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The "Pathophysiology of the Nervous System" paper contains a case study that explores stimulant psychosis caused by the use of speed, its diagnosis, the pathophysiology of amphetamines, prehospital interventions, and general treatment of the condition…
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Case Study Essay
Several conditions arise from drug abuse and overdose including stimulant psychosis, which results from amphetamine and cocaine overdose. The abuse of amphetamine has been rampant across the world following its availability in market. These drugs stimulate the central nervous system of an individual resulting into different body responses such as changes in the heart rate, blood pressure among other systemic processes controlled by the central nervous system (CNS) (Greene, Kerr & Braitberge 2008). In the case study provided, Bruisers, who was found semi-unconscious and had some history in drug abuse, most likely had an overdose of amphetamine. The description of Bruiser by his brother Danny plays an important role in aiding paramedics to isolate possible cause of his condition because most of his behaviour such as violence and drunkenness suggest a possible overdose of amphetamines. Danny suspected that his brother was either under the influence of heroin or speed because of his previous habits.
The circumstances surrounding Bruiser’s condition including his association with a pharmacy robbery best suit a scenario in which the patient might have abused amphetamines from the pharmacy. The abuse of amphetamines has been dubbed ‘speed’ in the streets especially because of the changes that occur in the body following its abuse or overdose. Some of the symptoms associated with speed include increased blood pressure, increased heart rate, agitation, increased breathing rates, and enlargement of the pupil. The use of heroin could be eliminated on the basis of the paramedics’ diagnostics in which the blood pressure and the heart rate of the patient increased as opposed to the case of heroin abuse. Therefore, it would be appropriate to conclude that the patient was suffering from stimulant psychosis, which is associated with the abuse of amphetamines.
This case analysis explores stimulant psychosis caused by use of speed, its diagnosis, pathophysiciology of amphetamines, prehospital interventions and general treatment of the condition
Patient Assessment
Bruiser is found in a semi-conscious at Hindmarsh Square by report who reports the matter to an ambulance service. The paramedics found Bruiser in a Semi-conscious state, snoring slowly, and incontinent of urine. In addition, Bruiser had also vomited and had a strong smell of wine as well as a recent track mark in his left arm. Observations made by the paramedics included elevated blood pressure, increased heart rates, enlarged pupils, changes in respiratory rates and a pale, cold and dry skin. These symptoms clearly depict an overdose of speed or amphetamines. The circumstances surrounding the patient’s condition such as robbery of a pharmacy provide a supporting evidence for amphetamine or speed overdose as the cause of the condition. Some of the symptoms surrounding the use of speed include increased heart beat, breathing rates, elevated blood pressure, enlargement of the pupils, aggressiveness, and hostility, and finally psychosis (Batki & Harris 2004). In situations where speed overdose leads the patient into the amphetamine psychosis, the patient begins to hear mixed voices and have the fear that other people may intend to hurt him/her sets in. As indicated from the case study, Bruiser became aggressive and agitated after receiving the essential treatment provided by the paramedics as a life-saving intervention before reaching the hospital for full diagnosis and treatment. Such observations indicated resumption of the symptoms associated with speed abuse as the patient began to regain his full consciousness. To support the diagnosis, some of the observations made by the paramedics at the scene coincide with the symptoms of amphetamine abuse especially the increase in the heart rate, blood pressure as well as the changes in respiratory rates.
Although the observations indicated by the paramedics show decreased respiratory rate, this may be associated with the toxic levels of amphetamines that cause slowed breathing rate (Goldman 2000). Since the patient had been reported as a user of both speed and heroin, the counter stimulating effects such as the decreased breathing rate could be associated with his previous use of heroin or even combination of the two that would have turned lethal. Bruiser also portrayed unique physical symptoms such as the dry, cold and pale skin, which characterize amphetamine abuse. However, it could be difficult to rule-out the possibility of the victim having combined the two drugs. This is because in many cases, abuse of amphetamines or speed does not lead to unconscious, though the semi-unconsciousness and the decreased respiratory rate could be associated with an overdose of the drug. Abuse of amphetamines or methamphetamine may also cause renal failure associated with rhabdomyolysis.
