COPD

Question 1

Define COPD

Answer 1

A heterogenous lung condition that exhibits chronic respiratory symptoms e.g., dyspnea due to abnormalities of the airways e.g., bronchi/alveoli, that cause persistent & often progressive airway obstruction

COPD is an obstructed airway which results in a reduction in flow of air

Question 2

Describe the key features of COPD

Answer 2

1. Chronic inflammatory disease that causes airway obstruction
2. Patients have obstructive spirometry
3. COPD is not fully reversible
4. Obstruction is progressive
5. Often caused by smoking. but genetic & environmental factors may be involved
6. Patients may experience flare-ups

Question 3

What does COPD also refer to?

Answer 3

Chronic bronchitis
Emphysema
Chronic irreversible asthma

Question 4

Define chronic bronchitis

Answer 4

The prescence of chronic/recurrent increase in bronchial secretions great enough to be coughed up. Secretions must be present for a minimum of 3 months per year during most days

It refers to long-term inflammation of the bronchi

Question 5

Define emphysema

Answer 5

Refers to abnormal enlargement of the alveoli with a destruction in alveoli walls

An indicator is an increased T cell and macrophage count
Alveolar walls are lost by loss of epithelial and endothelial cells

Emphysema results in loss of elastic recoil, creating high compliance and airway obstruction, reducing SA and increasing dead space in the airways. Loss of elasticity results in gas trapping/hyperinflation where air remains in alveolus during expiration
Barrel chest will develop which indicates chronic overinflation

Question 6

Describe the differences between chronic bronchitis and emphysema

Answer 6

Emphysema is a disease of the lung parenchyma whereas chronic bronchitis is a disease of the airways

Question 7

What is the impact of COPD in the UK?

Answer 7

900,000 ppl are diagnose
Costs 800 mil annually
Currently 4th in leading death cause, rose to 3rd in 2020
1-8 emergency admissions
82 people die daily
Takes up 1 mil+ beds annually

Question 8

What are the risk factors of COPD?

Answer 8

1. smoking
2. high exposure to dust & fumes
3. low birth weight
4. recurrent resp infections
5. chronic IV drug use
6. Genetic predisposition

Question 9

Describe the pathophysiology stages of COPD

Answer 9

1. Airway inflammation & remodelling
2. Development of emphysema: gas trapping, impaired gas exchange & airflow limitation
3. Oxidative stress

Question 10

Describe S1: Airway inflammation & remodelling

Answer 10

Chronic inflammation is triggered by exposure to irritants e.g., smoking
Immune system defends against toxins via:
-epithelium acting as a physical barrier to foreign bodies
- The mucocillary escalator removes foreign particles
- Inflammatory response can remove pathogens, e.g., increased conc of macrophages
- long-term changes occur tissue heals, but increased connective tissue forms leading to remodelling

Question 11

Describe the role of WBC in airway inflammation

Answer 11

Macrophages and nuetrophils release cytokines and chemotactic factors as well as proinflammatory cytokines, proteases and growth factors

Question 12

Describe the effects of inflammatory mediators on the airways

Answer 12

They cause fibrosis of airways resulting in the narrowing of airways, increased mucus production & hyperplasia (overgrowth) of goblet cells.
Impairs the cillia lining so less mucus can be cleared from the airways which creates a greater risk of infections

Question 13

Describe the effects of inflammatory mediators on the alveolar walls

Answer 13

There is an imbalance between proteases and antiproteases
The proteases digest connective tissue such as elastin & collagen, this leads to the destruction of the alveolar wall & supporting structures destruction.
This causes an increase in air space formation (bullae), creating a reduction in lung elasticity

Question 14

Describe remodeling and mucociliary dysfunction

Answer 14

TGF-B, a growth factor stimulates fibroblast production which produce collagen and an extracellular matrix.
This forms as scar tissue, resulting in the narrowing of the airways

Mucus glands become enlarged in airway walls, leading to increased mucus production and impairment of the mucociliary escalator. This results in mucus accumulation and reduction in airflow.

Question 15

Describe oxidative stress

Answer 15

Occurs when there is an imbalance between free radicals and antioxidants (over-production of free radicals & reduction in AO)
Free radicals react with other molecules resulting in harmful oxidation

OS is caused by inhaled toxins, which cause inflammation, the release of elastase to digest elastin (protease), and the inactivation of anti-proteases.
This results in abnormal tissue repair, alveolar wall obstruction & Mucus hypersecretion.
Antiproteases protect the lung tissue from action of proteases

Question 16

Describe the genetic predisposition for COPD

Answer 16

Having a A1AT defciency can result in a genetic predisposition to COPD as it can lead to lung & liver damage

