PHARMACOLOGY 2109 | Respiratory Drugs



Essential for life: 5–6 minutes without breathing can cause death.
Provides oxygen for cellular activity.
Removes excess acids and bases through gas exchange.
ALLERGIC RHINITIS


Allergic rhinitis (hay fever) = inflammation of the nasal mucosa
caused by allergens.
Not life-threatening but affects millions → needs pharmacotherapy to
control symptoms and prevent complications.
Signs & Symptoms:
 Like the common cold:
 Tearing eyes, sneezing, nasal congestion, postnasal drip,
itchy throat
 Possible complications:
 Loss of taste/smell, sinusitis, chronic cough, hoarseness, ear
infections in children
Causes
 Allergens (antigens): pollens, mold spores, dust mites, foods,
animal dander.
 Non-allergenic irritants: smoke, fumes, pollutants.
 Genetic predisposition increases risk.
Types
1. Seasonal allergic rhinitis – occurs during high pollen seasons
(spring/fall).
2. Perennial allergic rhinitis – year-round due to indoor allergens
(dust, pets, mold).
3. Mixed – some patients react to both seasonal and perennial
allergens.
Pathophysiology:
Allergen exposure
Immune system reaction = IgE produce
Mast cell activation
Release of chemical mediators
Inflammatory Response
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PHARMACOLOGY 2109 | Respiratory Drugs




Mast cells (connective tissue cells) and basophils (WBCs) in nasal
mucosa react to allergens.
Immediate hypersensitivity reaction: histamine release → sneezing,
itching, watery eyes.
Delayed reaction (4–8 hrs): ongoing inflammation → chronic
congestion.
Symptoms mimic inflammation because histamine is the main
mediator.
Treatment Goals: Prevent occurrence and Relieve symptoms
Histamine
 is a chemical mediator of inflammation that plays a central role in
allergic reactions.
 expose an allergen, mast cells and basophils release histamine,
triggering a cascade of physiological effects that lead to the
characteristic symptoms of an allergic response.
Role of Histamine in the Body
A. Source and Release
 Released from mast cells and basophils during allergic or
inflammatory reactions.
 Acts locally on surrounding tissues and blood vessels.
B. Physiologic and Pathologic Effects
 Mild allergic reactions:
 Itching (pruritus)
 Increased mucus secretion
 Nasal congestion
 Severe allergic reactions (anaphylaxis):
 Bronchoconstriction → difficulty breathing
 Vasodilation → hypotension
 Edema → tissue swelling
C. Histamine Receptors
1. H1 Receptors – found in smooth muscles, endothelial cells, and
sensory nerves; responsible for allergic symptoms.
2. H2 Receptors – located in the gastric mucosa; stimulate secretion of
gastric acid, leading to peptic ulcer formation.
Therapeutic Management:
A. H1 Receptor Antagonists (Antihistamines)
 commonly known as antihistamines, are drugs that selectively block
histamine from binding to H1 receptors, thereby preventing or
reducing allergic symptoms.
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PHARMACOLOGY 2109 | Respiratory Drugs
Therapeutic Uses of Antihistamines
 Primary Use – Allergic Rhinitis
 Relieve sneezing, rhinorrhea (runny nose), nasal congestion, and
itchy eyes/nose/throat.
 Most effective when taken prophylactically
 May lose effectiveness with long-term use (tolerance).
Pharmacologic Effects and Mechanism of Action
Mechanism of Action
 Block histamine binding to H1 receptors → prevent vasodilation,
capillary permeability, and smooth muscle contraction → reduce
allergy symptoms.
Additional (Anticholinergic) Effects
 Many antihistamines also block acetylcholine, producing
anticholinergic effects, such as:
 Drying of mucous membranes → less nasal congestion and
tearing
 Possible adverse effects: dry mouth, urinary hesitancy, blurred
vision
Classification and Characteristics
 First-Generation
- Ex. Diphenhydramine, Clemastine, Chlorpheniramine
- Cross blood-brain barrier; cause drowsiness and anticholinergic
effects
 Second-Generation
- Ex. Loratadine, Desloratadine, Fexofenadine, Cetirizine
- Less sedating; preferred for daytime use
Adverse Effects and Precautions
Common Adverse Effects
 Sedation and drowsiness (especially with first-generation agents)
 CNS depression—enhanced when taken with alcohol or other
sedatives
 CNS stimulation (rare): insomnia, nervousness, tremors
Anticholinergic Adverse Effects
 Dry mouth
 Urinary hesitancy (especially problematic in patients with
prostatic hypertrophy)
 Constipation
Other Therapeutic Applications - antihistamines are used in
several other conditions due to their anticholinergic and CNS
effects:
1. Vertigo and Motion Sickness
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PHARMACOLOGY 2109 | Respiratory Drugs
 Suppress the vomiting center in the medulla.
