COPD

Question 1

COPD definition?

Answer 1

Common, preventable and treatable disease that is characterised by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.

Question 2

What does COPD represent?

Answer 2

A spectrum of disease in which several pathological processes occur

Question 3

Prevalence of COPD?

Answer 3

• common lung condition
• 2-15% in industrialised countires
• thord most common cause of death and 5th most common cause of disability globally
• more common in men - those over 40 - becomes more common with age
• prevalence increasing in women by next decade = COPD will effect men and women equally

Question 4

Aetiology of COPD?

Answer 4

→ most encountered risk factor = tobacco smoke
→ 80% COPD patients have significant smoking history

Other environmental risk factors:

• indoor air pollution e.g. biomass fuels used for indoor cooking + heating
• occupational dusts/chemicals
• marijuana smoking

Question 5

Genetic risk factors of COPD?

Answer 5

• a1-antitrypsin deficiency affecting 2% of COPD patients

A deficiency createas a protease-antiprotease imbalance, resulting in unopposed neutrophil elastase action and thus alveolar destruction and early onset emphysema.

Question 6

What is a-1 antitrypsin?

Answer 6

A serum acute-phase protein produced in the liver; it acts as an antiprotease in the lung and inhibits neutrophil elastase.

Question 7

What is neutrophil elastase?

Answer 7

A protein released by neutrophils during inflammation to destroy bacteria and host tissue.

Question 8

What are the 3 overall (general) stages of COPD and what occurs?

Answer 8

𝑶𝒙𝒊𝒅𝒂𝒕𝒊𝒗𝒆 𝒔𝒕𝒓𝒆𝒔𝒔
Oxidants in cigarette smoke act directly on epithelial and goblet cells, causing inflammation.

𝑰𝒏𝒇𝒍𝒂𝒎𝒎𝒂𝒕𝒐𝒓𝒚 𝒄𝒆𝒍𝒍 𝒂𝒄𝒕𝒊𝒗𝒂𝒕𝒊𝒐𝒏
Cigarette smoke stimulates epithelial cells, macrophages + neutrophils to release inflammatory mediators and proteases (neutrophil elastase).

𝑰𝒎𝒑𝒂𝒊𝒓𝒆𝒅 𝒎𝒖𝒄𝒐𝒄𝒊𝒍𝒊𝒂𝒓𝒚 𝒄𝒍𝒆𝒂𝒓𝒂𝒏𝒄𝒆 𝒕𝒉𝒖𝒔 𝒍𝒆𝒂𝒅𝒊𝒏𝒈 𝒕𝒐 𝒓𝒆𝒕𝒂𝒊𝒏𝒆𝒅 𝒎𝒖𝒄𝒖𝒔 𝒔𝒆𝒄𝒓𝒆𝒕𝒊𝒐𝒏𝒔
Cilia damaged within ME so are unable to beat the mucus out of the lungs in the same way, leaving mucus behind (retention of secretions).

Question 9

What is emphysema (pathological process) ?

Answer 9

→ cigarette smoke induces the release of neutrophil elastase from neutrophils
→ in healthy lung tissue - antiproteases neutralise these proteases; however in COPD the volume of proteases produced overwhelms antiproteases.
→ destroys alveolar attachments
→ destruction in connective tissue which holds alveoli open (septa)
→ septa broken down - alveoli destroyed - airways collapse = airway obstruction
→ air is trapped in lungs which cannot escape (as airways have collapsed)

Question 10

What does destruction of the parenchyma (from emphysema) lead to?

Answer 10

Increased compliance of the lung and causes a mismatch in ventilation:perfusion

Increased compliance i.e. reduced elastic recoil of the lungs, means the lungs do not deflate as easily, contributing to air trapping.

Bullae (dilated air space >10mm) form, which may rupture, causing pneumothoraces (collapsed lung).

Question 11

FRC changes in a person with COPD?

Answer 11

Lungs are hyperinflated - cannot breathe fully out making it difficult to take deep breaths.

TLC same as normal breathing.
RV and FRC elevate (static airtrapping)

During exercise in COPD, FRC begins to increase as Vt increases, and the TLC begins to increase, indicating dynamic hyperinflation along with increased air trapping.

Question 12

What is chronic bronchitis? (pathological process)

Answer 12

MUCUS HYPERSECRETION
→ Cigarette smoke causes hyperplasia and hypertrophy of mucus secreting glands found in the submucosa of the large cartilaginous airways.

→ Hyperplasia of the intraepithelial goblet cells occurs at the expense of the ciliated cells in the lining epithelium. Less cilia increasing risk of retained secretions. Regions of epithelium may undergo squamous metaplasia.

→ Small airways become obstructed by intraluminal mucus plugs, mucosal odema, smooth-muscle hypertrophy and peribronchial fibrosis. Secondary bacterial colonisation of retained products occurs.

Question 13

What is the result of mucus hypersecretion?

Answer 13

Sputum left behind (warm + wet) = breeding ground for bacteria which could lead to infection.

Question 14

What is hyperplasia?

Answer 14

An organ or tissue increases in size due to an increase in the number of cells e.g. more mucus secreting glands

Question 15

Clinical features of COPD?

Answer 15

• progressive shortness of breath
• reduced exercise tolerance
• persistent cough
• chronic sputum production
• weight loss and peripheral muscle weakness or wasting may occur (due to not wanting to move as much because of lung condition).

Question 16

Diagnosis and investigations for COPD

Answer 16

Spirometry can be used to diagnose COPD

A postbronchodilator forced expiratory volume in 1 second (FEV!)/forced vital capacity (FVC) ratio of <0.7 (70%) confirms the presence of persistent airflow limitation and thus COPD.

Question 17

GOLD stages of COPD in relation to percentage of predicted FEV1 value?

Answer 17

mild = 80%
moderate = 50-79%
severe = 30-49%
very severe = less than 30%

Question 18

Management of COPD?

Answer 18

→ Management is holistic and incorporates both pharmacological and conservative treatments

→ There is no cure for COPD and no treatment available that can reverse the damage caused to the lungs by exposure to tobacco smoke or other noxious particles

→ The aim of treatment in COPD is to control symptoms and reduce exacerbations of disease

Question 19

What is pulmonary rehabilitation?

Answer 19

→ One of the few interventions in COPD proven to reduce symptoms, improve QOL and survival.

→ Pulmonary rehabilitation normally occurs in an outpatient setting with MDT aiming to coordinate optimum management.

→ Courses usually last 6-12 weeks and aim to improve patients’ exercise tolerance and provide management strategies enabling patients to cope with symptoms of breathlessness.

Question 20

What drugs can be used for a COPD patient?

Answer 20

• Inhaled bronchodilator therapy - controls symptoms of breathlessness
• Initially, patients start with a short-acting B2 - Agonist (SABA) and or short-acting muscarinic antagonist (SAMA) inhaler, using only when symptomatic
• Then long-acting inhalers (LABA + LAMA)
• Inhaled cortiosterioids may also be added in at a later stage - combination inhalers and variety of different delivery methods available to ensure effective drug delivery.
• As disease progresses further = triple inhaler therapy: LAMA,LABA AND ICS

Question 21

Typical physiotherapy problems for those with COPD?

Answer 21

→ increased work of breathing
→ dyspnoea
→ retained secretions
→ reduced exercise tolerance

Question 22

What treatment methods could be applied to a COPD patient?

Answer 22

→ ACBT - breathing control, thoracic expansion (with hold), cough/huff
→ positions of ease
→ pacing
→ if in ward, vibrations + shaking
→ bubble PEP
→ pursed lip breathing
→ breathing retraining with metronome
→ relaxation