Week 4- COPD

Question 1

prevalence of COPD in over 45?

Answer 1

5%

Question 2

mortality of COPD 10yrs after diagnosis

Answer 2

50%

Question 3

currently COPD is the – leading cause of disease?

Answer 3

5th, by 2030 its predicted to be the 3rd

Question 4

Is COPD reversible?

Answer 4

it is both reversible and non reversible, the structural changes cant be undone

Question 5

Common symptoms of COPD

Answer 5

shortness of breath, wheezing, coughing and increased mucous production

Question 6

How many die from COPD?

Answer 6

1 in 20

Question 7

COPD prevalence increases with…

Answer 7

age. 29% of over 75s have COPD

Question 8

Causes of COPD…

Answer 8

1. Smoking
   
   • passive smoking incldued
   • life long smokers have a 1 in 2 chance of dev COPD
   • number 1 cause of COPD
2. Frequent lung infections as a child
   
   • causes decreased lung function
3. genetic reasons
   
   • alpha-1 def
4. occupational dust and chemicals
5. indoor smoke from wood, coals etc.

Question 9

COPD risk factors

Answer 9

• smoking is a major cause
  
  • cessations slows progression and can be best treatment
• gender
  
  • more males affected than females
• prematurity
  
  • predisposes to childhood chest infections
• asthma
  
  • seems to be an asthma and COPD overlap
• a1 antitrypsin deficiency
• e-cigarettes

Question 10

Major fetaures of COPD

Answer 10

• Progressive decline in lung functin
• chronic bronchitis
  
  • excessive phelgm/sputum, cough and breahtlessness
• emphysema
  
  • breakdown of alveolar walls, driven by elastase(from neutrophils) induced damage
• *most patients have both

Question 11

COPD pathology

Answer 11

• emphysema ( disrupted alebolar attachments)
• mucous hypersecretion
• inflammation, fibrosis increase inflammatory cells
• decreased alveoli–> decreased area for exchange –> decreased O2 supply–> feeling of breathlessness

Question 12

2 COPD presentations

Answer 12

1. blue bloater
   
   • clinical diagnosis: daily productive cough for 3 months or more, in at least 2 consecutive years
   • overweight and cyanotic(lack of O2)
   • elevated haemoglobin because body overcompensating for hypoxia
   • peripheral oedema
   • rhonchi and wheezing(related to cough)
2. pink puffer
   
   • path diagnosis: permanent enlargement and destruction of airspace distal to the terminal bronchiole
   • older and thin
   • severe dysponea
   • quiet chest
   • x-ray shows hyperinflation and flattened diaphragm
     
     • makes it harder to breathe out because of increased deadpsaces. the air goes in but doesn’t come out easily

Question 13

in compariosn to normal lung fucntion, COPD patients…

Answer 13

have a slower rate of expiration, decreased FEV1, reduced peak expiratory flow, and extreme coving. all fo these indicate obstruction

Question 14

non pharmacological treatments for COPD

Answer 14

assess severity via FEV1, identify and avoid risk factors, cease smoking, flu vaccine, treat co-morbidities, assess exercise capacity

Question 15

pharmacological treatments for COPD aim to…

Answer 15

• treat symptoms
• prevent exacerbations
• preferably, oral corticosteroids should be limited short-course post-exacerbation

a stepwise approach is recommended, irrespective of disease severity, until adequate control has been achieved

Question 16

Types of dilators of COPD

Answer 16

• M3 antagonists
  
  • oppose tonic parasymp drive (Ach)
  • reduces mucous
• B2-adrenoreceptors agonists
  
  • oppose all contractors
  • stimulates mucocillarly clearane
  • inhibits release of inflamm mediators from mast cells
• LAMA/LABA
  
  • combination of the 2 is preferred over short acting or single therpaires as we don’t see acute attacks in COPD
  • usually for additive dilator effects in COPD

Question 17

Why are LAMA/SAMAs more important for COPD?

Answer 17

Ach is more important in COPD than other allergic mediators to contract the airways

Question 18

Averse effects of M3 antagonists

Answer 18

• dry throat( local anti-SLUD)
• acute infection
• flu-like symptoms
• trouble breathing

Question 19

Adverse effects and limitations of B2 agonists?

Answer 19

• tachycardia via B1
• muscle tremor via B2
• mask inflamm
• potential for receptor down regulation
• densentisation/tolerance

Question 20

cigarette smoke exposure mouse models

Answer 20

1. peristalitic pump cigarette smoke exposure
2. nose-only cigarette smoke exposure
3. whole body cigarette smoke exposure

Question 21

After exposing a mouse model to smoke for 3 days…

Answer 21

increased inflammatory cells were found in flushed out lungs, increased cells in lung parenchyma but no remodelling in the short term

cigarette smoke also caused a twitchy contraction and gradual narrowing both to with increased exposure to bronchoconstriction

reduced/impaired relaxation to salbutamol after cigarette smoke exposure. the relaxation is not sustained in exposed models

Question 22

Corticosteroids for COPD

Answer 22

• Less effective in COPD than in asthma but it is still widely prescribed as we don’t have other treatments
• still targets inflamm but poor efficacy in reducing inflammation due to macrophages and neutrophils
• do not affect symptoms
• inhalation can still reduce frequency and severity of exacerbations
  
  • as eosinophils play a big role in exacerbations
• orally its used to treat exacerbations
  
  • only a short course to minimise adverse side effects

Question 23

The approved treatment for long term maintenance for moderate to severe COPD is…

Answer 23

daily triple inhaler therapy(LABA/LAMA/ICS)

as severity increases we introduce steroids aswell

Question 24

a1-antitrypsin deficiency and COPD

Answer 24

Alpha-1-antitrypsin is an endogenous substance that inhibits activity of the trypsin enzyme elastase. If the lungs lack a1-antitrypsin coating it leaves them open for damage by neutrophilic elastase( autodegradation occurs). The mutations means that the a-1-antitrypsin cannot lead the liver and causes liver damage.

Question 25

a1-antitrypsin replacement therapy

Answer 25

Question 26

Progression of COPD

Answer 26

Question 27

Elastase and MMPs in COPD

Answer 27

Question 28

effects of e-cigarettes

Answer 28