Video Comparer 1 06 ^NEW^ Crack Cocaine

Video Comparer 1 06 ^NEW^ Crack Cocaine

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Cracks in the System: Twenty Years of the Unjust Federal Crack Cocaine Law(2006): In the 20 years following passage of the Anti-Drug Abuse Act of 2006, many of the myths surrounding crack cocaine were dispelled, making it clear that there was no scientific or penological justification for the 100:1 sentencing ratio.

The other major tech platforms, led by Facebook (the cocaine in this extended analogy), have rushed to compete, creating a "digital crack epidemic," according to a research note by the analysts titled "Has TikTok ruined the Internet?"

It's an extreme comparison, given the real crack epidemic devastated communities and killed thousands. And the Bernstein analysts were not suggesting TikTok will actually kill anyone. But their research note, and the severe description of TikTok's addictiveness, illustrates the platform's success and potential impact on the digital economy.

A comprehensive examination of the 100-to-1 crack versus powder cocaine sentencing disparity under which distribution of just 5 grams of crack carries a minimum 5-year federal prisonsentence, while distribution of 500 grams of powder cocaine carries the same 5-year mandatory minimum sentence.

Crack cocaine use disorder (CUD) has been related to sex differences. This work aimed to compare the severity of drug use and the severity of other negative related outcomes in males and females with CUD. A total of 1344 inpatients (798 males and 546 females) with crack cocaine use disorder (CUD) were evaluated by a detailed multidimensional clinical assessment, including addiction severity and trauma exposure. Linear regression predicted higher drug use severity (β = 0.273, p < 0.001) and more problems in domains related to childcare issues (β = 0.321), criminal involvement (β = 0.108), work-related problems (β = 0.281) and social support impairments (β = 0.142) for females, all with p < 0.001. Alcohol problems were predicted to be higher in males (β = -0.206, P < 0.001). Females had higher rates of other mental disorders, particularly trauma and stress-related disorders (OR: 3.206, CI: 2.22, 4.61). Important sex differences also emerged in trauma history and HIV infection prevalence. CUD has a more severe clinical presentation among females facing early abstinence. Sex differences in the CUD course indicate the need for consideration of sex-specific interventions and research.

Cocaine abuse is a major worldwide health problem. Patients with acute cocaine toxicity may require urgent treatment for tachycardia, dysrhythmia, hypertension, and coronary vasospasm in order to prevent pathological sequelae such as acute coronary syndrome, stroke, and death. This activity reviews the evaluation and management of cocaine toxicity and highlights the role of the interprofessional team in caring for affected patients.

Objectives:Describe the toxicokinetics of cocaine toxicity.Describe the typical history and physical exam findings for a patient with cocaine toxicity.Summarize the management options for cocaine toxicity.Explain the importance of improving care coordination among the interprofessional team to enhance the delivery of care for patients with cocaine toxicity.Access free multiple choice questions on this topic.

Cocaine abuse is a major worldwide health problem. Patients with acute cocaine toxicity presenting to the emergency department (ED) may require urgent treatment for tachycardia, dysrhythmia, hypertension, and coronary vasospasm, leading to pathological sequelae such as acute coronary syndrome, stroke, and death.[1][2][3]

Over the past few decades, body packers have also presented to the emergency department following bag ruptures. The other problem is that many patients have also ingested other illicit agents, including alcohol, which makes management difficult. While cocaine can adversely affect every organ in the body, its most lethal effects are on the cardiovascular system.

Cocaine abuse is a major public health problem, with an estimated 20 million users worldwide, based on the most recent United Nations World Drug Report. The number of frequent cocaine users, which had been declining since 2006 in North America, has experienced a recent increase, with an estimated 1% of the population reporting use. The Drug Enforcement Agency estimated that in 2012, 639,000 persons aged 12 or older had used cocaine for the first time within the previous 12 months in the United States (US), averaging approximately 1,800 initiates per day. In the US, cocaine was the most common drug of abuse resulting in hospital treatment, with 505,224 ED visits (40.3% of drug reported visits) in 2011 based on data from the Substance Abuse and Mental Health Services Administration. This translates to a rate of 162 ED visits per 100,000 population.[5][6]

Patients who abuse cocaine risk life-threatening consequences, including tachydysrhythmia, severe hypertension, acute coronary syndrome, stroke, acute myocardial and renal failure, seizure, hyperthermia, cocaine-induced rhabdomyolysis, and fetal/maternal morbidity and mortality.[7]

The adverse effects on the heart are due to the direct actions of cocaine by inhibiting the reuptake of catecholamines into the nerve endings. The increased catecholamine levels can induce life-threatening arrhythmias, and at the same time, the local anesthetic properties of cocaine further impair impulse conduction, leading to re-entry ventricular arrhythmias.

