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Pharmacy Stage 2 > Pathophysiology of COPD > Flashcards

Pathophysiology of COPD Flashcards

1
Q

What is COPD?

A

-persistent airflow limitation usually progressive and associated with an enhanced chronic inflammatory response in the airways and lungs to noxious particles or gases

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2
Q

What is the predominant cause of COPD?

A

smoking

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3
Q

What are the characteristics of the obstructed airflow in COPD sufferers?

A
  1. not fully reversible
  2. doesn’t change over months
  3. progressive in the long term
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4
Q

Two factors that contribute to the severity of COPD in patients?

A

Exacerbations and Comorbidities

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5
Q

When do exacerbations occur?

A

when symptoms worsen rapidly beyond normal day-to-day variations requiring a change in treatment.

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6
Q

Symptoms of COPD?

A
  1. chronic and progressive dyspnoea
  2. chronic cough
  3. chronic sputum production
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7
Q

Risk factors of COPD?

A
  1. genes

2. exposure to particles i.e. tobacco, dust, heating and cooking air pollution, outdoor air pollution

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8
Q

Two classes of COPD?

A
  1. chronic bronchitis

2. emphysema

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9
Q

what is chronic bronchitis?

A
  • a chronic cough with sputum production lasting at least 3 months
  • the bronchioles lose shape and are blocked with mucus.
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10
Q

what is emphysema?

A
  • a chronic cough caused by shortness of breath

- alveolar walls destroyed forming larger but fewer alveoli

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11
Q

what happens when an individual is exposed to COPD risk factors?

A
  1. neutrophils and macrophages accumulate in alveoli
  2. they become activated and release granules containing elastase and matrix metalloproteinases (MMP)
  3. resulting in damage and elastic tissue destruction
  4. hence inflammation
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12
Q

What is the protease/antiprotease imbalance theory?

A
  • this is when there is a deficiency in congenital or functional alpha1 anti-trypsin
  • hence causing an unbalance b/w the destructive protease activity and the protective antiprotease activity
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13
Q

define congenital and functional?

A

congenital - a trait since birth

functional - a trait developed as a result of an event

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14
Q

what is the consequence of tissue damage in the lung?

A

airway obstruction (dyspnoea)

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15
Q

Explain how tissue damage in the lungs causes dyspnoea in relation to elastic tissue?

A
  1. inflammatory infiltration of walls with neutrophils, macrophages, B cells and T cells
  2. loss of elastic tissue
  3. respiratory bronchioles collapse during expiration
  4. dyspnoea
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16
Q

Explain how tissue damage in the lungs causes dyspnoea in relation to thickening of bronchiole walls?

A
  1. Inflammatory infiltration of the walls with neutrophils, macrophages, B cells and T cells.
  2. Smooth muscle hypertrophy and fibrosis
  3. Bronchiole wall thickens
  4. Dyspnoea
17
Q

Explain how tissue damage in the lungs causes dyspnoea in relation to goblet cells?

A
  1. inflammatory infiltration of the walls with neutrophils, macrophages, B cells, T cells
  2. Goblet cell metaplasia with mucus accumulating in the lumen
  3. Dyspnoea
18
Q

What are the common causes of exacerbations?

A
  1. Viral upper respiratory tract infections

2. Infection of tracheobronchial tree

19
Q

What are the clinical presentations of COPD exacerbations?

A
  1. Dyspnoea
  2. Chest pain
  3. Cough
  4. Fever
  5. Altered mental status
20
Q

What are the comorbidities of COPD?

A
  1. Cardiovascular disease
  2. Osteoporosis
  3. Respiratory infections
  4. Anxiety and depression
  5. Diabetes
  6. Lung cancer
  7. Serious infections
  8. Bronchiectasis
21
Q

How is COPD diagnosed?

A
  • Using spirometry
  • chest radiograph
  • full blood count to check for anaemia and polycythaemia
  • BMI calculated
22
Q

What does a post-bronchodilator FEV/FVC value if less than 0.70 mean?

A

Shows presence of airflow limitations

Compare results to normal value for that age

23
Q

How can you differentiate between COPD an Asthma?

A
  1. If FEV AND FEV/FVC values return to normal after drug therapy
  2. If there’s a large response to bronchodilator or 30mg prednisolone after 2 weeks treatment
  3. Serial peak flow measurements show day-to-day variability
    (All these show signs of asthma and not COPD)
24
Q

What are therapeutic options for treating COPD?

A
  1. Smoking cessation (pharmacotherapy and NRT)
  2. Encourage regular physical activity
  3. Flu and pneumonia vaccines should be given
25
Q

Do any of the available treatments of COPD modify the long te decline in lung function?

A

Nope

26
Q

What are the two classes of bronchodilators?

A

Short-acting and long-acting

27
Q

What are short acting bronchodilators used to treat COPD?

A

They are bronchodilators that ease COPD symptoms that come and go.

28
Q

What are long acting bronchodilators used to treat COPD?

A

They are bronchodilators used to prevent breathing problems in those whose symptoms don’t go away.

29
Q

What are examples of short-acting bronchodilators?

A
  1. Anticholinergics (ipratropium)
  2. Beta2-agonists (albuterol)
  3. A combination of the two (ipratropium and albuterol)
30
Q

What are examples of long acting bronchodilators?

A
  1. Anticholinergics (tiotropium)
  2. Beta2-agonists (formeterol)
  3. Combination of the two
  4. Combination of beta2-agonist with a corticosteroid medicine
31
Q

Ipratropium is a muscarinic (m2) antagonist. How does this work as an anticholinergic?

A

Inhibits acetylcholine binding to muscarinic receptors on bronchial smooth muscle hence preventing signal transduction!

32
Q

What do anticholinergics do?

A

Dilate the airways preventing bronchospasm and reducing mucus production

33
Q

How do beta2-agonists work?

A
  1. They bind to the beta2-adrenergic receptor
  2. Adenylyl Cyclase is activated via Gs protein hence increasing cAMP levels and activating protein kinase A (PKA)
  3. PKA phosphorylates proteins that mediate bronchial smooth muscle relaxation causing them to relax

Pharmacy Stage 2 (85 decks)

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