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In this chapter and the next, we will look at all different kinds of drugs ranging from caffeine to crack and cocaine. Most drugs that will be discussed in this chapter exists for hundreds or even thousands of years. The use of drugs became alarming up till 2000. Since that year, the use of drugs by teenagers is stable. There is even a little decline and the decline of alcohol and tobacco use is bigger. Only the trend of marijuana use is an increasing one.
Drug schedule refers to the potential for abuse of a drug and this has been described by the Controlled Substance Act in 1970. Schedule I drugs do have less potential for abuse than schedules II to V.
Cocaine is extracted from the coca plant, which grows in the mountains of South America. People used to chew on the leaves of this plant, because it produced feelings of confidence. Nowadays, cocaine is most exported as cocaine sulphate or cocaine hydrochloride.
Cocaine compounds are extracted by crushing the leaves in a solution (such as kerosene, gasoline or alcohol). The liquid mixture that remains is processed under heat with sulfuric acid to isolate the cocaine alkaloids and to remove the waxy residues. The cocaine sulphate paste that remains contains about 60% cocaine and is then further processed into a water-soluble crystal composition called cocaine hydrochloride.
In South America, many of the waste products that originate during the extraction process of cocaine are dumped in the river. This has very harmful ecological consequences.
Cocaine alkaloid was first isolated in 1855 by Friedrich Gaedcke, he called it erythroxyline . Albert Niemann then called it cocaine. It was used as a local anesthetic, especially in eye and nose operations. It was also added to many drinks, given the stimulating effects and you could buy cocaine in local drugstores. Freud was enthusiastic about the substance and recommended it to other people. It was only in 1914 that the use of cocaine in all forms was banned by the Harrison Narcotic Tax Act and was described as a dangerous narcotic.
Cocaine hydrochloride is a water soluble substance that divides itself into cocaine-H + and Cl - ions after its administration. The positively charged cocaine ions are able to quickly pass cell membranes and enter the brain. Snorted and orally administered cocaine goes slower and will be absorbed less complete than intravenously administered, inhaled or vaporized cocaine.
Methylbenzoulecgonine is a composition that is the result of dissolving cocaine hydrochloride in a mild ammonia solution. This composition can be vaporized for inhalation and is called crack because of the cracking sound in this process. Crack can also be manufactured by heating cocaine hydrochloride in water and sodium ('sodium') bicarbonate. The cocaine rocks that arise as a result (called 'freebase' cocaine) are then heated until they can be vaporized. Inhalation causes peaks in plasma concentrations within 5 minutes.
Benzoylecgonine and ecgonine are the major metabolites of cocaine and can be found for weeks in both blood and body tissue. Cocaethylene is produced when cocaine is used together with alcohol. It can cause hypertension, ventricular arrhythmia and reduced blood flow with potentially fatal consequences.
Because cocaine binds to the dopamine transporter, it can pass through cell membranes in the brain. Cocaine binds to the dopamine transporter (DAT) and as a consequence blocks the normal reuptake of dopamine in the synaptic cleft, resulting in prolonged dopamine activity on postsynaptic receptors. Cocaine has similar effects on noradrenaline and serotonin receptors, but these are less important than the effects on the dopamine receptors. Blocking the dopamine transporter happens very quickly after the administration of cocaine. The rapid increase in dopamine activity in the mesolimbic system is believed to cause the pleasant effects of cocaine.
Place preference conditioning is a conditioning process in which one has a preference for the space where cocaine is administered. This has been shown by research with rats, a process that is evident from the rats' preference to spend time in the room where they were given cocaine. It is a demonstration of Pavlovian conditioning in which the signals of the specific context or space are associated with the use of drugs.
Cardiac toxicity is a dangerous effect of cocaine. It can cause myocardial infarction, arrhythmias and sudden death, because of the Na + channel blockade in neurons.
Amphetamines are compositions that are very similar to dopamine in chemical structures. The first used composition was ephedrine, also known as the old Chinese medicine ma huang. More recently the drug is called ephedra, which has been marketed as a substance for weight loss and it increases vigilance and performance. Although the effectiveness of this product remains controversial, it has been banned in the sports world. Due to many deaths, the drug has been completely banned since 2004.
