THERAPEUTICS I

COPD AND ALLERGIC RHINITIS

CHRONIC OBSTRUCTIVE
PULMONARY
DISEASE (COPD)
Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by chronic obstruction of lung
airflow that interferes with normal breathing and is not fully reversible.
Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation that is not fully
reversible. The most common conditions comprising COPD are chronic bronchitis and emphysema.

• Chronic bronchitis: chronic or recurrent excess mucus secretion with cough that occurs on most days for at
least 3 months of the year for at least 2 consecutive years.

• Emphysema: abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles,
accompanied by destruction of their walls, without fibrosis.

Chronic inflammatory changes lead to destructive changes and chronic airflow

limitation the most common cause is exposure to environmental tobacco smoke ,but other chronic
inhalational exposures can lead to COPD.
What is COPD……
• Progressive disease characterized by
airflow limitation that is not fully
reversible.
• Chronic bronchitis
• Emphysema
• Associated with an abnormal
inflammatory response of the
lung to noxious particles or gases,
mainly cigarette smoke.
What is COPD….
Chronic bronchitis Emphysema

• Chronic productive • Permanent enlargement

cough for at least 3 of the airspaces distal to
months in each of the 2 the terminal bronchioles
previous consecutive • Destruction of their walls
years without obvious fibrosis
• Chronic inflammation
• Inflammation in COPD is different from that seen in Asthma, use of
antiinflammatory medications and response to those medications are
different. Inflammation in asthma is mainly mediated through
eosinophils and mast cells. In COPD, the primary inflammatory cells
include neutrophils, macrophages and CD8+ T lymphocytes.
Causes and predisposing factors
• Tobacco smoking is the most common cause
• Indoor air pollution: Biomass fuel smoke (firewood,
charcoal and cow dung) exposure in poorly ventilated
kitchens
• Exposure to occupational dust and chemicals (cement,
paint, saw dust, fumes) without adequate protection
• It may frequently follow TB disease (residual symptoms) Occupational exposure to
dusts & chemicals also play a part
• Other risk factors: hereditary deficiency of α1-antitrypsin, asthma & airway hyper-
responsiveness
CLINICAL PRESENTATION
Initial symptoms include;
• chronic cough and sputum production; patients may experience cough for several years before
dyspnea develops.

• Physical examination is normal in most patients in milder stages.

• When airflow limitation becomes severe, patients may have cyanosis of mucosal membranes,
development of a “barrel chest” due to hyperinflation of the lungs, increased resting respiratory
rate, shallow breathing, pursing of lips during expiration, and use of accessory respiratory muscles.

• Patients experiencing COPD exacerbation may have worsening dyspnea, increased

sputum volume, or increased sputum purulence.
• Other features of exacerbation include chest tightness, increased need for bronchodilators,
malaise, fatigue, and decreased exercise tolerance.
• Rapid breathing, reduced chest expansion, with or without
increased use of accessory muscles of respiration, rhonchi,
cyanosis
• Decreased breath sounds, ankle swelling and other signs of
right heart failure
DIAGNOSIS

Diagnosis is based in part on patient symptoms and history of exposure

to risk factors such as tobacco smoke and occupational substances.

Classification of disease severity is based on assessment of airflow

limitation by spirometry, measurement of symptom severity, and
assessment of exacerbation frequency.
 Diagnosis of COPD
EXPOSURE TO RISK
SYMPTOMS FACTORS
Chronic cough tobacco
Chronic sputum occupation
shortness of breath indoor/outdoor pollution

è
SPIROMETRY
FEV1/FVC <70%
A diagnosis of COPD should be considered in any patient who has cough, sputum production, or dyspnea
and/or a history of exposure to risk factors. The diagnosis is confirmed by spirometry.
To help identify individuals earlier in the course of disease, spirometry should be performed for patients who
have chronic cough and sputum production even if they do not have dyspnea.
Spirometry is the best way to diagnose COPD and to monitor its progression and health care workers to care
for COPD patients should have assess to spirometry.
Differential diagnosis
• Asthma
• Congestive Heart failure
• Pulmonary embolism
• Pulmonary TB
TREATMENT
Goals of Treatment:
• Prevent or minimize disease progression
• relieve symptoms
• improve exercise tolerance
• improve health status
• prevent and treat exacerbations
• prevent and treat complications
• and reduce morbidity and mortality.
Inhalers are the preferred formulation for the treatment of
COPD.
Management- Goals
1
• Smoking cessation

2
• Reducing symptoms

3
• Minimizing the rate of decline in lung function

4
• Maintaining or improving the quality of life

5
• Preventing & treating exacerbations

6
• Limiting complications
NONPHARMACOLOGIC THERAPY

• Patients should receive education about their disease, treatment plans, and
strategies to slow progression and prevent complications.