In the case at hand, physical assessment indicated that the patient experienced incontinence of urine as well as vomiting, which also form part of symptoms associated with amphetamine abuse. The presence of track mark also provides supporting evidence for the use of amphetamine by the patient in question. This is because amphetamine administration can take place through different routes including oral, inhalation, and intravenous injections like most hard drugs (Yui et al. 1999). The intravenous route of administration produces effects in the body system within the shortest time possible compared with the other administration modes. Since most of the observations made in this case revolve around the abuse of amphetamines, as well as other evidences surrounding the scenario, the condition of the patient can be concluded to be an amphetamine or speed psychosis.
Pathophysiology of Amphetamine-induced Psychosis
Amphetamine-induced psychosis results from prolonged use or overdose of amphetamines just like other stimulant induced- psychosis. Amphetamines activate the sympathetic nervous system and stimulate adrenergic receptors resulting into central nervous system overstimulation. They induce the mental disorder through its impact on the central nervous system. The basic structure of amphetamine resembles that of norepinephrine, and its pharmacological properties parallel those of endogenous catecholamines. Amphetamines normally act as stimulants of the CNS in which they produce both adrenergic and sympathomimetic agonistic effects (Advokat 2007). Amphetamines, as sympathomimetic amines, stimulate the medullary respiratory centre and the reticular activating system. They cause stimulation of α and β receptors and release of nor-epinephrine and serotonin. These activities lead to increased levels of catecholamines in the synapse. In low levels, amphetamines result into elevated moods, enhanced physical activity, increased heart rate, and slight change in blood pressure. Amphetamines may be administered in either in form of its derivatives such as methamphetamine or amphetamine as the principle element thus bringing similar effects on both the central and peripheral systems. The drug functions through stimulating the release of neurotransmitters such as serotonin, noradrenaline, and dopamine.
Amphetamine may also inhibit the uptake of the three neurotransmitters, which in turn affect the nervous system in different ways. The inhibition process takes place through displacement of neurotransmitter substances from the vesicles as well as facilitating breakdown of the vesicular monoamine transporter (Wang et al. 2010). Amphetamines also function through inhibition of the monoamine oxidase that is responsible for metabolism of the neurotransmitters, and which cause their accumulation in the nervous system. The drug is readily absorbed through the gastrointestinal wall as well as the nasal mucosa responsible for the inhalation administration route.
The effect of amphetamine on the brain of an individual results from its ability to penetrate through the blood brain barrier unlike other forms of substances. The drug substance is further excreted through the urine in its uncharged form as facilitated by the organic cation transport system (Murray 1998). The hallmark of amphetamine-induced psychotic disorder entails the presence of paranoia. Amphetamine-induced psychotic disorder can be distinguished from paranoid schizophrenia by several differentiating characteristics associated with the former, including a predominance of visual hallucinations, hyperactivity, hyper sexuality, confusion, and incoherence as well as some evidence of disordered thinking.
Although positive symptoms of amphetamine-induced psychotic disorder and schizophrenia are similar, amphetamine-induced psychosis generally lacks the effective flattening and alogia of schizophrenia (Marshall & Werb 2009). Clinically, acute amphetamine-induced psychotic disorder can be completely indistinguishable from schizophrenia, and only the resolution of the symptoms in a few days or a positive finding in urine drug screen test eventually reveals the correct diagnosis.
The body system affected by amphetamine toxicity or overdose includes the nervous system, neuromuscular, cardiovascular, respiratory, gastrointestinal, and the ophthalmic systems. The effect of amphetamine on these body organs justifies the symptoms and observations made by the paramedics regarding the patient in the case study.
