Classification:

1. Adrenergic agonist

2. *Alpha₁, Alpha₂, Beta₁ and Beta₂

3. *Low doses are selective for Beta₁

Mechanism of action:

1. Agonist of adrenergic receptors

Clinical uses:

1. Anaphylaxis

2. Emergency treatment of cardiac arrest

3. Added to local anesthetic to decrease rate of vascular absorption

Adverse effects:

1. Excess sympathomimetic effect

2. Ineffective orally

Classification:

1. Classic Beta adrenergic agonist

2. *Beta₁ = Beta₂ (Beta selective)

3. *Not taken up into nerve endings like Epinephrine and NE

Mechanism of action:

Agonist of B receptors

Clinical uses:

1. Acute asthma (obsolete)

2. Emergency treatment of cardiac arrest

Classification:

Indirect-acting sympathomimetic

Mechanism of action:

Causes release of norepinephrine --> nonselective sympathetic effects

Clinical uses:

1. Hypotension

2. Bronchospasm (obsolete)

3. Nasal decongestant

Classification:

Beta₂ adrenergic selective agonist

Mechanism of action:

Beta₂ receptor agonist --> stimulates adenylyl cyclase  --> increase in cAMP in smooth muscle cells --> bronchodilation

Clinical uses:

1. Athsma (For acute attacks, not for prophylaxis)

2. COPD

Adverse effects:

1. Skeletal muscle tremor

2. Positive ionotropic effects

3. Smooth muscle relaxation

4. Tachycardia

Step 1 Pneumonic:

Beta₂ agonists stop MAST-R cells

Metaproterenol (acute asthma)

Albuterol (acute asthma)

Salmeterol & formoterol (long-term asthma)

Terbutaline (reduce pre-mature uterine contractions)

Ritodrine (reduce premature uterine contractions)

Classification:

Beta₂ adrenergic selective agonist (longer onset, longer duration of action)

Mechanism of action:

Beta₂ receptor agonist --> stimulates adenylyl cyclase  --> increase in cAMP in smooth muscle cells --> bronchodilation

Clinical uses:

1. Athsma (prophylaxis, not for acute attacks)

2. COPD

Step 1 Pneumonic:

Beta₂ agonists stop MAST-R cells

Metaproterenol (acute asthma)

Albuterol (acute asthma)

Salmeterol & formoterol (long-term asthma)

Terbutaline (reduce pre-mature uterine contractions)

Ritodrine (reduce premature uterine contractions)

Classification:

Beta₂ adrenergic selective agonist

Mechanism of action:

Beta₂ receptor agonist --> stimulates adenylyl cyclase  --> increase in cAMP in smooth muscle cells --> bronchodilation

Clinical uses:

1. Athsma (For acute attacks, not for prophylaxis)

2. COPD

Step 1 Pneumonic:

Beta₂ agonists stop MAST-R cells

Metaproterenol (acute asthma)

Albuterol (acute asthma)

Salmeterol & formoterol (long-term asthma)

Terbutaline (reduce pre-mature uterine contractions)

Ritodrine (reduce premature uterine contractions)

Classification:

Beta₂ adrenergic selective agonist

Mechanism of action:

Beta₂ receptor agonist --> stimulates adenylyl cyclase  --> increase in cAMP in smooth muscle cells --> bronchodilation

Clinical uses:

1. Athsma (For acute attacks, not for prophylaxis)

2. COPD

Step 1 Pneumonic:

Beta₂ agonists stop MAST-R cells

Metaproterenol (acute asthma)

Albuterol (acute asthma)

Salmeterol & formoterol (long-term asthma)

Terbutaline (reduce pre-mature uterine contractions)

Ritodrine (reduce premature uterine contractions)

Classification:

Beta₂ adrenergic selective agonist (longer onset, longer duration of action)

Mechanism of action:

Beta₂ receptor agonist --> stimulates adenylyl cyclase  --> increase in cAMP in smooth muscle cells --> bronchodilation

Clinical uses:

1. Athsma (For prophylaxis, not for acute attacks)

2. COPD

Step 1 Pneumonic:

Beta₂ agonists stop MAST-R cells

Metaproterenol (acute asthma)

Albuterol (acute asthma)

Salmeterol & formoterol (long-term asthma)

Terbutaline (reduce pre-mature uterine contractions)

Ritodrine (reduce premature uterine contractions)

Drug Class:

Methylxanthine --> purine derivative

Mechanism of Action:

1. Non-specific inhibition of phosphodiesterase --> inhibition of cAMP degradation to AMP --> thus, cAMP increases --> tachycardia and SM relaxation

2. Blockage of adenosine receptors

3. Increased Ca²⁺ release in skeletal muscle --> stronger diaphragm?

Clinical Use:

1. Asthma (not as effective as Beta₂ agonists)

2. Slow-release formulations for nocturnal asthma

Adverse Effects:

1. Tachycardia

2. Gastrointestinal distress, emesis

3. Tremor

4. Insomnia & headaches

5. Arrhythmias/seizures with large doses

Category:

Muscarinic competitive antagonist

Mechanism:

Quaternary ammonium (4^o) competitive antagonist of muscarinic receptors in airway --> prevents bronchoconstriction mediated by vagal discharge

*Designed to be aerosolized, thus it results in little systemic action. If given systemically, they are indistinguishable from other short-acting muscarinic blockers.

Clinical Use:

1. Asthma

2. COPD

Pneumonic:

Ipratropium = I-PRAy-that I can breath soon!

