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Pharmacology II > Respiratory System - Asthma & COPD > Flashcards

Respiratory System - Asthma & COPD Flashcards

1
Q

A chronic inflammatory disorder of the airways which involves complex interactions between many cells and inflammatory mediators which can result in inflammation, obstruction, increased airway responsiveness and episodic asthma symptoms.

A

Asthma

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2
Q

CLINICAL SIGNS & SYMPTOMS of Asthma:

A
  • SOB
  • Chest tightness
  • Wheezing
  • Tachypnea & tachycardia
  • Pulsus paradoxus
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3
Q

HALLMARK Pathophysiologic Features of asthma:

A
  1. Reversible narrowing of the bronchial airway
  2. Marked increased in bronchial responsiveness to inhaled stimuli.

PATHOLOGIC Features
- Lymphocylic
- Eosinophilic

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4
Q

2 DOMAINS FOR THE SPECTRUM OF ASTHMA’S SEVERITY:
1. Impairment
2. Risk

A

Impairment: based on the frequency & severity of symptoms, severity of the airflow obstruction on pulmonary function testing & the intensity of therapy required for maintenance of asthma control.

Classification:
Mild Intermittent - interval
Mild persistent - not on a daily basis
Moderate persistent - everyday
Severe persistent - throughout the day

Risk: Based on susceptibility to asthma exacerbations

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5
Q

Precipitating factors of acute asthma:

A
  • Allergens
  • Occupational exposures
  • Viral respiratory tract infections
  • Exercise
  • Emotions
  • Exposure to initants
  • Environmental exposures
  • Drugs
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6
Q

Asthmatic bronchospasm:

A
  1. Allergenic stimuli
    Mediated by IgE, produced in response to exposure to foreign proteins.
  2. Non-allergenic stimuli
    Exercise, Cigarette smoking, Cold air
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7
Q

Acute bronchoconstriction due to the release of histamine, tryptase, leukotrienes C4. D4 & prostaglandin D2

A

Early asthmatic response

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8
Q

Associated with an influx of inflammatory cells into the bronchial mucosa & with an increase in bronchial reactivity.
This is due to cytokines-produced by T2 lymphocytes especially interleukin (IL) 5,9 & 13.

A

Late asthmatic response

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9
Q

HYPOTHESIS:
Asthmatic bronchospasm (combination of mediators & exaggeration of responsiveness).
Drugs w/ different mode of action = effectively treat asthma.
Bronchospasm provoked by exposure to allergens might be reversed/prevented.

A

N/A

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10
Q

SYMPATHOMIMETIC AGENTS

A

ẞ2 Selective agonists:
Albuterol
Salmeterol
Metaproterenol
Pirbuterol
Terbutaline
(Short-acting)

a & ẞ Nonselective agonists:
Epinephrine

ẞ1 & ẞ2 agonists:
Isoproterenol

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11
Q

Available in SQ Indication is similar to epinephrine for severe asthma requiring emergency treatment when aerolized therapy is not available or has been ineffective.
Used to inhibit uterine contractions.

Principal A/E:
Skeletal muscle tremor
Nervousness
Occasional weakness

Dose:
Nebulizing solution:
- 2.5-5.0mg q 20 mins x3 doses,
- 2.5-10.0mg q 1-4 hrs pr
- or 10-15mg/hr continuously

MDI: 4-8 puffs q 20 mins up to 4 hrs, then q 1-4 hrs prn

Oral: SR tab,
0.3-0.6 mg/kg/day (pedia)
4mg q 12 hrs (adults)

A

Terbutaline

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12
Q

Long-acting B-agonists (LABA):

A
  • Salmeterol
  • Formoterol

interact with inhaled corticosteroids (ICS) to improve asthma control.
Not to be used as monotherapy.
W/ high lipid solubility

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13
Q

Ultra long-acting ß-agonists:

A
  • Indacaterol
  • Olodaterol
  • Vilanterol
  • Bambuterol

Used for monotherapy in COPD.
Used in combination w/ ICS for asthma

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14
Q

SYMPATHOMIMETIC AGENTS
-MOA: ẞ-agonists stimulate ẞ2 receptors activating adenyl cyclase, which increases intracellular production of cyclic adenosine monophosphate (cAMP).

Dose: Via inhalation, Systemic administration

Toxicity:
Worsened hypoxemia
Cardiac arrhythmias
Decreased arterial oxygen tension
Tachyphylaxis

A

N/A

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15
Q

Rapid-acting bronchodilator. Stimulates a, B and B2.
Used for the treatment of the acute vasodilation and bronchospasm of anaphylaxis.
Bronchodilation within 15 min that lasts for 60-90 min.

A

Epinephrine

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16
Q

Potent non selective B, and B2 bronchodilator.
Bronchodilation in 5 min that lasts for 60-90 min.

