Ethyl alcohol (ethanol) is a clear liquid with a bitter taste. It can be used as an anesthetic, a poison, a foodstuff, an antiseptic, or a surface blood vessel dilator. It is an unstable Central Nervous System depressant that produces euphoria and disinhibition. Without question, alcohol is the most used psychoactive drug. Psychoactive effects: As it passes the blood-brain barrier after ingestion and affect the cerebral cortex, most people feel their inhibitions quickly disappear and sense a more relaxed social attitude concerning their interactions with others. As a depressant, alcohol has a relaxing effect, but also clouds one's inhibitions and judgment. Alcohol's effect on glutamate may impair the formation of new memories by suppressing activity at NMDA receptor sites. It is responsible as well for impairing complex thought and judgment while intoxicated. Effects on the body: It contains no nutrients to nourish the cell. It can pass through every tissue cluster in the brain and body if enough is consumed. Immediately after drinking, the mouth and esophagus begins to absorb small amounts via the mucous membranes. The stomach will rapidly assimilate about one-quarter of a dose, followed by complete absorption through the walls of the small intestine within 20 to30 minutes. The cardiovascular system is affected by low doses of alcohol through the dilation of peripheral blood vessels, while severe alcohol intoxication will create a depression of the entire cardiovascular system. Alcohol irritates the gastrointestinal tract through direct contact, as well as by stimulating the secretion of stomach acid and pepsin, which can cause gastritis and injury to the mucous membranes of the stomach lining. The presence of food can modify these effects to some extent and also slows the absorption rate of alcohol. Because alcohol is a diuretic, it over stimulates the production of urine in the kidneys. The liver is the primary organ of alcohol detoxification. It is the central filter for the blood and is the site of 90% of alcohol metabolism. With continued heavy intake of alcohol, the liver cells begin to accumulate fatty deposits that destroy the cells and produce scarring called cirrhosis. This disease occurs in, and is fatal to, about 10% of chronic alcoholic patients. Nearly every organ in the body is affected by heavy use of alcohol. Gastritis, diarrhea, and gastric ulcers are commonly associated with heavy drinking. A single heavy drinking episode can cause the pancreas to hemorrhage. The consumption of large amounts of alcohol can depress the respiratory center in the medulla, causing death. Strong evidence indicates links between alcohol and cancers that occur in the upper digestive tract, respiratory system, mouth, pharynx, larynx, esophagus, and liver. Besides liver damage (cirrhosis), alcoholics may develop pathology of the nervous system due to vitamin deficiencies, as well as experience neurological complications such as the Wemicke-Korsakoff syndrome. This chronic brain syndrome is the result of thiamin deficiency from poor absorption, metabolism, and storage of the vitamin in the prolonged presence of alcohol, as well as poor diet while drinking. It has as its most striking feature a dementia characterized by permanent short-term memory loss coupled with filling in the blanks of memory with exaggerated stories. Tolerance and dependence: In the presence of repeated drinking, tolerance to the effects of alcohol begins as the body adapts to try to maintain its normal functioning in the continual presence of a foreign chemical. The liver becomes more efficient in detoxifying alcohol, the cells of the brain become less and less sensitive to the intoxicating effects of the chemical, and the chronic drinker exhibits fewer of the behavioral effects of intoxication. In addition, while brain cells may be less sensitive, damage continues unabated to the brain and organs such as the liver. Risk of dependence on alcohol, both physically and psychologically, is moderate to high. The etiology is complicated and appears to be affected by such factors as genetics, biological changes, brain reward systems, and stress relief mechanisms. It is suggested that the younger the onset of drinking, the greater the chance of that person developing a clinically defined alcohol disorder. WITHDRAWAL The acute withdrawal syndrome generally appears within 12 to 72 hours after drinking has ceased. The earliest signs of withdrawal are associated with hyperarousal and can include anxiety, irritability, insomnia, loss of appetite, tachycardia (rapid heartbeat), and tremulousness. An “eye-opener” (i.e., a drink first thing in the morning) is a common solution to hyperarousal for the problem drinker. Hence, alcohol abuse interviews commonly include a question concerning morning drinking. Alcoholic hallucinosis occurs in about 25% of withdrawal