BLOG CRIADO PARA O ESTUDO E PESQUISA DA DEPENDÊNCIA QUÍMICA E DROGAS DE ABUSO, COM UMA VISÃO NEUROCIENTÍFICA, TENDO COMO OBJETIVO A PREVENÇÃO DA DEPENDÊNCIA QUÍMICA, ATRAVÉS DE CONHECIMENTO E INFORMAÇÃO SOBRE AS SUBSTÂNCIAS DE ABUSO, VISANDO ESCLARECER OS PROFISSIONAIS DA ÁREA DA SAÚDE, CIENTISTAS, ESTUDANTES OU PESSOAS INTERESSADAS NA ÁREA DAS CIÊNCIAS BIOMÉDICAS E DA SAÚDE, COM PARTICULAR INTERESSE EM NEUROCIÊNCIAS E DEPENDÊNCIA QUÍMICA.

terça-feira, 30 de março de 2010

VÍDEO EDUCATIVO SOBRE DEPENDÊNCIA QUÍMICA EDUCATIONAL VIDEO ON ADDICTION

Addiction no Yahoo! Vídeo


Interessante Vídeo em Inglês, que aborda o tema da Dependência Química. Para ver o Vídeo, basta clicar no título acima "Addiction no Yahoo! Vídeo".

Interesting Video in English, which addresses the issue of Chemical Dependency. To see the video, simply click on the title above.

Interesante video en Inglés, que aborda la cuestión de la Dependencia de Sustancias Químicas. Para ver el video, haz clic en el título anterior.



terça-feira, 9 de março de 2010

NEUROCIÊNCIA E DEPENDÊNCIA QUÍMICA: MECANISMOS DE AÇÃO DAS DIFERENTES DROGAS DE ABUSO




INTRODUÇÃO


O entendimento das bases neurofisiológicas da dependência química continua desafiando os pesquisadores. De acordo com estudos, o sistema dopaminérgico vem sendo considerado como o mais importante no que se refere ao uso abusivo de substâncias, sendo a via dopaminérgica mesocorticolímbica a mais referida. Juntamente com a dopamina, outros neurotransmissores em conjunto parecem colaborar para a atividade da via dopaminérgica com o chamado “sistema de recompensa”. Incluem-se à dopamina, por exemplo: o ácido gama-aminobutírico (GABA), o glutamato, a serotonina e os peptídeos opióides. Além de atuar sobre o sistema de recompensa, o sistema dopaminérgico apresenta importante função sobre o sistema motor, além de funções refinadas de cognição e memória. Já o sistema opióide é responsável pelo componente hedônico (de prazer) do sistema de recompensa cerebral além de estar relacionado também à dor e ao processamento das emoções.
Quando observamos os mecanismos de ação das diferentes drogas de abuso verificamos que todas apresentam uma relação direta ou indireta com um ou mais destes neurotransmissores.

Mecanismos de ação das diferentes droga de abuso


Cocaína

A cocaína se liga aos transportadores de dopamina (DAT), serotonina (5-HTT) e noradrenalina. Entretanto, os efeitos subjetivos e comportamentais desta substância são geralmente atribuídos à sua ação sobre o sistema dopaminérgico. Acredita-se que 50% de ocupação de transportador de dopamina seja necessário para que um indivíduo perceba os efeitos da substância e que, para a sensação de euforia, pelo menos 60% dos sítios de DAT devem estar ocupados. Nas três vias de administração – aspirada, injetada e fumada (crack) - a ocupação de DAT é superior a 60% .
A cocaína per se provoca efeitos deletérios indiscutíveis, mas quando é ingerida concomitante ao álcool, leva a formação de um metabólito conjugado chamado cocaetileno. Esse metabólito apresenta propriedades psicoativas importantes e uma meia-vida muito maior do que se a cocaína e o álcool fossem ingeridos separadamente e seu acúmulo leva rapidamente a um quadro de intoxicação.


Metanfetamina e Ecstasy (MDMA -3,4-metilenodiox,metanfetamina)

As drogas classificadas como derivados anfetamínicos podem atuar no Sistema Nervoso Central (SNC) de formas distintas. Seu alvo principal são as monoaminas cerebrais: dopamina, serotonina e noradrenalina. Assim, farmacologicamente são classificadas como agonistas indiretos pois não atuam específicamente sobre receptores monoaminérgicos pós-sinápticos mas, indiretamente da seguinte forma:

1º Impedem a recaptação dos neurotransmissores através do bloqueio competitivo do transportador de dopamina e noradrenalina e em altas doses, também de serotonina;

2º Inibem a atividade das enzimas de metabolismo (monoaminoxidase - MAOA e MAOB);

3º Estimulam a liberação do neurotransmissor independente de Ca++ (ou seja independente da despolarização do botão sináptico).


