short acting Muscarinic Agonist (SAMA) – Ipratropium Bromide or
• Short acting Beta Agonist (SABA) – Salbutamol

as required

Step 2

If patient has exacerbation’s or persistent breathlessness (FEV1<50%) give:

• LABA + Inhaled Corticosteroid (combination inhaler)

or

• LAMA (Tiotropium)

Step 3

If patient had persistent exacerbations & breathlessness give:

LABA + LAMA + Inhaled Corticosteroid

Question 20

Other pharmacological therapies

Answer 20

Oral corticosteroids - only used in short courses for exacerbations of COPD

Mucolytics - e.g. carbocysteine often prescribed; help in sputum expectoration

Oral theophyllines - may be used in some cases

Question 21

Other therapies in COPD

Answer 21

Smoking cessation - only intervention shown to slow disease progression

Pulmonary Rehabilitation - exercise programme to improve general fitness

Vaccinations - influenza (annually), pneumococcus (5 yearly)

Diet - weight loss is recommended if the patient is obese to reduce respiratory effort. A low BMI is associated with impaired pulmonary status, decreased diaphragm mass, lower exercise capacity and increased mortality rate. Therefore, nutritional supplemenetation may be necessary

Self management plan- on how to respond promptly to symptoms of an exacerbation. Rescue course of antibitocs and corticosteroids at home with advive when to start (eg sputum becomes purulent

Question 22

How to assess long term prognosis in COPD patients

Answer 22

The Bode index is a new scoring system that incorporates

• Body Mass Index
• Airflow Obstruction
• Dyspnoea (MRC)
• Exercise (6 minute walk test)

It predicts mortality of COPD,

Higher score promotes a worse prognosis

Question 23

Acute management of COPD

Answer 23

Assess severity!- symptoms, ABG, CXR

ONAP

O- oxygen - controlled 24-28%, regular ABGs at 1 hours aim to maintain spO2 without increasing paCo2. Patients depend on degree of hypoxaemia to maintain respiratory drive and therefore, low concentrations of oxygen are given via a venturia mask so as not to reduce respiratory drive.

N- neubuliser - nebulised salbutamol 2.5-5mcg and ipratropium bromide 0.5mg qds, consider IV aminophylline if not improving

Antibiotics- if signs of bacterial infection (purulent sputum, increased sputum volume, increase WCC, increased CRP)

Predisolone - steroid 30-40mg OD

DVT prophylaxis (LMWH), monitor fluid balance and nutrution, manage co-morbidities

Patients with life-threatening resp failure willl require ventillatory assistance. Bilevel positive airway pressure (BiPAP) avoids the need for intubation and mechicanical venitilation/

Question 24

Genetics of COPD

Answer 24

Alpha 1 antitrypsin defiency

• 1-3% of COPD patients
• serine protease inhibitor
• M alleles normal variant
• SS and ZZ homozzygotes have clincial significane

unable to counterbalance destructive enzymes

Question 25

Indications for the use of Non-Invasive ventilation

Answer 25

• Non-invasive ventilation (NIV) (eg bi-level positive airway pressure (BPAP) should be considered for any patient with respiratory acidosis/hypercapnia and worsening respiratory distress (RR> 30/min) who have failed to respond to optimal medical treatment and controlled oxygen
• Worsening respiratory acidosis on treatment is a sensitive indicator of a deteriorating patient and may require admission to ICU
• Respiratory stimulants are rarely used to increasing availability of non-invasive ventilator support. Doxapram 1.5-4.0 m/min by slow IV infusion may help in short term to arouse the patient and to stimulate coughing

Question 26

Indications for home oxygen therapy

Answer 26

• This can prolong life expectancy of COPD patients. Longer it is given the greater the increase in life expectancy.
• Assessment for home oxygen should include blood gas measurement made 3 weeks apart in a stable patient receiving bronchodilator treatment
• Should be given @1-2L/min via nasal prongs for at least 15 hours a day. This aims to achieve improved survival rates (50% improvement in 3 year survival)
• Qualifiying criteria
  
  • pO2 <7.3pKa (on two separate occasions when COPD is stable at least 3 weeks apart)
  • pO2< 8pKa with evidence of secondary polycythaemia, nocturnal hypoxaemia or evidence of cor pulmonale
• warn patient about risk of fire and explosion with smoking