MCC EENT pharm

First generation antihistamine

-brompheniramine

-cyclizine

-cyproheptadine,

-diphenhydramine (Benadryl)

-hydroxyzine

-meclizine

-promethazine

First generation antihistamines crosses BBB (caused drowsiness)

Second/third generation antihistamines

-azelastine (intranasal)

-cetirizine (zyrtec)

-loratadine (claritin)

-fexofenadine (allegra)

-olopatadine (nasal/ophthalmic)

-ketotifen (ophthalmic)

don't cross BBB

Antitussives

Opiates: codeine

Non-opioid central: dextromethorphan

Local anesthetic: benzonatate

Bronchodilators

β2 agonists

SABA (Short-Acting Beta-Agonists)

-albuterol

-levalbuterol

-terbutaline

LABA (Long-Acting Beta-Agonists)

-formoterol

-salmeterol

-vilanterol

-arformoterol

Bronchodilators

Antimuscarinics

SAMA (Short-Acting Muscarinic-Antagonists)

-ipratropium

LAMA (Long-Acting Muscarinic-Antagonists)

-tiotropium

-umeclidinium

Decongestants

Oral:

pseudoephedrine >>phenylephrine

Intranasal:

-oxymetazoline

-tetrahydrozoline

-naphazoline

Expectorants

Guaifenesin

Guaifenesin may aid mucus clearance but has limited evidence.

Corticosteroids

Inhaled (ICS): budesonide, fluticasone, beclomethasone

Oral: prednisone, prednisolone

Injectable: hydrocortisone, methylprednisolone

Intranasal: fluticasone, beclomethasone, flunisolide, budesonide

Leukotriene Inhibitors

Receptor antagonists:

-montelukast

5-lipoxygenase inhibitor:

-zileuton

Mucolytics

N-acetylcysteine

Anti-IgE Monoclonal Antibody

Omalizumab

(Note: Dupilumab blocks IL-4/IL-13 signaling, not IgE.)

Antihistamines MOA

Reversibly and competitively bind H1 receptors (inverse agonists), stabilizing them in the inactive state

-some also block muscarinic and α-adrenergic receptors.

Antihistamines Uses

Allergic rhinitis, urticaria, conjunctivitis; motion sickness and insomnia (first-gen only)

-hydroxyzine for anxiety and pruritus.

H1 receptor - bronchial smooth muscle, nasal epithelium, brain

H2- in the gut and heart, mast cells

Antihistamines: Adverse Effects

Sedation, impaired coordination (first-gen

-dry mouth, urinary retention (antimuscarinic)

-hypotension and dizziness (α-blockade).

Antitussives: Codeine

MOA: μ-opioid receptor agonist in the medullary cough center

-used for dry, nonproductive cough

-Side effects: may cause sedation and constipation.

Antitussives: Dextromethorphan

MOA: NMDA receptor antagonist; suppresses cough reflex centrally;

Side effects: can cause hallucinations and abuse potential at high doses.

dayquil/robitussin

Antitussives: Benzonatate

(aka Tessalon perles)

MOA: Peripherally anesthetizes stretch receptors in lungs and pleura; reduces cough reflex

Side effects: may cause hypersensitivity, bronchospasm, confusion.

Bronchodilators: β2 Agonists

MOA

Stimulate β2 receptors → activate adenyl cyclase → increase cAMP → activate protein kinase A→ bronchodilation.

Bronchodilators: β2 Agonists

Use

SABA for rescue of acute bronchospasm

LABA for maintenance or with inhaled corticosteroids.

Bronchodilators: β2 Agonists

Side effects

Tremor, nervousness, tachycardia, palpitations; tolerance with overuse; LABA monotherapy increases asthma-related deaths.

LABAs must never be used as monotherapy in asthma.

Single maintenance and reliever therapy (SMART)

For asthma: Single maintenance and reliever therapy (SMART)- inhaled corticosteroid (budesonide) + LABA (formoterol) is superior therapy than SABA alone (albuterol)

No risk of bronchospasm caused by albuterol

Bronchodilators: Antimuscarinics

MOA

Block M3 receptors → prevent bronchoconstriction and mucus secretion.

Bronchodilators: Antimuscarinics

Uses

First-line for COPD

-combined with β2 agonists for severe asthma.

Bronchodilators: Antimuscarinics

Side effects

Dry mouth, bitter taste, possible urinary retention; avoid eye exposure (glaucoma risk).

Decongestants: Pseudoephedrine (oral), oxymetazoline (nasal)

MOA

α1-adrenergic agonists cause vasoconstriction of nasal mucosa → reduce edema and congestion.

