Based on Trevor’s symptomology, he is currently experiencing neuroleptic malignant syndrome that is an adverse reaction to anti-psychotic medications and anti-depressant medications (Benzer, 256). Trevor is currently unconscious thus; describing an adverse reaction to the medications he currently has taken copious amounts of (Benzer, 256). From a pathophysiological standpoint, there is a decreased amount of dopamine receptors, due to an initial blockade, and a decreased performance from the dopamine receptor D2 (Benzer, 256). With the initial decrease performance in the dopamine receptors, there is an adverse reaction with glutamate (Benzer, 257). Glutamate is released more frequently causing catonia subsequently, causing neurotoxicity and
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The symptomology is characterized by delirious thoughts, agitation, acidosis, and also a life threat of hyper adrenergic autonomic dysfunction (Chan, 352). Current studies show the symptomology shows that excited delirium is caused by a deregulated dopamine transportation method by specific sympathomimetic (Davis, 5). With the dysfunctional regulation of dopamine, the transportation system leads to an increased amount of dopamine to be released at the synaptic cleft (Davis, 5). Within the hypothalamus, dopamine receptors are responsible for overall thermo regulation, thus, causing a rapid increase in overall body temperature (Davis, 5). Based on Trevor’s symptomology, hyper dopaminergic release will result in hyperthermia and a dysfunctional hypothalamus, subsequently causing an excessive release of catecholamine’s to be released and furthering acute stress on the heart, causing cardiomyopathy (Davis, …show more content…
With excessive agitation, strenuous activity, and possible sympathomimetic use, Trevor’s skeletal muscles are at risk of developing atrophy and the release of toxic intracellular contents that will eventually enter the circulatory system (Mohr, 234). From a pathophysiological standpoint, the result of rhabdomyolosis is the affect on sodium, calcium, potassium, and myoglobin (Mohr, 234). Firstly, sodium will flow freely through the cell membrane, causing oedema to muscle cells, posing a threat to Trevor by causing intravascular hypovolemia (Mohr, 234). With the affect on calcium, destruction of the cell membrane will cause calcium to damage the electrical gradient and cause serum hypocalcaemia, thus leading to deposits of calcium to be release into renal and muscle tissues and cause a lactic acidosis (Mohr, 234). When those ions become affected, potassium is then affected by the decrease in overall membrane integrity, thus causing the resting membrane potential to become prolonged and cause ventricular irritability (Mohr, 234). When the muscle starts to catabolize, myoglobin is released and blocks the tubules in the kidney (Mohr, 235). Based on muscle catabolization and myoglobin being released, nephrotoxicity occurs causing kidney failure and hyperkalemia (Mohr, 235). Therefore, with significant changes due different intracellular ions, Trevor is at risk for kidney
The symptomology is characterized by delirious thoughts, agitation, acidosis, and also a life threat of hyper adrenergic autonomic dysfunction (Chan, 352). Current studies show the symptomology shows that excited delirium is caused by a deregulated dopamine transportation method by specific sympathomimetic (Davis, 5). With the dysfunctional regulation of dopamine, the transportation system leads to an increased amount of dopamine to be released at the synaptic cleft (Davis, 5). Within the hypothalamus, dopamine receptors are responsible for overall thermo regulation, thus, causing a rapid increase in overall body temperature (Davis, 5). Based on Trevor’s symptomology, hyper dopaminergic release will result in hyperthermia and a dysfunctional hypothalamus, subsequently causing an excessive release of catecholamine’s to be released and furthering acute stress on the heart, causing cardiomyopathy (Davis, …show more content…
With excessive agitation, strenuous activity, and possible sympathomimetic use, Trevor’s skeletal muscles are at risk of developing atrophy and the release of toxic intracellular contents that will eventually enter the circulatory system (Mohr, 234). From a pathophysiological standpoint, the result of rhabdomyolosis is the affect on sodium, calcium, potassium, and myoglobin (Mohr, 234). Firstly, sodium will flow freely through the cell membrane, causing oedema to muscle cells, posing a threat to Trevor by causing intravascular hypovolemia (Mohr, 234). With the affect on calcium, destruction of the cell membrane will cause calcium to damage the electrical gradient and cause serum hypocalcaemia, thus leading to deposits of calcium to be release into renal and muscle tissues and cause a lactic acidosis (Mohr, 234). When those ions become affected, potassium is then affected by the decrease in overall membrane integrity, thus causing the resting membrane potential to become prolonged and cause ventricular irritability (Mohr, 234). When the muscle starts to catabolize, myoglobin is released and blocks the tubules in the kidney (Mohr, 235). Based on muscle catabolization and myoglobin being released, nephrotoxicity occurs causing kidney failure and hyperkalemia (Mohr, 235). Therefore, with significant changes due different intracellular ions, Trevor is at risk for kidney