 Common drugs: Meclizine (Antivert), Dimenhydrinate
(Dramamine).
 Should be taken before travel or symptom onset.
2. Parkinson’s Disease and Drug-Induced Tremor
 Diphenhydramine may be used for its anticholinergic properties
to manage tremors.
3. Insomnia
 Diphenhydramine and Doxylamine (Unisom) act as mild
sedatives.
 Should be used for short-term less than weeks due to
tolerance.
4. Urticaria (Hives) and Skin Rashes
 Reduce itching and redness.
 Available as oral or topical preparations.
Nursing Considerations and Patient Education
 Assess for allergies, respiratory status, and sedation level before
administration.
 Instruct patients to avoid driving or operating machinery if drowsy.
 Advise avoiding alcohol and CNS depressants.
 Encourage adequate fluid intake and frequent mouth care for dry
mouth.
 Educate that these medications are preventive, not curative, for
allergic reactions.
B. Intranasal Corticosteroids



First-line therapy due to their superior efficacy in controlling
inflammation and preventing recurrence.
Corticosteroids, also known as glucocorticoids, are synthetic drugs
that mimic the action of cortisol, a hormone produced by the adrenal
cortex.
They exert potent anti-inflammatory and immunosuppressive
effects, making them valuable in managing a wide range of allergic
and inflammatory conditions.
Rationale for Intranasal Administration
Systemic vs. Local Use
 Systemic corticosteroids (oral or parenteral) can cause serious
side effects such as adrenal suppression, weight gain, and
osteoporosis with long-term use.
 Intranasal corticosteroids, however, act locally on the nasal
mucosa with minimal systemic absorption, making them safe
and well-tolerated for long-term therapy.
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PHARMACOLOGY 2109 | Respiratory Drugs
Mechanism of Action: When applied to the nasal mucosa,
intranasal corticosteroids:
Suppress the release of inflammatory
mediators (e.g., histamine, leukotrienes,
prostaglandins).
Reduce tissue edema
Cause mild vasoconstriction = decreased nasal
congestion
Inhibit recruitment of inflammatory cells
(eosinophils, basophils, lymphocytes)
Administration and Pharmacologic Considerations
Route and Devices -Delivered via a metered-dose nasal spray,
ensuring a consistent dose per application; commonly administered
OD or BID, depending on the formulation.
Onset and Duration - no immediate relief—unlike
decongestants/sympathomimetics; peak response: achieved after 1
to 3 weeks of continuous use; Most effective for prophylactic use.
Examples of Common Intranasal Corticosteroids
 Fluticasone (Flonase)
 Mometasone (Nasonex)
 Budesonide (Rhinocort)
Nursing Considerations and Patient Teaching
 Teach correct spray technique (head slightly tilted forward, avoid
septum).
 Emphasize daily adherence for optimal results.
 Inform that symptom relief is gradual, not immediate.
 Encourage saline nasal sprays for dryness.
 Instruct to report persistent epistaxis or irritation.
 Evaluate for improvement in nasal congestion and sneezing after
1–3 weeks.
C. Decongestants


used to relieve nasal congestion; a common symptom of allergic
rhinitis, sinusitis, or the common cold.
primarily by reducing swelling of the nasal mucosa, improving
airflow and relieving obstruction.
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PHARMACOLOGY 2109 | Respiratory Drugs

may be administered orally or intranasally, and are often
combined with antihistamines to provide broader relief from allergy
or cold symptoms such as sneezing and rhinorrhea.
Mechanism of Action
Most decongestants are classified as sympathomimetics, meaning they
mimic the effects of the sympathetic nervous system.
 Specifically, they stimulate alpha-adrenergic receptors in the nasal
mucosa.
