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This PowerPoint file is a supplement to the video presentation. Some of the educational content of this program is not available solely through the PowerPoint file. Participants should use all materials to enhance the value of this continuing education program. Poisoning: Stimulants and Hallucinogens Paul R. Lockman, BSN, PhD Assistant Professor Department of Pharmaceutical Sciences School of Pharmacy Texas Tech University Health Sciences Center Amarillo, Texas EMS/Nursing I 80612/30812 Objectives 1. Recognize the mechanism of action of stimulant/ dissociative anesthetic drugs. 2. Identify the symptoms of drug toxicity. 3. Identify general measures for treating drug overdoses. EMS/Nursing I 80612/30812 Cocaine 1. 2. 3. Define cocaine’s mechanism of action with regard to neurotransmission Identify symptoms of toxicity for cocaine Define a treatment protocol for an individual with cocaine toxicity General Comments Central nervous system (CNS) stimulants: a group of drugs that are loosely classified on their ability to elicit sympathomimetic clinical symptoms Differential diagnosis for CNS stimulant overdoses hypoglycemia hypo- or hyperthermia subarachnoid hemorrhage Cocaine Background Relevant neuroanatomy: dopaminergic-rich areas of the brain nucleus accumbens primary area considered in addiction processes Cocaine Background Grays Anatomy 20th US Edition Review of Neurotransmission Neurons communicate by chemical signals Incoming action potential causes opening of voltage-gated calcium channels Calcium influx causes neuronal vesicles to fuse with plasma membrane Review of Neurotransmission Released transmitter diffuses to receptors on postsynaptic membrane (e.g., ion channels) and causes response Transmitters also activate presynaptic receptors (feedback control) Cocaine: Mechanism of Action Cocaine: Mechanism of Action Blocks the presynaptic uptake of the amine neurotransmitters [i.e., norepinephrine (NE), dopamine (DA), and serotonin (5HT)] Dopamine blockade may cause euphoria and activate the reward system Cocaine: Mechanism of Action Serotonin blockade may add to the euphoria and agitation NE blockade leads primarily to cardiovascular events Strong correlation between DA reuptake inhibition and clinical CNS symptoms ~47% blockade = “high” described primarily as euphoria ~60-77% blockade = psychostimulation and agitation Cocaine: Symptoms Cocaine CNS stimulation occurs rostral to caudal (i.e., cortex stimulation first followed by the lower motor centers) Cocaine: Symptoms CNS symptoms appear in the following order (cortex brain base) restlessness excitement increased motor activity hyperthermia increased respiratory rate vomiting Cocaine: Neurologic/ Psychologic Effects Significant agitation seizures CNS neuronal irritability along with hyperthermia are attributed to most cocaine fatalities Tactile hallucinations picking, scratching bugs under the skin Cocaine: Neurologic/ Psychologic Effects Cocaine: Neurologic/ Psychologic Effects May also have spontaneous neurovascular accident ruptured aneurysm stroke Cocaine-induced Hyperthermia Increased heat production through increased motor activity Liver stimulation of glucose metabolism Direct stimulatory effect on thermoregulatory center in the hypothalamus Cocaine: Cardiovascular Effects Initially there is transient bradycardia (secondary to stimulation of the vagal nuclei): not clinically relevant Hypertension: resultant from central reuptake inhibition of norepinephrine and epinephrine Cocaine: Cardiovascular Effects Pronounced tachycardia: increased release of norepinephrine from adrenergic neurons (primarily in the adrenal medulla) Cocaine: Cardiovascular Effects Chromaffin cells found in the adrenal medulla are homologous to sympathetic ganglia innervated by preganglionic sympathetic nerve terminals uses acetylcholine as stimulant cells then secrete epinephrine (not norepinephrine) into blood Cocaine: Dysrhythmias Primarily tachydysrhythmias atrial fibrillation (A-fib) A-flutter supraventricular tachycardia premature ventricular contractions torsades ventricular fibrillation (V-fib) Cocaine: Dysrhythmias May also see conduction delays cocaine has anesthetic properties (for clinical use) blocks sodium channels Skeletal Muscle and Pulmonary Effects Ischemia secondary to vasoconstriction and increased oxygen demand from an increased workload may result in rhabdomyolysis Skeletal Muscle and Pulmonary Effects Pulmonary complications pulmonary edema secondary to pulmonary vasculature effects alveolar hemorrhage Cocaine Toxicity Evaluation and Treatment Benzodiazepines and thermal cooling are the only measures shown to have significant efficacy in reducing cocaine mortality!!!!! General Measures Protect staff and patient Lavage/activated charcoal/ cathartic Probably not that effective unless the patient has ingested a large quantity of cocaine in an attempt to evade arrest. Even then cocaine is rapidly and well absorbed from the gastrointestinal (GI) tract. Body Packers J Kelly, M Corrigan, RA Cahill, and HP Redmond Body Packers Abdominal x-ray may reveal large amount of drug usually swallowed in a condom charcoal and a lot of it, repeat doses often whole bowel irrigation: goal is to move the packages down the GI tract without rupture Body Packers Abdominal x-ray may