Lakhasly

Clinical Significance

Hyperthermic syndromes caused by medications include serotonin syndrome, neuroleptic malignant syndrome, anticholinergic toxidrome, and malignant hyperthermia.Excess T4 and T3 lead to an increased basal metabolic rate, thus increasing the body temperature, ATP turnover, and oxygen consumption.Clinical Significance

Hyperthermic syndromes caused by medications include serotonin syndrome, neuroleptic malignant syndrome, anticholinergic toxidrome, and malignant hyperthermia.Excess T4 and T3 lead to an increased basal metabolic rate, thus increasing the body temperature, ATP turnover, and oxygen consumption.Malignant Hyperthermia (MH) occurs due to a genetic alteration of ryanodine receptor 1 (RYR1) in the muscle cells, leading to skeletal muscle hypermetabolism upon exposure to depolarizing muscle relaxants (succinylcholine), halogenated anesthetics (halothane, isoflurane, desflurane, enflurane, ether, or sevoflurane), or, rarely, excessive heat or vigorous exercise.Malignant Hyperthermia (MH) occurs due to a genetic alteration of ryanodine receptor 1 (RYR1) in the muscle cells, leading to skeletal muscle hypermetabolism upon exposure to depolarizing muscle relaxants (succinylcholine), halogenated anesthetics (halothane, isoflurane, desflurane, enflurane, ether, or sevoflurane), or, rarely, excessive heat or vigorous exercise.Anticholinergic toxidrome is caused by ingesting medications with anticholinergic properties, including antihistamines, antidepressants, Parkinson drugs, mydriatics, antispasmodics, and antipsychotics.Anticholinergic toxidrome is caused by ingesting medications with anticholinergic properties, including antihistamines, antidepressants, Parkinson drugs, mydriatics, antispasmodics, and antipsychotics.Neuroleptic Malignant Syndrome (NMS) develops from using neuroleptics (dopamine antagonists), with signs and symptoms typically occurring within the first few weeks of treatment.Physical exam findings include hyperthermia, flushing, anhidrosis, dry mucous membranes, mydriasis, urinary retention, and altered mental status.In MH, once a cell depolarizes, the defective RYR1 becomes hyperactivated, causing excessive calcium release, inappropriate muscle contraction, and increased metabolic rate, all leading to excessive heat production.Neuroleptic Malignant Syndrome (NMS) develops from using neuroleptics (dopamine antagonists), with signs and symptoms typically occurring within the first few weeks of treatment.Physical exam findings include hyperthermia, flushing, anhidrosis, dry mucous membranes, mydriasis, urinary retention, and altered mental status.In MH, once a cell depolarizes, the defective RYR1 becomes hyperactivated, causing excessive calcium release, inappropriate muscle contraction, and increased metabolic rate, all leading to excessive heat production.Treatment includes stopping the offending drug, cooling methods, and administering cyproheptadine, a 5HT-2 receptor antagonist.Treatment includes stopping the offending drug, cooling methods, and administering cyproheptadine, a 5HT-2 receptor antagonist.Carbonic anhydrase inhibitors, such as acetazolamide and topiramate, can cause transient hypohidrosis and lead to heat intolerance, especially in children.An overactive thyroid gland releases excess T4 and T3, hormones that affect the basal metabolic rate of cells.

Clinical Significance

Hyperthermic syndromes caused by medications include serotonin syndrome, neuroleptic malignant syndrome, anticholinergic toxidrome, and malignant hyperthermia.

Serotonin syndrome develops from the use of serotonergic antidepressants, and it is typically seen within 24 hours of starting or changing therapy. Physical exam findings include hyperthermia, hyperreflexia, and myoclonus. Treatment includes stopping the offending drug, cooling methods, and administering cyproheptadine, a 5HT-2 receptor antagonist.

Neuroleptic Malignant Syndrome (NMS) develops from using neuroleptics (dopamine antagonists), with signs and symptoms typically occurring within the first few weeks of treatment.
Physical exam findings include hyperthermia, lead pipe rigidity, and hyporeflexia. Treatment includes stopping the offending drug, cooling methods, and administering a D2 agonist (bromocriptine).

Anticholinergic toxidrome is caused by ingesting medications with anticholinergic properties, including antihistamines, antidepressants, Parkinson drugs, mydriatics, antispasmodics, and antipsychotics. Physical exam findings include hyperthermia, flushing, anhidrosis, dry mucous membranes, mydriasis, urinary retention, and altered mental status. Treatment is generally supportive and symptom-specific, with the administration of physostigmine utilized for severe toxicity.

Malignant Hyperthermia (MH) occurs due to a genetic alteration of ryanodine receptor 1 (RYR1) in the muscle cells, leading to skeletal muscle hypermetabolism upon exposure to depolarizing muscle relaxants (succinylcholine), halogenated anesthetics (halothane, isoflurane, desflurane, enflurane, ether, or sevoflurane), or, rarely, excessive heat or vigorous exercise.