episodes, usually within the first 24 hours. It includes true auditory and visual hallucinations, illusions, and misperception of real environmental stimuli. Convulsive seizures, or “rum fits,” can occur with acute alcohol withdrawal. These seizures are most often of the grand mal variety, in which the eyes roll back in the head; body muscles contract, relax, and extend rhythmically and violently; and loss of consciousness occurs. About a third of alcoholics who have seizures in withdrawal develop delirium tremens. Delirium tremens, or DTs, is the most serious form of withdrawal. Without medical intervention, mortality rates are as high as 20%. With medical help, there still remains a 1% to 2% death rate. TOXIC AND LETHAL EFFECTS Comas can occur at BALs of 0.40%. Alcohol becomes lethal in higher concentrations by depressing the respiratory center in the medulla.
Opium is derived from the poppy flower. The main active ingredient is morphine alkaloid, which is widely used because it is the most effective and most powerful painkiller available. Other effects and signs of usage include euphoria, drowsiness, constricted pupils, nausea, possible respiratory distress, coma, and death. Other derivatives include heroin, codeine, hydromorphone, hydrocodone, oxymorphone and Oxycodone, as well as a number of synthetic medical compounds, including esiridine, methadone, fetanyl, and propoxyphene. Psychotic effects: The opioid drugs reduce both the perception of pain and the reaction to it. They also produce euphoria, which leads to their abuse. In addition, they reduce anxiety and stress and produce sleep. Injection continues to be the predominant method of heroin use, with intravenous injection providing the greatest intensity and most rapid onset of euphoria (7 to 8 seconds). Intramuscular injection produces euphoria in 5 to 8 minutes; while sniffing or smoking requires 10 to 15 minutes for peak effects to occur. Although nasal ingestion does not produce as intense or as rapid a rush, all forms of heroin administration are addictive. Recent scientific demonstration of receptors in the central nervous systems of both animals and humans, followed by the discovery that the body makes its own opiate-like substances, has greatly enhanced the understanding of the action of opioids. Administered opioids are thought to act at the neuronal synapses, either by acting as a neurotransmitter decreasing the transynaptic potential or by modulating the release of a neurotransmitter post synaptically. This appears to be the basis of their analgesic effect and may be similar to the action of the body's endogenous opioids. Effects on the body: Respiratory depression can occur because the drugs inhibit the respiratory brain stem mechanism, in particular the responsiveness to carbon dioxide. Suppression of the cough reflex is a well-known effect of the opioids. All opioid agonists constrict the pupils except meperidine, which in large doses may dilate them. Opioids also activate the brain stem chemoreceptor trigger zone to produce nausea and vomiting. Truncal rigidity may occur with some opioids, thus reducing thoracic compliance and interfering with ventilation. The effect is most apparent with high doses of highly lipid-soluble opioids like fentanyl. Peripheral effects occur with the cardiovascular, gastrointestinal, genitourinary, endocrine, immune, and integumentary systems. Most opioid drugs in therapeutic doses do not have significant effects on the heart, cardiac rate and rhythm, or blood pressure in the supine position. Meperidine (Demerol) is an exception because its antimuscarinic action can result in tachycardia. Opioids do produce peripheral vasodilation, reduce peripheral resistance, and inhibit the baro-receptor reflex. Therefore, when patients in the supine position raise their upper torsos, they may suffer orthostatic hypotension and may have syncope. Therefore, precautions should be taken with patients who have decreased blood volumes. The opioids constrict biliary smooth muscle, which may cause biliary colic. Constriction of the sphincter of Oddi may result in reflux of biliary secretions and elevated plasma amylase and lipase levels. In addition, the drugs decrease large intestine motility, leading to constipation. In the Opioid Dependence stomach, motility is decreased, and tone is increased. Gastric acid secretion is decreased. The opioids depress renal function, probably because they decrease renal plasma flow. Ureteral and bladder tone are increased, and increased urethral sphincter tone may lead to urinary retention. In addition, mu receptor agonists have an antidiuretic effect. Opioids also enhance renal tubular sodium reabsorption. Occasionally uterine colic caused by a renal stone is made worse by opioid-induced increase in ureteral tone. Opioid-induced uterine tone may prolong labor. The opioid analgesics