Depression overdoses

Contraindications for antipsychotic therapy are few they may include Parkinson s disease, hepatic failure, hypotension, bone marrow depression, or use of CNS depressants. Overdoses of antipsychotics are rarely fatal, except for thioridazine, which is associated with major ventricular arrhythmias, cardiac conduction block, and sudden death. For other agents gastric lavage should be attempted even if several hours have elapsed since the drug was taken, because gastrointestinal motility is decreased and the tablets may still be in the stomach. Moreover, activated charcoal effectively binds most of these drugs and can be followed by a saline cathartic. The hypotension often responds to fluid replacement or pressor agents such as norepinephrine. 

PCP intoxication typically produces miosis, nystagmus, hypertension, tachycardia, salivation, flushing, sweating, ataxia, and CNS stimulation or depression. Overdose of PCP is dangerous, as the user becomes violent and emergency treatment is required. It is necessary to keep the user calm and not leave him alone. Withdrawal symptoms of PCP are tremor, seizures, diarrhea, piloerection, and vocalizations. 

IAsu ].p-ANP(7-28). aminosuccinic acid aspartic acid, aminosultopride amisulpnde. amiodarone [ban, inn, usan) (Cordarone ) is a benzofuran derivative, a (Class III) antiarrhythmic used mainly to treat ventricular arrhythmias, amiphenazole [ban, inn] (DHA 245 amifenazole) is a phenylthiazole and has similar properties as doxapram as a CNS STIMULANT and RESPIRATORY STIMULANT. It was previously used intramuscularly to treat barbiturate and other CNS DEPRESSANT overdose. 

The second-generation antidepressants, particularly RIMAs and SSRJs, are much less toxic ia overdose than the older TCAs and irreversible MAO inhibitors. However, similar to first-generation antidepressants, the therapeutic effect only becomes manifest after several weeks. Up to one-third of depressed patients are nonresponders. Ideally, an antidepressant would combine a more rapid onset of action with greater clinical efficacy and a higher responder rate, as well as even better tolerability. 

A thiazole derivative that incorporates a fragment of the amphetamine molecule shows some CNS stimulant activity more specifically, the compound antagonizes the depression caused by overdoses of barbiturates and narcotics. Reaction of benzalde-hyde with sodium cyanide and benzenesulfonyl chloride gives the toluenesulfony1 ester of the cyanohydrin (141). Reaction of this with thiourea leads directly to aminophenazole (143) It is probable the reaction proceeds by displacement of the tosylate by the thiourea sulfur to give 142 addition of the amino group to the nitrile followed by tautomerization affords the observed product. ... 

Opiate overdose is a medical emergency that can result in respiratory and CNS depression. The opioid receptor antagonist naloxone immediately reverses cardiorespiratory depression. However, repeated naloxone administration is required, since the effects of naloxone last for 30 min, while opioid agonists can remain at potentially lethal blood levels for several hours. 

This drug is used for complete or partial reversal of narcotic depression, including respiratory depression. Narcotic depression may be due to intentional or accidental overdose (self-administration by an individual), accidental overdose by medical personnel, and drug idiosyncrasy Naloxone also may be used for diagnosis of a suspected acute opioid overdosage. 

Although rare, benzodiazepine toxicity may occur from an overdose of the drug. Benzodiazepine toxicity causes sedation, respiratory depression, and coma. Flumazenil (Romazicon) is an antidote (antagonist) for benzodiazepine toxicity and acts to reverse die sedation, respiratory depression, and coma within 6 to 10 minutes after intravenous administration. The dosage is individualized based on the patient s response, widi most patients responding to doses of 0.6 to 1 mg. However, die drug s action is short, and additional doses may be needed. Adverse reactions of flumazenil include agitation, confusion, seizures, and in some cases, symptoms of benzodiazepine withdrawal. Adverse reactions of flumazenil related to the symptoms of benzodiazepine withdrawal are relieved by die administration of die benzodiazepine. 

Adverse reactions seen with magnesium administration are rare. If they do occur, they are most likely related to overdose and may include flushing, sweating, hypotension, depressed reflexes, muscle weakness, and circulatory collapse (see Display 58-2). 

Despite the risks of benzodiazepine dependence and overdose among alcoholic patients beyond the period of acute withdrawal, there may be a role for the judicious use of benzodiazepines in treating these patients. To the degree that early relapse, which commonly disrupts alcoholism treatment, is a result of continued withdrawal-related symptoms (e.g., anxiety, depression, insomnia) that can be suppressed by low doses of benzodiazepines, retention in treatment could be enhanced by the use of benzodiazepines (Kissin 1977). Moreover, for some patients, benzodiazepine dependence, if it does occur, may be more benign than alcoholism. 

Major gastrointestinal effects include decreased gut motility and changes in secretion of gastric and intestinal fluids. Morphine and most p receptor agonists cause pupillary constriction. Some tolerance to this effect may develop, but addicts with high opioid levels will still have miosis. Respiratory depression is the usual cause of death from opioid overdose. 

Death from overdose of barbiturates may occur and is more likely when more than 10 times the hypnotic dose is ingested. The barbiturates with high lipid solubility and short half-lives are the most toxic. Thus the lethal dose of phenobarbital is 6—10 g, whereas that of secobarbital, pentobarbital, or amo-barbital is 2-3 g. Symptoms of barbiturate poisoning include CNS depression, coma, depressed reflex activity, a positive Babinski reflex, contracted pupils (with hypoxia there may be paralytic dilation), altered respiration, hypothermia, depressed cardiac function, hypotension, shock, pulmonary complications, and renal failure. 

The lethal dose of mescaline varies because of the development of tolerance to the action of the drug. After a massive overdose, hypotension, bradycardia, CNS depression, and respiratory failure may be life threatening. Fatal intoxications from mescaline are rare, and fatalities associated with mescaline use are usually attributed to traumas resulting from altered perceptions. 

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. 

Tricyclic antidepressants (TCAs) are effective for all depressive subtypes, but their use has diminished because of the availability of equally effective therapies that are safer on overdose and better tolerated. In addition to inhibiting the reuptake of NE and 5-HT, they also block adrenergic, cholinergic, and histaminergic receptors. 

Overdose fatalities are rare unless benzodiazepines are taken with other CNS depressants. 

Side effects are increased blood pressure and heart rate, respiratory depression, apnea, muscular hypertonus, and dystonic reactions. In overdose, seizures, polyneuropathy, increased intracranial pressure, and respiratory and cardiac arrest may occur. 

An analysis of 19 deaths from PCP overdose that occurred in two California counties from 1970 to 1976 showed that 12 were accidental, five suicidal, and two homicidal. Eight of the 12 accidental deaths were from drowning. Blood concentrations ranged from 1,250 to 2,300 ng/ml. Virtually all patients with levels of 1,000 ng/ml or more had coma, with the possible evolution of death due to medical complications, seizures, or respiratory depression. Levels greater than 2,000 ng/ml were almost always fatal (12). 

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