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pt > L 22 and 23 drugs used in asthma > Flashcards

L 22 and 23 drugs used in asthma Flashcards

1
Q

asthma

A

-Episodic bronchospasm resulting from an exaggerated bronchoconstrictor response
to various stimuli
-Bronchial hyperreactivity from chronic bronchial inflammation
-Episodic bronchospasm causes dyspnea, cough, and wheezing.
-Affects ~5% of adults and 7-10% of children.
-Over 3,000 fatality cases per year in US

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2
Q

types of asthma

A

-asthma is a heterogenous disease triggered by a variety of inciting agents
-extrinsic asthma (allergic asthma or classical asthma)
-intrinsic asthma

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3
Q

extrinsic asthma

A

-Hypersensitivity reaction induced by exposure to an extrinsic antigen (ex. dust mite, molds, and pollens)
-Commonly associated with other allergy in the patient as well as in other family members
-The onset is usually early in life.
-Elevated serum IgE levels and eosinophil count
-Driven by T H2 subset of CD4+ T cells

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4
Q

intrinsic asthma

A

-Nonimmune triggering mechanism (ex. aspirin, viral infection, cold, psychological stress, exercise)
-No personal or family history of allergy
-Serum IgE levels are normal.

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5
Q

extrinsic asthma attacks in two phases

A

-Acute bronchoconstriction (immediate asthmatic response) – 30-60 min after inhalation of
antigen
-Sustained bronchoconstriction (late asthmatic response) – 4-8 hours later after the immediate asthmatic response

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6
Q

acute bronchoconstriction

A

-immediate asthmatic response (IAR)
-Occurs after sensitization.
-Mediated by IgE, produced in response to exposure to foreign proteins
-IgE binds to FceR-1 on mast cells in the airway mucosa.

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7
Q

mast cells release ___

A

histamine, tryptase, leukotrienes (LTC 4 and LTD 4) and
prostaglandin D 2 (PGD 2)

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8
Q

Re-exposure to the allergen triggers the release of

A

mediators from the mast cells (mast cell degranulation).

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9
Q

Mediators cause the smooth muscle

A

contract and vascular leakage

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10
Q

direct stimulation of subepthelial vagal (parasympathetic receptors provoke

A

reflex bronchoconstriction

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11
Q

sustained bronchconstriction

A

-Late asthmatic response (LAR)
-3-6 hours after the early asthmatic response

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12
Q

sustained brochoconstriction is caused by the activation of TH2 cells and cytokine production

A

-ex. IL5, IL9, and IL13
-Attract and activate eosinophils.
-Stimulate mucus hypersecretion by bronchial epithelial cells.
-Stimulate IgE production by B lymphocytes

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13
Q

sustained bronchoconstriction activation of eosinophils

A

-Releases major basic protein (MBP), eosinophil cationic protein (ECP), peroxidase, which cause tissue damage.
-Amplifies and sustains the inflammation without additional exposure to the triggering antigen

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14
Q

airway remodeling in asthma: epithelium

A

Hyperplasia
Hypersecretion

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15
Q

airway remodeling in asthma: basement membrane

A

thickening

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16
Q

airway remodeling in asthma: smooth muscles

A

hypertropy

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17
Q

pharmacological treatment of asthma

A

-Sympathomimetics
-Inhaled corticosteroids (ICSs)
-Leukotriene pathway inhibitors
-Methylxanthine drugs
-Antimuscarinic agents
-Cromolyn and nedocromil
-Monoclonal antibodie

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18
Q

sympathomimetics

A

bronchodilators
“relievers”

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19
Q

inhaled corticosteroids (ICSs)

A

Anti-inflammatory steroids
“controllers”

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20
Q

leukotriene pathway inhibitors

A

5-lipoxygenase inhibitor
LTD 4 antagonists

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21
Q

mechanisms of sympathomimetics

A

-Binds to b 2 adrenergic receptors in the bronchial smooth muscle.
-Increases the cAMP concentration à relax the muscle cells

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22
Q

types of sympathomimetics

A

-nonselective
-beta selective
-beta 2 selective

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23
Q

nonselective sympathomimetics

A

Epinephrine (IV injection to relieve a severe attack)

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24
Q

beta selective sympathimimetics

A

-affects the heart, which has beta 1 adrenergic receptors
-isoproterenol: displaced by beta 2 selective drugs

25
Q

beta 2 selective sympathomimetics

A

-most used for the treatment of asthma
-short-acting and long-acting beta 2 agonist

26
Q

beta 2 selective agonist structure activity relationship

A

-Bulky N-substitutions à b 2 selective
-Substitutions in the phenyl ring (ex. resorcinol, salicyl alcohol) à b 2 selective and resistant to catechol-o-methyltransferase (COMT)
-Mostly racemic mixture (ex. levalbuterol); only R-isomer is active.

