PHARCARE 2

3E-PH

Smoking

Submitted by:
#5 Ambagan, Eldrick Justin B.
#6 Banton, Bianca Paola B.

Submitted to:
Asst. Prof. Agnes L. Castillo, PhD

I.

Definition:

Nicotine is an alkaloid that can be found in the tobacco plant, Nicotania

tabacum. This chemical is the most relevant psychoactive compound in
cigarette smoke but not the only. It is a potent euphoriant which induces
arousal and state of well-being. This alkaloid can improve attention time
and performance and has good effects on cognition. It is an anti-anxiety
and antidepressant. It is also very addictive.
Nicotine can be ingested, injected or can be administered through
smoke.
Smoking is a way for nicotine to enter the body using dried tobacco
leaves. It can be done through cigarettes, cigars or pipes. Cigarette
smoking is the most common.
In the cigarette smoke, there are more than 6000 chemicals.
Some of them are:
Gas Phase:
Carcinogens: nitrosamines, hydrazine, vinyl chloride, arsine, nickel
carbonyl, formaldehyde
Tumor initiator: urethane
Cilia toxic agent: formaldehyde, hydrogen cyanide, acrolein,
acetaldehyde
Toxic agent: hydrogen cyanide, nitrogen oxides, ammonia, pyridine,
carbon monoxide
Others: volatile chlorinated olefins and nitro-olefins
Particulate Phase:

Carcinogens: N-nitrosonornicotine, polonium-210, nickel

compounds, cadmium compounds, arsenic, pyrene, fluroanthene,
benzo(g,h,i)perylene, naphthalenes, 1-methylindoles, 9methylcarbazoles, catechol, 3- and 4- methyl-catechols
Tumor initiator benzo(a)pyrene, 5-methylchrysene,
benzo(j)fluoranthene, benzo(a)anthracene
Cilia toxic agent phenol, cresol
Toxic agent nicotine, minor tobacco alkaloids, bladder carcinogen

The most important of them are:

Nicotine colorless weak base with pKa of 8.5. It is water soluble

and has a bitter taste.
Tar carcinogenic aromatic hydrocarbons. It is whats left after
nicotine and moisture are removed.
Carbon monoxide has higher affinity to red blood cells than
oxygen
Smoking causes approximately 400, 000 deaths in the United States
each year and it is the leading cause of actual death in the same country.

II.

Stages

1. Initiation phase of experimenting with cigarettes; still not regular

smokers

Usually teens
Some people will not like it, some people do and will continue
smoking
2. Maintenance smoking behavior is already established
- there are changes in the body caused by continuous smoking
and addiction
3. Cessation trying to stay off cigarettes and stop smoking
- Can be caused by disapproval of loved ones, higher taxes for
cigarettes, etc.
- The smoker can undergo withdrawal symptoms: cravings
most persistent; depression first three months of cessation;
weight gain because of increased appetite first 6-8 weeks of
cessation; bradycardia, gastrointestinal discomfort,
irritability, anxiety and difficulty concentrating.
4. Relapse struggle with their craving to smoke and go back to their
smoking habits again.

III.

Mechanism of Action

IV.

Types

Smoke is first inhaled into the lungs. Then, its lipid solubility helps it to
be rapidly absorbed into the alveolar surface and into the pulmonary
capillary blood. Once the chemicals are in the blood, it will circulate
around the body and most specially, it will enter the brain. Within 8
seconds, nicotine is already in the brain.
Naturally, acetylcholine activates with nAChR. The nicotinic
acetylcholine receptors (nAChR) are ligand-gated ion channels which open
when activated. Once it reaches the brain, nicotine mimics the action of
acetylcholine. When the nAChRs open, the entry of ions like calcium and
sodium is allowed. This sends signals to different systems to produce
neurotransmitters.
Nicotine binds to the nicotinic acetylcholine receptors (nAChR) in the
mesocorticolimbic dopaminergic system, which is responsible for reward
and pleasure, and in the locus ceruleus, which is responsible for cognitive
function. The other neurochemical systems are cholinergic, glutamatergic,
-aminobutyric acid (GABA) and opioid peptide systems. These systems
control the release of dopamine, norepinephrine, glutamate, vasopressin,
serotonin, GABA, beta-endorphins and other neurotransmitters.
Nicotine also binds with nicotinic cholinergic receptors that result in
sympathetic nervous stimulation and with higher doses; it results in
parasympathetic nervous stimulation.
The negative effects of withdrawal are caused by the activation of
extrahypothalamic corticotropin-releasing factor (CRF). This receptor
produces negative behavior when activates and when it is blocked, the
negative withdrawal symptoms are prevented.
Liver metabolizes 80-90% of nicotine. The rest of nicotine and its
metabolites like cotinine and nicotine-1-N-oxide are excreted in the urine.
The half-life of nicotine is about two hours.