Differential Diagnosis
The diagnosis to Bruiser resembles other stimulant-induce psychosis as well as schizophrenia. Amphetamine-induced disorder resembles primary mental disorders thereby posing a great challenge in differentiating between amphetamine-induced psychosis and schizophrenia. Intoxication by cocaine, hallucinogens, and PCP present a similar picture and can sometimes be distinguished from amphetamine intoxication only through urine or serum toxicology (Nelson et al. 2010). The health professionals needed to determine all the diagnostics in order to delineate the exact cause of the Bruiser’s condition. However, mydriasis, history of recent drug use, and speed of onset can be limiting factors in the accuracy of the diagnosis. Physicians handling cases associated with amphetamine dependence or abuse should ensure that they distinguish amphetamine abuse from cocaine, PCP, and hallucinogens dependence or abuse (Yui et al. 1999).
Illicit drug urine test provides a confirmatory test for the presence of amphetamine or methamphetamine especially in delineating the cause of stimulant-induced psychosis. In case amphetamine abuse or overdose is suspected as the main cause of the stimulant-induced psychosis, amphetamines should indicate positive on methamphetamine or amphetamine test. Amphetamines can also be detected in stomach contents through a hospital lab test. Since the paramedics in the case involving Bruiser had provided an observational view involving ECG, blood pressure, respiratory rate, among other common diagnostic measures, urinalysis would play an important role in identifying the main cause of the patient’s condition.
Other important diagnostic measures that could resolve the patient’s condition dilemma would include the measure of blood gas or metabolic acidosis. Other differential diagnostic measures would involve determination of other stimulants such as methylxanthines such as caffeine, nicotine, and serotonergic medications, which could also lead to a similar condition or exacerbate the patient’s condition (Murray 1998). Such tests would ensure that the medical practitioners provide the best medical intervention and avoid other detrimental effects that may result from drug combination. Particularly stimulants such as amphetamine and cocaine produce almost similar psychotic states, often with persecutory delusions and disturbed behaviour including aggression hence the need to establish the exact stimulant behind the patient’s condition (Dawe, Geppert, Occhipinti & Kingswell 2004). Since the information provided by the family member implied that Bruiser was not new in the drug abuse realm, the medical practitioners should be able analyse the stimulant or substance behind the patient’s condition. The differential diagnosis would enable the physicians at the hospital level to establish whether the condition is associated with schizophrenia or stimulant-induced psychosis. For conditions indistinguishable from schizophrenia, proper diagnosis can be accomplished after investigation of physical factors especially where the condition is suspected to be triggered by drug misuse and trial of antipsychotic treatment.
Prehospital Intervention
Clinical observations and the patient’s history with heroine and speed led to suspicion of stimulant psychosis that required administration of sedative drugs as the first measure to counter agitation or aggressive. Continued monitoring of the patient was maintained to ensure that he does not develop any further complications before the hospital treatment. Paramedics or people attending to people suffering from amphetamine psychosis are highly discouraged from administering any other medication other than drugs capable of producing sedation. This is ideally because treatment of psychosis that entails high loading of antipsychotics may catalyse bad side effects hence exacerbating the patient’s condition (Moore 2010). The victim required reassurance that the environment they are in or are being transferred to is not harmful in any way as a way of handling the problem of fear associated with the condition. A person under stimulant-induced psychosis lives in a state of fearing being attacked and always ready to defend him or herself. Any unplanned approach to the victim may increase the victim’s state of aggression and agitation, which may culminate into physical injury (Moore 2010). Physical restraint may not work well especially for victims with acute behavioural disturbances because this may cause harm if the disturbances increase. Stimulant use may also be a possible risk factor for sudden death of individuals being physically restrained hence sedation using appropriate drugs provides a humane alternative in that it guarantees safety and humble time for physiological monitoring.
