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Pc Lint 9 0 Crack Cocaine __LINK__



  • processing.... Drugs & Diseases > Emergency Medicine Cocaine Toxicity Updated: Dec 31, 2020 Author: Lynn Barkley Burnett, MD, EdD, JD; Chief Editor: Sage W Wiener, MD more...

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  • Emergency Department Care Therapeutic Dilemmas Cardiovascular Concerns Pulmonary Concerns Neurologic Concerns Dystonic Reactions Metabolic Concerns Hyperthermia Cocaine-Induced Rhabdomyolysis GI concerns Body Packing and Body Stuffing Psychiatric Concerns Other Considerations Topiramate Consultations Prevention Show All Medication Medication Summary

Benzodiazepines Cardiovascular agents GI agents Nutrients Show All Questions & Answers Media Gallery Tables References Overview Practice Essentials Despite being overshadowed by opioids in recent years, cocaine remains one of the most common causes of drug-related emergency department (ED) visits in the United States. [1] Although nearly every organ system can be affected by cocaine toxicity, most patients present with cardiovascular complaints. [2]




pc lint 9 0 crack cocaine



Acute cocaine toxicity has three reported phases. In fatal cases, the onset and progression are accelerated, with convulsions and death frequently occurring in 2-3 minutes, though sometimes in 30 minutes.


Central nervous system (CNS) findings: Mydriasis, headache, bruxism, nausea, vomiting, vertigo, nonintentional tremor (eg, twitching of small muscles, especially facial and finger), tics, preconvulsive movements, and pseudohallucinations (eg, cocaine bugs)


The general objectives of pharmacotherapeutic intervention in cocaine toxicity are to reduce the CNS and cardiovascular effects of the drug. These are accomplished by using benzodiazepines initially and then controlling clinically significant tachycardia and hypertension while simultaneously attempting to limit deleterious drug interactions.


The ancient Incas of Peru believed the coca plant to be a gift from the gods. However, cocaine, derived from coca leaves, is a modern-day curse to the emergency physician. [3] Aside from alcohol (and not including tobacco-related illnesses), cocaine has been the most common cause of drug-related ED visits in the United States, accounting for 505,224 ED visits in 2011, according to the Drug Abuse Warning Network (DAWN). [4] Marijuana or hashish constituted the second leading cause at 455,668 visits. Heroin-related visits accounted for 258,482 visits.


Across the spectrum of acute and chronic effects, nearly every organ system can be affected. Trauma is often associated with cocaine use. Even the absence of cocaine, after a cocaine binge, may precipitate an ED visit due to withdrawal symptoms.


Use of cocaine spans thousands of years, with a duality of effects noted throughout history. Knowledge of its mind-altering function dates to at least 2000 BC. For centuries, indigenous mineworkers in Andean countries have used cocaine derived from the chewing of coca leaves as an endurance-enhancement agent. Spanish physicians reported the first European use of coca for medicinal purposes in 1596. Cocaine was not isolated from coca leaves until 1859. Nevertheless, by 1863, Vin Mariani, a wine fortified with 6 mg of cocaine alkaloid extract per ounce, was marketed in France. By 1880, the US pharmaceutical company Parke-Davis sold a fluid extract containing 0.5 mg/mL of crude cocaine.


In 1884, William Stewart Halsted performed the first nerve block using cocaine as the anesthetic. Halsted subsequently became the first cocaine-impaired physician on record. That same year, Sigmund Freud published the essay "Uber Coca," in which he advocated the use of cocaine in the treatment of asthma, wasting diseases, and syphilis. As with Halsted, Freud also became dependent on cocaine. In 1885, John Styth Pemberton registered French Wine Cola in the United States. The popular product, which contained 60 mg of cocaine per 8-oz serving, was later renamed Coca-Cola.


By 1893, occasional reports of fatality were associated with cocaine use, and in 1895, The Lancet reported a series of 6 deaths. By 1909, more than 10 tons of cocaine was being imported into the United States each year. Many over-the-counter medical products and elixirs had been created. One product for nasal application, called Dr. Tucker's Asthma Specific, contained 420 mg of cocaine per ounce.


The Harrison Narcotics Act of 1914 banned nonprescription use of cocaine-containing products. The resulting reduction in the use of cocaine marked the end of the first American cocaine epidemic. In the 1950s, amphetamine gradually replaced cocaine as the most common stimulant of abuse. However, this trend reversed in the 1970s, with crack ushering in the second epidemic of US cocaine use in 1985.


