Warung Bebas

Monday, 4 April 2011


Ideally, therapeutics for nicotine addiction should be available for the 80% of the world’s smokers who live in low- and middle-income countries. Within those countries, smokers have the lowest income, are the least educated, and have the poorest access to health care.
Thus, from a world view, cost of therapeutics and access become important considerations. Prevention is obviously an important strategy, but strategies to prevent tobacco addiction must deal with a politically powerful and wealthy multinational industry promoting use of tobacco . The tobacco industry in the United States alone spent 6 billion dollars in 1998 to market cigarettes, about 18 million dollars each day. More is spent promoting tobacco use elsewhere in the world. Although successful prevention strategies exist, well-funded competition encouraging tobacco use will remain .

More intensive therapeutics typically include behavioral interventions combined with NRT delivered over a series of sessions. Individual or group behavioral treatments appear almost equally effective. Intensive treatment programs are effective in assisting even very dependent smokers to stop for a few months. However, as with other addictions, relapse is a major problem. Initial quitting rates of 50% to 60% at 1 month typically decrease to 20% to 30% at 1 year. Various relapse-prevention procedures have been tried. None has proven clearly effective. Most tobacco addicts repeat the quitting process on average every 3.5 years and try three or four times before finally stopping forever (66). In that respect, stopping smoking is similar to overcoming addictions to other psychoactive drugs. Tobacco addiction treatment programs are cost-effective. Average treatment costs per year of life saved are $1,000 to $2,000 per year for brief counseling alone and $2,000 to $4,000 per year of life saved with more intensive counseling and pharmacotherapy to aid in smoking cessation. Smoking cessation treatments are less costly per year of life saved than are enerally accepted therapies for hypertension, hypercholesterolemia, and other chronic disorders.

Therapeutics: Clinical Guidelines
Guidelines for treating tobacco dependence were published in 2000 by the United States Public Health Service. The detailed report resulted from critical review of approximately 6,000 peer-reviewed articles on tobacco addiction therapeutics and 50 metaanalyses based on that literature.
The major general conclusions were as follows:
1. Tobacco dependence is a chronic condition warranting repeated treatment until bstinence is achieved.
2. Effective treatments for tobacco dependence exist. All tobacco users should be offered treatment.
3. Clinicians and health care systems must institutionalize consistent identification, documentation, and treatment
of every tobacco user at every visit.
4. Brief tobacco dependence treatment is effective. Every tobacco user should be offered at least brief treatment.
5. There is a strong relationship between the intensity of tobacco dependence counseling and effectiveness.
6. Three types of counseling are especially effective: practical counseling, social support as a part of treatment, and social support outside of treatment.
7. Five pharmacotherapies for tobacco dependence are effective: nicotine gum, nicotine inhaler, nicotine nasal spray, nicotine patch, and bupropion. At least one of these medications should be prescribed in the absence of contraindications.
8. Tobacco dependence treatments are cost-effective when compared with other medical and disease prevention interventions. Health insurance plans should include as a
benefit the counseling and pharmacotherapies identified as effective in the guideline.
Contemporaneous reviews of tobacco addiction therapeutics and an extensive report on tobacco addiction pharmacology and therapeutics from the Royal College of Physicians offered similar conclusions. A summary review from the Cochrane Tobacco Addiction Review Group identified and summarized evidence of efficacy for tobacco addiction therapeutics. Details of the 20 systematic reviews are available on the Internet in the Cochrane Library. The reviews used a similar strategy and reviewed much the same literature on tobacco addiction therapeutics as did the Public Health Service review. The Cochrane reviews considered the results from randomized controlled trials having at least 6 months of followup. Sustained abstinence or point prevalence quit rates were used in the metaanalysis as necessary. Simple advice from physicians presented during routine care was studied in 31 trials that included 26,000 smokers in a variety of clinical settings. Brief advice increased quit rate more than no advice (odds ratio, 1.69; 95% confidence interval, 1.5 to 1.98). Individual counseling was better than brief advice or usual care. Group therapy was more effective than selfhelp materials alone but not consistently better than interventions with more personal contact. Self-help informational material and printed descriptions of behavioral strategies had a small treatment effect.