Long-term use of cocaine can also alter cardiac histology leading to fibrosis, myocarditis, and contraction band necrosis. Cocaine significantly increases myocardial oxygen requirements, heart rate, and cardiac output. In patients with even mild coronary disease, these hemodynamic changes, plus its vasoconstriction ability, can trigger an acute coronary syndrome.

Asides from the myocardium, cocaine can also increase the risk of ischemic stroke. Cocaine can also cause seizures by lowering the threshold for seizure initiation. Chronic use of cocaine can lower the density of dopamine receptors leading to extrapyramidal symptoms, dystonia, bradykinesia, akinesia, and akathisia.

A high risk of death is the ability of cocaine to induce delirium. These patients are often at risk for sudden death. Excited delirium is often associated with aggression, hyperactivity, extreme paranoia, hyperthermia, incoherent screaming, and unusual strength. Individuals who develop excited delirium tend to be more sensitive to the elevated levels of catecholamines.

Another feature of cocaine toxicity is hyperthermia, which may be as high as 45 C. Hyperthermia is a marker for poor prognosis and is often associated with muscle breakdown, renal and liver injury, encephalopathy, disseminated intravascular coagulation (DIC), and metabolic acidosis.

Cocaine can be snorted, swallowed, injected, or smoked. Its pharmacodynamics involves multiple complex mechanisms, although its half-life is short at about 1 hour. This drug binds and blocks monoamine (dopamine, norepinephrine, and serotonin) reuptake transporters with equal affinity. Monoamines accumulate in the synaptic cleft resulting in enhanced and prolonged sympathetic effects. The principal actions of cocaine on the cardiovascular system are from alpha- and beta-1-adrenoceptor stimulation resulting in increased heart rate, systemic arterial pressure, and myocardial contractility, which are major determinants of myocardial oxygen demand. Cocaine and its metabolites may cause arterial vasoconstriction hours after use.[7] Epicardial coronary arteries are especially vulnerable to these effects, leading to decreased myocardial oxygen supply. Cocaine-induced platelet activation and thrombus formation are another deleterious effects caused by alpha-adrenergic- and adenosine diphosphate-mediated increase in platelet aggregation. Plasminogen activator inhibitor is also increased following cocaine use, thereby promoting thrombosis. Similar to local anesthetics such as lidocaine, cocaine blocks sodium channels and interferes with action potential propagation. This Vaughn-Williams class IC effect increases the risk of conduction disturbance and tachyarrhythmias. Adding to its complex toxicity, cocaine targets muscarinic acetylcholine, N-methyl-D-aspartate (NMDA), sigma, and kappa-opioid receptors.[8]

These patients present to the hospital with agitation, chest pain, anxiety, psychosis, and blunt and penetrating traumatic injuries. They are frequently hypertensive and tachycardic. They may be unwilling to disclose their cocaine use, and clinicians must consider a wide spectrum of diagnoses during the initial evaluation, such as withdrawal syndromes, thyrotoxicosis, acute psychosis, sepsis, pheochromocytoma, anticholinergic toxicity, serotonin and neuroleptic malignant syndromes, and intracranial hemorrhage.

Depending on the patient's presentation, laboratory testing for suspected cocaine toxicity can include a complete blood count, comprehensive chemistry panel, troponin, B-type natriuretic peptide, creatinine kinase, urinalysis, urine toxicology screen, and electrocardiogram. Imaging may also include chest x-ray, abdominal x-ray for suspected body packers or stuffers, and head CT if altered mental status suggests intracranial hemorrhage.[9][10]

Creatine kinase may be useful for the detection of rhabdomyolysis. Urinalysis may detect myoglobinuria. A urine drug screen is a must to detect other illicit substances. Most cocaine disappears from the body within 24 hours, but the metabolite, benzoylecgonine, may persist for weeks. This metabolite can also cause neurotoxicity.

The chest x-ray may show signs of pulmonary edema, pneumothorax, or even aspiration pneumonia. The abdominal x-ray may reveal swallowed packets of cocaine. Because of false negatives with the plain x-rays, a contrast-enhanced study or CT scan is recommended. The risk of bag rupture increases with time, so it is important to make the diagnosis promptly.

Patients with cocaine toxicity need to be stabilized, and attention should be paid to the ABCDEs. The patient's fever should be managed, and one should rule out hypoglycemia as a cause of the neuropsychiatric symptoms. A pregnancy test should be ruled in women of childbearing age. The treatment should be based on clinical symptoms, and one should avoid physical restraints. 2b1af7f3a8