The administration of sedative was then followed by determination of essential body functions such as heart rate, respiratory rate, blood pressure, and BCG are important in ascertaining the condition of unconscious victim before administering any medication to the patient. These observations help in determining the first essential intervention needed to save the life or stabilize the patient before diagnosis of the condition responsible for the unconsciousness. Observations made at the point of accident or emergency play an important role in helping health professionals in diagnosing the patient’s condition at the hospital level. The patient was then prepared carefully and transferred to the ambulance to be taken to hospital.
In assessment of toxicity, clinical observations of potentially toxic signs and symptoms emerge more relevant than estimation of the administered dosage of a drug. Observations may include any possible dilation of the pupils, changes in the colour of the skin, and general appearance such as skin suppleness. While still in the ambulance, paramedics are expected to monitor core temperature as severe hyperthermia may develop, cardiac monitoring, serum electrolytes, renal and hepatic functions. In some instances, rapid cooling is required if the temperature of the patient rises above 41 degrees Celsius, which may be achieved through a cooling shade, application of ice parks to neck, armpit, and groin but under health professional supervision. Some of these steps are evident from the case study of Bruiser in which the paramedics provided several clinical observations to this effect. The paramedics should inform other hospital-based healthcare providers to prepare for admission of the patient possibly through phone calls. The paramedics provided the hospital with all the observation made at the point of the emergency in order for them to prepare for the patient treatment.
After the first treatment, patients showing signs of stimulant intoxication-induced psychosis and aggression should be stabilized in a medically supervised setting for 2-3 days in which antipsychotics and tranquillizers can be administered to reduce the symptoms (Pates & Riley 2009). Treatment of psycho stimulant toxicity demands for prompt supportive care and well supervised use of medication. Individuals attending to victims of psychostimulant toxicity are discouraged from ipecac-induced emesis intervention because a clear role for gastric decontamination after oral intake has not been established (Greene, Kerins & O’Connor 2005). Gastric lavage emerges dangerous due to possible neurological and cardiovascular toxicity and the benefit of activated charcoal remains doubtful.
Treatment of the Amphetamine Psychosis
The general treatment of patients with all psychostimulant-induced psychosis is similar to treatment of acute mania or schizophrenia. The first step in treating victims of psychostimulant-induced psychosis involves creation of an environment that the patient can perceive as safe. Patients with acute agitation or violence may require administration of non-specific rapid sedation in order to control the dangerous behaviour and allow for assessment and management. Researchers have proposed benzodiazepines as a specific agent in circumstances where ongoing antipsychotic medication after acute treatment may not be required. Parenteral midazolam may be effective in controlling agitated or aggressive patients due to the sedative effects on the body system (Mclver 2006).
Antipsychotics such as Haloperidol are also important because of their prompt sedation, ability to cause less hypotension, fewer anticholinergic side effects, and less decrease in threshold compared to other neuroleptics (Shoptaw, Kao & Ling 2008). Other drug derivatives have been introduced into the market such as droperidol with improved properties including high efficacy and easy elimination from the body system. However, some of these agents are still at their clinical trials and much research is still required before their acceptance for hospital use in interventions for this condition. Several pharmacological studies have indicated increased potency in the use of combination regimes such as the combination of benzodiazepines and antipsychotics. Such regimes have proven to be safer and effective options, and indicate that combination of therapies as superior to single-agent regimes. It is worth noting that individuals recovering from psycho stimulants use suffer from a withdrawal syndrome such as crash or a brief period of recovery that last for a few days following binge use. This syndrome has been disregarded from being any significant clinical withdrawal to a mere process of recovery from a period of CNS overstimulation characterized by excessive sleeping, eating, and irritability of mood.