A

Isoproterenol

17
Q

MOA: at high concentration inhibit several members of PDE enzyme family in vitro, increasing the intracellular CAMP & in some tissues cGMP.
Inhibition of cell surface receptors for adenosine.
Enhancement of histone deacetylation.

• Theophylline-tea (1,3 dimethylxanthine)
• Theobromine - cocoa (3,7 dimethylxanthine)
• Caffeine - coffee (1,3,7 trimethylxanthine)

The cause for the decline of theophylline use in asthma:
- Toxicities
- Serum level monitoring: narrow therapeutic index

A

Methylxanthine Drugs

18
Q

A theophylline-ethylenediamine complex

A

Aminophylline

19
Q

Selective inhibitor of PDE4.
Reduces the frequency of exacerbations of COPD Approved by the US FDA as treatment for COPD

A

ROFLUMILAST

20
Q

METHYLXANTHINE DRUGS Effects:

CNS - mild cortical arousal with increased alertness & defence fatigue
Cardiovascular - (+) chronotropic and inotropic effects on the heart.
Gl - stimulates secretion of both gastric and digestive enzymes
Kidney - theophyline is a weak diuretic
- Smooth muscle - bronchodilation
- Skeletal muscle - improve contractility

A

N/A

21
Q

Antimuscarinic agent:

A

Atropine
Ipratropium bromide

Longer acting antimuscarinic agent:
Tiotropium, aclidinium, umeclidinium - used for maintenance therapy of COPD.

22
Q

A potent competitive inhibitor of acetylcholine at postganglionic muscarinic receptors, as a bronchodilator.

A

Atropine

23
Q

A selective quaternary ammonium derivative of atropine which can be inhaled in high doses because of its poor absorption into the circulation and poor entry into the CNS.
As effective as albuterol in patients with COPD who at least partially reversible obstruction.

A

Ipratropium bromide

24
Q

Suppress the inflammatory response and decrease hyperresponsiveness
MOA: Corticosteroids binds to glucocorticoid receptors on the cytoplasma of the cells.
Effect: Contraction of engorged vessels on bronchial mucosa.
Potentiation of the effects of beta receptor agonists.
Inhibition of the infiltration of asthmatic airways by lymphocytes, eosinophils and mast cells
Clinical use: improves all indices of asthma control.
Dose: for severe asthma exacerbations 30-60mg of prednisone per day.
IV dose of 0.5-Img/kg of methylprednisolone q 6-12 hr.
The dose is decreased after airway obstruction has improved.
Systemic treatment must be discontinued in 5 to 10 days

A

CORTICOSTEROIDS

25
Q

Inhaled Corticosteroids (ICS):
Average daily dose: 800mcg of inhaled beclomethasone is equivalent to 10-15mg/d of oral prednisone for the control of asthma.

A

Beclomethasone
Budesonide
Ciclesonide
Flunisolide
Fluticasone
Mometasone
Triamcinolone

26
Q

Oropharyngeal candidiasis - specialized problem of inhaled topical corticosteroids

Ciclesonide: A prodrug activated by bronchial esterases with less candidiasis.

Chronic use can cause: Increased the risk of osteoporosis & cataracts.

A

N/A

27
Q

TARGETED (MONOCLONAL ANTIBODY) THERAPY: Anti-IgE Monoclonal antibodies
- Monoclonal antibody, raised in mice and then humanized, making it less likely to cause sensitization when given to human subjects
MOA: Inhibits the binding of IgE to its receptor
- SQ a 2-4 hrs
- Also proven effective as a treatment for chronic recurrent urticaria
- For peanut allergy

A

Omalizumab

28
Q

TARGETED (MONOCLONAL ANTIBODY) THERAPY: Anti-IL-5 Therapy
• Mepolizumab
• Reslizumab
- These drugs are humanized monoclonal antibodies targeting IL-5
• BENRALIZUMAB - targeting IL-5 receptor
- These drugs were developed for the treatment of eosinophilic basthma.

A

N/A

29
Q

A disease state characterized by airflow limitation that is not fully reversible (WHO).
Major forms:
1. Chronic bronchitis - excessive mucus production
2. Emphysema - alveolar enlargement distal to the terminal bronchioles

Causes:
Smoking
Exposure to irritants
History of respiratory infection
-Social, economic & hereditary factors

A

COPD

30
Q

Occurs in older patient and is associated with neutrophilic rather than eosinophilic inflammation.
Poorly responsive even to high doses of ICS therapy.
Treatment is similar to asthma

A

COPD

31
Q

Approved for the treatment of COPD.
A selective PDE inhibitor that improves pulmonary function and reduces exacerbation frequency.

A

Roflumilast

Pharmacology II (8 decks)

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