Nicotine Replacement Therapeutics
NRT decreases the discomfort of nicotine withdrawal. The relatively stable brain nicotine levels resulting from NRT should facilitate a desensitized state for some nicotinic cholinergic receptors. Because some nicotinic receptor subtypes are more desensitized than others, both nicotine agonistic and desensitization mechanisms could operate together in NRT. In a nicotine-induced desensitized state, norepinephrine release normally stimulated by endogenous acetylcholine would be diminished. Other neurotransmitter release normally stimulated by endogenous acetylcholine could be diminished as well. The resulting NRT modulation of mood states in itself could be rewarding. In addition, some blunting of the reinforcing effects of cigarettes smoked during cessation lapses is likely during NRT. However, the mechanisms of NRT still remain uncertain because the intensity of withdrawal alone is not a good predictor of success for ultimately stopping smoking. Even though withdrawal symptoms can be diminished by NRT, other mechanisms, learning coping skills, and replacing some of the positive effects of nicotine are important as well. Whatever the mechanisms, NRT is clearly effective and safe for helping smokers to quit. The ochrane review of clinical trials with nicotine gum, transdermal nicotine patches, nasal spray, and inhalers concluded that NRT enhanced early cessation and reduced early relapse when compared with placebo. All products enhanced quitting smoking about twofold. Quitting rates, depending on intensity of concurrent behavioral interventions, ranged from 10% to 30% of patients with a 1-year follow-up. Higher nicotine doses were more effective, although the dose–response function is shallow. NRT did not appear to have significant dependence potential or to cause significant harm. Characteristics of long-term NRT users resembled those of treatment failures. It appeared many would be smoking or smoking more if NRT were not available. However, 70% to 90% of addicted smokers fail to stop smoking despite NRT. Why? Most studies included only nicotine-addicted smokers, so the usefulness of NRT for less addicted smokers remains uncertain. Although recommendations have been made for use of combinations of NRT products, for example, patch plus spray, patch plus gum, or higher-dose NRT, too few trials preclude clear evidence of effectiveness. Long-term reduction in smoking by concomitant use of NRT while smoking continues is being investigated. Nicotine inhalers and skin patches have been used safely and with sustained reduction in smoking for up to 30 months.
Particularly for highly dependent smokers, nicotine replacement from patches and gum probably delivers nicotine to the brain too gradually and without the transient but rewarding brief surges in brain nicotine levels from puffing on a cigarette. Nicotine nasal sprays or inhalers more closely approximate smoking in this respect, but only partially so, and clinically they do not offer advantages to patch failures. An inhaled nicotine aerosol would, in principle, be an ideal substitute nicotine delivery system, but despite many attempts, a practical inhaled aerosol system providing the control over dose offered by a tobacco cigarette has not been brought to market.

Non–Nicotine Replacement Pharmacotherapies
The consequences of neuroadaptive changes in brain function associated with chronic nicotine exposure should, in principle, be modified by appropriate neurochemical interventions. Pharmacotherapies mimicking nicotine’s neurochemical effects by increasing or modulating brain levels of dopamine, epinephrine, serotonin, and other neurotransmitters should correct the neurochemical deficiency states associated with nicotine withdrawal. Pharmacotherapies may also mimic some of nicotine’s actions on brain reward systems. Nicotinic receptor antagonism offers an additional strategy. Although treatment with anxiolytics did not improve outcome, antidepressants, bupropion, and nortriptyline increased quit rates. The mechanisms by which antidepressant drugs benefit smoking cessation are yet to be determined. The neurochemical consequences of chronic nicotine exposure have similarities to the effects of some antidepressants.