Mainstream smoke emission coming from the smoker. This smoke is

already filtered through the cigarette and altered by the respiratory tract
of the smoker.
Sidestream smoke smoke directly from burning cigarettes. This is a main
concern because this smoke still has high concentration of toxic
chemicals.
Types of smokers:
Firsthand smoker the one who uses cigarettes/cigars/pipes
Secondhand smoker the one who accidentally inhales the smoke coming
from the firsthand smoker

V.

Causes

VI.

Diseases/Outcome

The most rampant causes of smoking in individuals can be divided into

three aspects: social, economic and cultural. Social aspects include
parental or siblings cigarette use, peer pressure, type of school and
availability. The economy is also a factor in smoking because tobacco is a
multi-billion dollar industry. It gives employment to people from the
manufacture to marketing of the products. The government takes a huge
amount of taxes from the tobacco companies thats why prohibition of
cigarette smoking is hard to implement.
Smoking also depends on ones culture. For example, some ethnic
tribes uses tobacco in their religious ceremonies. But aside from that,
media plays a huge role in the promotion of cigarette smoking. Some
advertisements and movies portray a rugged, independent, masculine and
sophisticated image of the smoker which encourage the people to smoke.
Diseases associated with cigarette smoking:
Cardiovascular atherosclerotic vascular disease: coronary artery
disease, carotid vascular disease, mesenteric, renal, iliac,
abdominal aortic aneurism; peripheral vascular disease:
thromboangitis obliterans, deep venous thrombosis, pulmonary
embolus; cardiac disease: angina pectoris, coronary artery spasm,
arrhythmia
Malignancy respiratory tract: lung cancer (squamous cell,
adenocarcinoma, large cell, small cell), laryngeal cancer, oral
cancer; other tissues: esophagus, pancreas, bladder, uterine cervix,
kidney, anus, penis, stomach, liver, leukemia
Lung disease COPD: emphysema, chronic bronchitis, asthma;
other lung diseases: idiopathic pulmonary fibrosis, histiocytosis X,
respiratory bronchiolitis, Goodpastures syndrome, sleep apnea,
pneumothorax
Gastrointestinal disease peptic ulcer disease: gastric, duodenal;
gastroesophageal reflux; chronic pancreatitis; Chrons disease;
colonic adenomas
Dermatologic disease skin wrinkling, psoriasis
Reproductive disease ovarian failure; pregnancy related:
prematurity, premature rupture of membranes, spontaneous

abortion; decreased sperm quality; fetal effects: low birth weight,

impaired lung growth, sudden infant death syndrome, febrile
seizures, reduced intelligence, behavioral disorders, atopic
disease/asthma
Parental smoking (effects on children) asthma, rhinitis, otitis,
pneumonia, increased risk to smoke
Rheumatologic disease osteoporosis, rheumatoid arthritis
Psychiatric depression, schizophrenia
Oral disease periodontal disease, loss of taste
Loss of olfaction
Infectious disease tuberculosis, pneumococcal infection,
meningococcal infection
Endocrine disease altered hormonal secretion, graves disease,
antidiuresis, goiter
Renal glomerulonephritis
Benign prostatic hypertrophy
Cataracts

Three main diseases acquired from cigarette smoking:

1. Chronic Obstructive Pulmonary Disease (COPD) a progressive disease
characterized by reduced airflow in the lungs resulting in difficulty in
breathing. This can be caused by emphysema which is the
enlargement or damage in the alveoli, chronic bronchitis which is the
inflammation of the alveoli resulting into accumulation of mucus,
and/or small airways disease which is the narrowing of small
bronchioles.
Cigarette smoke directly cause cell death in the lungs because
of the oxidants present. Indirectly, it causes the activation of
macrophages and epithelial cells that produce proteinases and
chemokines followed by the immune and inflammatory cells. Some of
these cells lead to lung destruction and matrix proteolysis while some
cells excrete elastolytic proteinases that destroy the extracellular
matrix of the lung. If the matrix and the elastin is not repaired or
repaired ineffectively, there will be alveolar enlargement.
2. Lung Cancer rapid growth of abnormal cells in the lungs that form
tumors
Cigarette smoke has carcinogens which are both tumor initiators and
tumor promoters. The most important carcinogens in the smoke are
polycyclic aromatic hydrocarbons and nitrosamines. These chemicals
lead to somatic cell mutations and altered cellular functions that
results to epithelial cell abnormalities, from mild metaplastic changes
through severe dysplasia and finally, to cancer.
3. Cardiovascular Disease