Maconha

O principal componente psicoativo da maconha é o Δ9-tetrahidrocanabinol (THC). Seu mecanismo de ação do THC ainda não foi completamente elucidado, mas acredita-se que ele atue no SNC através de receptores canabinóides CB1 e CB2. As áreas cerebrais com maior densidade de receptores CB1 são o córtex frontal, núcleos da base, cerebelo e hipocampo. Estudos com animais têm demonstrado que o THC e a anandamida (canabinóide endógeno mais estudado), aumentam a concentração de dopamina no estriado e no sistema mesolímbico5 .

Nicotina

A nicotina é a principal substância do cigarro responsável pelos efeitos psicoativos e pela dependência de tabaco. No entanto, há milhares de compostos químicos na fumaça do cigarro e alguns deles podem contribuir para os efeitos comportamentais e tóxicos do tabaco. Nicotina é um agonista direto em receptores colinérgicos nicotínicos onde age acetilcolina endógena e estão amplamente
distribuídos no SNC. Os receptores nicotínicos implicados na ação da Nicotina6 estão localizados no sistema dopaminérgico mesocorticolímbico.

Álcool

Os mecanismos pelos quais o álcool atua no cérebro assim como as alterações cerebrais produzidas pelo seu consumo crônico ainda não estão compreendidos sendo que a maioria dos estudos indica a participação dos sistemas dopaminérgicos, serotoninérgicos e principalmente gabaérgicos.
O sistema de recompensa associado ao uso do álcool, além dos neurônios dopaminérgicos da área tegmental ventral e núcleo accumbens, inclui também estruturas que usam o ácido gama-aminobutírico (GABA) como transmissor, tais como o córtex, cerebelo, hipocampo, colículos superiores, inferiores e a amígdala.

Opióides

Os opióides modulam a liberação de neurotransmissores como a acetilcolina, serotonina, noradreanlina, além de outros peptídeos, como a substância P. O locus coeruleos, responsável pela maior parte da produção de noradrenalina no SNC, apresenta-se estimulado na síndrome de abstinência a opiáceos, o que provoca os típicos sintomas de estimulação simpática.
O sistema de recompensa aos opiáceos, além das estruturas antes mencionadas inclui também áreas que usam como neurotransmissores opiáceos endógenos, tais como o núcleo arqueado, a amígdala, o locus coeruleos e a área cinzenta periaquedutal dorsal.