 Activation of these receptors causes vasoconstriction, which
reduces blood flow, diminishes edema, and decreases nasal
congestion.
Routes of Administration
Intranasal Decongestants
 Examples: Oxymetazoline (Afrin) and Phenylephrine (NeoSynephrine, Vicks).
 Available over-the-counter as nasal sprays or drops.
 Produce a rapid onset of action, often within minutes, making them
useful for immediate relief.
 Systemic absorption is minimal, thus systemic side effects are rare.
Warning: Rebound Congestion
 Rebound congestion (rhinitis medicamentosa) occurs with prolonged
use (more than 3–5 days).
 It is characterized by hypersecretion of mucus, nasal swelling, and
worsening congestion once the drug effect wears off.
Oral Decongestants
 Common agents: Pseudoephedrine and Phenylephrine.
 Onset of action is slower compared to intranasal forms.
 Less effective for severe congestion, but do not cause rebound
congestion.
Potential Adverse Effects (Systemic):
 HPN, Central nervous system (CNS) stimulation — insomnia, anxiety,
restlessness
 Palpitations or tachycardia in sensitive patients
Nursing Considerations
 Educate to limit the use of intranasal decongestants to 3–5 days.
 Monitor for HPN, tachycardia, or insomnia in patients taking oral
forms.
 Caution in patients with cardiovascular disease, hyperthyroidism, or
glaucoma.
 Encourage adequate hydration and humidified air to relieve dryness.
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PHARMACOLOGY 2109 | Respiratory Drugs
COMMON COLDS
-
is a viral infection that primarily affects the upper respiratory tract.
Transmission: The virus spreads through droplets, direct contact, or
contaminated surfaces.
Incubation period: Typically, 1 to 3 days after exposure.
Duration: self-limiting, usually resolving within 7 to 10 days.
Pathophysiology
virus invades the nasal mucosa
triggers an inflammatory response
release of chemical mediators
(Histamine, prostaglandin, and cytokines
s/sx
Note: the symptoms are primarily due to inflammation, and not direct
viral damage, treatment focuses on symptom relief rather than
eradication of the virus.
S/Sx:
 Nasal congestion and rhinorrhea (runny nose)
 Sneezing
 Sore throat
 Cough
 Mild headache or malaise
 Occasionally, low-grade fever
Therapeutic Management:
ANTITUSSIVE
-
cough is a protective reflex mechanism designed to clear the airways of
mucus, foreign particles, and irritants.
- It involves:
 Stimulation of cough receptors in the respiratory tract (larynx,
trachea, bronchi).
 Transmission of impulses to the cough center in the medulla
oblongata.
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PHARMACOLOGY 2109 | Respiratory Drugs
Forceful expulsion of air to remove secretions or irritants.
- Antitussives are drugs that suppress or dampen the cough reflex.
- While this reflex is essential for airway protection, not all coughs are
beneficial.
 Productive coughs (with sputum) help clear the lungs and should not
be suppressed.
 Dry, hacking, nonproductive coughs, however, can be irritating and
may disturb sleep or cause throat discomfort—these are the types
best treated with antitussives.

Definition and Classification
Classified into two major groups based on their mechanism of action:
1. Opioid Antitussives
- are the most effective agents for suppressing cough.
Mechanism of Action: act centrally on the medulla, raising the
cough threshold and reducing the urge to cough.
Common Drugs: Codeine and Hydrocodone
Key Pharmacologic Points:
 Effective at low doses and low risk of dependence when used short
term in cough suppression.
 Often combined with other drugs such as antihistamines or
decongestants in cough and cold preparations.
Precautions and Adverse Effects
 Respiratory depression in cases of overdose.
 Use with caution in asthma and other respiratory diseases
because they may cause bronchoconstriction.
 Sedation, constipation, and nausea may also occur.
2. Non-Opioid Antitussives
- safer alternatives, especially for mild to moderate coughs.
2.1. Dextromethorphan - most commonly used non-opioid
antitussive. Also acts in central medulla = raise cough threshold, but
without analgesic or addictive properties.
Adverse Effects:
 Generally mild at therapeutic doses.
 At high doses, it may produce CNS effects such as:
 Hallucinations
 Slurred speech
 Euphoria
 Drowsiness
 Lack of motor coordination
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PHARMACOLOGY 2109 | Respiratory Drugs
2.2. Benzonatate (Tessalon)
- Another non-opioid antitussive, but with a different
mechanism of action.