Amphetamine was first synthesized in 1887. Around 1930 it came onto the market under the name Benzedrine as an antihistamine inhaler. Dextroamphetamine (Dexedrine) is structurally related to amphetamine and was introduced to treat narcolepsy, attention deficits, nasal congestion and obesity. In 1940, amphetamines were used to treat nearly 40 different disorders.
In 1960 the production of amphetamines increased, due to the use for weight loss. The funds were also used extensively by students and athletes, with sometimes deadly consequences. In 1970 the use of amphetamines was limited to only medical applications (narcolepsy and attention disorders).
Metamphetamine was first synthesized from ephedrine in 1893 and became very popular in the United States in 1980 due to its strong euphoric effects. It differs structurally from amphetamine by the added methyl group (CH3), which increases the solubility in fat. As a result, it can only cross the blood-brain-brain barrier a few seconds after the injection. Pure metamphetamine has a crystal form, which explains the name Crystal Meth.
Amphetamines can be administered in various ways, including: taking a pill orally (peak plasma concentration 2-3 hours), sniffing (inhalation through the nose), smoking and intravenous injection (peak plasma concentration 5 minutes). The metabolic half-life of amphetamines is between 10 and 15 hours.
Amphetamines increase the synaptic concentrations of noradrenaline and dopamine through different mechanisms. The first is that they bind to the presynaptic membranes of dopaminergic and noradrenergic neurons to increase the release of norepinephrine and dopamine from synaptic vesicles. They also block reuptake transporters of norepinephrine and dopamine.
Besides, amphetamines increase the dopamine activity by different mechanisms. They ensure that the dopamine transporters occur in reserve, through which vesicular dopamine is transported back into the terminal. Furthermore, this "free" dopamine is transported to the synaptic gap.
The contribution to behavioral stimulation and euphoria of amphetamines is also complex. They do this via the mesolimbic-mesocortical pathways in the ventral tegmental area (VTA). The euphoria is mediated in these regions of the brain and dopamine neurons from the VTA project tot the frontal cortex. This is called the mesocortical pathway.
A known composition structurally related to amphetamines is XTC (ecstasy) or also MDMA (methylenedioxymethamphetamine). The popularity of this drug began in 1970 when it was used as an aid for psychotherapy. The recreational use increased rapidly and the drug has been banned by the FDA since 1985. Users of this drug report euphoria, increased self-perception, an increase in sensations and promotion of intimacy with others. Dangerous side effects can include an increased heart rate and blood pressure, intense sweating and, severe tooth grinding (breaking of the teeth is not uncommon).
The neurotoxic consequences of MDMA are the strongest effects. This includes the significant damage to cortical serotonergic and dopaminergic neurons. These degenerative effects can persist for years after use of the drug. Even low to average use reduces or worsens many cognitive domains.
MDMA is a potent dopamine agonist. This means that it directly increases serotonin activity by enhancing the release of serotonin during neuronal signaling and by preventing reuptake. The dopamine activity in the nucleus accumbens is increased by blocking dopamine transporters and indirectly activating serotonergic neurons that regulate dopamine activity in the VTA.
LSD stands for 'lysergic acid diethylamide'. The strong hallucinogenic effects can occur in any modality, but the most striking hallucinations are visual. Color and movement is disturbed and music or sound can be observed with greater intensity and complexity. The hallucinations are sometimes described as synaesthesia. LSD was synthesized for the first time in 1938 by Albert Hoffman, who became an increasingly strong proponent of his responsible use during his lifetime.
Two hours after oral intake, peaks in plasma concentrations will be reached. The drug crosses the blood-brain brain barrier and is quickly distributed over the body tissue. LSD is the most powerful means of all psychoactive drugs. However, there is still no confirmed lethal dose. Psilocybin is a psychedelic composition that has been found in a specific type of mushroom. The pharmacological properties of LSD and Psilocybin are comparable to each other. However, research focuses more on LSD, so the emphasis in this book is more on LSD.
There are a number of harmful side effects of LSD known: increase in body temperature, heart rate and blood pressure, pupil dilation, dizziness, and nausea. The psychological side effects are: confusion, acute panic and, noticeable disturbances in both time and space. Because some users report flashbacks that persist long after using LSD, there is a separate category for the Hallucinogen Persistent Perception Disorder created in DSM-5. To get this diagnosis, one may not have used a hallucinogenic drug recently and show no signs of drug intoxication. For more information about the diagnostic criteria, see page 229. There is no agreement about the treatment of this disorder.