A BEHAVIORAL/SYSTEMS APPROACH TO THE NEUROSCIENCE OF DRUG ADDICTION

Drug addiction is presently viewed as a complex neuroadaptive process through which drugs of abuse alter cellular and molecular aspects of neural function in such a way as to render the brain circuits mediating various behavioral effects of these drugs more, or less, responsive to those effects. This process guides behavior in maladaptive directions during which severe physical and social consequences engulf and disable the addict. Cellular and molecular mechanisms of tolerance, sensitization (reverse tolerance), and dependence are rapidly being identified for almost all classes of abused drugs, and both established and new molecules are being investigated intensively using the most modern and advanced technologies available to neuroscience (Nestler, 2001b ,d ). As the neurobiology of drug addiction has advanced, the discovery of precise cellular and molecular adaptations related to the addictive process has been substantial. Alterations in many molecules have been newly implicated. From long-suspected involvement of the cAMP pathway in tolerance to and dependence on opiates (Sharma et al., 1975 ), we have identified a dedicated role of cAMP-related molecules in the actions of several drugs of abuse. The cAMP-dependent protein kinase and the cAMP response element-binding protein are but two examples. Molecules that interact both upstream and downstream of these effectors are also implicated and include various neurotransmitter receptors, inhibitory and stimulatory G-proteins, protein kinases and phosphatases, ion channels, immediate early genes, and gene transcription factors (for review, see Berke and Hyman, 2000 ; Nestler, 2001a ,b ). At the cellular level, alterations in synaptic and whole-cell plasticity accompany sensitization and withdrawal (Bonci and Williams, 1996 ; Zhang et al., 1998 ; Thomas et al., 2001 ; Ungless et al., 2001 ), as do structural changes in dendrites (Robinson and Kolb, 1997 , 1999 ).
Clearly, dopamine (DA) is the molecule most directly implicated in the positive reinforcing (rewarding, pleasurable) effects of all drugs of abuse. The ability of addictive drugs to enhance DA neurotransmission, particularly within the mesocorticolimbic DA system, is a well documented commonality among the various classes of abused drugs (for review, see Wise and Bozarth, 1987 ; Koob, 1992 ; White, 1996 ; Spanagel and Weiss, 1999 ). This DA reward system, which originates in the midbrain ventral tegmental area (VTA; A10 DA neurons) and projects to the nucleus accumbens (NAc), prefrontal cortex (PFC), and other limbic areas, has long been the major focus of our attempts to identify cellular and molecular mechanisms underlying addiction. However, the past decade has witnessed an emerging willingness to place the DA system within a broader context of neuronal circuitry engaged by specific drugs and particular behavioral sequences involved in the acts of drug seeking, drug taking, and recovery from drug actions (withdrawal, relapse, etc.).
One critical component of this broader conceptualization of drug reward circuitry is the glutamate neuronal system innervating and directly influencing the mesocorticolimbic DA system. Glutamatergic inputs to the VTA and NAc, arising from the PFC, hippocampus, and basolateral amygdala, have all been implicated in addiction. Indeed, a recurring theme in modern addiction research is the extent to which neuroadaptations responsible for various aspects of the addiction process are similar to those responsible for other forms of neural plasticity studied in cellular models of learning, such as long-term potentiation and long-term depression (Wolf, 1998 ; Berke and Hyman, 2000 ; Nestler, 2001c ); however, glutamate is not the only other system under intense scrutiny. We have long been baffled by the role of other monoamine transmitters in the actions of drugs of abuse. In recent years, a new emphasis on both serotonin and norepinephrine has reemerged, along with clear implications for various neuropeptide systems, including the opioid peptides and the stress-related peptides of the hypothalamus-pituitary-adrenal axis (Kreek and Koob, 1998 ). Moreover, as will be seen in several of the mini-reviews, brain GABAergic and cholinergic systems are fruitful avenues for continued research. Finally, conceptualization of the role of DA pathways has been enlarged to include the nigrostriatal system as it becomes engaged in stereotypic responses that define the process of addiction (Everitt and Wolf, 2002 ).
A concerted interplay between cellular/molecular and behavioral/systems neuroscience with respect to the process of addiction has never been so crucial. Identifying the systems involved in specific behaviors directs cellular/molecular studies of both acute and chronic drug actions. Similarly, identification of new molecules selectively altered by repeated drug administration, perhaps in brain areas not "routinely" considered with addiction circuits, can expand our concepts of brain circuitry modulating the addiction process. We are fortunate that the neuroscientists who have agreed to provide the six mini-reviews in this series work at both levels of analysis, thereby providing a comprehensive multidisciplinary perspective on the neurobiology of addiction. In putting together the teams of scientists to provide these reviews, I have specifically paired two investigators who do not necessarily collaborate directly, so that they mold perhaps different perspectives to provide a consensus as to the most important new developments in drug addiction research. As these reviews emphasize, our efforts to tie specific brain circuits to precise aspects of behavioral changes has broadened considerably the number of affected brain regions and highlighted the need to expand cellular and molecular studies to these areas. This has been made possible by the refinement of sophisticated behavioral approaches coupled to systems neuroscience.
When surveying the advances made with respect to the neuroscience of drug addiction, it is easy for the nonspecialist to get the incorrect impression that brain circuits have evolved to allow maladaptive patters of behavior. Actually, brain reward circuits subserve a much more critical evolutionary function: reward induced by natural reinforcers such as food and sexual interactions. Accordingly, we begin our series of reviews with a look at how the neuroscience of natural rewards is related to addictive drugs. Kelley and Berridge (2002) review current thinking of how the DA reward system encodes specific aspects of the reward process and how such encoding is impacted by natural rewards. They also provide compelling arguments for commonalities in the actions of natural rewards and drugs of abuse within both traditional reward areas and brain regions not normally considered within such circuitry.
After considering natural rewards, the next three reviews focus on the major classes of illicit drugs of abuse: psychomotor stimulants (amphetamine, cocaine), opiates (morphine, heroin), and cannabinoids (marijuana). In a somewhat expanded mini-review, Everitt and Wolf (2002) summarize the rapidly expanding field of psychostimulant addiction from a systems perspective. We have allowed this more detailed treatment not only because more work has focused on this class of drugs but also because these authors provide excellent descriptions of most of the sophisticated behavioral procedures that are also touched on in the other mini-reviews. The interested reader would be well served by first reading this mini-review to become familiar with the animal models used to study drug-seeking, conditioned reinforcement, and behavioral sensitization.
As pointed out by De Vries and Shippenberg (2002) , in contrast to psychostimulants, considerably less is known regarding the mechanisms of opiate addiction and relapse to opiates after withdrawal. Their commentary in this regard is well informed given that these authors could just as easily have reviewed the psychostimulants. This is another feature of the scientists whom I have chosen to participate in this series; many of them work across different drug classes, giving unique perspectives on the similarities and differences between various drugs of abuse. In this case, De Vries and Shippenberg emphasize that recent findings challenge previous notions regarding the role of one neurotransmitter or brain region in opiate addiction and point to activity of several neurotransmitter and neuropeptide systems in brain circuits mediating mood and affect underlying the addiction process.
Maldonado and Rodriguez de Fonseca (2002) tackle the job of integrating an explosive recent literature regarding the perhaps controversial concept of cannabinoid addiction. As social issues swirl with respect to the medical use and possible decriminalization of marijuana, neuroscientists have taken advantage of the relatively recent cloning of cannabinoid receptors, the identification of endogenous cannabinoids, and the development of specific and potent cannabinoid compounds to begin the identification of circuits involved in cannabinoid reward, dependence, and withdrawal. Maldonado and Rodriguez de Fonseca (2002) beautifully integrate discoveries at the behavioral/systems level with those at the cellular/molecular level to argue persuasively that addiction to cannabinoids shares common features with other drugs of abuse. The remarkable interactions between cannabinoid and opioid systems are particularly emphasized.
The last two mini-reviews turn to the two major licit drugs of abuse: alcohol and nicotine. Weiss and Porrino (2002) describe the unique challenges in alcohol addiction research that emerge from the multiple molecular targets of ethanol in several brain circuits. We have come far from the days of considering ethanol as a "modifier of membrane fluidity." Specific binding sites for ethanol within GABA-A and NMDA receptors provide particular challenges given the almost ubiquitous expression of these receptors throughout the nervous system. Weiss and Porrino (2002) clearly and concisely review the involvement of DA, opioid, and other systems in ethanol motivation and reward, adaptations relevant for the transition to dependence and relapse, and issues relevant to the treatment of alcoholism.
Finally, Picciotto and Corrigall (2002) team up to review the neuronal system involved in behaviors related to nicotine addiction and the molecular genetics that have identified which subtypes of nicotinic acetylcholine receptors are implicated in distinct brain regions. Nicotine presents its own challenges given that one does not typically identify this drug as exerting the profound euphoria associated with other drugs of abuse. Yet the DA reward system is again clearly implicated in the addictive properties of nicotine, but so are several other neurochemical systems and brain circuits. One primary example is the involvement of the pedunculopontine tegmental nucleus, a brain region not traditionally linked to the actions of other drugs of abuse, in the acquisition of nicotine self-administration [however, see Bechara et al. (1998) ].
Although not addressed in this set of reviews, it is important to point out that brain imaging studies have clearly indicated that many of the brain structures related to drug reward systems are also engaged by other rewards such as money (Knutson et al., 2001 ), romantic love (Bartels and Zeki, 2000 ), and maternal attachment (Lorberbaum et al., 1999 ). As one progresses through this series of mini-reviews, it will become apparent that there are many commonalities between different drugs with respect to the systems involved in similar aspects of behaviors associated with the addiction process. Yet there are also many important differences. I am hopeful that the reader will sense the excitement that exists in the neurobiology of addiction and the need for continued research to identify what some refer to as the molecular "switch" (Leshner, 1998 ) and the various components of the "spiraling distress-addiction cycle" (Kreek and Koob, 1998 ) that underlies the transition from drug taking to drug addiction.