- Chemically related to local anesthetics such as tetracaine.
Mechanism of Action:
 Suppresses cough by anesthetizing stretch receptors in the
lungs, which prevents the cough reflex from being
triggered.
Adverse Effects:
 May cause sedation, nausea, headache, or dizziness.
 If the capsule is chewed or broken, it can numb the mouth
and pharynx, potentially leading to choking or aspiration.
Clinical Tip: Always instruct patients to swallow benzonatate
capsules whole.
Clinical Considerations and Nursing Responsibilities
1. Assess the Type of Cough
o Only nonproductive coughs should be suppressed.
o Productive coughs must be maintained to clear secretions.
2. Monitor for Adverse Reactions
o Watch for respiratory depression with opioids.
o Observe for CNS side effects with non-opioid antitussives.
3. Educate the Patient
o Avoid concurrent alcohol or CNS depressants.
o Emphasize dose adherence.
o Encourage hydration to soothe throat irritation.
4. Evaluate Effectiveness
o Relief of dry, irritating cough.
o Improved sleep and comfort.
EXPECTORANT AND MUCOLYTICS
Mechanism of Action and Therapeutic Purpose
A. Expectorants
- Expectorants increase bronchial secretions and reduce the
viscosity of mucus = mucus thinner and easier to expel through
coughing.
- The goal is to convert a dry, nonproductive cough into a
productive cough that effectively clears the airways.
Drug Example: Guaifenesin (Mucinex)
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PHARMACOLOGY 2109 | Respiratory Drugs
Mechanism of Action: Increases the hydration of respiratory
tract secretions, reducing their viscosity and promoting easier
clearance by coughing.
Clinical Use: dry, nonproductive cough; sometimes beneficial in
productive coughs by facilitating mucus clearance.
Adverse Effects: May cause nausea, dizziness, or drowsiness
in some patients.
B. Mucolytics
- Mucolytics chemically break down the structure of mucus
molecules, directly reducing their thickness and stickiness.
A. Acetylcysteine (Mucomyst)
Mechanism of Action: Breaks down disulfide bonds within
mucus proteins, directly reducing the viscosity of bronchial
secretions.
Clinical Uses: Cystic fibrosis, Chronic bronchitis, COPD, and
Conditions with thick, tenacious mucus
Adverse Effects:
 Bronchospasm (especially in asthmatic patients)
 Unpleasant odor like rotten eggs due to its sulfur content
 Nausea or irritation of the respiratory tract
Special Use:
Acetylcysteine (Acetadote) is also given intravenously as an
antidote for acetaminophen overdose, where it restores hepatic
glutathione levels and prevents liver damage.
B. Dornase Alfa (Pulmozyme)
Mechanism of Action: An enzyme that breaks down DNA
molecules in thick mucus, decreasing its viscosity.
Clinical Use: maintenance therapy in cystic fibrosis, helping
to clear secretions and prevent infections.
Adverse Effects: may cause hoarseness, sore throat, or chest
pain, but generally well tolerated.
Nursing and Clinical Considerations
1. Assessment
o Evaluate the type of cough and sputum characteristics (color,
amount, viscosity).
o Assess for underlying respiratory disorders such as asthma, COPD,
or cystic fibrosis.
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PHARMACOLOGY 2109 | Respiratory Drugs
2. Administration and Monitoring
o For mucolytics, use a nebulizer and ensure proper inhalation
technique.
o Monitor for bronchospasm or signs of respiratory distress during
administration.
o Encourage fluid intake to enhance mucus clearance.
3. Patient Education:
o Advise patients not to use OTC cough products in children under 6
years old.
o Instruct on proper inhaler or nebulizer use for mucolytics.
o Emphasize the importance of not suppressing productive coughs
with antitussives when mucus clearance is necessary.
4. Expected Outcome
o Thinner secretions.
o Improved airway clearance.
o Decreased frequency and intensity of coughing.
Asthma and other Pulmonary Disorders
Why Inhalation Is Effective? Aerosol therapy delivers drugs directly to their
site of action, minimizing systemic side effects compared to oral or
intravenous routes.
