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Pharmacology > Treatment Of Asthma And COPD > Flashcards

Treatment Of Asthma And COPD Flashcards

1
Q

What is asthma

A

A chronic inflammatory disorder of bronchial airways that result in airway obstruction in response to external stimuli

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2
Q

How is airway inflammation caused

A

Antigens elicit the production of IgE antibodies. These antibodies attach themselves to the surface of mast cells and basophils.
Exposure to the same antigen after some time results in antigen-antibody reaction on lung mast cells which trigger the release of histamine and cysteinyl leukotrienes, agents that produce bronchoconstriction, mucus secretion and pulmonary edema.

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3
Q

What other chemotactic mediators are produced by mast cells

A

Leukotriene B4
Cytokines

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4
Q

Symptoms of asthma

A

Acute bronchoconstriction
Shortness of breath
Chest tightness
Rapid respiration
Wheezing
Cough

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5
Q

Two classes of anti asthmatic drugs

A

Bronchodilators
Anti-inflammatory agents

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6
Q

Classes of bronchodilators

A

B2- agonists
Antimuscarinics
Xanthine derivatives

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7
Q

Classes of anti-inflammatory agents

A

Corticosteroids
Mast cell stabilisers
Leukotriene antagonists
Anti-IgE monoclonal antibody
Long acting B2 agonists

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8
Q

Mention long acting and short acting B2 agonists

A

Long acting
- Salmeterol
- Formoterol

Short acting
- Albuterol
- Fenoterol
- Terbutaline

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9
Q

MOA of B-agonists

A

They bind to B-adrenergic receptors which are abundant on airway smooth muscle cells and stimulate adenyl cyclase and increase the formation of intracellular cAMP, thereby relaxing airway smooth muscles and inhibiting release of bronchoconstricting mediators from mast cells.

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10
Q

Difference between selective and non selective B-agonists

A

Non selective B-agonists activate both a and B adrenoreceptors while selective B-agonists activate B1 and B2 adrenoreceptors, having higher affinity for B2-adrenoreceptors (the predominant subtype in the airway)

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11
Q

Example of non selective B-agonists

A

Epinephrine

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12
Q

What is the drug of choice to treat acute anaphylaxis

A

Epinephrine

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13
Q

What is the time epinephrine takes to work and the duration of action

A

Within 15 mins

60-90 mins

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14
Q

Disadvantages of epinephrine

A
  • Not effective orally
  • Hyperglycaemia
  • CVS side effects (tarchycardia, arrythmia, hypertension)
  • Not suitable for patients with hypertension and heart failure
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15
Q

Ways to administer short acting B2 agonists

A

Inhalation
Orally
IV
Subcutaneous

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16
Q

What is the onset and duration of action for short acting B2 agonists

A

15 to 30 mins

4 to 6 hours

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17
Q

Duration of action for long acting selective B-agonists

A

12 hrs

18
Q

Administration of long acting selective B-agonists

A

Inhalation

19
Q

What class of drug is used to treat nocturnal asthma

A

Long acting selective B-agonists

20
Q

What class of drugs are combined with long acting selective B2- agonists

A

Corticosteroids

21
Q

Advantages of long acting selective B2-agonists

A
  • Minimal CVS effects so suitable for asthmatic patients with hypertension or heart failure
22
Q

What is the MOA of muscarinic receptor antagonists

A

Block muscarinic receptors (M2, M3)

23
Q

Examples of Antimuscarinics

A

Ipratropium
Tiotropium

24
Q

Administration of Antimuscarinics

A

Aerosol Inhalation

25
Q

Which bronchodilators are the main choice in COPD

A

Antimuscarinics

26
Q

Examples of xanthine derivatives

A

Methylxanthines
Theophylline

27
Q

Adverse effects of theophylline

A

Gastric pain, vomiting
Tremors
Hypotension
Convulsions
Insomnia

28
Q

MOA of theophylline

A

Raised intracellular cAMP by inhibiting phosphodiesterase

  • Antagonism of adenosine (a potent bronchoconstrictor) at A2 receptors
29
Q

What is the MOA of anti inflammatory agents

A

Reduce the number of inflammatory cells in the airways and prevent blood vessels from leaking fluid into the airway tissues

30
Q

What do corticosteroids do in the airways

A

Reduce the number of inflammatory cells in asthmatic airways (eosinophils, T-lymphocytes, mast cells, and dendritic cells)
Achieved by
- suppressing the production of chemotactic mediators and adhesion molecules
- inhibiting the survival in the airways of inflammatory cells

31
Q

How do corticosteroids perform their job

A

Inhibition of phospholipase A2
Upregulate B2 receptors

32
Q

Routes of administration for corticosteroids

A

Inhalation (budesonide and fluticasone)

Orally (Prednisone)

Injection ( Hydrocortisone and dexamethasone)

33
Q

Onset of action for corticosteroids

A

2 to 4 weeks

34
Q

Maximum action duration

A

9 to 12 months

35
Q

List mast cell stabilisers

A

Nedocromil

36
Q

MOA of mast cell stabilisers

A

Stabilization of mast cell membrane

37
Q

Administration of mast cell stabilisers

A

Inhalation

38
Q

Which asthma prophylaxis is more preferred in children than adults

A

Mast cell stabilisers

39
Q

Examples of leukotriene receptor antagonists

A

Zarfilukast
Montelukast
Pranlukast

40
Q

Examples of anti-IgE antibodies

A

Omalizumab

41
Q

MOA of monoclonal antibodies

A

Prevents IgE binding with it’s receptors on mast cells and basophils leading to decrease in release of allergic mediators

42
Q

Treatment of COPD

A
  • Inhaled bronchodilators
  • Inhaled glucocorticoids
  • Oxygen therapy

Pharmacology (3 decks)

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