stimulate the release of antidiuretic hormone, prolactin, and somatropin but may inhibit the release of luteinizing hor- mone. Patients receiving chronic opioid therapy may have low testosterone levels resulting in decreased libido, energy, and mood. Women may experience dysmenorrhea or amenorrhea. Opioids modulate the immune system by effects on lymphocyte proliferation, antibody produc- tion, and chemotaxis. In addition, leukocytes migrate to the site of tissue injury and release opioid peptides, which help counter inflamma- tory pain. However, natural killer cell cytolytic activity and lymphocyte proliferation are usually inhibited by opioids, which may play a role in tumor progression. Opioids produce flushing and warming of the skin, sometimes accompanied by sweating, urti- caria, and pruritus. Although peripheral hista- mine release is an important contributor, all opioids can cause pruritus via a central (spinal cord and medulla) action on pruritoceptive neural circuits. When opioids are administered by the epidural or spinal routes, their usefulness may be limited because of intense pruritus of the lips and torso. It is believed that chronic morphine use produces marked structural changes in the dopamine neurons in the brain's ventral segmental area (VTA). In research studies with mice, the size of mesolimbic dopamine neurons originating in the VTA showed a dramatic decrease, and the shape of the neurons also changed. No changes were observed in non dopaminergic neurons. Thus, the opioids affected exactly those brain cells implicated in continuing drug use. Tolerance and dependence: The risk of dependence of opioids, both physical and psychological, is high. Physiological tolerance and dependence results from brain changes after prolonged use, while psychological tolerance and dependence are a result of linking learned associations between drug effects and environmental cues. These phenomena of tolerance to and physical dependence (neuroadaption) on opioids appear to be receptor site-specific. Endogenous molecules have been identified with opioid activity and at least 12 peptides have been discovered, including the beta-endorphins and dynorphines. These long-chain peptides are believed to bind to their own specific opioid receptors. Stimulation of opioid receptors located in critical cells, such as those located in the locus coeruleus, produce a decrease in cell firing, ultimately causing the cells to become hyper excitable. Tolerance to opioids can develop quite rapidly in frequent users, and experiments have verified that a clinical dose of morphine (60 milligrams a day) in an individual can be increased to 500 milligrams per day in as little as 10 days. Over time, the brain substitutes administered chemical opiates for natural endorphins, causing effects such as euphoria to become less intense. As the body accommodates to the presence of chemical opioids, long-term usage produces a ”threshold effect,” after which time the chronic opioid user will use the drug just to function in a normal state, no longer getting high. Withdrawal: Opoid withdrawal causes flu like symptoms. The symptoms of withdrawal include feelings of dysphoria, nausea, repeated yawning, sweating, tearing, and a runny nose. It is during this period that subjects experience craving or”drug hunger” for repeated exposure to the drug. The symptoms of opiate withdrawal are the result of interactions between the opioid and other neurotransmitter systems. People going through opioid withdrawal can experience serious distress and physical discomfort. For the most commonly misused opioids, withdrawal symptoms start to peak two or three days after the last use. Acute physical symptoms improve after five to seven days from last use; however, the psychological symptoms of intense cravings, anxiety and low mood, as well as sub acute physical symptoms, may last for weeks, even months. The persistence of these symptoms is a factor in relapse risk Overdose: Mortality figures indicate that death by overdose on heroin/morphine is highly prevalent throughout the nation. This phenomenon occurs because an important effect of narcotics is to depress the respiratory centers response to blood levels of carbon dioxide. In addition, this effect is additive with alcohol or other sedative hypnotics, which increases the danger of fatal overdose.