Types of Inhalation Devices
1. Nebulizer – commonly used un acute settings for severe respiratory
distress.
2. Dry Powder Inhaler (DPI) – examples: Turbuhaler and Rotahaler.
3. Metered-Dose Inhaler (MDI) - requires coordination between
inhalation and activation of the device.
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PHARMACOLOGY 2109 | Respiratory Drugs
Difference between the two:
 DPI: Breath-activated, no propellant, dry powder form, needs strong
inhalation effort.
 MDI: Uses propellant, requires coordination, produces a mist,
suitable with spacer.
Advantages of Aerosol Therapy
 Rapid onset of drug action, direct delivery to the target site
(bronchioles and alveoli).
 Lower systemic toxicity compared to oral medications.
 Provides immediate relief for bronchospasm, an acute constriction of
the airways.
Disadvantages and Nursing Considerations
 Only 10–50% of the drug may reach the lower respiratory tract.
 Systemic absorption can still occur, leading to potential adverse
effects.
 Proper patient education is essential:
ASTHMA
- chronic inflammatory disorder of the airways characterized by reversible
bronchoconstriction and airway hyperresponsiveness.
- most common chronic respiratory diseases.
- Asthma involves two major pathophysiologic components:
1. Bronchoconstriction – narrowing of the airway due to smooth muscle
contraction.
2. Inflammation – swelling of the airway mucosa and increased mucus
secretion.
Clinical Manifestations
 Shortness of breath (dyspnea)
 Wheezing and Coughing (often worse at night or early morning)
 Chest tightness
 Difficulty speaking during attacks
 In severe cases: cyanosis, use of accessory muscles, and panic due to
hypoxia
Goals of Asthma Management
Focuses on two therapeutic goals:
1. To terminate acute bronchospasms in progress
→ achieved with quick-relief (rescue) medications.
2. To prevent and reduce the frequency of future attacks
→ achieved with long-term (maintenance) medications.
Pharmacologic Therapy
A. Quick-Relief (Rescue) Medications - used to provide immediate
symptom relief during an acute asthma attack.
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PHARMACOLOGY 2109 | Respiratory Drugs
1. Short-Acting Beta₂-Adrenergic Agonists (SABAs)
- first-line agents for relieving acute bronchoconstriction.
There are two main receptor subtypes:
 Beta₁ receptors: Primarily located in the heart, responsible for
increasing heart rate and contractility.
 Beta₂ receptors: Found mainly in the bronchial smooth muscles,
uterus, and vascular smooth muscle.
Mechanism of Action
beta₂ receptor is stimulated
causes relaxation of bronchial smooth
muscle
=
Bronchodilation
(open the airways)
Classification of Beta-Adrenergic Agonists in Two Ways:
I. Based on receptor selectivity
 Nonselective Beta Agonists - act on both beta₁ and beta₂
receptors; effective bronchodilators but produce undesirable
cardiac side effects due to beta₁ stimulation.
Examples: Epinephrine and Isoproterenol (Isuprel).

Selective Beta₂ Agonists - only the beta₂ receptors found in the
lungs, minimizing cardiac effects; largely replaced nonselective
agents in asthma pharmacotherapy.
II. Based on duration of action.
 Short-Acting Beta Agonists (SABAs) - “rescue drugs” — used
to abort or terminate acute asthma attacks; onset within
minutes but duration of 2-6hrs.
Example: Pirbuterol (Maxair), Albuterol

Intermediate-Acting Beta Agonists - Used for intermittent
control of symptoms; duration up to 8hrs.
Example: Terbutaline
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PHARMACOLOGY 2109 | Respiratory Drugs

Long-Acting Beta Agonists (LABAs) - maintenance therapy in
patients with persistent asthma; Onset: Relatively slow — not
suitable for acute attacks; duration: Up to 12 hours
Example: Salmeterol
Caution: The FDA issued a black box warning due to
increased reports of asthma-related deaths among those
misusing LABAs as rescue medication.
Remember: LABAs should never be used alone for asthma
control. They must be combined with inhaled corticosteroids or
other controller drugs.
Adverse Effects
Generally safe, systemic exposure — especially from oral or
parenteral routes — may lead to:
 Tremors and nervousness
 Tachycardia or palpitations
 Angina or dysrhythmias in patients with cardiac impairment
 Tolerance development with chronic use, leading to decreased
effectiveness
Nursing Considerations
 Patient education on proper inhaler technique.