reveal large amount of drug serial radiographs to evaluate GI clearance may remove in operating room if needed (if packages rupture, high mortality rate) Neurologic Symptoms Assessment: physical exam agitation tactile hallucinations Treatment: benzodiazepines, such as lorazepam or diazepam (benefit is from reduction of the seizure threshold as well as diminishment of psychomotor agitation) Hyperthermia Hyperthermia blanket Ice Environment Fans Aggressive fluid resuscitation unless significant pulmonary edema noted Pulmonary Symptoms Treatment primarily supportive in nature maintain airway as needed assess for respiratory rate: may have some respiratory alkalosis provide supplemental oxygen: goal is to supplement to provide for the increased demand and workload of the organs Cardiovascular Symptoms Myocardial ischemia ECG (electrocardiograph): if ST elevation is present treat as a typical myocardial infarction –Morphine –Oxygen –Nitrates –Aspirin Cardiovascular Symptoms Myocardial ischemia cardiac enzymes • evaluate CPK (creatine phosphokinase) specifically • must evaluate in serial fashion (i.e., 2 and 6 hours) • if normal, myocardial infarction unlikely Dysrhythmias Evaluate ECG (again in a serial fashion every hour) Benzodiazepines to reduce workload of heart Atrial dysrhythmias origin thought to be from CNS should respond to cooling and sedation Dysrhythmias Ventricular dysrhythmias early on in the management the dysrhythmia probably originates from the local anesthetic effect of cocaine on the myocardium Dysrhythmias Ventricular dysrhythmias • treatment is sodium bicarbonate • will overwhelm the sodium channels, providing improved conductance Dysrhythmias Ventricular dysrhythmias late in management the dysrhythmia may originate from ischemic cardiac tissue: treatment includes sodium bicarbonate and lidocaine Amphetamines 1. 2. 3. 4. Define the mechanism of action of amphetamines with regard to neurotransmission Identify symptoms of toxicity for amphetamines Define a treatment protocol for an individual with amphetamine toxicity Differentiate the clinical toxicity of various amphetamines Mechanism of Action Can block the reuptake of dopamine and serotonin similar to cocaine, however it is not significant to major clinical symptoms Mechanism of Action Regional Distribution Lateral tegmental area, with projections which overlap those of the locus coeruleus but target the hypothalamus Largest site of synthesis is locus coeruleus, in midbrain (just a few hundred cells); it sends axons to almost every other region of the nervous system Regional Distribution Grays Anatomy 20th US Edition Clinical Symptoms in Autonomic Nervous System NE release results in peripheral stimulation of α and β receptors in the autonomic nervous system (ANS): Clinical Symptoms in Autonomic Nervous System results in continual fight or flight response hypertension tachycardia dysrhythmias myocardial infarction and/or ischemia Clinical Symptoms in Autonomic Nervous System results in continual fight or flight response hyperthermia rhabdomyolysis dehydration Clinical Symptoms NE in the locus coeruleus anorexia hypervigilance Increased dopamine/serotonin in mesolimbic area results in altered perception/ psychosis Amphetamines do not have the ability to block sodium channels like cocaine Hallucinogenic Amphetamines: Distinction and Symptoms Designer amphetamines are created by substituent substitutions allowing the molecule greater interaction with the presynaptic NE transporter (i.e., allows either greater or lesser synaptic distribution) Methylenedioxymethamphetamine (MDMA) MDMA has less stimulant effect than regular amphetamines but 10x greater serotonergic effect widely abused by college and high school students has many common names: M&M, Adam, E, Ecstasy, MDM Reported clinical symptoms (in addition to the amphetamine symptoms listed above) enhances pleasure euphoria enhancement of socialization ataxia restlessness confusion Toxic Doses for Amphetamine Treatment should be based upon clinical symptoms and measures required alleviate those symptoms Toxic Doses for Amphetamine Amphetamine: low dose increased vigilance, delayed sleep anorexia reduced sensation of fatigue euphoria increased motor and speech activity typically, motor and intellectual tasks can be performed more rapidly but with more errors Toxic Doses for Amphetamine Amphetamine: high dose paranoid psychosis, tactile hallucinations convulsions with potentially lethal consequences tachycardia hypertension strokes arrhythmias General Measures for Treatment Protect staff and patient Airway, breathing, and circulation (ABCs) Lavage/activated charcoal/ cathartic Specific Measures Hyperthermia ice fans environment aggressive fluid resuscitation Neurologic symptoms assessment: physical exam agitation tactile hallucinations Specific Measures Treatment: benzodiazepines, such as lorazepam or diazepam Benzodiazepines and thermal cooling are excellent measures in reducing amphetamine mortality!!!!!!!!!! Urinary Acidification Principle is similar to urinary alkalinization that aids in the elimination of weak acids (e.g., aspirin, phenobarbital, chlorpropamide, etc.) Urinary Acidification Amphetamines are a weak base: acidification of the urine will theoretically ionize the molecule in the urine; the drug is trapped and cannot be absorbed back