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Pulmonary > Treatment of Asthma and COPD > Flashcards

Treatment of Asthma and COPD Flashcards

1
Q

Describe MOA of Sympathomimetics (B2-adrenergic receptor agonists)

A

Increase levels of cAMP, which promotes bronchodilation

  • Intracellular levels of cAMP can be increased by B-agonists (increase rate of its synthesis by adenylyl cyclase) or by PDE-inhibitors such as theophylline, which slos the rate of degradation.
  • Bronchoconstriction can be inhibited by muscarinic antagonists and possibly by adenosine antagonists

Some inhibitory effect on the release of mediators from mast cells and on **microvascular permeability **

Promote to a small degree **mucociliary transport **

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2
Q

Name the sympathomimetic bronchodilators

A

Non-specific: Epinephrine, Ephedrine, Isoproterenol

B2-specific (quick onset-short duration): Albuterol, Terbutaline

B2-specific (slow onset-long acting i.e. LABA): Salmeterol, Formoterol (used only in combination with steroids as they donot prevent inflammation)

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3
Q

What are the adverse reactions of sympathomimetics?

A
  • N/V, headache
  • Fall in BP and increased HR (because heart has B2AR) and cardiac arrythmias (hypokalemia leading to QT prolongation)
  • Arterial oxygen tension (PaO2) may decrease
  • CNS toxic effects which include agitation, convulsions, coma and respiratory vasomotor collapse
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4
Q

Name the Cholinergic Antagonists (Bronchodilators)

A

Atropine: competitive Ach-muscarinic blockade

  • reduces airway smooth muscle constriction
  • decrease in mucus secretion
  • enhane B2-mediated bronchodilation
  • adverse reactions: pupillary dilation and cycloplegia, on contact

Ipratropium: quaternary compound, is poorly absorbed with no significant systemic effects

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5
Q

What is the drug that is a combined anti-cholinergic and B2 agonist?

A

Combivent

Combined therapy produces a greater improvement in lung fucntion than either ipratropium or albuterol alone

Indicated for COPD

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6
Q

What are the methylxanthines?

A

Aminophylline (theophylline + diethylamine)

Theophylline

They are combined bronchodilators and anti-inflammatory agents!

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7
Q

What are the actions of methylxanthines?

A

Inhibits PDE, which results in accumulation of cAMP that produces bronchodilation. Anti-inflammatory by blocking the effect of adenosine on mast cells and also causes the deacetylation of histones.

  • Increased levels of cAMP
  • Inhibits muscle adenosine receptors
  • Decreased release of mediators
  • Bronchodilation
  • Anti-inflammatry effects
  • Positive inotropic and chronotropic effects
  • Increased CNS activity
  • Increased gastric acid secretion
  • Weak diuretic
  • Increased skeletal muscle strength (diaphgram)
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8
Q

What are the adverse reactions to Methylxanthines?

A
  • 5-10ug/mL serum levels may cause n/v, nervousness, headache and insomnia
  • Serum levels >20ug/mL cause vomitting, hypokalemia, hyperglycemia, tachycardia, cardiac arrythmias, tremor, neuromuscular irritability and seizures
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9
Q

Cromolyn Sodium (Anti-inflammatory) MOA

A

MOA:

  • May alter the activity of Cl- channels
  • Inhibit degranulation of mast cells in the lung
  • Inhibit inflamatory response by acting on eosinophils
  • Inhibit cough by thier action on airway nerves
  • Reduce bronchial hyperactivity associated with excercise- and antigen-inhaled asthma
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10
Q

Cromolyn Sodium (Anti-inflammatory) Adverse Effects

A

No systemic toxicity

Unpleasant taste

Irritation of trachea: cough, and bronchospasm can occur after inhalation

Rare adverse effects: chest pain, restlessness, hypotension, arrhythmias, n/v, CNS depression, seizures and anorexia

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11
Q

Name the Glucocorticoids/Corticosteroids (Anti-inflammatory)

A

All end in “sone” or “sonide”

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12
Q

Which of the corticosteroids has the best pharmacokinetics?

A

Ciclesonide has the best PK

  • very rapidly cleared from the mouth so will not cuase the oropharyngeal candidiasis
  • high lipophilicity
  • high binding to the glucocoriticoid receptors
  • high protein binding which reduces systemic absorption
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13
Q

What are the pharmacological actions of corticosteroids?

A
  • Decrease production of inflammatory cytokines
  • Reduce mucus secretion
  • Reduce bronchial hyperactivity
  • Enhance the effect of B-2 adrenergic agonists
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14
Q

What are the adverse consequences of corticosteroids?