• Smoking cessation is the most important intervention to prevent development

and progression of COPD. Reducing exposure to occupational dust and fumes as
well as other environmental toxins is also important.

• Pulmonary rehabilitation programs include exercise training, breathing

exercises,optimal medical treatment, psychosocial support, and health education.

• Administer the influenza vaccine annually during influenza season.

 PHARMACOLOGIC THERAPY
Treat patients with intermittent symptoms and low risk for
exacerbations (Group A) with short-acting inhaled bronchodilators as needed.
When symptoms become more persistent (Group B), initiate long-acting
inhaled bronchodilators.
For patients at high risk for exacerbations (Groups C and D),
consider inhaled corticosteroids (ICS) combined with long-acting
bronchodilators.
• Short-acting inhaled bronchodilators (β2-agonists or anticholinergics)
are initial therapy for patients with intermittent symptoms; they
relieve symptoms and increase exercise tolerance.

• Long-acting inhaled β2-agonists or anticholinergics relieve symptoms,

reduce exacerbation frequency, and improve quality of life and health
status. They are recommended for moderate to severe COPD when
symptoms occur on a regular and consistent basis, when short-acting
agents provide inadequate relief, and for patients at risk for
exacerbation
Sympathomimetics (β2-Selective Agonists)

β2-Selective agonists cause relaxation of bronchial smooth muscle and

bronchodilation and may also improve mucociliary clearance.
Administration via metered-dose inhaler (MDI) or dry-powder inhaler
(DPI) is at least as effective as nebulization therapy and is usually
favored because of cost and convenience.
Sympathomimetics (β2-Selective Agonists)

• Short-acting β2-agonists (SABA) are preferred over other short-acting

sympathomimetics (isoproterenol, metaproterenol, isoetharine) because they have greater
β2 selectivity and longer durations of action (4–6 hours). Inhalation is preferred over oral
and parenteral administration in terms of efficacy and adverse effects.
• SABA can be used for acute relief of symptoms or on a scheduled basis to
prevent or reduce symptoms. If patients do not achieve adequate control with a
SABA alone, it is reasonable to add ipratropium bromide.
• Recommended doses of SABA are as follows:
salbutamol / Albuterol inhalation aerosol and inhalation powder 1 to 2 inhalations every 4
to 6 hours

Terbutaline oral tablets 2.5 to 5 mg 3 times daily, 6 hours apart (maximum 15

mg/day)
Sympathomimetics (β2-Selective Agonists)
• Long-acting β2-agonists (LABA) are dosed every 12 to 24 hours on a
scheduled basis and provide bronchodilation throughout the dosing
interval.
• In addition to providing greater convenience than SABA for patients
with persistent symptoms,LABA produce similar or superior
improvements in lung function, symptom relief, reduced exacerbation
frequency, and need for hospitalization. These agents are not
recommended for acute relief of symptoms.
• Recommended doses by inhalation for maintenance therapy are as
follows:
Salmeterol inhalation powder 1 inhalation every 12 hours
Formoterol inhalation powder 1 inhalation every 12 hours
Anticholinergics
When given by inhalation, anticholinergics (also known as muscarinic antagonists)
produce bronchodilation by competitively inhibiting cholinergic receptors in
bronchial smooth muscle.