Atherosclerosis when plaque made of fats, cholesterol and

calcium accumulate in the arteries blocking or slowing down the
blood flow. This can lead to myocardial infarction, angina
pectoris or stroke.
Cigarette smoke and the toxins it has, causes endothelial injury
which is associated with atherosclerosis. The smoke also causes
tachycardia which again, cause endothelial injury. Smoking also
contributes to the increase of oxidized low-density lipoproteins
which are atherogenic.

Other effects:

VII.

Increases carboxyhemoglobin levels (carbon monoxide in the

blood)

Prevention/Treatment

Behavioral Treatment
The treatment model is based on a theory of change that
proposes that for individuals to change their behavior they must be motivated or
ready to change and have the skills to execute the change in behavior effectively

The general rationale of behavioral treatment is that through

skills training, the automatic chain of events (Antecedent Behavior
Consequences) leading to smoking can be disrupted, and smoking behavior can be
replaced with alternative behaviors.
Motivation
Defined as the desire and intention to discontinue an
old behavior and initiate a new behavior.
Thought to be determined by cognitive processes
involved in weighing the personal pros versus cons of
persisting with the old behavior and weighing the
personal pros versus cons of initiating the new
behavior
Motivation is dynamic as it can vary within an
individual across time and circumstances
Therefore external influences that help smokers shift
their beliefs regarding the pros and cons of smoking
versus quitting may enhance motivation and ultimately
result in their initiating a cessation attempt
Cessation Stage Interventions
Self-Management
Critical component of behavioral smoking
interventions
Refer to strategies intended to rearrange
environmental cues that trigger smoking or
alter the consequences of smoking
Patients begin to intervene in trigger situations
to break up the smoking behavior chain
(situationurgesmoke) by using one of three

general strategies: avoid the trigger situation,

alter or change the trigger, or use an alternative
or substitute in place of a cigarette.
Social Support
Positive social support within (the clinician) and
outside of treatment has been shown to
increase cessation rates
Social support can be a source of motivation for
quitting and of positive reinforcement for
maintaining abstinence
Also may provide a buffer against stressful life
events that might precipitate a relapse
Includes making specific requests to family and
friends about steps they can take to support the
patients abstinence efforts
Maintenance
Maintenance is a critical issue for smoking
cessation programs.
Most commonly used maintenance strategies
are based on the relapse prevention model
Extending behavioral treatment and
pharmacotherapy may improve cessation
outcomes
Identifying and Coping with High-Risk Situations
for Relapse
Relapse prevention theory proposes that the
ability to cope with high-risk situations
determine individuals probability of maintaining
abstinence.
High-risk situations involve the ff. elements:
Negative moods
Positive moods
Social situations involving alcohol
Being in the presence of smokers
High-risk situations are functionally similar to
trigger situations
Managing Slips
When patients experience a slip to smoking,
they often progress to further smoking and
relapse
Preventing slips is the best way to achieve
smoking abstinence and this point should be
stressed to all patients
A slip is an important time for the clinicians to
assess motivation or commitment to quitting
Lifestyle Change
Replacing a negative addiction (such as
smoking) with a positive addiction by