 Reinforce that short-acting beta agonists are for acute relief,
while long-acting ones are for maintenance.
 Monitor for cardiac symptoms, especially in elderly or cardiac
patients.
 Encourage regular follow-up and adherence to prescribed
controller medications.
2. Anticholinergics
- vital role in managing asthma and COPD
Mechanism of Action
REMEMBER!
Parasympathetic nervous system (PNS)  Through the
neurotransmitter acetylcholine = bronchoconstriction and increased
mucus secretion.
By blocking the parasympathetic system mimics the effects of
sympathetic activation, resulting in bronchodilation — like the
action of beta₂-agonists, but through a different pathway.
Clinical Applications
Anticholinergics are primarily indicated for:
 Bronchodilation in asthma.
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PHARMACOLOGY 2109 | Respiratory Drugs

Maintenance therapy in COPD, including chronic bronchitis
and emphysema
NOTE: beneficial in older adults or patients with cardiac disease,
where beta₂-agonists may cause unwanted tachycardia or
arrhythmias.
Common Anticholinergic Drugs in Respiratory Therapy
a. Ipratropium (Atrovent)
- Most prescribed for both asthma and COPD.
- Onset of action: Slower than most beta₂-agonists.
- Example: Combivent – a fixed-dose combination of
ipratropium + albuterol in a single metered-dose inhaler (MDI).
b. Tiotropium (Spiriva)
- prophylaxis and management of bronchospasm in patients
with COPD, including chronic bronchitis and emphysema.
- Longer duration of action than ipratropium.
- ideal for long-term maintenance.
c. Aclidinium (Tudorza Pressair)
- Approved in 2012 specifically for COPD treatment.
- rapid onset and sustained broncho dilating effect.
Pharmacokinetics and Route of Administration
Oral or parenteral forms caused significant systemic side effects:
 Blurred vision,
 Constipation, and
 Urinary retention,
 Tachycardia.
To minimize systemic toxicity, inhaled formulations were developed;
limiting absorption into the bloodstream — making them safer and more
tolerable for long-term use.
Adverse Effects
Common Adverse Effects
 Dry mouth - Due to decreased salivary secretion
 GI distress - Constipation or mild abdominal discomfort
 Headache - Mild and transient
 Anxiety or nervousness - Occasionally reported
Note: Systemic anticholinergic effects are rare when the drug is inhaled
properly.
Combination Therapy and Clinical Considerations
Anticholinergics + Beta₂-adrenergic agonists often yields superior
bronchodilation compared to either drug alone.
This dual mechanism — one blocking parasympathetic constriction, the
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PHARMACOLOGY 2109 | Respiratory Drugs
other stimulating sympathetic relaxation - provides a synergistic effect
that improves airflow and symptom control.
Nursing Considerations:
 Educate patients on the proper use of inhalers to ensure maximum
lung deposition.
 Encourage rinsing the mouth after inhalation to reduce dryness or
irritation.
 Assess for urinary retention in elderly males (especially with prostatic
hypertrophy).
 Monitor breathing patterns and respiratory status before and after
administration.
 Reinforce that these drugs are for maintenance therapy, not acute
rescue during asthma attacks.
3. Systemic Corticosteroids
-
Corticosteroids are considered the most potent natural antiinflammatory agents known to medicine.
Mechanism of Action
Corticosteroids suppress activation of
inflammatory cells.
(eosinophils, mast cells, and macrophages)
WHILE
Increase production of anti-inflammatory
mediators.
=
 Reduced mucus production
 Decreased airway edema
 Diminished airway obstruction
NOTE: Corticosteroids not directly cause bronchodilation, it enhances
responsiveness of bronchial smooth muscles to beta-adrenergic
agonists.
Routes of Administration: systemically or by inhalation
 Inhaled Corticosteroids (ICS) - for long-term prevention of
asthma attacks; suppress airway inflammation without major
systemic adverse effects; not effective for acute attacks.
Onset of effect: improvement within 1–2 weeks, with maximum
benefit after 4–8 weeks.
Often combined with a long-acting beta agonist (LABA) for additive
effects.