Short-acting muscarinic antagonists (SAMA) for COPD include primarily ipratropium bromide. It
has a slower onset of action than SABA (15–20 min vs 5 min for albuterol). It may be less suitable
for as-needed use but is often prescribed in this manner. Ipratropium has a more prolonged effect
than SABA, with the peak effect occurring in 1.5 to 2 hours and the duration up to 8 hours. If
patients do not achieve adequate control with ipratropium alone, it is reasonable to combine it
with an SABA.
The most frequent patient complaints are dry mouth, nausea, and, occasionally, metallic taste.
Because it is poorly absorbed systemically, anticholinergic side effects are uncommon (e.g.,
blurred vision, urinary retention, nausea, and tachycardia).
Anticholinergics
• The recommended doses for maintenance COPD treatment
are as follows:
Ipratropium bromide inhalation aerosol 2 inhalations four times per day
Ipratropium bromide nebulization solution 500 mcg every 6 to 8 hours

• Long-acting muscarinic antagonists (LAMA) available recommended doses

for maintenance treatment are as follows:
Tiotropium bromide inhalation spray 2 inhalations once daily.
Glycopyrrolate inhalation powder 1 inhalation twice daily
Combination Anticholinergics and Sympathomimetics

Combination of an inhaled anticholinergic and β2-agonist is often used, especially as

the disease progresses and symptoms worsen.
Combinations allow the lowest effective doses to be used and reduce adverse effects
from individual agents.
Combination of both short- and long-acting β2-agonists with anticholinergics
provides added symptomatic relief and improvements in pulmonary function.

Recommended doses for COPD maintenance therapy include:

Ipratropium plus albuterol inhalation spray 1 inhalation four to six times per day
Ipratropium plus albuterol nebulization solution one 3-mL vial four
times per day by nebulization with up to two additional 3-mL doses allowed per
day, if needed.
 Methylxanthines

Theophylline and aminophylline produce bronchodilation by inhibiting

phosphodiesterase and other mechanisms.

Chronic theophylline use in COPD may improve lung function. Subjectively, theophylline reduces
dyspnea, increases exercise tolerance, and improves respiratory drive.

Methylxanthines have a very limited role in COPD therapy because of drug interactions and
interpatient variability in dosage requirements. Theophylline may be
considered in patients intolerant of or unable to use inhaled bronchodilators. It may
also be added to the regimen of patients not achieving optimal response to inhaled
bronchodilators.
Corticosteroids
Corticosteroids reduce capillary permeability to decrease mucus.

Appropriate situations for corticosteroids in COPD include

(1) short-term systemic use for acute exacerbations and
(2) inhalation therapy for chronic stable COPD in select patients.
Chronic systemic corticosteroids should be avoided in COPD management because of questionable benefits and high
risk of toxicity.

Inhaled corticosteroid therapy may be beneficial in patients with severe COPD and at
high risk of exacerbation who are not controlled with inhaled bronchodilators.

Side effects of inhaled corticosteroids are mild and include hoarseness, sore throat, oral candidiasis, and skin bruising.
Severe side effects such as adrenal suppression, osteoporosis, and cataract formation occur less frequently than with
systemic corticosteroids, but clinicians should monitor patients receiving high-dose chronic inhaled therapy.
• Combination of inhaled corticosteroids and long-acting bronchodilators is
associated with greater improvements , health status, and exacerbation
frequency than either agent alone.
• Availability of combination inhalers makes administration of both
drugs convenient and decreases the total number of inhalations needed daily.
examples include:
Budesonide plus formoterol inhalation aerosol (Symbicort)
Fluticasone plus salmeterol inhalation
For patients with more symptoms and at high risk of exacerbation, triple
therapy (LABA plus LAMA plus inhaled corticosteroid) may be considered as a
first or second choice.
Management
Non Pharmacological Pharmacological
Smoking Β2-agonists- salbutamol, R-salbutamol,
pirbuterol & terbutaline; Salmeterol,
cessation formoterol & aformoterol
Pulmonary Anticholinergics –ipratropium & tiotropium
rehabilitation
Long term oxygen Methylxanthines- theophylline,
therapy aminophylline