As with many pharmacotherapies, recognition that bupropion could be useful for treating tobacco addiction resulted from serendipitous observations. Smokers being treated with bupropion for depression reported less desire to smoke or greater success in stopping smoking. Bupropion is structurally related to phenethylamines resembling an anorectic drug diethylproprion and is believed to assist smoking cessation by blocking neuronal uptake of dopamine and norepinephrine and possibly by decreasing firing of the locus ceruleus. Bupropion and some other antidepressants functionally antagonize some nicotinic cholinergic receptors in muscle and autonomic ganglia and reduce receptor response to nicotine. Whether antidepressant drugs similarly antagonize brain nicotine receptors is undetermined.Bupropion was effective judging from two large trials and two smaller unpublished ones. Bupropion alone or combined with a nicotine patch was more effective than the patch alone. Although the drug caused dry mouth and insomnia, serious side effects were uncommon. Bupropion was as effective in patients with a history of depression as with those without such a history. When given to a group of smokers not trying to quit permanently, bupropion decreased some withdrawal symptoms but had no effect on craving. Bupropion was a more cost-effective therapeutic agent for tobacco addiction than NRT.

Other Therapies With and Without Utility
Clonidine shares some pharmacologic effects of bupropion and tricyclic antidepressants. The Cochrane review of six clinical trials of clonidine found increased smoking quit rates, but side effects of sedation and postural hypotension posed problems for many patients. Sensory stimulants mimic mouth and airway sensory responses to smoking that become associated with the pharmacologic effects of nicotine and thus become reinforcers. Ascorbic acid aerosols and citric acid inhalers evaluated in cessation trials reduce craving and some withdrawal symptoms over the short term. The effects of opiate antagonists on cigarette smoking have been studied to examine how opioid systems modulate smoking behavior and to determine whether opioid antagonists could be useful to aid in smoking cessation. Naloxone precipitates opiate withdrawal-like symptoms and increases desire to smoke. The effects of naloxone or naltrexone on ad libitum smoking over brief periods in a laboratory were inconsistent, but some smokers smoked less.
A clinical trial compared naltrexone, 50 mg daily for 12 weeks, or placebo, with or without transdermal nicotine. Only transdermal nicotine increased abstinence rates.

Naltrexone had no effect on cessation rates. Transdermal nicotine reduced craving and cigarette smoking in smokers who did not quit. Naltrexone had no such effects. Another 4-week trial of naltrexone or placebo found no difference in smoking 6 months later. Thus, the clinical trial data indicate no useful role for opioid antagonists in smoking cessation therapy despite the suggestive laboratory results.
Nicotinic receptor antagonism offers another possible strategy. A nicotine antagonist mecamylamine has been investigated as a cessation aid both alone and in combination with NRT. Mecamylamine started before quitting smoking and continued afterwards appeared useful in two studies. Combined use of mecamylamine and nicotine patch increased quit rate more than nicotine alone, a finding leading to consideration of mecamylamine blockade of nicotine’s rewarding effects.
Circulating antibodies binding nicotine in blood and preventing its reaching the brain would be functionally equivalent to a receptor antagonist’s preventing nicotine receptor access. Antibodies have been induced by immunization of rats with nicotine linked to an immunogen.
Immunized animals had reduced brain nicotine concentrations and reduced behavioral and cardiovascular effects after intravenous nicotine. Whether immunization alters the reinforcing effects of nicotine remains to be determined. Lobeline, a nonpyridine alkaloid and partial nicotine receptor agonist from the Indian tobacco plant (Lobelia inflata),has long been used in proprietary smoking treatments. Although no longer marketed in the United States, lobeline is available elsewhere. No clinical trials had more than a 6-month follow-up. The drug was judged unproven by the Cochrane review.
ACTH has been suggested to aid smoking cessation, based on the notion that nicotine increases ACTH and cortisol release and that during nicotine withdrawal, there may be a state of hypoadrenocorticism. Uncontrolled trials with small numbers of smokers given a few ACTH injections during the first week after quitting reported high quit rates or decreased smoking, but without controlled clinical trials, ACTH must still be considered unproven.
Silver acetate has long been available as an over-the-counter smoking deterrent in the form of chewing gum, lozenges, and spray. A reaction with cigarette smoke produces an unpleasant metallic taste, the basis for this aversive therapy.
Several clinical trials reported short-term efficacy, particularly in less addicted smokers. Whenever the urge to smoke is great, it is easy to stop silver acetate use, so it does not appear an effective therapeutic for severe nicotine addiction.
The effectiveness of other aversion therapies, acupuncture, hypnotherapy, and exercise was at best considered uncertain.