increasing participation in activities that are

incompatible with smoking and are a source of
pleasure
Patients are encourages to set aside time as
often as possible (ideally, on a daily basis) for
this purpose
Ex. exercise
Pharmacological Treatment
Nicotine Replacement Therapy (NRT)
Remains a mainstay of pharmacotherapy for the
treatment of tobacco dependence.
To date, the US FDA has approved five nicotine
replacement products:
Nicotine gum
Nicotine patches
Nicotine nasal spray
Nicotine vapor inhaler
Nicotine lozenges
Available in the Philippines:
Nicotine gum (Nicorette)
Nicotine patch (Nicotinell TTS)
Nicotine gum
OTC Product
Available in 2mg or 4mg doses
4mg dose recommended for use in smokers who
smoke 25 or more cigarettes a day
Effective as monotherapy or in combination with other
NRT
Patients bite into gum and then park the gum
between the cheek and gum for several minutes
before chewing it again
This cycle allows for buccal absorption and should be
repeated over a period of 30 minutes per piece of gum
Nicotine patch
Delivers a steady dose of nicotine for 24 hours after a
single application
Available without a prescription in doses of 7, 14, and
21 mg
Standard-dose nicotine patch therapy is 21mg/24
hours
High-dose nicotine patch therapy (>21mg/day) has
been shown to be safe and well tolerated in patients
who smoke more than 20 cigarettes per day
Nicotine nasal spray
Delivers nicotine directly to the nasal mucosa and has
been observed to be effective for achieving smoking
abstinence.

 Deliver nicotine more rapidly than other NRTs and

reduces withdrawal symptoms more quickly than
nicotine gum
Each spray contains 0.5mg of nicotine, and one dose is
one spray in each nostril (1mg total)
Recommended dosing is one to two doses per hour,
not to exceed five doses per hour or 40 doses per day
Can be used with in combination with other NRT or
with Bupropion SR
Nicotine vapor inhaler
A plastic holder into which a cartridge containing a
cotton plug impregnated with 10mg of nicotine is
inserted.
Although the device is called an inhaler, this is a
misnomer because little of the nicotine vapor reaches
the pulmonary alveoli even with deep inhalations
Delivers a nicotine vapor that is absorbed across the
nasal mucosa
Recommended initial dose of inhaler when used alone
is 6 to 16 cartridges per day.
Recommended length of treatment is approximately 12
weeks
Lends itself to being used in combination with other
NRTs or Bupropion SR
Nicotine lozenges
OTC product
Available in 2 and 4mg doses
4 mg dose for use in high dependence smokers (time
to first cigarette of the day <30 min after arising)
Although method of delivery (transbuccal) is similar to
that of nicotine gum, the lozenge is simpler to use and
likely will demonstrate improved patient compliance
Non-Nicotine Products
Bupropion SR
First non-nicotine pharmacologic treatment approved
for treament of tobacco dependence.
A monocyclic antidepressant that inhibits the reuptake
of both norepinephrine and dopamine
Does not appear to work through its antidepressant
activity. Rather, the efficacy of bupropion in smoking
cessation is hypothesized to stem from its
dopaminergic activity.
Also has been to shown to have an antagonist effect
on nicotinic acetylcholine receptors
Treatment should be initiated about 1 week before the
patients stop date at an initial dose of 150mg/day for
3 days then 150 twice daily.
Usual length of treatment is 6 to 12 weeks

 Varenicline
Newest first-line drug for treating tobacco dependence
Blocks nicotine from binding to the receptor
(antagonist effect) and stimulates (agonist effect)
receptor-mediated activity leading to the release of
dopamine which reduces craving and nicotine
withdrawal symptoms.
In trials, varenicline was more effective for achieving
smoking abstinence compared to placebo or bupropion
SR
Not recommended for use in combination with NRT
Some case reports have suggested that varenicline
could exacerbate psychiatric symptoms in individuals
with severe mental illness.
Available in the Philippines as Champix
Nortriptyline
Tricyclic antidepressant recommended as a second-line
drug for treating tobacco dependence
Thought to be as effective as bupropion in helping
smokers to stop smoking and that the mechanism of
action of each is independent of their antidepressant
effects.
Clonidine
Centrally acting alpha-agonist that can be used as a
second-line drug
Available in both oral and transdermal forms
Transdermal form is easier to use with a recommended
dose of 0.2mg/day for 3 to 10 weeks

VIII. Laws

Republic Act No. 9211

Tobacco Regulation Act of 2003
An act regulating the packaging, use, sale, distribution and
advertisements of tobacco products and for other purposes.
The act mandated the following:
Smoking is prohibited in public places like schools, hospitals,
airports, train stations and the like
Mandated that smoking areas shall be designated in places that
are open to the general public and private workplaces
Prohibited sale of tobacco products to minors
Prohibited sale or distribution of tobacco products within 100
meters of a school, public playground, or places frequented by minors
Required retailers to verify age of buyer in case of doubt
Required manufacturers and advertisers to shows warnings on
packaging and advertisements of tobacco products
Restrictions with regards to sponsorship of tobacco brands

IX.

References

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