Primary Drug Name: Spiriva
(Spiriva)
Generic name: Tiotropium bromide
What is Spiriva Asthma Medication?
Spiriva (tiotropium bromide inhalation powder) is indicated for
the long-term, once-daily, maintenance treatment of bronchospasm
associated with chronic obstructive pulmonary disease (COPD), including
chronic bronchitis and emphysema.
Each capsule contains 22.5 microgram tiotropium bromide monohydrate
equivalent to 18 microgram tiotropium. The delivered dose (the dose
that leaves the mouthpiece of the HandiHaler device) is 10 microgram.
Spiriva consists of a dry powder for inhalation. The active ingreidiant
in Spiriva is tiotropium bromide 18mcg intended for oral inhalation
using the Handihaler Device. The dry powder or capsule is not intended
for oral consumption.
The dry powder is delivered from the Handihaler device at a rate
of 20L/min.
The capsules are light green hard capsules, containing a white or
yellowish white powder, with product code and company logo printed
on the capsule.
The typical shelf life of Spiriva is 18 months. However, the typical
shelf life of an opened capsule is 9 days. top of page
How should Spiriva Asthma
Medication be Used?
SPIRIVA is taken once a day, using the HandiHaler device. Taking
SPIRIVA requires four steps: Open the blister and the HandiHaler
device, insert the SPIRIVA capsule, press the HandiHaler button
and inhale your medication.
The following are the instructions for the patient on how to inhale
from the Spiriva capsule by means of the HandiHaler.
Remember to carefully follow your doctor’s instructions for
using Spiriva. The
HandiHaler is especially designed for Spiriva. You must not use
it to take any other
medication. You can use your HandiHaler for up to one year to take
your medication.
The HandiHaler
1 Dust cap
2 Mouthpiece
3 Base
4 Piercing button
5 Centre chamber
1. Open the dust cap by pulling it upwards. Then open the mouthpiece.
2. Remove a Spiriva capsule from the blister (only immediately before
use) and place it in the centre chamber. Put the Spiriva capsule
in the centre chamber (5), as
illustrated. It does not matter which way the capsule is placed
in the chamber.
3. Close the mouthpiece firmly until you hear a click, leaving the
dust cap open.
4. Hold the HandiHaler with the mouthpiece upwards and press the
green button completely in once, and release. This makes holes in
the capsule and allows the medication to be released when you breathe
in.
5. Breathe out completely. Important: Please avoid breathing into
the mouthpiece at
any time.
6. Raise the HandiHaler to your mouth and close your lips tightly
around the
mouthpiece. Keep your head in an upright position and breathe in
slowly and deeply but at a rate sufficient to hear the capsule vibrate.
Breathe until your lungs are full;
then hold your breath as long as comfortable and at the same time
take the
HandiHaler out of your mouth. Resume normal breathing. Repeat step
5 and 6 once, this will empty the capsule completely.
7. Open the mouthpiece again. Tip out the used capsule and dispose.
Close the
mouthpiece and dust cap for storage of your HandiHaler. top of page
Spiriva Dosage and Administration
The recommended dosage of SPIRIVA HandiHaler is the inhalation of the contents of one SPIRIVA capsule, once-daily, with the HandiHaler inhalation device.
No dosage adjustment is required for geriatric, hepatically- impaired, or renally- impaired patients.
However, patients with moderate to severe renal impairment given SPIRIVA should be monitored closely.
SPIRIVA capsules are for inhalation only and must not be swallowed.
top of page
What are Spiriva Side Effects?
Common Spiriva Side Effects: With SPIRIVA the
most commonly reported adverse drug reaction was dry mouth. Dry
mouth was often mild and usually resolved during continued treatment.
Other reactions reported in individual patients and consistent with
possible anticholinergic effects included constipation, increased
heart rate, blurred vision, glaucoma, urinary difficulty, and urinary
retention.
Several organ systems and functions are under control of the parasympathetic
nervous system and thus can be affected by anticholinergic agents.
Possible adverse events attributable to systemic anticholinergic
effects include dry mouth, dry throat, increased heart rate, blurred
vision, glaucoma, urinary difficulty, urinary retention, and constipation.
In addition, local upper airway irritant phenomena were observed
in patients receiving tiotropium bromide. An increased incidence
of dry mouth and constipation may occur with increasing age. top of page
Spiriva - How Supplied
SPIRIVA capsules, containing 18 mcg tiotropium, are light green.