NEUROBIOLOGIA DE LAS DROGAS DE ABUSO


Diversos neurotransmisores se han implicado en los efectos de las drogas de abuso (GABA, glutamato, acetilcolina, dopamina, serotonina, o las endorfinas). De estos, la dopamina se ha asociado de forma consistente con el efecto de refuerzo de la mayoría de las drogas de abuso. Estas aumentan las concentraciones de dopamina extracelular en regiones límbicas, incluyendo el núcleo accumbens. Específicamente, dichos efectos de refuerzo parecen deberse a su capacidad para sobrepasar la magnitud y la duración de los incrementos rápidos de dopamina que desencadenan los refuerzos naturales como la comida o el sexo. Dichas diferencias cuantitativas y cualitativas con respecto al incremento de dopamina que las drogas inducen explicarían porqué los refuerzos naturales no conducirían a la adicción.
El efecto sobre la dopamina es directo en algunas drogas (cocaína, anfetamina, éxtasis), mientras que otras sustancias afectan a neurotransmisores implicados en la regulación de la dopamina (nicotina, alcohol, opiáceos o marihuana).
Según parece, y a diferencia de lo que se creía hasta ahora, los incrementos de dopamina no se relacionan directamente con la recompensa, sino con la predicción de recompensa y con la “relevancia”. La relevancia se refiere a la capacidad de ciertos estímulos o cambios ambientales para producir una activación o desencadenar un cambio atencional-conductual. La relevancia, que añadida a la recompensa, se aplica a los estímulos aversivos, nuevos e inesperados, afecta a la motivación para buscar la anticipada recompensa y facilita el aprendizaje condicionado. Esto proporciona una perspectiva diferente de las drogas, ya que implica que los incrementos de dopamina inducidos por las drogas motivarán inherentemente la búsqueda de más droga, independientemente de si los efectos de la droga son conscientemente percibidos como placenteros o no.
Los incrementos de dopamina inducidos por las drogas facilitan asimismo el aprendizaje condicionado, de manera que los estímulos neutros que se asocian con la droga quedan condicionados (por ejemplo encuentros con cierta gente, ciertos lugares como discotecas, etc.). Una vez condicionados, pueden por sí mismos aumentar la dopamina y desencadenar el deseo de consumir. Esto puede explicar el riesgo de las personas con una adicción de recaer cuando se exponen a un entorno en el que previamente se ha consumido la droga, y englobaría parte de lo que Ingelmo y cols. han denominado el “contexto drogado” (Ingelmo y cols., 2000).


