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Respiratory > Asthma > Flashcards

Asthma Flashcards

1
Q

SABA drugs

A

Albuterol and terbutaline

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2
Q

Inhaled corticosteroids drugs

A 
Beclomethasone
Budesonide
Mometasone
Fluticasone
Ciclesonide
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3
Q

Leukotriene pathway inhibitor drugs

A

Zileuton
Zafirlukast
Montelukast

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4
Q

LABA drugs

A

Formoterol and salmeterol

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5
Q

Antimuscarinic drugs

A

Ipratropium and tiotropium

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6
Q

Methlxanthine drugs

A

Theophylline

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7
Q

Sympathomimetic agents MOA

A
  • Primary mechanism: relax airway smooth muscle via b2-adrenergic activation; increase cAMP
  • Inhibit the release of bronchoconstricting mediators from mast cells
  • May inhibit microvascular leakage and increase mucociliary transport by increasing ciliary activity
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8
Q

Why do nebulizers require a higher dose versus an inhaler?

A

The particles are larger

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9
Q

Beta2-agonists adverse effects of inhaled

A

Tremulousness
Heart palpitations/arrhythmias
Cough/throat irritation
Contraindications: Cautiously use in patients with CV disease

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10
Q

Corticosteroids MOA

A
  • Presumed to act by their broad anti-inflammatory actions
    • Inhibits production of inflammatory cytokines
    • Inhibits the infiltration of asthmatic airways by lymphocytes, eosinophils, and mast cells
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11
Q

Corticosteroids clinical use

A
  • Aerosol controller therapy (minimal systemic absorption)
  • Improves severity of symptoms, tests of airway caliber and bronchial reactivity, frequency of exacerbations, and quality of life
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12
Q

Corticosteroids adverse drug reactions

A

Oropharyngeal candidiasis, hoarseness, adults - possible risk of osteoporosis and cataracts
Children - slight delay in rate of growth

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13
Q

Leukotriene pathway inhibitors MOA

A

Block leukotriene D4 receptor (except zileuton)

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14
Q

LTC4 and LTD4 exert many effects in asthma, including…

A

Bronchoconstriction
Increased bronchial reactivity
Mucosal edema
Mucus hypersecretion

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15
Q

Leukotriene pathway inhibitors are less effective than inhaled corticosteroids for…

A

Airway caliber, bronchial reactivity, airway inflammation

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16
Q

Zileuton has been linked to…

A

Severe hepatotoxicity

17
Q

Principal advantage for leukotriene pathway inhibitors

A

Oral formulations

18
Q

Ingestion of aspirin causes…in some asthmatics

A

Profound bronchoconstriction and symptoms of systemic histamine release (flushing and abdominal cramping)

19
Q

Leukotriene inhibitors ____ the response to aspirin challenge

A

Reduce

20
Q

Cromolyn and nedocromil MOA

A
  • Altering the function of delayed chloride channels in the cell membranes&raquo_space;inhibiting cell activation
    • Mast cells&raquo_space; inhibition of degranulation
    • Eosinophils&raquo_space; inhibition of the inflammatory response to inhaled allergens
21
Q

Cromolyn and nedocromil clinical use

A
  • Non-seasonal asthma symptoms and reduced need for bronchodilators
  • Allergic rhinoconjunctivitis
  • Adverse drug reactions are minimal due to poor drug absorption
  • Usage has diminished due to low-dose corticosteroid
22
Q

LABA

A
  • Potent selective agonists with a long duration of action (12+ hours; high lipid solubility)
    • Can dissolve in the smooth muscle cell membrane in high concentrations
    • Interact with inhaled corticosteroids to improve asthma control
    • Have no anti-inflammatory actions of their own; not used as monotherapy
  • Salmeterol (a partial agonist)
  • Formoterol (a full agonist)
23
Q

LABA adverse effects

A

Asthma-related death (black box) + SABA effects

24
Q

Antimuscarinic agents clinical use

A

-Limited use (used for patients intolerant of beta-agonists)

25
Q

Iprotropium

A

Aerosolized or nasal spray emergency addon

Poorly absorbed into circulation and the CNS (minimize systemic atropine-like effects)

26
Q

Tiotropium

A

Long-acting antimuscarinic agent

Recently approved for the maintenance treatment of asthma in patients ≥6 years

27
Q

Methylxanthines (theophylline) MOA

A

At high concentrations, inhibit phosphodiesterase (PDE) enzymes&raquo_space; elevated levels of cAMP (or cGMP, tissue dependent)
Specifically PDE3 and PDE4 in the airway smooth muscle and on inflammatory cells
Inhibition of PDE3 relaxes airway smooth muscle
Inhibition of PDE4 in inflammatory cells reduces their release of cytokines and chemokines&raquo_space; decreases immune cell migration and activation
Inhibition of cell surface receptors for adenosine&raquo_space; adenosine can cause bronchoconstriction
Enhanced histone deacetylation (histone acetylation&raquo_space; inflammatory gene transcription)

28
Q

Theophylline pharmacodynamics

A

CNS (primarily caffeine but all have effects)
-Low doses: mild cortical arousal with increased alertness and deferred fatigue
-High doses: nervousness and tremor
-Very high doses: medullary stimulation and convulsions, maybe death
CV
(dose-dependent positive chronotropic and inotropic effects)
GI tract
(stimulates secretion of gastric acid and digestive enzymes)
Kidney (weak diuretics)
Smooth muscle (
bronchodilation)
Skeletal muscle
(strengthened contraction of isolated skeletal muscles in vitro; improve contractility and reverse fatigue of the diaphragm in patients with COPD)

29
Q

Theophylline clinical uses

A

Most potent bronchodilator of the methylxanthines

  • Relieves airflow obstruction in acute asthma
  • Reserved for patients in whom symptoms remain poorly controlled despite the combination of regular treatment with an inhaled anti-inflammatory and as needed use of a b2-agonist
30
Q

Theophylline cautions/adverse reactions

A 
Narrow therapeutic window (blood levels monitored)
Anorexia
Vomiting
Nausea
Abdominal discomfort
Headache and anxiety
Insomnia
Seizures
Arrhythmias
31
Q

Omalizumab

A
  • Anti-immunoglobulin E (IgE) monoclonal antibody
    • Binds free IgE&raquo_space; at its constant region
  • Prevents IgE from binding to the receptors on mast cells and other inflammatory cells
  • Does NOT activate IgE already bound to these cells&raquo_space; does not provoke mast cell degranulation
32
Q

Omalizumab clinical use

A

Reduction in frequency and severity of asthma exacerbations (works best with more severe disease states)

33
Q

Benralizumab

A
  • IL-5 receptor alpha antibody
  • Clinical: add-on maintenance treatment of severe asthma in adults and children >12 with an eosinophilic phenotype
  • Adverse effects: antibody production, headache, pharyngitis
34
Q

Mepolizumab and Reslizumab

A

Monoclonal antibodies against IL-5 (mep = subcutaneous; res = IV)
Clinical: eosinophilic severe asthma
Adverse effects: Mep - hypersnsitivity, headache, site reaction
Res - anaphylaxis (black box), oropharyngeal pain

Respiratory (9 decks)

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