LSD and Psilocybin are partial serotonin agonists with high affinity for 5-HT receptor subtypes. This is probably due to their molecular structure. Partial agonists are drugs that have an affinity for a receptor, but have a lesser effect than agonists or endogenous ligands (in this case serotonin).
The current theory is that the hallucinogenic effects of LSD and Psilocybin are mediated by partial agonism of 5-HT2A receptors in the brainstem and in multiple cortical areas (middle prefrontal cortex, cingularis anterior and the somatosensory cortex). Research on the patterns of neuronal signals (neuronal signaling) generated by hallucinogens is done with laboratory animals.
Marijuana is the name that is often used for cannabis sativa. Its use began tens of thousands of years before Christ. In 1900 the drug was mainly used for medicinal purposes. In 1937, however, the use of this drug in the United States was stopped by the Marijuana Tax Act. Cannabis was further controlled by the Controlled Substances Act in 1970. In 1992, William Devane and his colleagues isolated an endogenous cannabinoid, which they called anandamide.
THC stands for Delta 9-tetrahydrocannabinol. By heating marijuana, the THC vaporizes and enters the blood through the lungs. Only seconds after inhalation the blood-brain-brain barrier traverses. Peaks in the plasma concentration are reached within a few minutes. The concentration of THC is very variable and depends on the type of cannabis that is used and how the cannabis has grown. An average marijuana cigarette contains about 0.5 grams of plant material with a THC content of about 8.5 percent. The amount of THC that is inhaled is about 10-20 percent. This means that the bioavailability of THC in a cigarette is only about 5 milligrams.
Orally administered marijuana is absorbed slower and less completely. Peaks in plasma concentrations are reached one to four hours after ingestion. THC and its metabolites can be found in the body for a long time, up to 2 weeks after use.
In the case of frequent users of marijuana, metabolites can still be found three to four weeks after abstinence, as the THC has built up in the tissues and is only gradually metabolized.
THC has a direct interaction with neuronal signal systems. This theory is based on the fact that an extremely small dose of THC already has noticeable effects. For the exercise of this effect, THC must work directly on cell receptors and no non-specific effect can occur.
In 1988, cannabinoid (CB) receptors were found in rats using 'radioactive labeling'. Two types of CB receptors are now known:
CB1 receptors: This kind of CB receptors are located in the basal ganglia, the cerebellum, the hippocampus, the amygdala, the thalamus and the cortex. These receptors are in any case partly responsible for the behavioral effects of marijuana.
CB2 receptors: This kind of CB receptors are located on the presynaptic terminals of different types of neurons. All of these receptors are metabotropic G-protein coupled receptors that regulate the formation of cyclic AMP.
These receptors provide a process of neuronal suppression, which is a common type of short-term neuronal plasticity. The depolarization of a neuron causes a reduction in the GABA-mediated neural inhibition.
Dronabinol (Marinol) is a synthetic THC extract of marijuana. In the United States it can be used as a remedy for nausea and vomiting as a result of chemotherapy and radiation therapy against cancer. Nabilone (Cesamet) is a fully synthesized THC. It can be used in the United States to treat nausea and vomiting due to cancer therapy and to treat anorexia and weight loss due to AIDS.
A number of other medical conditions may also benefit from marijuana treatment, including: sight threatening ocular pressure associated with glaucoma; chronic and phantom pain on the limbs; withdrawal symptoms due to opiate and alcohol addictions; muscle spasms in patients with multiple sclerosis, Huntington's disease and Parkinson's disease.
The effects of THC are mild euphoria, anxiolysis and disturbances in the perception of time. Furthermore, it can cause confusion and an increased feeling of fear in some (especially frequent) users. Furthermore, THC damages cognitive and motor functioning. Harmful effects on memory have been known for some time, these are probably mediated by CB1 receptors in the hippocampus.