Crack (cocaine free base), which is generally sold in the form of "rocks," may also be sold in large pieces called slabs. These are approximately the size and shape of a stick of chewing gum and are sometimes scored to form smaller pieces. Crack cocaine differs from cocaine salt in that it is stable to pyrolysis and can be smoked. Users of cocaine in its crack form tend to be young adults aged 18-30 years who live in the central city and who are from low socioeconomic backgrounds. However, in 1986, the National Office of Drug Control Policy reported that young inner-city drug users were beginning to disdain crack as a ghetto drug. In Miami, for example, crack use had become unfashionable, and individuals continuing to use it, particularly blacks, were trying to hide it from their peers.


Cocaine powder (cocaine salt) is currently marketed to adults from all ethnic backgrounds and socioeconomic groups, predominantly white men older than 30 years who live in the central city. In several locales, cocaine is mentioned as a club drug, but it is not as prominent as methamphetamine and some hallucinogens in the club environment. It cannot be smoked, but is well absorbed transmucosally.


From January 2013 and December 2017, the average retail price per pure gram of cocaine decreased while the average purity increased. The price decreased 28.2%, from $213 to $153, while purity increased 38.6%, from 46.4% to 64.3%. [5]


The chemical name for cocaine is benzoylmethylecgonine. It is derived from the leaves of Erythroxylon coca, a shrub indigenous to Peru, Bolivia, Mexico, the West Indies, and Indonesia. Cocaine is a bitter crystalline alkaloid with the molecular formula of C17 H21 NO4. Ecgonine, an important part of the cocaine molecule, is an ester-type local anesthetic that belongs to the tropane family, which also includes atropine and scopolamine.


The primary effect of cocaine is blockade of norepinephrine reuptake; its secondary effect is marked release of norepinephrine. These effects act synergistically to increase norepinephrine levels at the nerve terminal. Cocaine also causes moderate release and reuptake-blockade of serotonin and dopamine. Its marked local anesthetic effects are caused by sodium channel blockade, which inhibits the conduction of nerve impulses, decreasing the resting membrane potential and the amplitude of the action potential while simultaneously prolonging the duration of the action potential. In the heart, cocaine acts as a Vaughan Willaims IC sodium channel blocker.


Cocaine enters the United States in the form of a hydrochloride salt, having undergone numerous steps in refinement from the original coca leaf. In its hydrochloride form, cocaine may be absorbed topically across all mucosal membranes, including the oral, nasal, GI, rectal, urethral, and vaginal membranes. It may also be injected intravenously or ingested. Ingested cocaine is poorly absorbed from the stomach because it is a weak base with a pKa of 8.6, but it is readily absorbed from the duodenum. Cocaine may be inhaled through a straw or rolled-up paper currency, or snorted from a coke spoon, typically containing 5-20 mg of the drug. A 1-inch line typically contains 25-100 mg of the drug.


Crack is produced when the hydrochloride molecule is removed by ether extraction, which frees the basic cocaine molecule, or "freebase". Heating does not destroy freebase, rather it melts at 98C and vaporizes at higher temperatures. These physical properties allow it to be smoked.


Crack is lipid soluble and therefore rapidly absorbed in the pulmonary capillaries. The term crack describes the crackling sound heard when cocaine freebase is smoked. Crack may be smoked in a pipe bowl containing 50-100 mg or in a cigarette with as much as 300 mg. Smoking crack bypasses the vasoconstriction that results when cocaine is snorted; therefore, the effects are similar to taking cocaine intravenously. Crack smokers may aggressively inhale against a small pipe and then perform a Valsalva maneuver before exhaling against pursed lips or forcefully blow the drug into a partner's mouth. These techniques are reputed to enhance the euphoria of cocaine.


All of the cocaine injected intravenously is delivered to the circulatory system, versus 20-30% of cocaine that is ingested or inhaled. With repeated use, tolerance develops so that the intensity and duration of effect decrease. People who use cocaine long term may dose themselves as frequently as every 10 minutes, binge as long as 7 days at a time and use as much as 10 g/d. Reverse tolerance, with onset of seizures and paranoid ideation at decreased doses, has been observed in animals and is thought to occur in humans as well. 350c69d7ab


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