Marijuana and hashish are produced from the hemp plant, cannabis. As a psychoactive agent, it is used primarily to produce euphoria followed by relaxation. Cannabis is known by many names: marijuana, hash, pot, herb, weed, grass, ganja, or dope. Cannabis is usually smoked as cigarettes (joint, nail) or in a pipe (bong). The strength of the end product that comes from the hemp plant vary, owing to the climate and soil in which it is grown and the method of cultivation and preparation. Its potency and quality depend mainly on the type of plant that is grown. Bhang is identified as the least potent and cheapest and is made from the cut tops of uncultivated plants that contain low-resin content. Ganja is derived from the flowering tops and leaves of selected plants that have been carefully cultivated having a high content of resin and, therefore, being more potentiated to the user. Charas is the highest grade and is produced from the resin itself, obtained from fully mature plants. This highly potentiated source is generally referred to as hashish. Additionally, clandestine laboratories have developed a method of producing a liquid called ”hash oil,” which has been found to have more than 60% THC content compared with an average 30% in regular hashish. Psychoactive Effects: Smoking of cannabis can produce relaxation following, euphoria, loss of appetite, impaired memory, loss of concentration and knowledge retention, loss of coordination, as well as a more vivid sense of taste, sight, smell, and hearing. Stronger doses cause fluctuation of emotions, fragmentary thoughts, disoriented behavior, and psychosis. It may also cause irritation to the lungs and respiratory system and cancer. The short-term effects of marijuana include problems with memory and learning, distorted perception, difficulty in thinking and problem solving, loss of coordination, and increased heart rate. Long-term marijuana abuse indicates some changes in the brain similar to those seen after long term abuse of other major drugs. Effects on the body: Cannabis is generally smoked in a cigarette called a joint or a doobie. A marijuana cigarette contains 421 chemicals before ignition. There are 61 cannabanoids, including delta-1 tetrahydrocannabinol, which is the psychoactive agent. Neuroscience research findings have indicated the effects of this psychoactive agent on the modulation of mediotemporal and ventrostraital functions of the brain. There are also 50 different waxy hydrocarbons, 103 terpines, 12 fatty acids, 11 steroids, 20 nitrogen compounds, as well as carbon monoxide, ammonia, acetone, benzene, benzathracene, and benzoprene. When ignited, these chemicals convert into more than 2,000 other chemicals. As these are metabolized by the body, they convert to about 600 chemical metabolites. Cannabinoids have a half-life of 72 hours in the human body. When ingested, effects appear to be dose-dependent. Cannabinoids are lipid-soluble and store at megamicroscopic levels for indefinite periods of time in the body. Early research findings on cannabis have been mixed. However, more recent neuroscience research using structural imaging findings on CT or MR imaging, and conventional angiography clearly indicates that excessive use of cannabis leads to functional or structural impairment of the central nervous system. Chemicals found in marijuana and hashish are believed to interfere with the cell's ability to manufacture pivotal molecules, which grossly affects the substances necessary for cell division including DNA, RNA, and proteins. This causes an ”aging process” in particular clusters of cells found in the brain, liver, lungs, spleen, lymphoid tissues, and sex organs. One well-confirmed danger of heavy, long-term use is its ability to damage the lungs due to the fact that it burns 16 times ”hotter” than tobacco and produces twice as many mutagens (agents that cause permanent changes in genetic material). Biopsies have confirmed that cannabis smokers may be at an extremely high risk for the development of lung diseases including bronchitis, emphysema, and cancer. It is believed that some of marijuana's adverse health effects may occur because THC impairs the immune system's ability to fight disease. There is a prevalence of studies supporting the biological association of marijuana smoking with lung cancer. It is believed that long-term marijuana use causes mental or emotional deterioration. Amotivational syndrome, which includes symptoms of passivity, aimlessness, apathy, uncommunicativeness, and lack of ambition, has been attributed to prolonged marijuana use. Marijuana has the potential to cause problems in daily life or make a person's existing problems worse with depression, anxiety, and personality disturbances exacerbated with chronic marijuana use. One still needs to ask whether these symptoms result from the use of marijuana, the personality characteristics of heavy drug users—bored, anxious, depressed, listless, cynical, and rebellious or a combination. Marijuana has also been looked on as the “gateway drug,” or precursor to use of other, more dangerous drugs. Anyone who uses one drug may be interested in others for the same reasons. Users of one drug often find themselves in the company of users of other drugs, and therefore making them readily available. Marijuana smoke contains some of the same cancer-causing compounds as tobacco, usually in