A high dose of THC inhibits the release of glutamate in the afferent neurons in the basal ganglia, causing disturbed movement and even cataplexy. Furthermore, cannabinoids disrupt the normal cerebellar control of movement, independent of the central dopamine movement systems. Contrasting is the therapeutic effect of activation of these cannabinoid receptors in people with multiple sclerosis, Parkinson's disease and Huntington's disease.
An advantage of Marijuana over other antiemetic drugs is the fact that the side effects are often more tolerable for patients. Cannabinoids seem to work directly on the CB1 receptors in the area postrema, as a result of which the reflex to surrender is inhibited.
Initially the use of cannabinoids will cause an increase in blood pressure and heart rate. Frequent users, however, often have to deal with a fall in blood pressure as a result of vasodilation.
Recent research has shown that cannabinoids (and specifically CB2 agonists) inhibit immune responses and inflammation.
Tolerance appears with animals and people who receive an extremely high dose of a drug. There is still no evidence for tolerance after a dose that most users and patients receive. Chronic use can cause dependence, with abstinence causing withdrawal symptoms.
In a self-administration experiment with THC, animals had to press a lever to get the drug. In the fixed ration 10 (FR10) schedule, a small amount of it will be released every tenth press. These animals got around 40 to 50 injections in one hour. This means that THC does have abuse potential.
The different neurons in our brains, and in particular the interaction between them, are responsible for human behaviour. They do this by sending and receiving neurotransmitters. Knowledge of associated processes is very important to have a good understanding of the effect of psycho pharmaceuticals.
This chapter describes the functioning and interaction of neurons to get a better picture of how the brain responds to the environment and adapts to it.
The different neurons in our brains do not all look the same. The function and location of the neuron affects the size, shape and other properties of the neuron. The three most important neuronal groups are sensory neurons, motor neurons and interneurons. The sensory neurons pick up signals, the brain interprets these signals and the motor neurons then respond to this. In the central nervous system you find the interneurons which enables the transition between the other two groups of neurons.
The cell body is also called soma and is the largest part of the neuron. Here the metabolism of the cell takes place and you can find the nucleus with DNA.
Dendrites receive signals from surrounding neurons. The more dendrites a neuron has, the more information this neuron can receive. The location of the neuron affects the number of dendrites, for example, interneurons have more dendrites than neurons in the spinal cord.
The signal from the neuron is passed through the axon, which is an extension of the cell body and can have a length of a few millimetres to tens of centimetres. The axon hillock is the place where both the axon and the electrical signal start. Some axons have a myelin layer, especially the peripheral axons. The myelin is a glial cell that isolates the axon and enables an accelerated transportation.
The end of the axon is called the terminal button. Here, neurotransmitters are stored, released and in some cases reuptake takes place. A particular protein is very important for this reuptake, which will get more attention later in this chapter, as many psychotropic drugs work on this protein.
The neural transfer is the process by which the signal from the terminal button is transported to the dendrite of the next neuron (in the central nervous system). Signals are transmitted through nerves in the peripheral nervous system.
The lipid bilayer is a double layer of lipids that form the membrane of the neuron. This membrane enables that the neuron can have its own internal environment. In the membrane there are proteins which enable that glucose and ions can enter the cell and carry waste products out of the cell. By transporting the ions, the electric potential of the neuron changes. The important ions are An - , Cl - , Na + and K + . The sodium and chloride ions only enter the cell
.....read moreDepression is the most common psychological disorder. One out of ten adults have ever been diagnosed with depression. In general, 17% of all people, 24% of women and 12% of men. Depression in adolescence and among young adults can lead to suicide, among others. Suicide is number three of leading causes of death.
The diagnostic criteria are described in DSM-IV or DSM-V. At least five of the following symptoms must be experienced for at least two weeks:
Another form of depression is the reactive depression. This is often accompanied by a big change in someone's life. This depression is similar to a major depression, but it only disappears in a few weeks to a month, and in this type the period of depression alternates with periods of normal mood.
Deviations in serotonin and norepinephrine systems can cause depression. This is known because medications that act on these monoamines (serotonin and norepinephrine) reduce or cause the depression. Evidence for this is the drug Reserpine that was used for high blood pressure, but as a side effect it causes depression. Once the drug was stopped, the depression disappeared again. This is how the monoamine hypothesis of depression came about. In the first version of this one did not know which of the monoamines were responsible for the depression and how this was could be caused. A contradiction to the monoamine hypothesis is the lag time. This is the time between taking the medicine and when the medicine starts to work. In antidepressants, for example, two weeks may pass before changes in symptoms occur.