The HandiHaler inhalation device is gray colored with a green button.
It is imprinted with SPIRIVA HandiHaler (tiotropium bromide inhalation
powder), the Boehringer Ingelheim company logo, and the Pfizer company
logo. It is also imprinted to indicate that SPIRIVA capsules should
not be stored in the HandiHaler device and that the HandiHaler device
is only to be used with SPIRIVA capsules.
Six SPIRIVA capsules are
packaged in an aluminum/PVC/aluminum blister card. One blister card
consists of two blister strips, each containing 3 capsules and joined
along a perforated-cut line. After using the first capsule, the
2 remaining capsules should be used over the next 2 consecutive
days. Capsules should always be stored in the blister and only removed
immediately before use. The foil lidding should only be peeled back
as far as the STOP line printed on the blister foil to prevent exposure
of more than one capsule. The drug should be used immediately after
the packaging over an individual capsule is opened.
top of page
Spiriva Mechanism of Action
Spiriva - Tiotropium bromide is a long-acting, specific, muscarinic
receptor antagonist, in clinical medicine often called an anticholinergic.
By binding to the muscarinic receptors in the bronchial smooth musculature,
tiotropium bromide inhibits the cholinergic (bronchoconstrictive)
effects of acetylcholine, released from parasympathetic nerve endings.
It has similar affinity to the subtypes of muscarinic receptors,
M1 to M5.
In the airways, tiotropium bromide competitively and reversibly
antagonises the M3 receptors, resulting in relaxation. The effect
was dose dependent and lasted longer than 24h. The long duration
is probably due to the very slow dissociation from the M3 receptor,
exhibiting a significantly longer dissociation half-life than ipratropium.
As an N-quaternary anticholinergic, tiotropium bromide is topically
(broncho-) selective when administered by inhalation, demonstrating
an acceptable therapeutic range before systemic anticholinergic
effects may occur. The bronchodilation is primarily a
local effect (on the airways), not a systemic one. Dissociation
from M2-receptors is faster than from M3, which in functional in
vitro studies, elicited (kinetically controlled) receptor subtype
selectivity of M3 over M2. The high potency and slow receptor
dissociation found its clinical correlate in significant and long-acting
bronchodilation in patients with COPD.
The clinical development programme included four one-year and two
six-month randomised, doubleblind studies in 2663 patients (1308
receiving tiotropium bromide). The one-year programme consisted
of two placebo-controlled trials and two trials with an active control
(ipratropium). The two six-month trials were both, salmeterol and
placebo controlled. These studies included lung function and health
outcome measures of dyspnea, exacerbations and health-related quality
of life. In the aforementioned studies, tiotropium bromide, administered
once daily, provided significant improvement in lung function (forced
expiratory volume in one second, FEV1 and forced vital capacity,
FVC) within 30 minutes following the first dose which was maintained
for 24 hours.
Pharmacodynamic steady state was reached within one week with the
majority of bronchodilation observed by the third day. Tiotropium
bromide significantly improved morning and evening PEFR (peak expiratory
flow rate) as measured by patient’s daily recordings. The
bronchodilator effects of tiotropium bromide were maintained throughout
the one-year period of administration with no evidence of tolerance.
A randomised, placebo-controlled clinical study in 96 COPD patients
demonstrated that
bronchodilation was maintained throughout the 24 hour dosing interval
in comparison to placebo regardless of whether the drug was administered
in the morning or in the evening.
The following health outcome effect was demonstrated in the long
term (6-month and one-year) trials:
Tiotropium bromide significantly improved dyspnea (as evaluated
using the Mahler Transitional Dyspnea Index.). This improvement
was maintained throughout the treatment period.
Spiriva HandiHaler (tiotropium bromide inhalation powder) helps
patients manage their COPD symptoms by helping to keep lung airways
open (also known as bronchodilation) for up to 24 hours. SPIRIVA
is the only once-daily maintenance therapy for the bronchospasm
(airway tightening) that occurs with COPD.
Clinical studies showed that SPIRIVA improved lung function in COPD
patients. Studies also showed that patients using SPIRIVA needed
less rescue medication (like short-acting beta2-agonists). top of page
Chronic Obstructive Pulmonary Disease (COPD)
Chronic obstructive pulmonary disease, or COPD, is characterized
by abnormalities in the lungs that make it difficult to exhale normally.