A

Inhaled

  • oropharyngeal candidiasis, hoarseness and dry mouth
  • decreased bone mineral density in premenopausal women
  • decreased rate of growth in children

Oral (prolonged use)

  • glucose intolerance
  • increase BP and weight
  • bone mineralization
  • cataracts
  • immunosuppresion
  • retarded growth in children
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15
Q

Explain Cushingoid Syndrome

A

Related to the excessive use of glucocoritcoids

  • Weight gain, especially abdomen, face (moon face), neck and buffalo hump
  • Thinning and leg/arm muscle weakness
  • Thin skin, with easy bruising and stretch marks
  • Increased acne, facial hair growth, and scalp hair loss in women
  • A ruddy complexion on the face and neck
  • Often a neck skin darkening (acanthosis)
  • Child obestiy and poor growth in height
  • High BP (usually)
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16
Q

Name the two LT receptor blockers and describe their MOA (Anti-inflammatory)

A

LTB4 is a neutrophil chemoattractant

LTC4 and LTD4 mimic many Sx of asthma including bronchial hyper-reactivity, bronchoconstriction, mucosal edema, and increased mucus secretion

Monteleukast and Zafirlukast block LTD4 receptors

  • decrease bronchial reactivity and bronchoconstriction
  • decrease mucosal hypersecretion and mucosal edema
  • decrease airway inflammation
  • especially good for asprin-induced asthma
17
Q

What are the adverse effects of the LT antagonists?

A

Zafirlukast: GI disturbances, mild headache and elevation of liver enzymes in some patients. High doses in rodents have caused hepatic and bladder cancer and histocytic carcinoma

Monteleukast: GI disorders, layrngitis, pharyngitis, nausea, otitis, sinusitis and viral infections (more frequent in peds population). Possible association with suicidal ideation.

18
Q

Name the only LT synthesis inhibitor (Anti-inflammatory) and describe MOA

A

Zileuton

  • inhibits LTB4, C4, D4, E4 formation
  • decreases smooth muscle contraction and blood vessel permeability and reduces leukocytes migration to teh damaged area
  • causes hepatic enzyme elevation - LFTs required
  • CYP1A2 substrate and inhibitor - interaction with theophylline
  • most other effects mild and self-limiting
  • under evaluation for other inflammation-related diseases like RA, ulcerative colitis and acne
19
Q

Name the only anti-IgE antibody and describe the MOA

A

Omalizumab

  • binds to IgE and prevents IgE-instigated release of inflammatory mediators, which decreases allergic response
  • reduces severity and frequency of asthma attacks
  • reduces requirement of inhaled corticosteroids, improves long term asthma control
20
Q

What are the adverse effects of Omalizumab?

A
  • serious allergic rxns: difficulty breathing, closing of throat, swelling of face, lips or tongue, and hives
  • less erious effects: redness, bruising, warmth, burning, stinging, itching, pain or inflammation at injection site or sore throat or cold Sx
  • initial concenrs for tumors
  • increase in CV complications: MI, CAD, arrhythmias
  • contraindications: no known drug interactions
21
Q

What is COPD?

A

Progressive loss of airflow in lungs resulting in broncho-constriction that is not fully reversible. Primarily caused by chronic inflammation. The two common forms are bronchitis and emphysema.

  • Elastic parenchymal tissue is replaced by inelastic fibrotic tissue such that elastic recoil of lung is lost. Collapse of airways mid-exhalation leads to air trapping, loss of capacity and, in some cases, impaired gas exchange.
22
Q

Asthma vs. COPD

  • Age
  • Sx
  • Allergic Etiology
  • Treatment response to: bronchodilators, corticosteroids, smoking status, airflow limitation
A

Asthma

  • young (child)
  • variable dyspnea
  • allergic etiology in >50%
  • Treatment response to bronchodilators (reversible), corticosteroids (good), smoking status (nonsmokers affected), airflow limitation (can normalize after resolution of episode)

COPD

  • older (>40 y/o)
  • progressive dyspnea
  • no allergic etiology association
  • Treatment response to bronchodilators (partially reversible), corticosteroids (poor), smoking status (usually long smoking hx), airflow limitation (cannot normalize; progressive deterioration wtih advancing age)
23
Q

COPD Treatment Options

A

Smoking cessation (welbutrin)

Bronchodilators (B2 adrenergic receptor agonists)

  • Short acting to releive Sx: albuterol or terbutaline
  • Long acting: salmeterol/fluticasone, formoterol/budesonide, indacaterol, vilanterol/fluticasone

Antimuscarinic Agents: Ipratopium, Umeclidinium bromide/Vilanterol

Theophylline and derivatives

24
Q

Contraindicated Drugs in Airway Disease

A
  • Sedatives
  • Beta Blockers (if you need to use, then use selective B1 blockers such as atenolol)
  • Aspirin adn other COX inhibitors
  • ACE-I (increased levels of bradykinin and PGE2)
  • Local anesthetics containing epinephrine
25
Q

What is one respiratory stimulant?

A

Doxapram

  • post-anesthesia respiratory depression
  • drug-induced respiratory depression
  • acute hypercapnia in COPD
  • activates peripheral carotid receptors
  • narrow margin of safety
  • short acting (given IV)

Pulmonary (10 decks)

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