In MH, once a cell depolarizes, the defective RYR1 becomes hyperactivated, causing excessive calcium release, inappropriate muscle contraction, and increased metabolic rate, all leading to excessive heat production. The treatment of MH is to stop the offending drug and immediately administer dantrolene, a postsynaptic muscle relaxant. Rapidly cooling the patient, giving 100% oxygen, and regulating metabolic acidosis are also important.

Additionally, some medications can inhibit sweating and increase the risk of thermoregulatory dysfunction. Carbonic anhydrase inhibitors, such as acetazolamide and topiramate, can cause transient hypohidrosis and lead to heat intolerance, especially in children. M3 anticholinergic agents such as bladder antispasmodics, tricyclic antidepressants, and neuroleptics can also lead to heat intolerance.

Drugs such as salicylate and methyl salicylate can cause hyperthermia by uncoupling oxidative phosphorylation. Lastly, the recreational use of psychomotor stimulants is known to frequently cause hyperthermia. These drugs include amphetamine, methamphetamine, cocaine, heroin, and 3,4-methylenedioxy-methamphetamine, also known as MDMA or ecstasy.

Hyperthyroidism is a condition of an overactive thyroid gland that can lead to altered thermoregulation. An overactive thyroid gland releases excess T4 and T3, hormones that affect the basal metabolic rate of cells. Excess T4 and T3 lead to an increased basal metabolic rate, thus increasing the body temperature, ATP turnover, and oxygen consumption.Clinical Significance

Hyperthermic syndromes caused by medications include serotonin syndrome, neuroleptic malignant syndrome, anticholinergic toxidrome, and malignant hyperthermia.

Serotonin syndrome develops from the use of serotonergic antidepressants, and it is typically seen within 24 hours of starting or changing therapy. Physical exam findings include hyperthermia, hyperreflexia, and myoclonus. Treatment includes stopping the offending drug, cooling methods, and administering cyproheptadine, a 5HT-2 receptor antagonist.

Neuroleptic Malignant Syndrome (NMS) develops from using neuroleptics (dopamine antagonists), with signs and symptoms typically occurring within the first few weeks of treatment.
Physical exam findings include hyperthermia, lead pipe rigidity, and hyporeflexia. Treatment includes stopping the offending drug, cooling methods, and administering a D2 agonist (bromocriptine).

Anticholinergic toxidrome is caused by ingesting medications with anticholinergic properties, including antihistamines, antidepressants, Parkinson drugs, mydriatics, antispasmodics, and antipsychotics. Physical exam findings include hyperthermia, flushing, anhidrosis, dry mucous membranes, mydriasis, urinary retention, and altered mental status. Treatment is generally supportive and symptom-specific, with the administration of physostigmine utilized for severe toxicity.

Malignant Hyperthermia (MH) occurs due to a genetic alteration of ryanodine receptor 1 (RYR1) in the muscle cells, leading to skeletal muscle hypermetabolism upon exposure to depolarizing muscle relaxants (succinylcholine), halogenated anesthetics (halothane, isoflurane, desflurane, enflurane, ether, or sevoflurane), or, rarely, excessive heat or vigorous exercise.

In MH, once a cell depolarizes, the defective RYR1 becomes hyperactivated, causing excessive calcium release, inappropriate muscle contraction, and increased metabolic rate, all leading to excessive heat production. The treatment of MH is to stop the offending drug and immediately administer dantrolene, a postsynaptic muscle relaxant. Rapidly cooling the patient, giving 100% oxygen, and regulating metabolic acidosis are also important.

Additionally, some medications can inhibit sweating and increase the risk of thermoregulatory dysfunction. Carbonic anhydrase inhibitors, such as acetazolamide and topiramate, can cause transient hypohidrosis and lead to heat intolerance, especially in children. M3 anticholinergic agents such as bladder antispasmodics, tricyclic antidepressants, and neuroleptics can also lead to heat intolerance.

Drugs such as salicylate and methyl salicylate can cause hyperthermia by uncoupling oxidative phosphorylation. Lastly, the recreational use of psychomotor stimulants is known to frequently cause hyperthermia. These drugs include amphetamine, methamphetamine, cocaine, heroin, and 3,4-methylenedioxy-methamphetamine, also known as MDMA or ecstasy.

Hyperthyroidism is a condition of an overactive thyroid gland that can lead to altered thermoregulation. An overactive thyroid gland releases excess T4 and T3, hormones that affect the basal metabolic rate of cells. Excess T4 and T3 lead to an increased basal metabolic rate, thus increasing the body temperature, ATP turnover, and oxygen consumption.