Decongestants: Pseudoephedrine (oral), oxymetazoline (nasal)

Uses

Short-term relief of nasal obstruction. Max use 3 days

Decongestants: Pseudoephedrine (oral), oxymetazoline (nasal)

Side effects

Insomnia, tachycardia, headache; rebound congestion (rhinitis medicamentosa) if used >3 days

Causes vasoconstriction so avoid in hypertension, glaucoma, urinary retention, pregnancy.

Expectorants: Guaifenesin (mucinex)

MOA, Use, SEs

Increases hydration of respiratory secretions to thin mucus, easing clearance.

Uses: Symptomatic relief of thick mucus; limited evidence of efficacy.

AEs: Rare; nausea or stomach upset occasionally.

Little efficacy

Corticosteroids

MOA

-Suppress inflammatory gene expression and mediator release (via HDAC2 activation and PLA2 inhibition)

-reduce inflammatory cells in airways

-reduce capillary permeability and mucosal edema

-increase β2 receptor sensitivity (upregulation).

Corticosteroids

Uses

Inhaled/Intranasal:

-Maintenance therapy in asthma

-allergic rhinitis (most effective for congestion).

Systemic:

-Acute asthma/COPD exacerbations.

Corticosteroids

side effects

Inhaled/Nasal:

-Dysphonia (hoarse voice)

-oral candidiasis (thrush)

-nasal burning & epistaxis

Systemic:

-Adrenal suppression

-osteoporosis

-HTN

-hyperglycemia

-weight gain

-taper to avoid withdrawal.

Leukotriene Inhibitors

MOA

Montelukast blocks cysteinyl-LT1 receptors.

Zileuton inhibits 5-lipoxygenase, preventing leukotriene synthesis.

Leukotriene Inhibitors

Uses

Maintenance of mild to moderate asthma, prevention of exercise- or NSAID-induced bronchospasm.

Leukotriene Inhibitors

Side effects

-Liver enzyme elevation

-dyspepsia (abdominal pain)

-montelukast carries a boxed warning for neuropsychiatric effects (depression, suicidal ideation).

Mucolytics

MOA, Uses, Side effects

Break disulfide bonds in mucoproteins and DNA to liquefy secretions.

Uses: COPD or bronchitis with thick mucus; also antidote for acetaminophen overdose (IV form).

AEs: Unpleasant odor/taste, possible bronchospasm in sensitive patients.

Anti-IgE Monoclonal Antibody: Omalizumab

MOA

Binds free IgE, preventing its attachment to mast cells and basophils → less mediator release.

Anti-IgE Monoclonal Antibody: Omalizumab

Use

Moderate-to-severe allergic asthma not controlled by standard therapy.

Anti-IgE Monoclonal Antibody: Omalizumab

Side effects

Injection-site reactions, anaphylaxis (rare), high cost limits first-line use.

Aerosol Inhalation - drugs

The route is essential for drugs like β2 agonists, corticosteroids, cromolyn, and antimuscarinics.

-It minimizes systemic side effects compared to oral or IV routes.

-rapid onset with delivery to the lungs

Aerosol Inhalation - devices

Metered-dose inhaler (MDI): Slow, deep inhalation while pressing canister; hold breath 10 seconds.

Dry Powder Inhaler (DPI): Quick, deep breath; hold 5–10 seconds.

Soft Mist Inhaler (SMI): Slow mist, deep inhalation; hold 10 seconds.

Case 1: Seasonal Allergic Rhinitis

-Loratadine (anti-H1) reduces sneezing.

-Pseudoephedrine (α1-agonist) reduces nasal congestion/runny nose.

-Olopatadine (anti-H1) treats itchy, watery eyes.

-Intranasal glucocorticoids provide best overall symptom control.

Case 2: Chronic Nasal Congestion from Oxymetazoline

Diagnosis: rhinitis medicamentosa (rebound congestion from α-agonist overuse).

Management: discontinue oxymetazoline, switch to intranasal corticosteroid.

Case 3: Postnasal Drip, Clear Rhinorrhea, Sneezing, Stuffy Nose

Rapid relief: intranasal antihistamine (azelastine).

Add intranasal steroid for longer-term control.

Consider ipratropium (SAMA) for persistent rhinorrhea.

Asthma Treatment

Rescue:

-SABA (albuterol).

Maintenance:

-ICS + formoterol (SMART) regimen for both controller and reliever.

Severe disease:

-Add-on LAMA or biologic (omalizumab, dupilumab).

COPD Treatment

First-line maintenance:

-LAMA (most effective bronchodilator) > LABA …or LABA/LAMA combination.

Acute exacerbation:

-SABA + SAMA (Duoneb).

Inhaled corticosteroids:

-Consider in frequent exacerbations or asthma overlap.

NAC can thin mucus in COPD but doesn’t improve outcomes.