Cocaine respiratory

Cocaine. This lias a bitter taste, is mydriatic, produces local anaesthesia and is toxic. After absorption, or when taken internally, it acts chiefly by stimulation of the central nervous system, succeeded by depression. Since the two phases may be present in different areas simultaneously, a mixed result may ensue. With large doses the chief symptoms are those of medullary depression. Death is due to paralysis of the respiratory centre. The main use of cocaine in medicine is as a local anaesthetic. 

Large or quickly repeating doses over a period of hours can led to extreme anxiety, paranoia and even hallucinations. These effects usually disappear as the drug is eliminated from the body. The after-effects of cocaine and crack use may include fatigue and depression as people come down from the high. Excessive doses can cause death from respiratory or heart failure but this is rare. 

The treatment goals for acute intoxication of ethanol, cocaine/amphetamines, and opioids include (1) management of psychological manifestations of intoxication, such as aggression, hostility, or psychosis, and (2) management of medical manifestations of intoxication such as respiratory depression, hyperthermia, hypertension, cardiac arrhythmias, or stroke. 

BZ is usually disseminated as an aerosol with the primary route of entry into the body through the respiratory system the secondary route is through the digestive tract. BZ blocks the action of acetylcholine in both the peripheral and central nervous systems. As such, it lessens the degree and extent of the transmission of impulses from one nerve fiber to another through their connecting synaptic junctions. It stimulates the action of noradrenaline (norepinephrine) in the brain, much as do amphetamines and cocaine. Thus, it may induce vivid hallucinations as it sedates the victim. Toxic delirium is very common. 

The answer is local anesthetic properties it can block the initiation or conduction of a nerve impulse. It is biotransformed by plasma esterases to inactive products. In addition, cocaine blocks the reuptake of norepinephrine. This action produces CNS stimulant effects including euphoria, excitement, and restlessness Peripherally, cocaine produces sympathomimetic effects including tachycardia and vasoconstriction. Death from acute overdose can be from respiratory depression or cardiac failure Cocaine is an ester of benzoic acid and is closely related to the structure of atropine. 

Physical effects of high doses of ketamine include decreased respiration and heart rate, increased blood pressure, and the possibility of vomiting and convulsions. These can lead to cardiac and respiratory arrest, coma, and death. The risk of ketamine overdose is much greater when it is mixed with other drugs such as alcohol, Ecstasy, caffeine, or cocaine. Overdoses of ketamine have been reported when people boost the drug (take another dose before the first dose wears off) to prolong its psychedelic effects. 

As would be expected, khat overuse produces symptoms similar to those of other monoamine stimulants, such as cocaine or amphetamine, including signs of sympathetic overarousal. In the extreme this can involve a toxic psychosis. Disorders more frequently associated with chronic khat use in males are headaches, anorexia, insomnia, constipation, and respiratory illnesses (Kennedy et al. 1983). Females report higher incidences of acute gastritis, jaundice, bronchitis and hepatic diseases. Also, cathinone has toxic reproductive effects in humans and experimental animals (Islam et al. 1990). It decreases sperm count and motility, and increases the number of abnormal sperm cells. It also decreases plasma testosterone in rats. 

The use of cocaine for local anesthesia has been largely replaced by synthetic drugs that produce less psychoactive effects. However, cocaine is still used sometimes for topical anesthesia of the upper respiratory tract. 

Abuse of cocaine during pregnancy is associated with increased rates of prematurity, low birth weight, respiratory distress, bowel and cerebral infarctions, reduced head circumference, and increased risk of seizures (Keller and Snyder-Keller, 2000). Infants prenatally exposed to cocaine show abnormal habituation and impaired attention. 

Action on CNS Local anaesthetics stimulate CNS and produce restlessness, tremor, mental confusion, convulsion. In toxic doses, it causes respiratory depression, coma and death. Cocaine is a powerful stimulant while procaine and other agents produce less CNS stimulant effect. 

Addicts use cocaine intravenously or by snorting the powder. After intravenous injections, coma and respiratory depression can occur rapidly. It has been reported that fatalities associated with snorting usually occur shortly after the abrupt onset of major motor seizures, which may develop within minutes to an hour after several nasal ingestions. Similar results occur if the substance is taken by mouth Treatment is directed toward ventilatory support and control of seizures—although in many instances a victim may not be discovered in time to prevent death. It is interesting to note that cocaine smugglers, who have placed cocaine-filled condoms in their rectum or alimentary tract, have died (Suarez et al.. 1977). The structural formula of cocaine is given in Fig 1. 

At higher doses, cocaine can produce undesirable effects, including tremor, emotional lability, restlessness, irritability, paranoia, panic, and repetitive stereotyped behavior. At even higher doses, it can induce intense anxiety, paranoia, and hallucinations, along with hypertension, tachycardia, ventricular irritability, hyperthermia, and respiratory depression. In overdose, cocaine can cause acute heart failure, stroke, and seizures. Acute intoxication with cocaine produces these various clinical effects, depending on the dose these effects are mediated by inhibition of the dopamine transporter and in turn by the effects of excessive dopamine activity in dopamine synapses, as well as by norepinephrine and serotonin in their respective synapses. 