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PHARMACOLOGY 2109 | Respiratory Drugs

Systemic Corticosteroids - used for severe or unstable asthma
unresponsive to inhaled therapy; after stabilization, the patient is
switched to an inhaled corticosteroid for long-term control.
Short-term use only (typically 5–7 days) to minimize systemic
adverse effects.
Example: Oral prednisone.
Adverse Effects
 Inhaled Corticosteroids (Local Effects) - hoarseness (dysphonia);
oropharyngeal candidiasis (oral thrush) due to local
immunosuppression. Nursing Consideration: Rinsing the mouth after
each use can minimize this risk.
 Systemic Corticosteroids (Systemic Effects)





adrenal gland suppression and atrophy
peptic ulcer formation
hyperglycemia due to increased gluconeogenesis
growth retardation in children
osteoporosis with long-term use in adults Patients at risk
should undergo periodic bone mineral density testing.
NOTE: To minimize these risks, systemic therapy should be limited to
less than 10 days whenever possible.
Clinical Implications in Nursing Practice
 Monitoring patients for signs of systemic side effects, especially with
prolonged corticosteroid use.
 Educating patients on the importance of adherence to daily inhaled
therapy.
 Teaching correct inhaler techniques to ensure optimal drug delivery
and minimize local side effects.
 Encouraging patients to report symptoms such as oral white
patches, hoarseness, or signs of infection.
 Reinforcing that inhaled corticosteroids are preventive, not for
immediate relief during acute asthma attacks.
B. Long-Acting (Maintenance) Medications
- Used to control chronic inflammation and prevent future attacks.
 Inhaled Corticosteroids (ICS)
 Examples: Budesonide (Pulmicort), Fluticasone (Flovent)
 Mechanism: Suppresses airway inflammation and reduces mucus
production.
 Most effective long-term control therapy.
 Long-Acting Beta₂-Adrenergic Agonists (LABAs)
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PHARMACOLOGY 2109 | Respiratory Drugs
 Examples: Salmeterol (Serevent), Formoterol (Foradil)
 Mechanism: Maintains bronchodilation for up to 12 hours.
 Used only in combination with corticosteroids, not for acute
attacks.
C. Mast Cell Stabilizers
Mechanism of Action
 Inhibiting mast cells from releasing histamine and other chemical
mediators of inflammation, including prostaglandins and leukotrienes.
 By preventing this release, these drugs reduce airway inflammation,
decrease edema, and prevent bronchoconstriction.
In simple terms, they “stabilize” the mast cells to prevent inflammatory
cascades that trigger asthma attacks.
Therapeutic Role
 Used primarily for asthma prophylaxis (prevention), not for acute
attacks.
 Like corticosteroids, they must be taken daily to maintain their
preventive effect.
 Maximum benefit may take several weeks of consistent use.
NOTE: less effective than inhaled corticosteroids in managing chronic
asthma.
Drug Examples and Forms
a. Cromolyn (Intal)
Routes and Indications:
 Inhalation (MDI or nebulizer): Asthma prophylaxis
 Intranasal (Nasalcrom): Seasonal allergic rhinitis
 Ophthalmic (Crolom): Allergic conjunctivitis
 Oral (Gastrocrom): Systemic mastocytosis (FDA-approved), offlabel for ulcerative colitis and food allergies
Adverse Effects:
 Nasal irritation, burning, or congestion
 Throat irritation
 Rare: Bronchospasm and anaphylaxis
Special Note: Short half-life → requires 4–6 doses per day
b. Nedocromil (Tilade)
- Exhibit no serious systemic toxicity because of poor systemic
absorption.
- Effective for preventing asthma triggered by allergens or exercise.
Mechanism of Action: Prevents histamine release by stabilizing
mast cells.
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PHARMACOLOGY 2109 | Respiratory Drugs
D. Leukotriene Modifiers
Leukotrienes
- are chemical mediators of the immune and inflammatory response;
synthesized by mast cells, neutrophils, basophils, and eosinophils.
- when released into the airway, leukotrienes cause three key
pathophysiologic effects:
 Bronchoconstriction – tightening of airway smooth muscles
 Increased vascular permeability – leading to edema
 Airway inflammation and mucus secretion
- These effects contribute to airway obstruction and exacerbation
of asthma symptoms.