A1AT is needed to protect lung tissue from damage via trypsin, a deficiency therefore results in an imbalance between proteases and antiproteases
A1AT is formed, but is misshapen so cannot leave the liver
This occurs in 1-3000/5000 people
It gradually results in emphysema.
It can be triggered by mild smoke exposure

Question 17

What are the symptoms & signs of COPD

Answer 17

Symptoms: Cough, SOB, regular sputum production & frequent chest infections

Signs:
1. Clubbing of fingers
2. Cyanosis
3. Ankle oedema
4. Raised JVP
5. Wheezing
6. Chest hyperinflation

Additional features:
1. Weight loss
2. fatigue
3. waking at night
4. Resp failure
5. chest pain
6. Hemoptysis

Question 18

Describe the effects of emphysema e.g., on ventilation

Answer 18

Emphysema patients have an increased expiratory time, they breathe slower & more deeply to max ventilation. patients may have pursed-lip breathing to increase positive end expiratory pressure (PEEP) to prevent airway collapse.

Effect on ventilation:
Neutrophils produce elastase to target elastic fibers around the alveoli
The destruction of alveolar walls results in reduced ventilation due to elastase. Proteases destroy capillaries & therefore reduce perfusion.
Ventilation & perfusion are both therefore reduced, creating a matched deficit.
O2 & CO2 are well maintained, however PO2 eventually drops and CO2 increases

Question 19

Describe the effects of chronic bronchitis on ventilation

Answer 19

Bronchoconstriction & increased mucus production causes a chronic cough & wheezing.
The inability to ventilate alveoli leads to an imbalance between ventilation/perfusion which can cause hypoxemia & hypercapnia

Hypercapnia causes a drop in pH & cause resp acidosis
Hypoxemia will lead to polycythemia (blood thickens) as RBC number increases
Cyanosis occurs due to resp acidosis, hypoxemia and polycythemia

Question 20

Describe the effects of chronic bronchitis on ventilation (continued)

Answer 20

Hypoxia causes the vasoconstriction of pulmonary capillaries causing increased pulmonary vascular pressure & pulmonary hypertension.
Pulmonary hypertension can cause R-Side HF, which reduces bloodflow returning to L-side, this overall reduces CO & circulating blood volume.

A reduction in blood volume activates the RAAS causing oedema & fluid retention

Question 21

What is the effect of COPD in spirometry

Answer 21

Narrowed airways cause a reduction in airflow and prolonged expiration,

This causes a reduction in FEV1, a normal FVC, but a reduced FEV1/FVC % ratio,
An obstructed spirometry

As severity increases gas trapping & hyperinflation causes an increase in residual volume. The FVC may then also become reduced. The FEV1/FVC ratio will be in the lower limit number

TLC & RV increases due to hyperinflation.

Bronchodilators do not reverse effects

Question 22

Describe the psychosocial effects of COPD

Answer 22

Can have a mental effect, not seek treatment due to self-blame for being a smoker.

It can cause a strain on family dynamics, as COPD patients are limited to what they are capable of, limits ability to work

Question 23

Describe the treatment available for COPD

Answer 23

1. smoking cessation
2. Pharmacological therapy e.g., bronchodilators, oxygen, corticosteroids & others
3. Non-pharmacological therapy e.g., diet, end of life plans, self-care & surgery

Question 24

Define smoking cessation

Answer 24

Refers to the process of quitting smoking, overcoming physical addiction & psychological habits in order to improve health & wellbeing

This can be done by:
- group therapy
- online support
- nicotine replacement therapy e.g., patches, gum, nasal & mouth spray, lozengers and E-cigs
- stop smoking medication e.g., Zyban or Champix

Question 25

Describe the side effects of nicotine replacement therapy

Answer 25

1. Patches can cause skin irritation 2. Nasal spray can cause irritation of nose, eyes or throat 3. Symptoms of dizziness, stomach issues & headaches 4. It can cause sleep disruption & vivid dreams

Question 26

Describe the function of bronchodilators

Answer 26

They are used to relieve bronchoconstriction by relaxing the smooth muscle around the bronchioles. This enables easier airflow In COPD beta2-agonist & antimuscarinics are used. Despite COPD being irreversible bronchodilators are used to reduce lung hyperinflation to improve resp muscle function & better overall function

Question 27

Describe beta2-agonists & anticholinergics

Answer 27

anticholinergics e.g., Atrovent or spirivia, block the parasympathetic maintenance of bronchial tone and are more effective in COPD patients than asthma as there is increased parasympathetic activity in COPD. Receptors are most present in central airways Beta2-agonists e.g., Ventolin, relax the smooth muscle in airways, receptors are more prevalent in peripheral airways Beta2-agonists and anticholinergics work well together as they act on different receptors, at different locations & take different forms of action. This makes them have a great combined effect on bronchodilator pathways

Question 28

Describe the use of corticosteroids in treatment for COPD

Answer 28

They can be used to reduce inflammation as by inhaling steroids they have the ability to alter genes within leukocyte nuclei to dampen down inflammation. Recommended for those with severe COPD & give in combination with beta2-agonist and anticholinergic drugs. Overall, it reduces exacerbation rates, normal spirometry and health status, but does create a higher risk of pneumonia.

