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IMED3001 > Pharmacology of Asthma > Flashcards

Pharmacology of Asthma Flashcards

1
Q

What causes asthma?

A

Asthma is caused by recurrent narrowing of the airways due to reduction in lumen of airway passages.

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2
Q

What are the symptoms asthma?

A

Wheezing

Breathlessness

Cough

(variable intensity which increase at night)

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3
Q

What are common triggers of asthma?

A

Allergens

Respiratory Tract Viral infections

Exercise

Smoke

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4
Q

What causes airway narrowing in asthma?

A

Airway mucous

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5
Q

What key structures are found in the airways?

A

Lumen directly surrounded by epithelium which contains mucous secreting goblet cells, basement membrane surrounding epithelium, smooth muscle and submucosal glands surrounding the basement membrane and finally cartilage in the most superficial layer.

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6
Q

What do goblet cells do?

A

They produce mucous

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7
Q

What do cilia do?

A

They push mucous containing particulate matter towards the mouth where it can get expelled.

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8
Q

How do inflammatory molecules get into the airways?

A

Via submucosal blood vessels

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9
Q

How is the diameter of the airways controlled?

A

VIa smooth muscle contraction and relaxation.

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10
Q

What changes in the airway airway cause narrowing?

A

Increased thickness of airway wall

Increase in mucus production (Larger submucosal glands and more mucous secreting cells)

Constriction of airway smooth muscle

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11
Q

How is asthma managed?

A

It cannot be cured so long-term management strategy is to control symptoms (to maintain normal activity levels) and to reduce the risks.(minimizing risk of asthma attacks, airflow limitation, and medication side effects)

3 strategies employed:

1) Preventing/relieving bronchoconstriction with reliever medication.
2) Suppressing inflammation with controller medication (eg inhaled corticosteroids (ICS)
3) Inhibiting mucous secretion

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12
Q

What do reliever medications do?

A

They either prevent or reverse bronchoconstriction.

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13
Q

Why do airways narrow during an asthma attack?

A

They activate specific receptors (GPCRs) that are expressed on the surface of airway smooth muscle and can cause the smooth muscle to contract.

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14
Q

What are the proteins present on the surface of airway smooth muscles that cause contraction of smooth muscle during asthma?

A

NK (binds neuropeptide)

M3 (acetylcholine receptor aka muscarinic receptor)

H1 (Histamine receptor)

LT (Leukotriene receptor)

ETb (Endothelin receptor)

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15
Q

What happens when GPCRs on smooth muscle surface are bound by their ligands?

A

They increase Ca influx into the cell resulting in contraction and airway narrowing.

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16
Q

What are important features of reliever medications?

A

They need to act quickly

They need to act irrespective of the substances causing bronchoconstriction (i.e they need to use their own pathways to relax smooth muscles)

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17
Q

What is salbutamol?

A

A beta-2 receptor agonist which reverses airway narrowing.

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18
Q

How do beta-2 adrenoceptor agonists work?

A

They bind to and stimulate beta-2 adrenoceptors on airway smooth muscle inducing relaxation irrespective of bronchoconstrictors.

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19
Q

Do beta-2 adrenoceptors agonists inhibit inflammation?

A

No, not significantly

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20
Q

How are beta-2 adrenoceptor agonists administered?

A

By inhalation

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21
Q

What are LABAs? How are they different to their short term counterparts?

A

Long Acting Beta2 Agonists dilate bronchi for much longer than short-term beta2 agonists (which act for 4 - 6 hours)

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22
Q

Can all LABAs be used as relievers?

A

No, it depends on the onset of action.

23
Q

Which LABA can be used as a reliever?

A

eformoterol because it has a rapid onset of action (5 - 10 minutes)

24
Q

Which LABA can not be used as a reliever?

A

Salmeterol because it has a delayed onset of action (15 - 20 minutes)

25
Q

How are LABAs commonly used?

A

In combination with Inhaled CorticoSteroids (ICSs) which makes them available in a single inhaler

26
Q

What do muscarinic cholinoceptor antagonists do?

A

They inhibit contraction of smooth muscle that is induced by acetylcholine interaction with muscarinic receptor.

27
Q

How are muscarinic cholinoceptor antagonists administered?

A

Aerosol with slower onset of action than short-acting beta2 adrenoceptor agonists.