Surgery- Corticosteroids- Beclomethasone,

bullectomy, lung Budesonide, Fluticasone, Triamcinolone,
volume reduction Mometasone, ciclesonide
surgery & lung
Others-alpha antitrypsin, leukotriene modifiers e.g
transplantation zafirlucast, montelukast, mast cell stabilizer e.g.
nedocromil & antioxidant & mucolytic-N-
acetylcysteine, immunizations
• Smoking cessation slows rate of pulmonary function decline in patients with COPD. Can also reduce cough and sputum
production and decrease airway reactivity.
• Pulmonary rehabilitation results in improvements in dyspnea, exercise capacity, health status and health care utilization.
Hence indication in such circumstances. The program includes exercise training, nutrition counseling and education.
• Long term administration of oxygen longer than 15 hours per day to patients with chronic respiratory failure reduces
mortality and improve quality of life. Goal of oxygen therapy is raise oxygen saturation to at least 90% and or paO2 to at least
60mmHg to allow for oxygenation of vital organs. Continued for eternity if initiated when the patient was stable.
• Bronchodilators reduce symptoms and improve exercise tolerance and quality of life.
• Beta 2 agonists cause smooth relaxation by stimulating adenylcyclase to increase the formation of cAMP.
• Shorting acting Beta 2 for rescue therapy & associated with tachyphylaxis. Adverse of effects of Beta 2 agonists include
palpitations, tachycardia, hypokalemia, and tremor. Sleep disturbance may also occur.
• Anticholinergics produce bronchodilation by competitively blocking muscarinic receptors in bronchial smooth muscle.
Tiotropium has been shown to be superior to salmeterol and ipratropium hence preferred first line.
• Methylxanthines are phosphodiesterase inhibitor that increase intracellular cAMP.
• In symptomatic patients with severe COPD and frequent exacerbations, regular treatment with inhaled corticosteroids
decrease the number of exacerbations per year and improves health status.
• Immunizations- annual influeza vaccination, pneumococcal vacicination.
 Treatment algorithm for stable COPD
I: Mild II: Moderate III: Severe IV: Very Severe

FEV1/FVC < 70%

• FEV1 < 30%

• FEV1/FVC < predicted
• FEV1/FVC < 70% or FEV1 < 50%
70%
• FEV1/FVC < 70% predicted plus
• 50% < FEV1 < chronic
• 30% < FEV1 <
80% respiratory
• FEV1 > 80% predicted 50% predicted
failure
predicted
Active reduction of risk factor(s); influenza vaccination
Add short-acting bronchodilator (when needed)
Add regular treatment with one or more long-acting
bronchodilators (when needed); Add rehabilitation
Add inhaled glucocorticosteroids if
repeated exacerbations
Add long term
oxygen if chronic
respiratory failure.
Consider surgical
treatments
Treatment of COPD Exacerbations
• An exacerbation is a sustained worsening of the
patient’s symptoms from his or her usual stable state
that is beyond normal day to day variations.
• Acute in onset & sufficient to warrant a change in
management
• Commonly reported symptoms are worsening
dyspnea, increased sputum production & change in
sputum color.
• Often triggered by respiratory infections and air pollution.
• Antibiotics are indicated when there are specific signs of airway
infection e.g. change in sputum color or increased sputum production
or dyspnea or patients requiring mechanical ventilation.
TREATMENT OF COPD EXACERBATIONS
Goals of Treatment: The goals are to:
(1) prevent hospitalization or reduce length of hospital stay
(2) prevent acute respiratory failure and death
(3) resolve symptoms
(4) return to baseline clinical status and quality of life.
NONPHARMACOLOGIC THERAPY

• Provide oxygen therapy for patients with significant hypoxemia (eg,

oxygen saturation less than 90%).
PHARMACOLOGIC THERAPY

Bronchodilators

Dose and frequency of bronchodilators are increased during acute exacerbations to

provide symptomatic relief. Short-acting β2-agonists are preferred because of rapid
onset of action. Anticholinergic agents may be added if symptoms persist despite
increased doses of β2-agonists.

Theophylline should generally be avoided due to lack of evidence documenting

benefit. It may be considered for patients not responding to other therapies.
Corticosteroids
Clinical trial results suggest that patients with acute COPD
exacerbations should receive a short course of IV or oral
corticosteroids. Although optimal dose and duration are unknown,
prednisone 40 mg orally daily (or equivalent) for 10 to 14
days can be effective for most patients.

If treatment is continued for longer than 2 weeks, employ a tapering

oral schedule because of hypothalamic-pituitary-adrenal axis
suppression.
Antimicrobial Therapy
Antibiotics are of most benefit and should be initiated if at least two of the
following
three symptoms are present: (1) increased dyspnea, (2) increased sputum
volume, and (3) increased sputum purulence.