into blood, resulting in increased elimination and decreased toxicity Urinary Acidification However, acidification of the urine requires acidification of the blood leading to metabolic acidosis This acidosis coupled with the increased demand and ischemia at muscles can enhance the possibility of rhabdomyolysis PCP and Ketamine 1. Define mechanism of action, clinical symptoms and treatment for phencyclidine (PCP), and ketamine PCP and Ketamine Dissociative anesthetics are drugs which cause an altered sensory perception without losing consciousness Monoamine reuptake inhibition NMDA (N-Methyl-D-aspartic acid) antagonism Sigma opioid receptor: PCP associates with extremely high doses Clinical Symptoms: Ketamine and PCP Mechanism and symptoms are similar to amphetamines and cocaine, but must be at higher doses to have significant clinical effect Responsible for sympathomimetic and psychomotor effects Clinical Symptoms: Ketamine and PCP Symptoms resemble that of schizophrenia (sometimes unable to distinguish difference, except PCP symptoms usually recede within 4 weeks) Inhibition of sensory perception: produce a lack of response to external stimuli Clinical Symptoms: Ketamine and PCP Dissociative consciousness memory perception (including pain): diminution in all 5 senses Increase in motor activity Hallucinations typically are auditory Clinical Symptoms Unique to PCP Hallmark sign of PCP toxicity is delusion of superhuman strength and invulnerability (result of anesthetic and dissociative properties of drug) Clinical Symptoms Unique to PCP Other neurologic signs bizarre behavior cerebellar signs dystonic reactions Treatment of PCP and Ketamine Toxicity ABCs and supportive therapy as always Agitation and bizarre behavior: benzodiazepines are used to reduce symptoms Treatment of PCP and Ketamine Toxicity Decontamination ipecac contraindicated – possible seizures lavage, probably not activated charcoal/cathartic indicated if recent ingestion Treatment of PCP and Ketamine Toxicity Most individuals recover within 1-2 hours; however, some patients may be symptomatic for weeks Treatment of PCP and Ketamine Toxicity Protect the patient: primary symptoms of toxicity are a result of behavioral injury and or rhabdomyolysis from significant muscle exertion Acidification of urine is theoretical BUT NOT RECOMMENDED Poisoning: Stimulants and Hallucinogens If you have any questions about the program you have just watched, you may call us at: (800) 424-4888 or fax (806) 743-2233. Direct your inquiries to Customer Service. Be sure to include the program number, title and speaker. EMS/Nursing I 80612/30812 Release Date: 11/01/2012 The accreditation for this program can be found by signing in to www.ttuhsc.edu/health.edu EMS/Nursing I 80612/30812 This continuing education activity is approved by the Continuing Education Coordinating Board for Emergency Medical Services for 1.5 advanced CEH. You have participated in a continuing education program that has received CECBEMS approval for continuing education credit. If you have any comments regarding the quality of this program and/or your satisfaction with it, please contact CECBEMS at: CECBEMS -12200 Ford Road, Suite 478 Dallas, TX 75234 Phone: 972-247-4442 [email protected] EMS I 80612 The Texas Tech University Health Sciences Center Continuing Nursing Education Program is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation. Provider approved by California Board of Registered Nursing, Provider #CEP11800, for the designated number of contact hours for each program. Provider approved by Florida Department of Health Board of Nursing, Provider #FBN2060. Provider approved by West Virginia Board of Examiners for Registered Professional Nurses, Provider #WV1998-0262RN. Iowa Board of Nursing approved provider #325. Accepted by the North Carolina Board of Nursing. Reminder to all PARTICIPANTS, certificates should be retained for a period of four (4) years. Health.edu reports Florida Continuing Education (Contact Hours) to CE Broker. This activity provides 1.5 contact hours. Nursing I 30812 This activity is presented for educational purposes only. Participants are expected to utilize their own expertise and judgment while engaged in the practice of nursing. The content of the presentations is provided solely by presenters who have been selected for presentations because of recognized expertise in their field. Nursing I 30812 DISCLOSURE TO PARTICIPANTS Requirements of successful course completion: •Complete the program via video presentation, PowerPoint slides, audio presentation, and/or manuscript. •Complete the course evaluation. •Complete the posttest with a score of 80% or greater. •Complete the time utilized in course completion including the posttest. Nursing I 30812 Conflicts of Interest: Paul R. Lockman, BSN, PhD has disclosed that no financial interests, arrangements or affiliations with organization/s that could be perceived as a real or apparent conflict of interest in employment, leadership positions, research funding, paid consultants or member of an advisory board or review panel, speaker’s bureau, major stock or investment holder, or other remuneration. Commercial Support: There is no commercial support and/or relevant financial relationships related to this educational activity. 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