NEUROBIOLOGIA DE LA ADICCIÓN A LAS DROGAS


La adicción es probablemente el resultado de los cambios neurobiológicos asociados con alteraciones crónicas e intermitentes a niveles suprafisiológicos de los sistemas dopaminérgicos. Volkow y cols. (Volkow y cols., 2004) han postulado que las adaptaciones en estos circuitos dopaminérgicos hacen al adicto más sensible a los picos (incrementos rápidos) de dopamina que se producen con las drogas de abuso, y menos sensibles a los incrementos fisiológicos producidos por los refuerzos naturales (comida y sexo). Estas adaptaciones ocurren tanto a nivel de la fisiología celular (alteración de factores de transcripción, que regulan la expresión de determinados genes, algunos en particular implicados en plasticidad de las sinapsis), como a nivel morfológico en los circuitos cerebrales regulados por la dopamina. Por ejemplo, la administración crónica de cocaína o anfetaminas a roedores produce un aumento de la densidad tanto de dendritas como de espinas sinápticas en el núcleo accumbens y en la corteza prefrontal. Este cambio morfológico se cree que facilita un incremento de la valencia motivacional de la droga.
Igualmente, hay cambios a nivel de los neurotransmisores, no sólo para dopamina, sino también para el glutamato, el GABA, la serotonina o los opiáceos. Estos cambios determinan un funcionamiento alterado de determinados circuitos cerebrales, algunos de los cuales están implicados en la asignación de relevancia o el control de la inhibición; alteración que se asocia a conducta compulsiva (corteza orbitofrontal) y desinhibición (circunvolución anterior del cíngulo). Dichas anomalías en estas regiones frontales del cerebro pudieran estar tras la naturaleza compulsiva de la administración de la droga en los adictos o en su incapacidad para controlar las ansias de consumir cuando se encuentran expuestos a la droga. En adictos a cocaína, los estudios de neuroimagen muestran un descenso de la actividad dopaminérgica (estimada por la densidad de receptores D2) en la corteza orbitofrontal y en la región anterior de la circunvolución del cíngulo. La dopamina tiene una función inhibitoria, que al perderse podría redundar en un exceso de actividad en dichas áreas. Asimismo, parecen existir cambios a nivel de circuitos dopaminérgicos mesocorticales.

quinta-feira, 4 de março de 2010

CRACK: CONSIDERAÇÕES BIOPSICOSSOCIAIS



Informações Gerais sobre o Crack

Crack é uma droga feita a partir da mistura de cocaína com bicarbonato de sódio geralmente fumada. É uma forma impura de cocaína e não um sub-produto. O nome deriva do verbo "to crack", que, em inglês, significa quebrar, devido aos pequenos estalidos produzidos pelos cristais (as pedras) ao serem queimados, como se quebrassem.
Chega ao sistema nervoso central em dez segundos, devido ao fato de a área de absorção pulmonar ser grande e seu efeito dura de 3 a 10 minutos, com efeito de euforia mais forte do que o da cocaína, após o que produz muita depressão, o que leva o usuário a usar novamente para compensar o mal-estar, provocando intensa dependência. Não raro, o usuário tem alucinações, paranóia (ilusões de perseguição).
Seis vezes mais potente que a cocaína, o crack tem ação devastadora provocando lesões cerebrais irreversíveis e aumentando os riscos de um acidente vascular cerebral (AVC) ou de um infarto agudo do miocárdio (IAM).
Em relação ao seu preço, é uma droga mais barata que a cocaína.
O uso de cocaína por via intravenosa foi quase extinto no Brasil, pois foi substituído pelo crack, que provoca efeito semelhante, sendo tão potente quanto a cocaína injetada. A forma de uso do crack também favoreceu sua disseminação, já que não necessita de seringa — basta um cachimbo, na maioria das vezes improvisado, como uma lata de alumínio furada, por exemplo.

Efeitos do Crack no Organismo Humano

O crack eleva a temperatura corporal, podendo causar no dependente um acidente vascular cerebral. A droga também causa destruição de neurônios e provoca a degeneração dos músculos do corpo (rabdomiólise), o que dá aquela aparência característica (esquelética) ao indivíduo: ossos da face salientes, braços e pernas finos e costelas aparentes. O crack inibe a fome, de maneira que os usuários só se alimentam quando não estão sob seu efeito narcótico. Outro efeito da droga é o excesso de horas sem dormir, e tudo isso pode deixar o dependente facilmente doente.
A maioria das pessoas que consome bebidas alcoólicas não se torna alcoólatra. Isso também é válido para outras drogas. No caso do crack, o usuário se torna completamente viciado na droga, ficando dependente com apenas três ou quatro doses, às vezes até na primeira. Normalmente o dependente, após algum tempo de uso da droga, continua a consumi-la apenas para fugir do desconforto da síndrome de abstinência — depressão, ansiedade e agressividade —, comum a outras drogas estimulantes.
Após o uso, a pessoa apresenta quadros de extrema violência, agressividade que se manifesta a princípio contra a própria família, desestruturando-a em todos os aspectos, e depois, por consequência, volta-se contra a sociedade em geral, com visível aumento do número de crimes relacionados ao vício em referência.
O consumo de crack fumado através de latas de alumínio como cachimbo, uma vez que a ingestão de alumínio está associada a dano neurológico, tem levado a estudos em busca de evidências do aumento do alumínio sérico em usuários de crack.
O uso do crack — e sua potente dependência psíquica — frequentemente leva o usuário à prática de delitos, para obter a droga. Os pequenos furtos de dinheiro e de objetos, sobretudo eletrodomésticos, muitas vezes começam em casa. Muitos dependentes acabam vendendo tudo o que têm a disposição, ficando somente com a roupa do corpo. Se for mulher, não terá o mínimo escrúpulo em se prostituir para sustentar o vício. O dependente dificilmente consegue manter uma rotina de trabalho ou de estudos e passa a viver basicamente em busca da droga, não medindo esforços para consegui-la.
Embora seja uma droga mais barata que a cocaína, o uso do crack acaba sendo mais dispendioso: o efeito da pedra de crack é mais intenso, mas passa mais depressa, o que leva ao uso compulsivo de várias pedras por dia.
As chances de recuperação dessa doença, que muitos especialistas chamam de "doença adquirida" (lembrando que a adição não tem cura), são muito baixas, pois exige a submissão voluntária ao tratamento por parte do dependente, o que é difícil, haja vista que a "fissura", isto é, a vontade de voltar a usar a droga, é grande demais. Além disso, a maioria das famílias de usuários não tem condições de custear tratamentos em clínicas particulares ou de conseguir vagas em clínicas terapêuticas assistenciais, que nem sempre são idôneas. É comum o dependente iniciar, mas abandonar o tratamento.