Selection of empiric antimicrobial therapy should be based on the most likely

organisms: Haemophilus influenzae, Moraxella catarrhalis, Streptococcus
pneumoniae, and Haemophilus parainfluenzae. Site-specific sensitivities should
also be considered in drug selection.
• In uncomplicated exacerbations, recommended therapy includes a macrolide
(azithromycin or clarithromycin), second- or third-generation cephalosporin, or
doxycycline.
• Avoid trimethoprim–sulfamethoxazole because of increasing pneumococcal resistance.
• Amoxicillin and first-generation cephalosporins are not recommended because of β-lactamase
susceptibility.
• Erythromycin is not recommended because of insufficient activity against H. influenzae.

In complicated exacerbations where drug-resistant pneumococci, β-lactamaseproducing H.

influenzae and M. catarrhalis, and some enteric gram-negative organisms may be present,
recommended therapy includes amoxicillin/clavulanate or a fluoroquinolone with enhanced
pneumococcal activity (levofloxacin, gemifloxacin, or moxifloxacin)
• In complicated exacerbations with risk of Pseudomonas aeruginosa,
recommended therapy includes a fluoroquinolone with enhanced
pneumococcal and P. aeruginosa activity (levofloxacin). If IV therapy
is required, a β-lactamase-resistant penicillin with antipseudomonal
activity or a third- or fourth-generation cephalosporin with
antipseudomonal activity should be used.
Treatment Algorithm for Management
of COPD Exacerbation
Initiate or increase bronchodilator therapy
Consider antibiotics

Reassess within hours

Resolution or improvement No resolution or improvement

of signs and symptoms
ADD oral corticosteroids
Continue management
Step down when possible Reassess within hours

Review long term Worsening of signs/symptoms

management

REFER to hospital
• Antibiotics should be used in patients with COPD exacerbations who; have all
three cardinal symptoms (increased dyspnea, increased sputum volume, and
increased purulence; have increased sputum purulence along with one other
cardinal symptom or experience a severe exacerbation requiring mechanical
ventilation)
• Common organisms include: Mild (S. pneumoniae, H-influenzae, Moraxella
catarrhalis, chlamydia pneumonia, virus), moderate (+ resistant pneumococci,
E-coli, enterobacter spp, Klebsiella pneumoniae), severe (+ p. aeruginosa)
• Common classes of antibiotics- 1st line beta lactam e.g. amoxicillin+ clavulinic,
tetracycline, Cotri; alternative macrolides, 2nd or 3rd generation cephalosporins;
alternative in moderate- fluoroquinolones; severe – antipseudomonal e.g.
quinolones, piperacillin-tazobactam, ceftazidime, cefepime.
ALLERGIC RHINITIS

• Allergic rhinitis involves inflammation of nasal mucous membranes in

sensitized individuals when inhaled allergenic particles contact
mucous membranes and elicit a response mediated by
immunoglobulin E (IgE).
• There are two types: seasonal and persistent (formerly called
“perennial”) allergic rhinitis.
ALLERGIC RHINITIS

• Airborne allergens enter the nose during inhalation and are processed by
lymphocytes, which produce antigen-specific IgE, sensitizing genetically predisposed
hosts to those agents. On nasal reexposure, IgE bound to mast cells interacts with
airborne allergens, triggering release of inflammatory mediators.
An immediate reaction occurs within seconds to minutes, resulting in rapid release of
preformed and newly generated mediators from the arachidonic acid cascade.

• Mediators of immediate hypersensitivity include histamine, leukotrienes,

prostaglandin, tryptase, and kinins. These mediators cause vasodilation, increased
vascular permeability, and production of nasal secretions.
• Histamine produces rhinorrhea, itching, sneezing, and nasal obstruction.
A late-phase reaction may occur 4 to 8 hours after initial allergen exposure due to
cytokine release from mast cells and thymus-derived helper lymphocytes. This
inflammatory response causes persistent chronic symptoms, including nasal
congestion.
CLINICAL PRESENTATION

• Seasonal (hay fever) allergic rhinitis occurs in response to specific allergens (pollen
from trees, grasses, and weeds) present at predictable times of the year (spring and/or
fall) and typically causes more acute symptoms.

• Persistent allergic rhinitis occurs year-round in response to nonseasonal allergens (eg,

dust mites, animal dander, and molds) and usually causes more subtle, chronic
symptoms.Many patients have a combination of both types, with symptoms year-round and seasonal
exacerbations.