Generally, two distinct diseases are involved: emphysema and chronic
bronchitis. According to the World Health Organization (WHO), 75%
of deaths from COPD that occur in developed countries are directly
related to smoking tobacco. Emphysema and chronic bronchitis cause
excessive inflammatory processes that eventually lead to abnormalities
in lung structure that permanently obstruct airflow (hence the term
"chronic obstructive"). Asthma usually can be controlled,
but some asthmatics have permanently narrowed airways and suffer
COPD.
COPD is the 4th-leading cause of death in the United States. An
estimated that 16.4 million Americans have been diagnosed with COPD;
however, just as many people have some form of lung impairment but
have not been diagnosed with COPD. According to the American Lung
Association, approximately 14 million people suffer from chronic
bronchitis, the seventh leading chronic condition in the United
States. There are an estimated 1.9 million people suffering with
emphysema. Of these, 55.5% are men and 44.5% are women.
COPD may go unnoticed in its early stages because it is often confused
with asthma, a bad cough, or a natural part of aging. Also, many
people think of COPD as a disease that only affects the elderly,
when in fact, almost 50% of patients are under age 65 and some people
start having symptoms in their early 40s.
Symptoms of COPD tend to develop gradually and can begin in a person's
early 40s. They may be worse some days than others, or they may
be bad all the time. The important thing is to identify the symptoms
early and get treatment. top of page
Order Spiriva from Canada
Spiriva is an expensive drug when purchased in the United States.
The reason for the expensive price in the US is because the US Government
does not regulate prices on Spiriva arthritis medication and therefore
Spiriva is most expensive when bought in the United States. There
are alternative international sources for Spiriva and Canada is
well known for its safe yet much more affordable rx medication.
Canada is a reliable and proven alternate source for Americans who
cannot afford Spiriva at American costs. The Canadian Government
regulates all drugs including Spiriva and so drug prices in Canada
are much cheaper. Savings of up to 90% on drugs are possible when
purchasing Spiriva from Canadian pharmacies.
Another factor determining the cheap prices from Canada is the US
to Canadian dollar currency exchange rate. The American dollar can
go much further when ordering prescription medications such as Spiriva
from Canada. top of page
Ordering Spiriva Asthma Medication from Canada
Is Spiriva from Canada Safe?
Q. Is it safe to order Spiriva Asthma
Medication from Canada?
A. Spiriva form Canada is as safe as Spiriva from the US. Take
Precautions when searching Canadian Online Pharmacies. top of page
COPD Risk Factors
Tobacco use is the number one COPD risk factor. Heavy smokers are
at greatest risk. Cigarette smokers are at greater risk than cigar
and pipe smokers. All smokers are at greater risk than lifelong
nonsmokers. Smoking tobacco causes 80% to 90% of COPD cases. An
agent in tobacco smoke stimulates inflammation in the lungs, leading
to destruction of the alveoli and narrowing of the airways. While
smoking is related to most cases of emphysema, only 15% to 20% of
smokers develop the disease. What other factors contribute to the
development of "smokers emphysema" remains unclear.
Having alpha-1-antitrypsin (AAT) deficiency, also called familial
emphysema, is another risk factor. People with familial emphysema
have a hereditary deficiency of alpha-1-protease inhibitor. When
there is a deficiency of AAT, the activity of elastase—an
enzyme that breaks down elastin—is not inhibited and elastin
degradation occurs unchecked. Individuals with a severe genetic
deficiency of AAT usually have symptoms by the time they reach early
middle age. It is critical that people with this deficiency never
smoke. Approximately 1% to 3% of all cases of emphysema are due
to AAT deficiency. Familial emphysema, or alpha1-antitrypsin (AAT)
deficiency-related emphysema, is caused by the hereditary deficiency
of a protein called alpha1-antitrypsin. This deficiency leads to
uncontrolled destruction of the alveoli and emphysema. Occupational
exposure to dust, fumes, and gases appears to contribute slightly
to lung function decline and chronic bronchitis. The role of air
pollution in COPD remains controversial. top of page
Common Symptoms of COPD
Chronic Cough - It is often the first symptom
of COPD to develop. It is often discounted as smoker's cough or
the effect of cold weather.