higher concentrations. Someone who smokes five joints per day may be taking in as many cancer- causing chemicals as someone who smokes a full pack of cigarettes every day. Cancer of the respiratory tract and lungs may be promoted by marijuana smoke, since it contains irritants and carcinogens. Tobacco smoke and marijuana smoke may work together to change the tissues that line the respiratory tract. Marijuana smoking could contribute to early development of head and neck cancer in some people. Smoking marijuana has been linked to testicular cancer. Long-term health risks of marijuana use include immune system effects, cardiovascular effects, respiratory effects, reproductive effects, behavioral effects, and cancer. Marijuana use also puts users at risk for various types of accidents. Coinciding with the increasing rates of cannabis use due to medical marijuana has been the recognition of a new clinical condition known as cannabinoid hyperemesis syndrome. This syndrome is characterized by cyclic episodes of nausea and vomiting and abdominal pain. Despite the well established antiemetic properties of marijuana, there is increasing evidence of its paradoxical effects on the gastrointestinal tract and central nervous system. Long-term cannabis use can impair the immune system’s ability to fight off microbial and viral infections. Both animal and human studies have shown that marijuana impairs the ability of T-cells in the lungs’ immune defense system to fight off some infections. Users with preexisting coronary artery disease or cerebrovascular disease may experience myocardial infarctions, congestive heart failure, or stroke. Peripheral vasodilatation causes postural hypotension, which may lead to dizziness or syncope. Cannabis arteritis is a very rare peripheral vascular disease similar to Buerger’s disease. High doses of THC cause a drop in testosterone level, decreased sperm production, and compro- mised sperm motility and viability. THC alters the normal ovulatory cycle by decreasing follicle-stimulating hormone, luteinizing hormone, and prolactin secretion. It crosses the placenta and impairs placental development, fetal nourishment, and placental gas exchange. For this reason, it is implicated in low birth weight, growth restriction, preeclampsia, spontaneous miscarriage, and stillbirth. It also accumu- lates in breast milk. Children of chronic users (greater than five joints per week) were found to have lower verbal and memory scores at age 2 years. A possible increased risk of nonlymphoblastic leukemia, rhabdomyosarcoma, and astrocytoma exists in children whose mothers use cannabis during their pregnancies. Psychiatric/Behavioral Long-term use of marijuana also can lead to a series of attitude and personality changes known as “amotivational syndrome.” This syndrome is characterized by a diminished ability to carry out long-term plans, a sense of apathy, decreased attention to appearance and behavior, and decreased ability to concentrate for long periods of time. These changes can also include poor performance in school. Long-term marijuana use has been shown to cause a decline in IQ of up to eight points. Marijuana use can cause relationship problems and antisocial behavior, such as lying and stealing money. It leads to lower life satisfaction, financial difficulties, and a greater chance of being unemployed. Marijuana use has been shown to increase the risk of schizophrenia two fold in vulnerable individuals. Tolerance and dependence: Many individuals who develop a dependency on marijuana are susceptible to other dependencies because of anxiety, depression, or feelings of inadequacy. In general, there appears to be both a psychological and physical potential for dependency. Signs of possible misuse of marijuana include animated behavior and loud talking, followed by sleepiness, dilated pupils and bloodshot eyes, distortions in perception, hallucinations, distortions in depth and time perception, and loss of coordination. An overdose of marijuana can cause fatigue, lack of coordination, paranoia, and psychosis. Withdrawal: Studies since the 1970s have suggested a marijuana withdrawal syndrome, characterized by insomnia, restlessness, loss of appetite, and irritability. A 1999 study conducted at Harvard Medical School confirmed higher levels of aggression in marijuana users during withdrawal when compared with the infrequent or former marijuana user. Research also reported by Bartholomew et al. (2010) indicated that cannabinoid (THC or synthetic forms of THC) withdrawal in chronically exposed animals leads to an increase in the activation of the stress-response system and changes in the activity of nerve cells containing dopamine. It should be noted that dopamine neurons are involved in the regulation of motivation and reward, and are directly or indirectly affected by all drugs of abuse including cannabis.