The current version of the monoamine hypothesis states that depression is the result of neural degeneration in the hippocampus and the frontal cortex. This is because monoamine neurons no longer produce growth factors here. An important protein in this is the Brain derived neurotropic factor BDNF . BDNF is a protein that ensures that cells survive and receptors and new neurons grow. If this does not happen, the neurons in the hippocampus and frontal cortex can no longer communicate properly. Chronic treatment with antidepressants leads to an improvement in activity. However, it takes some time before it recovers. There are genetic characteristics that cause these receptors to work worse so that someone is more susceptible to develop a
.....read moreFear is a learned emotional and physiological response to events in the environment. It affects behavior, heart rate, hormone release and physical sensations. Through these experiences people learn to avoid dangerous situations. Before there is fear, signals first have to be sent to the brain. This goes with the help of the amygdala nuclei that are located in the temporal lobes. In this area, sensory information from a threat will be sent. The rest of the information from this threat, is sent via the amygdala to other parts of the brain, such as the hypothalamus, punch and medulla. The amygdala is the most important brain structure that has to do with anxiety. Without the amygdala, there are almost no emotional reactions. In addition, the hypothalamus controls the release of hormones and the punch and medulla provide responses to anxiety such as stiffening, heartbeat and facial expression.
Two other areas in the prefrontal cortex are also very important in anxiety. These are the ventromedial prefrontal cortex and the orbitofrontal cortex. These areas ensure that the context of the situation gets an emotional charge and thus lead to the behavior of the person. They receive information from the amygdala, thalamus and ventral tegmentum. Subsequently they send information back to the hypothalamus and cingulate cortex and they also send stop signals back to the amygdala. The cingulate cortex receives input about the state of the body and connects an emotion to it. An example are physiological reactions (heartbeat, breathing, facial expressions etc.) and behavior, these different stimuli are taken together under the emotion anxiety. As soon as the emotion can be ignored, stop signals are sent to the amygdala and there are no physical reactions to the emotion anymore. This is all part of a direct fear response. People can also worry for a longer time. This is another form of anxiety in which there are no emotional stimuli to cause the fear response, but where thoughts alone trigger enough. Fear because of worry can lead to various anxiety disorders that will be discussed further in this summary.
The person suffers from repeated unexpected panic attacks and is afraid of another attack or the consequences of such an attack for at least one month. Often the greatest fear is the fear of dying during an attack. During a panic attack there must be extreme anxiety and at least four of the following symptoms occur: palpitations/accelerated heartbeat, sweating, shaking or stiffening, shortness of breath, suffocation, chest pain, nausea, dizziness/fainting, depersonalization, anxiety for loss of control, fear of death, paraesthesia (numb/tingling) and shivers/heat shakes. A panic disorder can also lead to agoraphobia, in which a person no longer dares to go outside because of fear of a subsequent panic attack in a place where he/she cannot escape from the situation.
Opium has been used for thousands of years as a medicine and for religious or ritual purposes. Early medical texts already describe opiates as narcotics. The main active substance in opium is morphine. This substance became popular as an anesthetic drug since the 1850s. It has also been used against coughing, as a medicine for fever and diarrhea. Morphine is still widely used today. Since the discovery of morphine, a lot of research has been done to discover an anti-pain medication that is less addictive. This led to, among other things, heroin.
Because opium and heroin were widely available since the nineteenth century, opium addiction became popular. At the beginning of the twentieth century, a legal attempt was made to stop this addiction, unfortunately this had little effect.
In opiates, the pharmacologically active substances are morphine, codeine and thebaine alkaloids. Alkaloids are natural constituents that are available in different forms and contain nitrogen. Various attempts have been made to synthesize alkaloids. That is why the book distinguishes between opiates (natural and formed from opium) and opioids (synthetically produced anesthetics).
