Asthma & COPD Flashcards

1
Q

Name a systemic corticosteroid

A

methylprednisolone

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2
Q

Name an aerosol corticosteroid

A

fluticasone

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3
Q

Name a beta2 adrenergic agonist that is short acting?

A

albuterol

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4
Q

Name a beta2 adrenergic agonist that is long acting?

A

salmeterol

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5
Q

Name a short-acting muscarinic antagonist

A

ipratropium bromide

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6
Q

Name a long-acting muscarinic antagonist

A

tiotropium

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7
Q

Name a methylxanthine phosphodiesterase inhibitor

A

theophylline

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8
Q

Name a leukotriene pathway inhibitor

A

montelukast

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9
Q

Name an IgE inhibitor

A

omalizumab

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10
Q

What is the main mechanism for maintenance drugs?

A

**prevent **asthma attacks . . . they affect

airway responsiveness/reactivity

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11
Q

Which group of drugs affect airway resistance?

A

quick relief meds, relieve bronchoconstriction

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12
Q

What is the deposition of inhaled drugs?

A

Particles too small will come right back out.
Those that are too big will be swallowed.
2-5 micrometers = optimal and will be inhaled

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13
Q

Which are the most effective sites to pharmacologically target to prevent asthma attacks?

A

CS, IgE, leukotriene inhibitors >> neutrophils

muscarinic antagonists, B2 agonists, methylxanthines >> cholinergic reflex, bronchoconstriction

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14
Q

What is the most effective treatment in **preventing **asthma attacks?

A

inhaled glucocorticoids (ICS)

ICS suppress inflammation . . . DO NOT CURE disease.

In hrs, antiinflammatory effect; maximal benefit weeks/mo. Add B2 agonist before raising steroid dose.

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15
Q

True/False: 17 alpha substitution increases the topical activity of corticosteroids.

A

True.

Why?

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16
Q

How do corticosteroids suppress inflammatory gene transcription?

A

Recall: the corticosteroid gets translocated to the nucleus where it directly affects gene translation (stops acetlyation).

17
Q

Name the effects of corticosteroids on airway cells

A

*corticosteroids increase the transcription of beta 2 receptors

18
Q

What are two main adverse affects with corticosteroids?

A

inhalation >> oropharyngeal candidiasis and dysphonia

high dose/systemic >> HPA suppression (bone resorption, skin thinning, growth retardation)

19
Q

When are systemic glucocorticoids used?

A

with asthma exacerbations

  • short term 3-10 days, must withdraw over 1-2 weeks
20
Q

When do you use B2 agonists in asthma?

A

short acting: rescue
long acting: + ICS

*most asthmatics can be controlled with ICS + B2 agonist
NOTE: B2 agonists increase glucocorticoid nuclear translocation (complement each other)

21
Q

Bronchodilators

A
22
Q

What is the difference between albuterol and salmeterol?

A

albuterol

  • short acting 3-5 min
  • peak 30-60 min
  • duration 3-6 hr
  • *salmeterol**
  • duration >12 hr
23
Q

MOA of B2 agonists

A
24
Q

When do you know that asthma is not adequately controlled?

A

Using rescue inhaler >2x/week

25
Q

True/false: Long acting B2 agonists should NOT be prescribed unless accompanied by ICS.

A

True

combination inhaler preferred

* HOWEVER, LABA can be prescribed alone in COPD

26
Q

When would you use an inhaled muscarinic antagonist?

A

IF patient intolerant of B2 agonists.

27
Q

What’s the different between ipratropium and tiotropium?

A
  • *ipratropium**
  • short acting 15-30 min
  • duration 3-4 hrs
  • *tiotropium**
  • duration >24hrs
28
Q

True/false: anticholinergic drugs inhibit vagally mediated airway tone, producing bronchodilation.

A

True

29
Q

Which asthma drug has a narrow therapeutic window and needs plasma level monitoring?

A

theophylline

30
Q

What is the goal of anti-IgE therapy?

A

Neutralize serum IgE, thus there is no allergen induced activation of immune cells.

31
Q

What asthma drug is cheapest and most expensive?

A

cheap: theophylline
expensive: anti IgE monoclonal antibody

32
Q

True/false: COPD is defined as the presence of airflow limitation that is not fully reversible.

A

True

33
Q
A
34
Q

True/false: there is no sympathetic innervation of bronchiole smooth muscle, but there are Beta 2 receptors on the lung.

A

True

35
Q

Conceptual model for immunopathogenesis of asthma

A

2 phases

early reaction

driven by mast cell and histamine

late reaction

more inflammatory mediators