Symptoms include;
 clear rhinorrhea
 sneezing
nasal congestion
postnasal drip
allergic conjunctivitis
pruritic eyes, ears, or nose.
ALLERGIC RHINITIS
CLINICAL PRESENTATION
• In children, physical examination may reveal dark circles under the eyes
(allergic shiners)

• Patients may complain of loss of smell or taste, with sinusitis or polyps the
underlying cause in many cases.
• Postnasal drip with cough or hoarseness can be bothersome.
ALLERGIC RHINITIS
• Untreated rhinitis symptoms may lead to insomnia, malaise, fatigue, and
poor work or school performance.

• Allergic rhinitis is associated with asthma; 10% to 40% of allergic rhinitis

patients have asthma.

• Complications include recurrent and chronic sinusitis and epistaxis.

DIAGNOSIS

• Medical history includes careful description of symptoms, environmental

factors and exposures, results of previous therapy, use of medications,
previous nasal injury or surgery, and family history.

• Microscopic examination of nasal scrapings typically reveals numerous

eosinophils. peripheral blood eosinophil count may be elevated

• Allergy testing can help determine whether rhinitis is caused by immune

response to allergens. Immediate-type hypersensitivity skin tests are
commonly used.
Percutaneous testing is safer and more generally accepted than intradermal
testing, which is usually reserved for patients requiring confirmation.
TREATMENT

Goals of Treatment:
• Minimize or prevent symptoms
• prevent long-term complications
• minimize or avoid medication side effects
• provide economical therapy
• maintain normal lifestyle.
 NONPHARMACOLOGIC THERAPY
Avoiding offending allergens is important but difficult to accomplish, especially for
perennial allergens.
• Mold growth can be reduced by keeping household humidity less than 50% and removing obvious growth
with bleach or disinfectant.

• Patients sensitive to animals benefit most by removing pets from the home, if
feasible.
• Reducing exposure to dust mites by encasing bedding with impermeable
covers and washing bed linens in hot water has little benefit, except perhaps in
children.

• Steps to prevent poor air quality in homes include avoiding wall-to-wall carpeting, using
moisture control to prevent mold accumulation, and controlling sources of pollution such as cigarette
smoke.

• Patients with seasonal allergic rhinitis should keep windows closed and minimize time spent outdoors
during pollen seasons. Filter masks can be worn while gardening or mowing the lawn.
PHARMACOLOGIC THERAPY

Antihistamines
Histamine H1-receptor antagonists bind to H1 receptors without activating
them,
preventing histamine binding and action. They are effective in preventing the
histamine response but not in reversing its effects after they have occurred.
Oral antihistamines are divided into two categories:
(1) nonselective (first-generation or sedating antihistamines)
(2) peripherally selective (second-generation or nonsedating antihistamines).
The sedating effect may depend on ability to cross the blood–brain barrier.
Most older antihistamines are lipid soluble and cross this barrier
easily. Peripherally selective agents have little or no central or autonomic
nervous system effects.
 Antihistamines
• Symptom relief is caused in part by an anticholinergic drying effect that reduces
nasal, salivary, and lacrimal gland hypersecretion. Antihistamines antagonize
increased capillary permeability, wheal-and-flare formation, and itching.

• Drowsiness is the most frequent side effect, and it can interfere with driving ability or adequate
functioning. Sedative effects can be beneficial in patients who have
difficulty sleeping because of rhinitis symptoms.
Adverse anticholinergic such as dry mouth, difficulty in voiding urine, constipation,
and cardiovascular effects may occur.
• Antihistamines should be used with caution in patients predisposed to urinary retention and in
those with increased intraocular pressure, hyperthyroidism, and cardiovascular disease.

• Other side effects include loss of appetite, nausea, vomiting, and epigastric distress.