Morphine and heroin are injected directly into the blood stream although Codeine and opioids are often taken orally. Once opiates are in the body, they can quickly pass through the blood-brain barrier. For example, only a few seconds after administration, heroin has already reached the brain. This works differently with morphine and codeine. Because of their solubility in water, only twenty to thirty percent reach the brain, while the rest is excreted again. In the liver, morphine and heroin are both converted to morpine-6-glucuronide, which is an active metabolite. Morphine and its metabolite have a half-life of 1-3 hours, so it works relatively long as an anesthetic.
Opiates have different effects on neural activity including sedation, euphoria and respiratory depression.
Pain can occur in many different ways. The pain receptors are called nociceptors. The pain signals are transmitted via fast myelinated fiber webs and via slow unmyelinated fiber webs. The myelinated fiber webs cause a sharp, rapid pain, while the unmyelinated fiber webs cause dull and slow pain. This pain often comes after the short, sharp pain in tissue damage. The perception of pain differs per person. Depression makes people more prone to pain.
The excitatory neurotransmitter substance P is released upon activation of the nociceptors. Opiates in the spinal cord can modulate pain. They do this by modulating the activity of serotonin and noradrenergic neurogen in the medulla. The release of substance P is inhibited.
There are different areas of the brain that play a role in the perception of pain. The cingulate cortex plays a role in feeling pain or the sensation of pain. Damage to this area does not stop make you feel pain, but that you do
.....read moreIn the United States, the lifetime prevalence of substance abuse and dependence is about 15% of the population. When tobacco is included in this estimate, it comes down to 45%. This prevalence has remained relatively stable over the past ten to twenty years.
Addiction is not always the same as dependence. An addiction is the result of specific neural changes that result from the use of drugs. These are drugs that affect dopamine activity in mesolimbic and mesocortical systems. Not all drugs that provide a dependency produce these neural changes. Alcohol, cocaine, amphetamine, opiates and tobacco do produce this, among other things.
Addiction can occur suddenly or it can develop over the years. The common threat in addiction is the pattern of destruction in the personal and family life of the addict. People with an addiction deny the pain they do to others as well as the negative financial and physical consequences that the addiction has. Alcohol addiction includes comorbid depression, bipolar disorder and anxiety disorders. Treatment of substance abuse is not often successful and is rarely completed on a first attempt.
The DSM-IV-tr makes no distinction between drug dependence and drug addiction. Drug addiction disorders are classified by the degree of deterioration and by the presence of tolerance and/or withdrawal symptoms. An individual can thus be dependent of a substance, without having a disorder. The diagnosis of a substance dependency disorder replaces a substance abuse disorder, where it is a requirement that the additional symptoms be present for a longer period of time. If this is not (yet) the case, then there is a substance dependency disorder.
Not all behavioural and neurobiological characteristics of addiction are present in all cases of dependence. An important characteristic is the intense desire or the strong motivation to take drugs, despite the serious adverse consequences. This desire is often even present after years of abstinence. The critical difference between drug dependence and drug addiction is caused by neural changes that result from the use of certain drugs. The reaction of the brain, produced by addictive substances, is due to the effect of the drugs on the reward (reward pathway) of the brain. This system is an evolutionary change that helps to allocate hedonistic values to stimuli. It also provides motivation for seeking sexual partners and for reproduction. The changes because of addictive drugs, benefit the reward system, which keeps the motivation going to search for drugs and to take them.
The critical neural structures where the path consists of: the nucleus accumbens and the ventral tegmental area (ventral tegmental area, VTA). Research on this system originated by James Olds and his student Peter Milner in 1954. They experimented with electrical stimulation in the septum of rats.
The reward system consists of:
The mesolimbic dopamine system: VTA,
.....read moreIn this chapter and the next, we will look at all different kinds of drugs ranging from caffeine to crack and cocaine. Most drugs that will be discussed in this chapter exists for hundreds or even thousands of years. The use of drugs became alarming up till 2000. Since that year, the use of drugs by teenagers is stable. There is even a little decline and the decline of alcohol and tobacco use is bigger. Only the trend of marijuana use is an increasing one.
Drug schedule refers to the potential for abuse of a drug and this has been described by the Controlled Substance Act in 1970. Schedule I drugs do have less potential for abuse than schedules II to V.
Cocaine is extracted from the coca plant, which grows in the mountains of South America. People used to chew on the leaves of this plant, because it produced feelings of confidence. Nowadays, cocaine is most exported as cocaine sulphate or cocaine hydrochloride.