Conclusion
From the clinical observation made by paramedics, description of the patient and the circumstance surrounding the patient’s condition as well as some physical symptoms and literature, Bruiser’s condition can be associated with stimulant-induced psychosis. Amphetamine or speed-induced psychosis is characterized by similar symptoms displayed by the victim including agitation, aggressiveness, incoherence, increased heart rate, changes in respiratory rates, and blood pressure. The circumstance surrounding the incidence in the case scenario also provides support for the possibility that the victim was involved in amphetamine overdose, which could have come from the pharmacy broken into. The differential diagnosis that could easily identify the stimulant responsible for the psychosis includes amphetamine urine test as well as testing other stimulants such as nicotine, cocaine, PCP, and hallucinogens. For amphetamine-induced psychosis, a positive amphetamine or methamphetamine test should be recorded. Prehospital intervention for this condition requires immediate administration of sedatives in case of increased agitation and aggression in order to avoid further physical injury of the victim. Paramedics should also ensure proper recording of clinical observations such as blood pressure, heart rate, respiratory rates, and blood glucose levels among other important physiological indicators before administration of any medication to the patient. Amphetamine- induced psychosis can be treated using different forms of sedative agents and antipsychotic pharmaceutical products.
References
Advokat, C 2007, ‘Update on amphetamine neurotoxicity and its relevance to the treatment of ADHD’, Journal of Attention Disorders, vol 11. no. 1, pp. 8-16.
Batki, S & Harris, D 2004, ‘Quantitative drug levels in stimulant psychosis: relationship to symptoms severity, catecholamines and hyperkinesia’, The American Journal on Addiction, vol.13, pp. 461-470.
Dawe, S, Geppert, L, Occhipinti, S & Kingswell, W 2004, ‘A comparison of the symptoms and short-term clinical course in inpatients with substance- induced psychosis and primary psychosis,’ Journal of Substance Abuse Treatment, vol. 40. no.1, pp.95-101.
Goldman, H 2000, Review of general psychiatry, McGraw-Hill Professional: New York.
Greene, S, Kerins, M & O’Connor, N 2005, ‘Prehospital activated charcoal: the way forward’, Emergency Medicine Journal, vol 22, no.10, pp. 734-737.
Greene, S, Kerr, F & Braitberge, G 2008, ‘Review article: amphetamines and related drugs of abuse’, Emergency Medicine Australasia, vol. 20, pp. 391-402.
Marshall, D & Werb, D 2009, ‘Health outcomes associated with methamphetamine use among young people: a systematic review’, Society for the Study of Addiction, vol. 105, pp. 991- 1002.
Mclver, C, McGregor, C, Baigent, M, Spain, D, Newcombe, D & Ali, R 2006, ‘Guidelines for the medical management of patient with methamphetamine- induced psychosis’, Government of South Australia, viewed 4 October, 2011, from:
Moore, E 2010, The amphetamine debate: the use of adderall, ritalin and related drugs for behavior modification, neuroenhancement and anti-aging purposes, McFarland: North Carolina.
Murray, J 1998, ‘Psychophysiological aspect of amphetamine-methamphetamine abuse’, The Journal of Phychology, vol 132. no. 2, pp. 227-237.
Nelson, L, Lewin, N, Howland, M.A, Hoffman, R, Goldfrank, L, Flomenbaum, N 2010, Goldfrank's Toxicologic Emergencies, 9th edn, McGraw: New York.
Pates, R & Riley, D 2009, Intervention for amphetamine misuse, John Wiley and Sons: Hoboken.
Shoptaw, S, Kao, U & Ling, W 2008, ‘Treatment for amphetamine psychosis’, Cochrane Database of Systematic Reviews, vol. 4, pp.2-7.
Wang, Pei, L, Fletcher, P.J, Kapur, S, Seeman, P & Liu, F 2010, ‘Schizophrenia-induced sensitized state and acute amphetamine exposure all show a common alteration: increased dopamine D2 receptor dimerization’, Molecular Brain, vol 3, pp. 25.
Yui, K, Goto, K, Ikemoto, S, Ishiguro, T, Angrist, B, Duncan, G.E, Sheitman, B.B, Lieberman, J.A, Bracha, S.H & Ali, S.F 1999, ‘Neurobiological basis of relapse prediction in stimulant-induced psychosis and schizophrenia: the role of sensitization’, Molecular Psychiatry, vol. 4, pp. 512-523.
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