They are not used as relievers but rather are used regularly for long-term control of asthma symptoms and can be used in addition to beta2-adrenoceptor agonists and glucocorticoids.

28
Q

What are the limitations of using muscarinic cholinoreceptor antagonists?

A

They are effective only against bronchoconstriction caused by acetylcholine.

They also have adverse-effects such as dry mouth and bitter taste.

29
Q

What common muscarinic cholinergic antagonist is used?

A

ipratopium bromide (atrovent which is not the same as atropine)

30
Q

Can muscarinic cholinergic antagonists be used to suppress inflammation?

A

Yes, in allergic asthma

31
Q

What is the best form of asthma control?

A

Inhaled Corticosteroids (ICS) are the front line therapy in maintaining Th2-driven eosinophilic asthma.

32
Q

How do ICS work?

A

Reduce expression of genes and proteins that drive Th2/eosinophilic inflammatory response often seen in asthma.

33
Q

Why are ICS drugs given in inhalation form?

A

To reduce side effects

34
Q

How must ICS drugs be taken to be effective?

A

They must be taken regularly

35
Q

What are the benefits of using ICS drugs?

A

Reduced airway inflammation

Less airway narowing

Improved lung function

Improved symptom scores

More symptom-free days.

Reduced asthma medication use

Fewer exacerbations and hospitalisations

36
Q

Do ICS drugs work as relievers?

A

No they must be taken regularly and prophylactically

37
Q

When are people more likely to take ICS?

A

When combined with LABAs.

38
Q

Why is asthma suboptimally controlled in up to 20% of patients?

A

Irregular use of medicaitons (poor use or non-adherence)

Incorrect inhaler technique

Inadequate treatment of comorbidity (obesity, smoking-related disease, GERD, drugs)

Asthma heterogeneity

True glucocorticoid resistance which is uncommon

39
Q

What asthma is treated more effectively by ICS?

A

Eosinophilic asthma

40
Q

What are leukotrenes (LTs)?

A

Potent mediators of inflammation which are upregulated by mast cells and eosinophils in asthma

41
Q

What receptors do Leukotrienes bind to?

A

CysLT

42
Q

How do LTs cause airway narrowing?

A

S-lipoxygenase converts arachidonic acid into LTA4 which is converted into LTC4, LTD4, and LTE4 which can combine with CysLT1 receptor which results in

Secretion of mucous

Contraction of Airway Smooth Muscle (ASM)

Leakage of blood via influx of eosinophils.

43
Q

How do LT receptor antagonists work?

A

They block CysLT1 receptor from being bound by LTC, LTD, LTE resulting in a decrease in narrowing.

44
Q

What are LT receptor antagonists used for?

A

Not used to relieve acure asthma attacks but can be used as add-ons for uncontrolled asthma

45
Q

How are LT receptor antagonists administered?

A

They can be administered orally

46
Q

What is omalizumab?

A

An anti-IgE medication that binds to free IgE preventing binding to IgE receptor.

47
Q

What are anti-IgE antibodies used for?

A

To treat uncontrolled severe allergic asthma in people with raised IgE and already taking ICS. (Expensive af so should only be used in very specific situations)

48
Q

How are anti-IgE antibodies administered?

A

Subcutaneous injections every 2 or 4 weeks.

49
Q

What is the problem with using anti IgE antibodies?

A

They are biological drugs making them expensive. (they are effective though so good for use on certain patients who would otherwise have stayed at hospital for extended periods of time)

50
Q

What do anti-IgE antibodies do?

A

They bind IgE antibodies preventing their allergic action.

51
Q

What is mepolizumab?

A

A monoclonal antibody to IL-5 which is important for activation of Th2/eosinophilic asthma.

52
Q

Who is meoplizumab most effective in?

A

In patients with high sputum eosinophils that continue to have asthma despite high doses of ICS.

53
Q

What is azithromycin?

A

Antibiotic with anti-inflammatory and mucoregulatory activity.

It has shown great promise in clinical trials with fewer exacerbations, less cough and sputum production, better quality of life, and fewer infections.

54
Q

What is the biggest limitation of using azithromycin?

A

It is an antibiotic so it can potentially cause antibiotic resistance.

IMED3001 (46 decks)

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