A 34-year-old woman with a history of renal insufficiency induced by long-term use of cocaine developed respiratory failure and was intubated and sedated with intravenous lorazepam (65 mg, 313 mg, and 305 mg on 3 consecutive days). After 2 days she had a metabolic acidosis, with hyperlactatemia and hyperosmolality. Propylene glycol, a component of the lorazepam intravenous formulation, was considered as a potential source of the acidosis, as she had received more than 40 times the recommended amount over 72 hours. Withdrawal of lorazepam produced major improvements in lactic acid and serum osmolality. 

The respiration is at first accelerated. During the spasms, it is irregular. The volume then diminishes. It may assume the Cheyne-Stokes type. Respiratory paralysis is the usual cause of death. This is also the first center to fail when the cocaine is applied locally to the fourth ventricle. 

Cocaine is a central nervous system (CNS) stimulant that causes a significant increase in heart rate, respiration, blood pressure, and body temperature. According to DAWN, one in thirteen cocaine users go to the hospital to be treated for severe reactions that could be life-threatening. Sudden death can result from heart failure, respiratory failure, seizures, strokes, and cerebral hemorrhage. There is no antidote for cocaine overdose. Even if the adverse reactions do not result in death, they can do permanent damage to the body. 

In 2000, heroin was second only to cocaine in the number of drug-related emergency room episodes reported to a national registry run by the Drug Abuse Warning Network. Heroin, listed as a principal agent in respiratory and cardiac emergencies, went from 33,884 episodes nationwide in 1990 to 94,804 in 2000—an increase of nearly 180%. 

Overdoses of cocaine are often rapidly fatal, victims dying within minutes from arrhythmias, seizures, or respiratory depression. Those who survive for 3 hours usually recover fully. Intravenous administration of diazepam, propranolol, or calcium channel-blocking drugs may be the best... 

Among the toxicants that increase respiratory rate are cocaine, amphetamines, and fluoroacetate (all of which are shown in Figure 6.11), nitrites (compounds containing the NOjion), methanol (CH3OH), salicylates, and hexachlorobenzene. Cyanide and carbon monoxide may either increase or decrease respiratory rate. Alcohols other than methanol, analgesics, narcotics, sedatives, phe-nothiazines, and opiates in toxic doses decrease respiratory rate. The structural formulas of some compounds that affect respiratory rate are shown in Figure 6.13. 

Some people have an exaggerated reaction to cocaine and overdose on small amounts. Chronic users become more sensitive to the toxic effects of the drug, and may experi ence serious problems after taking their accustomed dose. Seizures, elevated blood pressure, respiratory depression, coma, and death can follow. 

The clinical symptoms of cocaine intake are the following vasoconstriction, dilated and reactive pupils, hyperthermia, arrhythmias, increased blood pressure, dry mouth, increased sweating, tremors, dizziness, muscle spasms, hyperactivity, and insomnia. Cocaine-related deaths are generally caused by cardiac arrest or seizures followed by respiratory arrest [11],... 

Cocaine is a CNS stimulant that affects blood vessels and pupils, and increases body temperature, heart rate, and blood pressure. The euphoric effects of cocaine are quick and include reduced fatigue and mental clarity, as well as hyperstimulation. Research reports that the faster the absorption, the shorter the duration of action. The effects of cocaine in humans are variable (e.g., feeling of restlessness, irritability, and anxiety). Cocaine has powerful neuropsychological-reinforcing properties that are responsible for its repeated compulsive use. In some cases, the first dose may prove fatal. Cocaine-related death may be due to cardiac arrest or convulsion followed by respiratory arrest. In drug abuse, people mix cocaine with alcohol, leading to a chemical complex called cocaethylene, which intensifies the euphoria but can culminate in death. 

The hazards of cocaine specific for pregnant women include premature rupture of placental membranes, spontaneous abortion, abnormal labor, and several general medical risks (e.g., hypertension). Their babies typically have growth retardation with consequent lowered birthweight. Cocaine use is also related to sudden infant death syndrome, characterized by abnormal respiratory control, particularly during sleep. 

Death from cocaine often occurs within 2-3 minutes, suggesting direct cardiac toxicity, fatal dysrhythmias, and depression of medullary respiratory centers as common causes of death (11,12). Thus, cocaine s local anesthetic properties can contribute additional hazards when high doses are used, reminiscent of deaths reported in the era when it was used as a mucous membrane paste for nasopharyngeal surgery (13). 

Cocaine has a spectrum of pharmacological effects. It initially causes excitement and euphoria later, with higher doses, lower centers become involved, producing reduced coordination, tremors, hyper-reflexia, increased respiratory rate, and at times nausea, vomiting, and convulsions. These symptoms are eventually followed by CNS depression. 

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