Nicotine Addiction
Addiction is defined as a situation in which a drug unreasonably controls behavior. The primary criteria for drug dependence are highly controlled or compulsive use of a drug with psychoactive effects and the presence of drug-reinforced behavior. Additional criteria are stereotypic patterns of use, use despite harmful consequences, relapse following abstinence, and recurrent drug cravings.

What are the symptoms of nicotine addiction?
•    irritability
•    impatience
•    hostility
•    anxiety
•    depressed mood
•    difficulty concentrating
•    restlessness
•    decreased heart rate
•    increased appetite or weight gain

Complications of Nicotine addiction?
Nicotine dependence can affect several parts of your body. Common complications of nicotine dependence are:
•    Lung cancer
•    Dry skin
•    Emphysema
•    Chronic bronchitis
•    Increased risk of heart disease.
•    Esophageal cancer
•    Larynx cancer
•    Throat cancer
•    Oral cancer
•    Infertility
•    Pregnancy and newborn complications
•    Dull senses

Dependence-producing drugs often produce “tolerance,” physical dependence, and pleasant effects. Smoking fits these definitions of an addictive behavior.  Approximately 40 percent of smokers attempt to quit annually, yet less than 5 percent do. Most smoking cessation tempts fail within the first two weeks; on average, four or more attempts are necessary before long-term cessation is achieved.
Even in patients with cardiovascular disease, cancer, or chronic obstructive pulmonary disease where stopping smoking is critical to halt further deterioration of their medical condition, fewer than 50 percent quit.
The agent largely responsible for maintaining smoking addiction is nicotine. Animal models demonstrate nicotine’s addictive potential, and several lines of evidence suggest that nicotine is addictive in humans as well. In addition to the difficulty in quitting, research shows that smokers adjust their smoking habits to maintain relatively stable concentrations of nicotine, that the reinforcing effects of nicotine are blocked by pretreatment with the nicotine receptor antagonist mecamylamine, and that quitting smoking is associated with cravings and a characteristic withdrawal syndrome. Nicotine’s neurobiological effects are complex and not entirely understood. Nicotine binds to nicotinic acetylcholine receptors located in the brain, autonomic ganglia, and neuromuscular junctions.
Such binding leads to the release of a number of neurotransmitters and hormones including dopamine, serotonin, norepinephrine, acetylcholine, vasopressin, and beta-endorphin. The release of these substances modulates many of the subjective, cognitive, and behavioral effects associated with smoking, such as increase in pleasure, improved mood, increased attention, enhanced cognition and motor performance, and weight loss.
Chronic use of nicotine results in the development of “tolerance,” which decreases the effect of a given dose of the drug. Tolerance is the result of morphological changes in the brain, such as receptor desensitization and inactivation as well as upregulation of receptor number. As a result of this neuroadaptation, cessation of tobacco use results in a withdrawal syndrome, characterized by depressed mood, insomnia, irritability, frustration or anger, anxiety, difficulty concentrating, restlessness, decreased heart rate, and increased appetite or weight gain. These symptoms generally peak at one week and gradually decrease over time, sometimes eventually reaching lower levels than were experienced while smoking. Thus, nicotine addiction is maintained not only by the subjective positive effects that smokers experience, but also by the desire to avoid the negative symptoms associated with nicotine withdrawal.
The potential for abuse or addiction to a drug is generally determined by the magnitude of the positive reinforcing effects and the speed of drug delivery to the brain. Typically, the relationship between drug dose and the reinforcing effect of the drug is characterized by an inverted U-shaped curve. Administration of an addictive drug will increase until its toxicity reduces the overall desirable effects and therefore decreases its reinforcing effects.
Generally, the more quickly the drug is delivered to the brain, the greater the potential for abuse. Nicotine from a smoked cigarette reaches the brain in ten to twenty seconds, with initial arterial nicotine concentrations far surpassing venous concentration.
Such rapid delivery contributes to its high abuse potential. Smokeless tobacco and nicotine gum, which take longer to reach the brain, have somewhat less abuse potential, and the nicotine patch, which is very slowly absorbed, has minimal abuse potential
Current and future pharmacological treatments aim to reduce tobacco use by targeting the mechanisms that reinforce tobacco use. Some treatments use agents that mimic the reinforcing effect of nicotine or reduce the negative effects (such as craving or withdrawal symptoms) associated with abstinence. Strategies being considered for future therapies include using agents that block the reinforcing effects of nicotine, prevent nicotine from crossing the blood brain barrier, and alter the metabolism of nicotine.