Sputum production - Patients often produce sputum (also called phlegm)
after coughing.
Shortness of breath (dyspnea) - In the early stages
of COPD, patients may experience breathlessness only during strenuous
activity (climbing stairs or exercising), and attribute this to
age or being out of shape, but gradually patients begin to feel
shortness of breath even during simple activities, like walking
across the room, and even at rest.
Emphysema
In the lung there are millions of tiny, thin-walled, elastic air
sacs called alveoli (see Anatomy of the Respiratory System). These
tiny sacs perform the crucial task of replenishing the blood with
oxygen (via inhalation) and ridding the body of carbon dioxide (CO2)
in exhalation. Emphysema is the enlargement of the alveoli accompanied
by destruction of their walls. In "smokers emphysema"
an agent in cigarette smoke sets off a self-perpetuating, low-grade
inflammation that causes the release of enzymes (elastase) from
inflammatory cells that break down collagen and elastin —
substances that maintain the structure and elasticity of alveoli
— in the alveolar walls. The NHLBI (National Heart, Lung and
Blood Institute) reports that this creates an imbalance between
the elastin-degrading enzymes and their inhibitors. They also found
that oxidants in cigarette smoke inactivate a significant number
of elastase inhibitors, thereby decreasing the amount of active
antielastase available to protect the lung and further upsetting
the elastase-antielastase balance.
This disruption of the alveolar walls and elastin leads to a decrease
in the elastic recoil of the lungs, limiting the ability of the
alveoli to passively shrink and to exhale. This accounts for the
main limitation to exhalation seen in severe COPD. The disruption
of the alveolar walls also leads to their increase in size, making
the lungs larger and placing the chest at a mechanical disadvantage.
Disruption of the alveolar walls also makes exchange of oxygen from
the alveoli to the capillaries and carbon dioxide from the capillaries
to the alveoli more difficult. Collapse of the bronchial walls occurs
when the cartilage in the bronchial walls has been weakened.
Familial emphysema
People with familial emphysema have a hereditary deficiency of alpha-1-protease
inhibitor, also called alpha1-antitrypsin (AAT). When there is a
genetic deficiency of AAT, the activity of elastase—an enzyme
that breaks down elastin—is not inhibited and elastin degradation
occurs unchecked. Individuals with a severe genetic deficiency of
AAT usually have symptoms by the time they reach early middle age.
It is critical that people with this deficiency never smoke.
Destruction of alveolar walls, capillaries, and attachments between
alveoli and bronchioles causes (1) susceptibility of airways to
compression and collapse, impeding airflow out of the lungs; (2)
entrapment of air in the alveoli; (3) poor air-gas exchange, that
is, reduced ability to inhale oxygen and exhale carbon dioxide (CO2),
resulting in increased levels of CO2 in the blood; (4) the development
of bullae (areas of lung extensively destroyed so that they become
large dilated air sacs); and (5) enlarged lungs.
Chronic Brochitis
Chronic bronchitis is the presence of cough productive of sputum
for 3 months per year, in 2 consecutive years. In chronic bronchitis,
tobacco smoke causes inflammatory cells (neutrophils and leukocytes)
to arrive in the bronchi. These cells worsen airway obstruction
by causing inflammation and thickening of the airways. Also, mucus-producing
glands deep within the lining of the airways become enlarged (hypertrophy)
and increase in number (hyperplasia), and the number of surface
cells that produce mucus (goblet cells) increases, resulting in
excessive secretion of mucus in the lungs. The resulting chronic
cough and expectoration affects the central conducting airway (see
Anatomy of the Respiratory System).
The function of mucus in the lungs is to trap and clear particles,
to dilute harmful substances, to lubricate the airways, and to humidify
inspired air. In chronic bronchitis, (1) the hyperplasia and hypertrophy
of the submucosal glands (mucus-producing glands deep within bronchial
walls) thicken the airway walls; (2) the resulting increased volume
of mucus that occurs plugs the airways; (3) columnar cells (cells
that line the surface of the airways) undergo changes that result
in the destruction of cilia — delicate hairlike structures
on columnar cells lining the airways that sweep mucus with offending
agents up and out of the lungs. The loss of cilia and the inability
to clear bacteria predispose the patient to lung infections. top of page
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