Question 29

Describe the use of combination inhalers in the treatment of COPD

Answer 29

Combo inhalers help reduce frequency of flare-ups & manage symptoms. They consist of a bronchodilator and a steroid medication. There is a large range of combo inhalers that can be used e.g., a short acting bronchodilator and a low dose of steroids or a much longer acting bronchodilator with higher doses of steroid. This ensures patient receives all their medication without having to inhale from multiple devices Triple therapy: includes drugs of LAMA, LABA & ICS

Question 30

What does LAMA, LABA, SAMA & SABA stand for?

Answer 30

LAMA: Long acting antimuscarinic agent LABA: long acting Beta2 agonist SAMA: Short acting antimuscarinic agent SABA: Short acting beta2-agonist

Question 31

Describe other drug therapy involved in COPD treatment

Answer 31

1. Antimicrobials are used to reduce likelihood of chest infections and reduce flare-ups 2. Mucolytics e.g., carbosteine reduces the volume of mucus production, reduces obstruction of the airways 3. Oxygen, can increase quality of life & exercise ability, used for those with type 2 resp failure, minimum usage of 15hrs per day 4. Treatment of anxiety and depression e.g., therapy or antidepressants

Question 32

Describe type 1 resp failure

Answer 32

Occurs when there is lack oxygen in the blood (hypoxaemia) despite normal or low levels of carbon dioxide (CO₂) in the bloodstream. It is characterized by low arterial oxygen levels (PaO₂), less than 60 mmHg, while carbon dioxide levels (PaCO₂) are normal or low ( less than 50 mmHg). This condition results in insufficient oxygen being delivered to tissues and organs, Known as a failure in gas exchange, there is a mismatch in ventilation & perfusion This could be due to diffusion impairment, which affects the alveolar-capillary membrane, reducing the ability of oxygen to diffuse into the blood, such as ILD Shunting of alveolar hyperventilation can also contributes.

Question 33

Describe type 2 resp failure

Answer 33

Described as a pump failure, lungs cannot effciently ventilate to remove excess CO2 resulting in hypercapnia. Damage or deformities in the respiratory muscles can cause type 2 resp failure as it reduces ability to ventilate effciently, shunting and increased dead space can also affect ventilation

Question 34

Describe O2 therapy on CO2 retention

Answer 34

In COPD patient they have a reduced sensitivity to CO2, the drive ti breathe is intitated by low O2 levels, known as the hypoxic drive. By supplementing O2 they hypoxic drive will be reduced leading to hypoventilation. This can lead to hypercapnia & lead to resp acidosis, where the blood pH drops and becomes more acidic. A pH of 6.8 or less is FATAL

Question 35

Describe the adv and disadv of O2 therapy

Answer 35

ADV: increases survival and improves haemodynamics DISADV: needs to be used for a minimum of 15hrs per day, does not relieve breathlessness, requires a prescription. Requires counselling and assessment

Question 36

Describe self-care, pulmonary rehab & surgery in treatment for COPD (non-pharmacological)

Answer 36

Self-care: patients are encouraged to take responsibility for their disease, Patients are recommended to get vaccines such as yearly flu jab, COVID & pneumonia. We provide patients with general advice & long-term treatment options e.g., bronchodilator Pulmonary rehab: aims to promote Exercise & educate patients. Encourage patients to exercise to increase tolerance, reduce breathlessness & increase muscle strength. As well as educating them on nutrition, COPD meds, Living with COPD and benefits/financial claims they can make Surgery: involves a range of procedures such as Bullectomy (removal of bullae), transplant, Lobectomy (removal of a lung lobe)

Question 37

Describe dietary changes, non-invasive ventilation & palliative care in treatment for COPD (non-pharmacological)

Answer 37

Diet: patients should aim to eat in a calorie deficit if they have a large BMI to lose weight, as well as eating nutritious and high protein foods to aid in muscle repair Non-invasive ventilation: use of a BiPAP machine Palliative care: patients and their family should be aware of end-stage diagnosis, as it can prevent death from uncontrollable/distressing symptoms, ensure cultural and spiritual needs are met & be aware that death for a patient may be imminent, helps the family prepare for life after the loss

Question 38

What can we do to improve COPD management

Answer 38

1. Early diagnosis to enable early treatment 2. Smoking cessation 3. Vaccinations 4. Practice inhaler technique 5. Education 6. Appropriate referrals e.g. O2 assessment & nutrition