• Taking medication with meals or a full glass of water may prevent gastrointestinal
(GI) side effects.
 Antihistamines
• Antihistamines are more effective when taken 1 to 2 hours before anticipated exposure to
the offending allergen.
Examples
First generation antihistamines
• Chlorpheniramine cyproheptadine
• Cetrizine promethazine
• Levocetrizine
• diphenhydramine
Second generation antihistamines
• Loratadine
• Desloratadine
• Ebastine
• Fexofenadine
• Olopatadine(nasal spray)
Decongestants

Topical and systemic decongestants are sympathomimetic agents that act on

adrenergic receptors in nasal mucosa to produce vasoconstriction, shrink
swollen mucosa, and improve ventilation. Decongestants work well in
combination with antihistamines when nasal congestion is part of the clinical
picture.
Topical decongestants are applied directly to swollen nasal mucosa via drops or
sprays.They result in little or no systemic absorption.
Examples
• Pseudoephedrine
• Phenylephrine
• Oxymetazoline(nasal spray)
Nasal Corticosteroids
Intranasal corticosteroids relieve sneezing, rhinorrhea, pruritus, and nasal congestion
with minimal side effects (see Table 76–2). They reduce inflammation by blocking
mediator release, suppressing neutrophil chemotaxis, causing mild vasoconstriction,
and inhibiting mast cell–mediated, late-phase reactions.
These agents are an excellent choice for persistent rhinitis and can be useful in
seasonal rhinitis, especially if begun in advance of symptoms. Some authorities
recommend nasal steroids as initial therapy over antihistamines because of their high
degree of efficacy when used properly along with allergen avoidance.
Side effects include sneezing, stinging, headache, epistaxis, and rare infections with
Candida albicans.
Some patients improve within a few days, but peak response may require 2 to 3
weeks. The dosage may be reduced once a response is achieved.
Blocked nasal passages should be cleared with a decongestant or saline irrigation
before administration to ensure adequate penetration of the spray.
Cromolyn Sodium

• Cromolyn sodium (Nasalcrom), a mast cell stabilizer, is available as a

nonprescription nasal spray for symptomatic prevention and treatment of allergic
rhinitis. It prevents antigen-triggered mast cell degranulation and release of
mediators, including histamine. The most common side effect is local irritation
(sneezing and nasal stinging).
Dosage for persons at least 2 years of age is one spray in each nostril three or four
times daily at regular intervals. Nasal passages should be cleared before
administration, and inhaling through the nose during administration enhances
distribution to the entire nasal lining.
For seasonal rhinitis, treatment should be initiated just before the start of the
offending allergen’s season and continue throughout the season.
In persistent rhinitis, effects may not be seen for 2 to 4 weeks; antihistamines or
decongestants may be needed during this initial phase of therapy.
• Ipratropium Bromide
Ipratropium bromide (Atrovent) nasal spray is an anticholinergic agent that may be
useful in persistent allergic rhinitis. It exhibits antisecretory properties when applied
locally and provides symptomatic relief of rhinorrhea.
The 0.03% solution is given as two sprays (42 mcg) two or three times daily.
Adverse effects are mild and include headache, epistaxis, and nasal dryness.
Montelukast
Montelukast (Singulair) is a leukotriene receptor antagonist approved for treatment
of persistent allergic rhinitis in children as young as 6 months and for seasonal
allergic rhinitis in children as young as 2 years. It is effective alone or in combination
with an antihistamine.
Dosage for adults and adolescents older than 14 years is one 10-mg tablet daily.
Children ages 6 to 14 years may receive one 5-mg chewable tablet daily. Children
ages 6 months to 5 years may be given one 4-mg chewable tablet or oral granule
packet daily
Montelukast is no more effective than antihistamines and less effective than
intranasal corticosteroids; therefore, it is considered third-line therapy after those
agents.
• IMMUNOTHERAPY
Immunotherapy is the process of administering doses of antigens responsible for
eliciting allergic symptoms into a patient with the intent of inducing tolerance to the
allergen when natural exposure occurs. Until recently, immunotherapy was only
available for subcutaneous injection; sublingual dosage forms are now available for a
limited number of allergens.
Beneficial effects of immunotherapy may result from induction of IgG-blocking
antibodies, reduction in specific IgE (long-term), reduced recruitment of effector
cells, altered T-cell cytokine balance, T-cell anergy, and alteration of regulatory T
cells.
Good candidates for immunotherapy include patients with a strong history of severe symptoms unsuccessfully
controlled by avoidance and pharmacotherapy and patients
unable to tolerate adverse effects of drug therapy. Poor candidates include patients
with medical conditions that would compromise the ability to tolerate an
anaphylactic-type reaction, patients with impaired immune systems, and patients with
a history of nonadherence.