CRACK COCAINE


Crack cocaine, crack or rock is a solid, smokable form of cocaine. It is a freebase form of cocaine that can be made using baking soda (sodium bicarbonate) or sodium hydroxide, in a process to convert cocaine hydrochloride (powder cocaine) into methylbenzoylecgonine (freebase cocaine).
Crack cocaine, often nicknamed "crack" after the sound made during its manufacture, appeared primarily in impoverished inner-city neighborhoods in New York, Los Angeles, and Miami in late 1984 and 1985. Because of the dangers for manufacturers of using ether to produce pure freebase cocaine, producers began to omit the step of removing the freebase precipitate from the ammonia mixture. Typically, filtration processes are also omitted. The end result is that the cut, in addition to the ammonium salt (NH4Cl), remains in the freebase cocaine after the mixture has evaporated. The "rock" that is thus formed also contains a small amount of water.
A spoon with a mixture of baking soda, cocaine and a small amount of water. When heated from below, small crack cocaine ‘rocks’ will begin to form in the mixture.
Baking soda is a base used in preparation of crack, although other weak bases may substitute for it. The net reaction when using sodium bicarbonate (NaHCO3, common baking soda) is

Coc-H+Cl– + NaHCO3 → Coc + H2O + CO2 + NaCl

Crack cocaine is usually purchased already in rock form, although it is not uncommon for some users to "wash up" or "cook" the cocaine into crack themselves. This process is done with baking soda (sodium bicarbonate), water, and a spoon. Once mixed and heated, the bicarbonate breaks down into carbon dioxide and sodium carbonate, which then reacts with the hydrochloride of the cocaine molecule, leaving cocaine as an oily free base. Once separated from the hydrochloride, the cocaine alkaloid floats to the top of the now leftover liquid. It is at this point that the oil is picked up rapidly, usually with a pin or long thin object. This pulls the oil up and spins it, allowing air to set and dry the oil, and allows the user and/or maker to roll the oil into the rock-like shape.
Crack vaporizes near temperature 90 °C (194 °F), much lower than the cocaine hydrochloride melting point of 190 °C (374 °F). Whereas cocaine hydrochloride cannot be smoked (burns with no effect), crack cocaine when smoked allows for quick absorption into the blood stream, and reaches the brain in 8 seconds. Coupled with the fact that crack is considered more potent than cocaine hydrochloride, users obtain an intense high much more quickly than with the normal method of insufflating ("sniffing" or "snorting") the powdered cocaine.

PSYCHOLOGICAL EFFECTS

Crack cocaine is a substance that affects the brain chemistry of the user: causing euphoria, supreme confidence, loss of appetite, insomnia, alertness, increased energy, a craving for more cocaine, and potential paranoia (ending after use). Its initial effect is to release a large amount of dopamine, a brain chemical inducing feelings of euphoria. The high usually lasts from 5–10 minutes, after which time dopamine levels in the brain plummet, leaving the user feeling depressed and low. When cocaine is dissolved and injected, the absorption into the bloodstream is at least as rapid as the absorption of the drug which occurs when crack cocaine is smoked, and similar euphoria may be experienced.
A typical response among users is to have another hit of the drug; however, the levels of dopamine in the brain take a long time to replenish themselves, and each hit taken in rapid succession leads to increasingly less intense highs. However, a person might binge for 3 or more days without sleep, while partying with occasional hits from the pipe.
Use of cocaine in a binge, during which the drug is taken repeatedly and at increasingly high doses, leads to a state of increasing irritability, restlessness, and paranoia. This may result in a full-blown paranoid psychosis, in which the individual loses touch with reality and experiences auditory hallucinations.
Stimulant drug abuse (particularly amphetamine and cocaine) can lead to delusional parasitosis (aka Ekbom's Syndrome: a mistaken belief they are infested with parasites).For example, excessive cocaine use can lead to formication, nicknamed "cocaine bugs" or "coke bugs," where the affected people believe they have, or feel, parasites crawling under their skin. These delusions are also associated with high fevers or extreme alcohol withdrawal, often together with visual hallucinations about insects.
People experiencing these hallucinations might scratch themselves to the extent of serious skin damage and bleeding, especially when they are delirious.