Mechanism of Action
it interferes the leukotriene pathway
Reduce airway inflammation
and
bronchoconstriction
Two main mechanisms by which these drugs act:
 Inhibition of Leukotriene Synthesis
 Zileuton (Zyflo CR) acts by inhibiting the enzyme
lipoxygenase, which prevents leukotriene formation.

Blockade of Leukotriene Receptors
 Zafirlukast (Accolate) and Montelukast (Singulair) act by
blocking leukotriene receptors on airway tissues,
preventing leukotrienes from exerting their effects.
NOTE: they are not direct bronchodilators; by reducing broncho
constrictive mediators, they indirectly improve airflow.
Clinical Uses: most effective for
 Persistent asthma not adequately controlled by inhaled
corticosteroids (ICS) or short-acting beta agonists (SABA).
 Exercise-induced bronchospasm (in some cases).
 Allergic rhinitis (especially montelukast).
‘Not first-line agents, but valuable adjunct therapy’
Adverse Effects
 headache, cough, nasal congestion
 Gastrointestinal upset (nausea, abdominal pain, or dyspepsia)
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PHARMACOLOGY 2109 | Respiratory Drugs
Special consideration:
 Older adults (≥65 years) may experience a higher incidence of
infections.
 Patients with hepatic impairment or chronic alcohol use should
avoid these drugs because they are extensively metabolized by
the liver.
Nursing Considerations
 Assessment
 Obtain baseline liver function tests (LFTs) before therapy.
 Evaluate the severity and control of asthma symptoms.
 Patient Education
 Emphasize that these drugs are for prevention, not for treating
acute attacks.
 Advise daily, consistent use, even when asymptomatic.
 Encourage patients to report signs of liver dysfunction such as
jaundice, fatigue, or dark urine.
 Monitoring
 Watch for drug interactions, particularly with theophylline and
warfarin (especially with zafirlukast).
 Reinforce adherence to concurrent inhaled corticosteroid therapy,
if prescribed.
Chronic Obstructive Pulmonary Disease
-
COPD is a progressive pulmonary disorder characterized by chronic
and recurrent obstruction of airflow in the lungs; not fully reversible
and gradually worsens over time.
The disease is marked by chronic inflammation, and loss of lung
elasticity.
There are three major conditions associated with COPD:
 Asthma – characterized by reversible airway obstruction and
hyperresponsiveness.
 Chronic Bronchitis – inflammation of the bronchi with excess
mucus production, resulting in productive cough and dyspnea.
 Emphysema – permanent enlargement and destruction of alveoli
leading to loss of gas exchange surface and severe dyspnea.
NOTE: asthma often grouped under COPD due to overlapping symptoms
and airway changes.
Pharmacologic Management: GOALS
 Relieve symptoms
 Prevent complications
 Slow disease progression
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PHARMACOLOGY 2109 | Respiratory Drugs
A. Bronchodilators
 Ipratropium (Atrovent) – anticholinergic that relaxes smooth
muscle and decreases mucus secretion.
 Beta₂-agonists – relieve bronchospasm and improve airflow
(short-acting or long-acting forms).
 Inhaled corticosteroids – reduce airway inflammation.
B. Mucolytics and Expectorants
 Help reduce mucus viscosity and facilitate clearance.
 Common examples: acetylcysteine or guaifenesin.
C. Oxygen Therapy
 Long-term oxygen therapy (LTOT) improves survival in severe
COPD by correcting chronic hypoxemia.
D. Antibiotics
 Indicated for patients with recurrent infections or acute
exacerbations.
E. Newer Agent: Roflumilast (Daliresp)
 A phosphodiesterase-4 inhibitor with anti-inflammatory effects.
 Reduces COPD exacerbations but not used for acute
bronchospasm.
Drugs to Avoid
 Beta-adrenergic antagonists (beta-blockers) – may cause
bronchoconstriction.
 Respiratory depressants such as opioids and barbiturates – can
suppress respiratory drive.
Nursing Implications and Patient Teaching
 Encourage smoking cessation — the most critical intervention that
can slow disease progression and reduce symptoms.
 Teach proper inhaler techniques and adherence to maintenance
therapy.
 Promote breathing exercises, adequate hydration, and balanced
nutrition.
 Educate about early signs of infection and when to seek medical
attention.
 Support psychological well-being and encourage participation in
pulmonary rehabilitation programs.
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