COPD Flashcards

1
Q

What does COPD stand for?

A

Chronic Obstructive Pulmonary Disease.

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2
Q

What is COPD?

A

This is a disease characterised by chronic bronchitis (inflammation of the lungs) and/or emphysema (constriction of the lungs) associated with airway obstruction and airway hyperreactiveiy. The disease cannot be cured, and is only partially reversible.

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3
Q

How does the disease start and then develop?

A

The disease starts off as obstructive, then develops to restrictive, destroying alvaeoli and reducing lung capicity.

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4
Q

What is the difference between Obstructive and Restricitve?

A

Obstructive: REduced airflow due to partial or complete obstruction. No change in total lung capacity.
Restrictive: Characterised by reduced lung expansion therefore leading to reduced total lung capcaity.

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5
Q

The cause of almost all COPD:

A

Smoking

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6
Q

What is the goal of management of COPD?

A

No cure, therefore goal is to reduce exacerbations and improve quality of life.
Stop Smoking is the best way to manage the progression of the disease.

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7
Q

What is the first-presnetaton that we would supect COPD?

A

> 35, with a ‘smoker’s cough’. Unlikely to see COPD any sooner because it takes time to progress.

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8
Q

What are the possible causes of COPD in the small % that are not smokers?

A

Passive smoking,
pollutants (where they used to work e.g. miners or cotton factory)
Rare genetic disease causing lung changes.

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9
Q

What is the COPD pathology.

A

Partially-reversible airflow obstruction. Inflammation is mainly driven by Neutrophils and not eosinophils (in ashtma), and predominently invades in the peripheral lung (towards the edges of the lung).
There is epithelial shedding, damage to cilia, oedema, and irreversible loss of lung elasticity. There is Emphysema also. There is no thickening of the basement membrane, no hypertrophy or hyperplasia which is different to asthma. COPD patients also have a hyper-reactive airway.

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10
Q

Is there mucous hypersecretion?

A

Yes but is less viscous than in asthma

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11
Q

What is Emphysema:

A

This is lung damage by inflammation of the alveoli, enlargement of the air spaces distal to the terminal bronchioles, reduced surface area and elasticity, airway collapse and therefore increased effort to breathe and flushed cheeks.

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12
Q

What Lymphocyte is involved in the COPD mechanism?

A

Type 1 T-helper lymphocyte (Th1)

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13
Q

What is teh mechanism of the disease?

A

Smoking or other irritants will cause a cascade of immune response mainly through resident macrophages in the lung through Th1. The end result is thinning (fibrosis) of the airways, Emphysema (less surface area for gas exchange), Alveolar wall destruction and mucous hypersecretion.

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14
Q

What are the Treatmetn options for managing the disease:

A
Main is remove irritant.
Corticosteroids
Beta agonists
Anticholinergics
Oxygen
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15
Q

How do corticosteroids work in this disease?

A

Work against eosinophils, not neutrophils therefore these are not effective for COPD. They also increase the risk of pneumonia

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16
Q

What is the first-line pharmacological treatment?

A

Sort acting bronchodilator inhaler:
1) SABA = short-acting Beta2 adrenoerceptor agonist.
e.g. Salbutamol or Terbutaline.
Immediate symptomatic relief by causing bronchodilation. They should be used before excericse to avoid an asthma attack.
or
2) Anticholinergics (Antimuscarinic inhalers) which block acetylcholine from causing bronchoconstriction e.g. Ipratropium
Both of these are used when required.

17
Q

What can be used if the 1st line treatment isn’t sufficient?

A

If more sever, regular inhaled treatment is required: A long-acting bronchodilator inhaler.
1) LABA = Long-acting Beta2adrenorecptor agonist e.g. Salmeterol with a onger duration of action of >12 hours. This drug must be given with a corticosteroid to avoid breakthrough attack e.g. Salmeterol + Fluticasone. Combination inhalers are available.
or
2) Long-acting antimuscarinic inhaler e.g. Tiotropium

18
Q

What if 2nd line therpay isn’t sufficient?

A

Triple therapy: Use a Combination inhaler of LABA and corticosteroid along with another inhaler of Long-acting antimuscarinic inhaler.

19
Q

If inhaled therapy isn’t sufficeint, what are the next steps?

A

Use oral Theophylline (xanthines) tablets which may prevent inflammatory cell activation and smooth muscle relaxation. They don’t give immediate relief of an attack, so still need SABA inhaler.

20
Q

What is the treatemtn in an emergancy episode of COPD exacerbation when B-agonists don’t work?

A

Aminophyline IV.

21
Q

What is the oxygen treatment?

A

RElieve symptoms, but patients have to carry it around in canisters which is bothersome.
Also danger of respiratory depression when too much oxygen is given.

22
Q

What is the efficacy of Corticosteroids in treating COPD?

A

Only reduce the exacerbations, they are not as effective as treating asthma because they targer eosinophils and not neutrophils.

23
Q

What are the investigations carried out to diagnose COPD?

A

1) spirometry - measure lung flow and capacity. Measure FEV1 and FVC. results are compared against predicted normal ranges and are base don sex, age, height, race. If the FEV <80%, and the FEV/FVC ratio is <0.7 then COPD possible
2) History and examination, smoking?
3) Chest x-ray
4) Full blood count
5) BMI