Category:

Muscarinic competitive antagonist

Mechanism:

Quaternary ammonium (4^o) competitive antagonist of muscarinic receptors in airway --> prevents bronchoconstriction mediated by vagal discharge

*Designed to be aerosolized, thus it results in little systemic action. If given systemically, they are indistinguishable from other short-acting muscarinic blockers.

Clinical Use:

1. Asthma

2. COPD

Adverse effects:

1. Atropine-like effects

*Since they are not readily absorbed systemically, there are relatively few side effects

Pneumonic:

It saves me from three (M₃) TIOS (uncles) that try to strangle (bronchoconstrict) me!!!

(drug = broncodilation)!

Category:

Mast Cell stabilizer

Mechanism:

1. Poorly understood, but prevents release of mast cell mediators

2. No bronchodilation activity, but can prevent bronchoconstriction caused by allergy

Clinical Use:

1. Asthma

2. Allergy

Adverse Effects:

1. Only local effects as it is very insoluble

2. Aerosol: cough or irritation

3. Possible drug allergy

Category:

Inhaled corticosteroid

Mechanism:

Binds cytosolic glucocorticoid receptor --> transocates into nucleus --> binds nuclear response elements --> transcription leads to antiinflammatory effects:

1. Reduced synthesis of arachidonic acid by phospholipase A₂

2. Inhibition of COX-2 expression --> reduction in leukotriene and prostaglandin synthesis

*May increase responsiveness of Beta₂ adrenoreceptors in airway

Clinical Use:

1. Asthma prophylaxis (moderate cases not fully responsive to Beta₂ agonists)

2. Allergic rhinitis

Adverse Effects:

1. Frequent aerosol administration --> small degree of adrenal suppression

2. Candidiasis from changes in oropharyngeal flora

3. Mild growth retardation in children

Category:

Systemic corticosteroid

Mechanism:

Binds cytosolic glucocorticoid receptor --> transocates into nucleus --> binds nuclear response elements --> transcription leads to antiinflammatory effects:

1. Reduced synthesis of arachidonic acid by phospholipase A₂

2. Inhibition of COX-2 expression --> reduction in leukotriene and prostaglandin synthesis

*May increase responsiveness of Beta₂ adrenoreceptors in airway

Other:

Increases gluconeogenesis and muscle catabolism --> maintains serum glucose levels --> increased release of amino acids, decreased peripheral glucose uptake, increased lipolysis, weak mineralcorticoid activity

Clinical Use:

1. Severe refractory chronic asthma

Adverse Effects:

1. Adrenal suppression

2. Growth retardation

3. Muscle wasting

4. Osteoporosis

5. Salt retention

6. Glucose intolerance

7. Behavioral changes

Category:

Systemic corticosteroid given parenterally

Mechanism:

Bind nuclear response elements --> reduce synthesis of arachidonic acid by phospholipase A₂ & inhibit expression of COX-2 --> reduction in leukotriene and prostaglandin synthesis

*May increase responsiveness of Beta₂ adrenoreceptors in airway

Clinical Use:

1. Status Asthmaticus

Adverse Effects:

1. Adrenal suppression

2. Growth retardation

3. Muscle wasting

4. Osteoporosis

5. Salt retention

6. Glucose intolerance

Category:

Leukotriene receptor blocker

Mechanism:

Blockage of the LTD₄ and LTE₄ receptors --> inhibition of signalling

Clinical Use:

Prevention of:

1. Exercise-induced asthma

2. Antigen-induced asthma

3. Aspirin-induced asthma

Adverse Effects:

1. Churg-Strauss syndrome (allergic granulomatous angiitis)

Category:

Lipoxygenase inhibitor

Mechanism:

Selective inhibitor of 5-lipoxygenase --> disruption of arachdonic acid conversion to leukotrienes

Clinical Use:

Prevention of:

1. Exercise-induced bronchospasm

2. Antigen-induced bronchospasm

3. Effective against aspirin allergy

Adverse Effects:

1. Occasional elevation of liver enzymes

Category:

Humanized anti-IgE murine monoclonal antibody

Mechanism:

Binds IgE that is on sensitized mast cells --> inhibits mast cell activation

Clinical Use:

1. Prophylaxis of asthma

Adverse Effects:

1. Expensive and must be administered parenterally

1.Activation of beta-2 receptors on bronchiolar smooth muscle

2.Beta-2 receptor (GPCR) increases cAMP production

3.Increased cAMP activates protein kinase A (PKA)

4.PKA phosphorylates myosin light chain kinase (MLCK)

5.Phosphorylated MLCK has a decreased affinity for
 (Ca²⁺)calmodulin

6.Results in less phosphorylation of myosin light chain

7.Leads to decreased activity of smooth muscle actin/myosin

8.Ultimately, leads to bronchodilation

Beta blockers:

- can precipitate acute attacks in asthmatics

- neutralizes most effective treatment for acute attacks

- precipitate asthma in patients undiagnosed athsmatic

- Selective Beta₁ blockers are not completely selective

Drug Class:

Methylxanthine --> purine derivative

Soluble ethelenediamine salt of theophylline

Mechanism of Action:

1. Inhibition of phosphodiesterase --> inhibition of cAMP degradation to AMP --> thus, cAMP increases

2. Blockage of adenosine receptors in CNS --> not related to bronchodilation

Clinical Use:

1. Status asthmaticus (IV) as adjunct with IV or inhaled sympathomimetic

Adverse Effects:

1. Tachycardia

2. Gastrointestinal distress

3. Tremor

4. Insomnia

5. Arrhythmias/seizures with large doses