1. http://www.americanheart.org/presenter.jhtml?identifier=4753
2. http://www.mamashealth.com/substance/nicotine.asp


An acute infectious disease of warm-blooded animals characterized by involvement of the nervous system resulting in death.

It is caused by the RABIES VIRUS, a rhabdovirus of the genus lyssavirus. RHABDOVIRUS: any group of rod-shaped RNA viruses with 1 important member, rabies virus, pathogenic to man. The virus has a predilection for tissue of mucus-secreting glands and the Central Nervous System. All warm-blooded animals are susceptible to infection with these viruses. LYSSAVIRUS: Greek – frenzy. A genus of the family Rhabdoviridae. There are 2 kinds of rabies. URBAN or CANINE RABIES are transmitted by dogs. SYLVATIC RABIES are transmitted from wild animals and bats which sometimes spread to dogs, cats and livestock.

MODE OF TRANSMISSION: It is commonly communicated to man through the saliva of an infected mammal by an exposure to an open break in the skin such as bites or scratch and inhalation of infectious aerosols such as from bats. In some cases, it is transmitted through organ transplants (corneal transplant), from an infected person.

MEDIA OF TRANSMISSION: Through saliva, tears, urine, serum, liquor and other body fluids.

The period between the exposure to the virus to the occurrence of the first symptom, is usually 2-8 weeks. It may be as short as 4 days or as long as 2 years depending on depth of laceration and site of wound. The virus moves along nerve axons passively about 3 millimeters per hour. It is not known how the virus remains viable or where it is located during prolonged incubation period.

SUSCEPTIBILITY AND RESISTANCE: All warm-blooded mammals are susceptible. Natural immunity in man is unknown.

There is yet no way of immediately segregating those who had acquired rabies infection from those who had been bitten by non-rabid sources. No tests are available to diagnose rabies in humans before the onset of clinical disease. The most reliable test for rabies in patients who have clinical signs of the disease is DIRECT IMMUNOFLUORESCENT STUDY of a full thickness biopsy of the skin taken from the back of the neck above the hair line. The RAPID FLUORESCENT FOCUS INHIBITION TEST is used to measure rabies-neutralizing antibodies in serum. This test has the advantage of providing results within 24 hours. Other tests of antibodies may take as long as 14 days. 
True rabies must be distinguished from RABIES HYSTERIA, a psychological condition in persons who think they have been bitten by a rabid animal. In such cases, a patient ordinarily attempts to emulate convulsive seizures. Patient receiving rabies vaccine treatment may develop paralysis attributable to a sensitization caused by the rabbit brain material in the vaccine. This paralysis may simulate paralytic rabies and may produce symptoms referable to cranial nerves, such as difficulty swallowing, paralysis of the masseter muscles and unilateral or bilateral facial paralysis. Encephalitis without paralysis may be caused by the vaccine treatment and in such cases the disease begins with high fever and headache with may be followed by convulsions and coma.

SIGNS & SYMPTOMS (most common)
a. Sensory change on or near Delirium 
b.the site of entry Insomnia 
c. Fever Convulsions 
d. Laryngeal spasme 
e. Salivation or foaming of the mouth 
f. Sense of apprehension, anxiety, irritabilty 
g. Acute attack: fever, muscle  twitching, hyperventilation and excess salivation 
h. Headache
The usual duration is 2-6 days without medical intervention. Death is often due to convulsion or respiratory paralysis.