Cocaine compounds are extracted by crushing the leaves in a solution (such as kerosene, gasoline or alcohol). The liquid mixture that remains is processed under heat with sulfuric acid to isolate the cocaine alkaloids and to remove the waxy residues. The cocaine sulphate paste that remains contains about 60% cocaine and is then further processed into a water-soluble crystal composition called cocaine hydrochloride.
In South America, many of the waste products that originate during the extraction process of cocaine are dumped in the river. This has very harmful ecological consequences.
Cocaine alkaloid was first isolated in 1855 by Friedrich Gaedcke, he called it erythroxyline . Albert Niemann then called it cocaine. It was used as a local anesthetic, especially in eye and nose operations. It was also added to many drinks, given the stimulating effects and you could buy cocaine in local drugstores. Freud was enthusiastic about the substance and recommended it to other people. It was only in 1914 that the use of cocaine in all forms was banned by the Harrison Narcotic Tax Act and was described as a dangerous narcotic.
Cocaine hydrochloride is a water soluble substance that divides itself into cocaine-H + and Cl - ions after its administration. The positively charged cocaine ions are able to quickly pass cell membranes and enter the brain. Snorted and orally administered cocaine goes slower and will be absorbed less complete than intravenously administered, inhaled or vaporized cocaine.
Methylbenzoulecgonine is a composition that is the result of dissolving cocaine hydrochloride in a mild ammonia solution. This composition can be vaporized for inhalation and is called crack because of the cracking sound in this process. Crack can also be manufactured by heating cocaine hydrochloride in water and sodium
.....read moreAlcohol is the most abused drug in the world. Given the availability and the large percentage of the population that uses it, it is not surprising that alcohol leads to the most common substance abuse disorder.
Distillation is a process in which alcohol is separated from other fermentation products by heating it. Although distillation can result in pure ethyl alcohol (ethanol), most spirits contain 40-50 percent alcohol.
Alcohol or ethanol is both soluble in water and fat and can easily spread through all cell membranes. Higher alcohol concentrations (stronger drinks) spread faster than lower ones. Ethanol passes the blood-brain barrier quickly, and peaks in plasma concentrations are reached between 30 to 60 minutes. The presence of food in the stomach and intestines slows the distribution of alcohol. The wall of the small intestine absorbs approximately eighty percent and the remainder will be absorbed by the stomach or is almost immediately excreted by perspiration, breathing or urine. Because all tissues, including the placenta, absorb alcohol so easily, a pregnant woman exposes her fetus to blood levels similar to their own.
The blood alcohol concentration (BAC) is expressed in the number of grams of alcohol per hundred milliliters of blood. A breath test can immediately determine the BAC by analyzing the breath of an individual. The breath contains alcohol that got into the lungs through the bloodstream. With a BAC of 0.06-0.1 you already have a much higher reaction time, problems with attention, reduced control over movements and significant limitations in cognitive functioning. With a BAC of 0.3-0.39 it becomes already very dangerous and you can get fatal symptoms. Above 0.4 it can be fatal.
Alcohol metabolism starts immediately after consumption. Approximately 90-95 percent of the alcohol is metabolized by the enzyme group alcohol dehydrogenase. The remaining five to ten percent is excreted by perspiration and breathing or is metabolized by another liver enzyme. This enzyme is called P450 and is essential for oxygen reactions that are involved in metabolism. Only a small fraction of alcohol is excreted via the urine.
Small amounts of alcohol dehydrogenase immediately begins to metabolize alcohol in the stomach. When alcohol enters the small intestine, it is quickly absorbed into the blood supply. This way it ends up in the liver, where the remaining part (80-85 percent) is metabolized. First-pass metabolism is alcohol that is metabolized by stomach and liver enzymes before it can reach the tissues. About 25-30 percent of the ingested alcohol falls below. The amount of metabolized alcohol depends on the availability of alcohol dehydrogenase and the coenzyme nicotinamide adenine dinucleotide (NAD). This coenzyme can be seen as a rate-limiting enzyme, because availability determines the rate of alcohol metabolism. Because men and women have different levels of alcohol dehydrogenase, they metabolize alcohol in different speeds.
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