27
Q

beta 2 selective agonist toxicities

A

-Tachycardia, arrhythmias – less of a concern for b 2 selective agonists
-Skeletal muscle tremors
-Induction of tachyphylaxis – reduction in the bronchodilator response upon regular uses

28
Q

short acting beta 2 agonist (SABA)

A

-Albuterol, terbutaline, metaproterenol, pirbuterol
-PRN for acute attacks

29
Q

long acting beta 2 agonist (LABA)

A

Salmeterol, formoterol
-Additional therapy for patients who is currently using inhaled glucocorticoids
-Not for acute attacks but for daily regular use
-No anti-inflammatory action; should not be used as monotherapy for asthma (black box warning).
-Commonly available as combination inhalers with corticosteroids

30
Q

metaproternol

A

-Resorcinol analogue of isoproterenol
-Somewhat selective for β 2 receptor
-least potent β 2 agonist
-5-min onset and 4-hr duration when inhaled
-Good oral bioavailability

31
Q

terbutaline

A

-N-t-butyl analogue of metaproterenol
-Greater b 2 selectivity
-3-fold greater potency than metaproterenol at b 2 receptors
-Good oral bioavailability

32
Q

albuterol

A

-Most widely used
-Salicyl alcohol in the phenyl ring à resistant to COMT
-5-min onset and 4-8 hr duration of action when inhaled.
-Levalbuterol is R-isomer.
-Greater potency, but more expensive

33
Q

pirbuterol

A

-Analogous to albuterol except the pyridine ring.
-Comparable duration of action as albuterol
-Less potent than albuterol

34
Q

salmeterol

A

-Available as a powder
-Greater lipid solubility; dissolve in cellular membranes.
-20-minute onset and 12-hr duration of action

35
Q

formoterol

A

-Available as a powder
-More rapid onset than salmeterol with a comparable duration of action
-Resistant to COMT and MAO

36
Q

inhaled corticosteroids

A

-maintenace therapy for persistent asthma
-not curative
-systemic or oral cortcosteroids are reserved for severe cases
-inhaled corticosteroids are the most effective way to minimize the systemic adverse effects

37
Q

inhaled corticosteroids adverse effects

A

-Candidiasis – can be treated with topical clotrimazole
-Can be reduced by having patients gargle water
and expectorate after each inhaled treatment
-Ciclesonide – 21-ester prodrug, associated with less candidiasis.
-Hoarseness – direct effect of corticosteroids on
the vocal cords
-Long term use may increase the risk of osteoporosis and cataracts
-In children, 1 cm reduction in their growth only
for the first year

38
Q

leukotrienes

A

-Produced from arachidonic acid by 5-lipoxygenase.
-Involved in many inflammatory diseases and in
anaphylaxis
-LTB 4 – potent neutrophil chemoattractant
-LTC 4 and LTD 4 – responsible for many
symptoms of asthma, such as bronchoconstriction, increased bronchial reactivity, mucosal edema, and mucus hypersecretion

39
Q

leukotriene pathway inhibitors

A

-improve asthma control and reduce the frequency of asthma exacerbations.
-Not as effective as inhaled glucocorticoids.
-Effective when taken orally, easier than inhalation for children.
-Reduce significantly the response to aspirin in aspirin-induced asthma (5- y10% of asthma patients)

40
Q

types of leukotriene pathway inhibitors

A

-5-lipoxygenase inhibitor – zileuton
-selective antagonists for the cysLT 1 receptor – zafirlukast, montelukast

41
Q

zileuton

A

-5-lipoxygenase inhibitor
-Racemic mixture
-N-hydroxy group is essential for inhibitory activity.
-Good oral bioavailability
-Alternative to LABA in addition to inhaled corticosteroids
-Not for acute asthma attack
-Requires periodic monitoring of liver function.