PHYSIOLOGICAL EFFECTS

The short-term physiological effects of cocaine include: constricted blood vessels; dilated pupils; and increased temperature, heart rate, and blood pressure. Large amounts (several hundred milligrams or more) intensify the user's high, but may also lead to bizarre, erratic, and violent behavior. Large amounts can induce tremors, vertigo, muscle twitches, paranoia, or, with repeated doses, a toxic reaction closely resembling amphetamine poisoning. Some users of cocaine report feelings of restlessness, irritability, and anxiety. In rare instances, sudden death can occur on the first use of cocaine or unexpectedly thereafter. Cocaine-related deaths are often a result of cardiac arrest or seizures followed by respiratory arrest.
An appreciable tolerance to cocaine’s high may develop, with many addicts reporting that they seek but fail to achieve as much pleasure as they did from their first experience. Some users will frequently increase their doses to intensify and prolong the euphoric effects. While tolerance to the high can occur, users might also become more sensitive (sensitization) to cocaine's anesthetic and convulsant effects, without increasing the dose taken: this increased sensitivity may explain some deaths occurring after apparently low doses of cocaine.

ADDICTION

Crack cocaine is popularly thought to be the most addictive form of cocaine, and one of the most addictive forms of any drug. However, this claim has been contested: Morgan and Zimmer wrote that available data indicated that "...smoking cocaine by itself does not increase markedly the likelihood of dependence.... The claim that cocaine is much more addictive when smoked must be reexamined." They argued that cocaine users who are already prone to abuse are most likely to "move toward a more efficient mode of ingestion" (that is, smoking).
The intense desire to recapture the initial high is what is so addictive for many users. Purer forms of crack cocaine will produce the feeling of euphoria: even after smoking diluted or fake crack for hours, one hit of real crack will produce euphoria. Hours of misery or tweaking can be reversed with one single hit of real crack. The memory of that type of high can cause addicts to buy large amounts of street crack, hoping for the real thing.
On the other hand, Reinarman et al. wrote that the nature of crack addiction depends on the social context in which it is used and the psychological characteristics of users, pointing out that many heavy crack users go for days or weeks without using the drugs.

HEALTH ISSUES

Because crack also refers to non-pure (or fake) versions of rock cocaine, the health issues also include risks beyond smoking cocaine. However, crack usage is less dangerous than speedballing or "snowballing" (mixing cocaine with heroin), which can lead to more fatalities than either drug used on its own.
When large amounts of dopamine are released by crack consumption, it becomes easier for the brain to generate motivation for other activities. The activity also releases a large amount of adrenaline into the body, which tends to increase heart rate and blood pressure, leading to long-term cardiovascular problems. It is suggested by research that smoking crack or freebase cocaine has additional health issues beyond other methods of taking cocaine. Many of these issues relate specifically to the release of methylecgonidine, and the specific effect of methylecgonidine on the heart, lungs, and liver.
Toxic adulterants: As noted previously, virtually any substance may have been added in order to expand the volume of a batch, or appear to be pure crack. Occasionally, highly toxic substances are used, with an indefinite range of corresponding short and long-term health risks. For example, if candle wax or macadamia nuts are procured (as a form of fake crack) they will burn in a crack pipe producing a noxious smoke.
Smoking problems: The task of introducing the drug into the body further presents a series of health risks. Crack can not be snorted like regular cocaine, so smoking is the most common consumption method. Crack has a melting point of around 90 °C (194 °F), and the smoke does not remain potent for long. Therefore, crack pipes are generally very short, to minimise the time between evaporating and losing strength. This often causes cracked and blistered lips, colloquially "crack lip", from having a very hot pipe pressed against the lips. The use of "convenience store crack pipes" - glass tubes which originally contained small artificial roses - may also create this condition. These 4-inch (10-cm) pipes are not durable and will quickly develop breaks; users will typically continue to use the pipe even though it has been broken to a shorter length. The hot pipe might burn the lips, tongue, or fingers, especially when shared with other people quickly taking another hit from the already hot short pipe.
Pure or large doses: Because the quality of crack can vary greatly, some people might smoke larger amounts of diluted crack, unaware that a similar hit of a new batch of purer crack could cause an overdose: triggering heart problems or rendering the user unconscious.
Pathogens on pipes: When pipes are shared, unless users rotate and push the pipe to the burnt, sterilized end, any bacteria or viruses from the previous user's mouth can be transferred: tuberculosis can be spread by saliva. In terms of harm reduction, mouth pieces (lengths of tubing added to the end of the glass pipe) should be used and not shared.
Pathogens in needles/spoons: When crack is cooked down, as in a spoon with vinegar or lemon juice, for injecting with a syringe, diseases can be spread. Sexually transmitted infections such as HIV can be passed through a shared needle (or shared spoon if the needle is emptied into the spoon). From a harm reduction perspective, clean injection equipment should always be used and never shared. Ascorbic acid is safer for use than vinegar.
As a comparison, studies have shown that long-term insufflation (snorting) of cocaine in powder form can, after extensive use, destroy tissues in the nasal cavity, and has been known to create deviated septa, potentially collapsing the nose.Addiction is widely considered a health issue. Many governments have made access to clean equipment and education regarding safer practices difficult, as the use of cocaine is illegal.