1.Responsible pet ownership
a) pet immunization, esp. cats, usually starting at 3 months of age and every year thereafter
b) don’t allow pets to roam around the streets
c) take care of your pets, keep them in good health – bathe, feed with clean adequate food and provide clean sleeping quarters
2.Thoroughly clean ALL BITES AND SCRATCHES made by any animal with strong medicinal soap or solution.
3.Responsible awareness. Report immediately rabid or suggestive of rabies domestic or wild animals to proper authorities (local government clinic, veterinarians or community officials).
4. Pre-exposure to high risk individuals. Veterinarians, hunters, people in contact with animals (zoo), butchers, lab-staff in contact with rabies, forest rangers/caretakers.
5.DOH Standard Protocol
a) If dog is apparently healthy, observe the dog for 14 days. If it dies or show signs suggestive or rabies, consult a physician.
b) If the dog shows signs suggestive of rabies, kill the dog immediately and bring head for lab examination. Submit for immunization while waiting for results.
c) If the dog is not available for observation (killed, died or stray), submit for immunization. *see DOH- Revised Guidelines on Management of Animal Bite Patients- 2007 for more complete guide B.

a. Local wound treatment. Immediately wash wound with soap and water. Treat with antiseptic solutions such as iodine, alcohol and other disinfectants.
b. Antibiotics and anti-tetanus as prescribed by physician.
c. Rabies – Specific Treatment. Post-exposure treatment is given to persons who are exposed to the rabies virus. It consists of active immunization (vaccination) and passive immunization (immune globulin administration).

a. ACTIVE IMMUNIZATION – aims to induce the body to develop antibodies and T-cells against rabies up to 3 years. It induces an active immune response in 7-10 days after vaccination, which may persist for one year or more provided primary immunization is completed MEDICAL AGENT: Human Diploid Cell rabies Vaccine (HDCV)

b.PASSIVE IMMUNIZATION – aims to provide IMMEDIATE PROTECTION against rabies which should be administered within the first 7 days of active immunization. The effect of the immune globulin is only short term. Rabies antibodies are introduced before it is physiologically possible for the patient to begin producing his own antibodies after vaccination. Some of the RIG is infiltrated around the site and the rest is given intramuscularly. MEDICAL AGENT: Rabies Immune Globulin (RIG)

* provide patient isolation
* handwashing. Wash hands before and after each patient contact and following procedures that offer contamination risk while caring for an individual patient. Handwashing technique is important in reducing transient flora on outer epidermal layers of skin.
* Wear gloves when handling fluids and other potential contaminated articles. Dispose of every after patient care. Gloves provide effective barrier protection. Contaminated gloves becomes a potential vehicle for the transfer of organisms.
* Practice isolation techniques. To prevent self-contamination and spread of disease.

(about the disease, cause of infection and preventive measures)
* assess patient’s and family’s level of knowledge on the disease including concepts, beliefs and known treatment.
* Provide pertinent data about the disease: 
a. organism and route of transmission 
b. treatment goals and process 
c. community resources if necessary
* allow opportunities for questions and discussions

3. ALTERED BODY TEMPERATURE: FEVER RELATED TO THE PRESENCE OF INFECTION. Since fever is continuous, provide other modes to reduce discomfort.
 * If patient is still well oriented, Inform the relation of fever to the disease process. The presence of virus in the body
* Monitor temperature at regular intervals
* Provide a well ventilated environment free from drafts and wind. 

4. DEHYDRATION related to refusal to take in fluids secondary to throat spasms and fear of spasmodic attacks.
•  Assess level of dehydration of patient.
* Maintain other routes of fluid introduction as prescribed by
* the physician e.g. parenteral routes Moisten parched mouth with cotton or gauze dipped in water 
* but not dripping.

1. Taber’s Cyclopedic Medical Dictionary 17th Edition. 1994. Singapore: Davis Company. Department of Health.2000.
2. Community Health Nursing Services in the Philippine Department of Health, 9th Edition.Philippines.DOH Smeltzer, Suzanne and Bare, Brenda. 2000.
3. Brunner & Suddarth’s Textbook of Medical-Surgical Nursing, 9th Edition. Philadelphia: Lippincott Williams and Wilkins


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