42
Q

monotelukast

A

-Blocks the binding of LTC 4, LTD 4, and LTE 4 to the receptor
-Once a day dosing
-Good oral bioavailability
-Reduces the frequency of asthma exacerbations
-Little toxicity

43
Q

methylxanthine drugs

A

-Theophylline (most effective, more specific for smooth muscle), theobromine, and caffeine
-Once a mainstay of asthma treatment but have almost replaced by b 2 selective agonists
-Still used in some countries due to its low cost

44
Q

mechanism of methylxanthine drugs

A

-inhibition of phosphodiesterase (PDE 3 and PDE 4) à increase in the cellular cAMP concentration –> bronchodilation and suppression of histamine release
-Block the action of adenosine, which causes bronchoconstriction and the release of histamine.
-Histone deacetylation, which suppresses inflammatory gene expression

45
Q

toxicity of methylxanthine drugs

A

-Nausea, vomiting, tremulousness, arrhythmias
-Narrow therapeutic index

46
Q

antimuscarinic agents

A

-anticholinergic agent
-Clinically valuable for patients who are intolerant of inhaled β agonists

47
Q

mechanisms of antimuscarinic agents

A

-Stimulation of cholinergic (parasympathetic) nerves causes bronchoconstriction and mucus secretion.
-Antimuscarinic drugs competitively inhibit the action of acetylcholine at muscarinic receptors

48
Q

ipratropium

A

-Bronchodilator
-Quaternary amine derivative of atropine
-Poorly absorbed into the circulation after inhaled.
-Minimal oral bioavailability
-Relatively free of systemic atropine-like effects

49
Q

mast cells stabilizers

A

-Cromolyn and nedocromil
-Once widely used for asthma management, especially in children.
-Inhibit mast cell degranulation.
-No direct bronchodilator action; should be used prophylactically (daily dosing).
-poorly absorbed into the systemic circulation and have little toxicity, but not as potent or as predictably effective as glucocorticoids.
-The current indication is allergic rhinoconjunctivitis as eye drops

50
Q

anti-IgE monoclonal antibody

A

Omalizumab
-Recognizes the portion of IgE that binds to its receptor (FceR-1 and FceR-2) on immune cells.
-Inhibits IgE binding to mast cells.
-Reserved for patients with severe asthma and allergic sensitization

51
Q

anti-IL-5 therapy

A

-IL-5 released from T H-2 cells attracts and activates eosinophils.
-Anti-IL-5 monoclonal antibodies (Mepolizumab and Reslizumab)
-Anti-IL-5 receptor monoclonal antibody (Benralizumab)
-Used as a maintenance therapy of severe asthma in patients with an eosinophilic phenotype

52
Q

short acting beta 2 agonist drugs

A

-Metaproterenol (Alupent ®)
-Terbutaline
-Albuterol
-Pirbuterol (Maxair ®)

53
Q

long acting beta 2 agonist drugs

A

Salmeterol (Serevent ®)
Formoterol

54
Q

inhaled corticosteroids drugs

A

-Triamcinolone acetonide (Azmacort ®)
-Beclomethasone dipropionate (Vanceril ®, Qvar ®)
-Flunisolide (Aerobid ®)
-Budesonide (Pulmicort ®)
-Mometasone furoate (Asmanex ®)
-Fluticasone propionate (Flovent ®)
-Ciclesonide (Alvesco ®)

55
Q

leukotriene pathway inhibitors drugs

A

-Zileuton (Zyflo ®)
-Zafirlukast (Accolate ®)
-Montelukast (Singulair ®)

56
Q

methylxanthine drugs to know

A

-Theophylline
-Theobromine
-Caffeine

57
Q

antimuscarinic agents drugs

A

Ipratropium (Atrovent ®)

58
Q

mast cells stabilizers drugs

A

Cromolyn (Gastrocrom ®)
Nedocromil (Tilade ®)

59
Q

monoclonal antibodies drugs

A

-Omalizumab (Xolair ®)
-Mepolizumab (Nucala ®)
-Reslizumab (Cinqair ®)
-Benralizumab (Fasenra ®)

pt (17 decks)

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