Crack (droga)


Crack o Piedra

El crack (también llamado piedra), es el nombre vulgar de un derivado de la cocaína, en concreto del resultado de hervir clorhidrato de cocaína en una solución de bicarbonato de sodio, el resultado es una pasta amarillenta e insoluble en agua que flota en la superficie y se endurece al enfriarse, luego es fácilmente recuperada en forma de "rocas". El término crack es una onomatopeya que sugiere el ruido que hacen las piedras de esta droga al calentarse por la evaporación de la cocaína en base que contienen, al liberarse de la mezcla con el bicarbonato de sodio. También recibe nombres vulgares entre los usuarios a esta droga, como rocas, chulas,"pops", piedras o rockstars, entre otros; a veces erróneamente se le confunde con el bazuco o paco que es la costra que queda en la olla donde preparan la cocaína y está compuesto por los alcaloides de la planta sin refinar ni purificar.

ELABORACIÓN

El crack se elabora en laboratorios clandestinos macerando las hojas de coca con queroseno. A la pasta resultante suele agregársele bicarbonato de sodio para aumentar el volumen y disminuir su costo, y hacer más manejable la sustancia. Posee un alto grado de impurezas, pero lo que hace imposible su consumo por vía nasal, peneana o intravenosa es que no es soluble en agua, ya que no es una sal de cocaína y por ello su forma de uso es pulmonar.

MODO DE CONSUMO

Dado que el crack se fuma, ingresa rápidamente al torrente sanguíneo, produciéndole al individuo una sensación de euforia, pánico, insomnio y la necesidad de repetir la toma de crack. Debido a la rapidez de los efectos, casi inmediatos, el crack se hizo muy popular en la década de los 80. Otra razón para su popularidad es que no cuesta mucho, económicamente hablando, procesarlo ni adquirirlo. Sus efectos secundarios son muy similares a los de la cocaína, solamente que el riesgo de padecer alguno de ellos es mucho más alto por las vía de consumo, propensa a producir accidentes cardio y cerebro vasculares.
Desde los años 80, el crack se fuma en pipa de vidrio, con ceniza de cigarro sobre una lata con orificios, en un gotero de cristal, en un cigarro como primo (nombre que se le da a un tabaco mezclado con cocaína), entre otras. Otro instrumento utilizado para consumir crack es un tubo metálico similar a una antena de radio (en muchos casos lo es) a la que se le introduce una suerte de alambre y se utiliza para fumar crack simulando una pipa. Este método es utilizado principalmente por adictos de muy pocos recursos y se conoce como "fumar en tubo".

ADICCIÓN

Durante los años 90, según el Instituto de Adicciones (Adictions Institute) aumentó enormemente el número de personas que consumen crack en Norteamérica.
El mayor problema con este derivado de la cocaína es que es altamente adictivo; aunque la adicción que provoca no es física, pero es psicológica y fuerte. Los usuarios de crack describen sus efectos como más intensos, pero de menor duración, lo que implica que su dosificación sea más continua. El uso del crack se ha vinculado con la violencia, pero no se puede asegurar que esto sea un efecto derivado del propio consumo de la droga, tanto como de los grupos social y económicamente más pobres, con un alto índice de violencia y delincuencia en sí mismos, que no pueden permitirse usar la cocaína y esta es su forma barata de acceso a la misma.
Algunos especialistas han querido ver la adicción al crack como intratable, pero académicos consideran que esto se asevera por ser una droga consumida por gente pobre que no puede pagar un tratamiento en centros especializados. Este es un segundo castigo que recae sobre los grupos más empobrecidos que consumen esta sustancia, mientras que los de alto poder adquisitivo, consumirían la base libre de cocaína y tendrían acceso a los recursos asistenciales si lo necesitasen.

TRANSTORNOS FÍSICOS

Entre ellos se ubican la disminución de la potencia sexual, cefalea, enfermedad de Parkinson y hemorragia cerebral, daños en el cerebro y pulmones (enfisema).

TRANSTORNOS PSICOLÓGICOS

•Depresión.
•Ansiedad.
•Psicosis similar a la ocurrida en la esquizofrenia.
•Bipolaridad.
•Paranoia.
•Miedos.

Informações Acadêmicas e Pessoais

Minha foto
Rio de Janeiro, RJ, Brazil