Hyperthermic reaction is a typical form of body heat balance disorder. The central link of pathogenesis is a temporary elevation of body temperature above the physiological norm, which occurs due to a transient predominance of heat production processes over heat loss mechanisms. A crucial characteristic of this condition is that, unlike fever, the body's own thermoregulatory mechanisms remain fully intact and continue to function.
Essence of the processTemporary predominance of heat production over heat loss with preserved thermoregulation
ClassificationBy origin, reactions are divided into endogenous, exogenous, and combined
Frequent triggersPainful stimulation, severe psychoemotional stress, or administration of certain drugs
Cellular mechanismUncoupling of tissue oxidation and phosphorylation processes
Classification and Endogenous Causes
According to their origin (etiology), all hyperthermic reactions are divided into three major groups: endogenous, exogenous, and combined. Endogenous disorders develop under the influence of internal factors and are subdivided into several types:
Psychogenic. They occur against the background of significant psychoemotional stress. Classic examples include stress reactions in students during exams or when solving vital problems. They also accompany mental disorders (e.g., hysteria) and various neurotic states. The main development mechanism is the powerful activation of the sympathoadrenal system.
Endocrine. Based on the activation of exothermic metabolic processes. The most frequent causes are catecholamine hyperproduction (observed in pheochromocytoma) and excess thyroid hormones (in hyperthyroid states). An important role here is played by the formation of specific substances—uncouplers of cellular oxidation and phosphorylation processes.
Neurogenic Hyperthermic Reactions
Neurogenic disorders belong to the endogenous group and are structurally divided into centrogenic and reflexogenic.
Centrogenic. They develop upon direct irritation of neurons in the thermoregulation center (primarily the department responsible for heat production), as well as associated zones of the cerebral cortex and brainstem. Etiological factors include hemorrhages, mechanical trauma, growing tumors, and aneurysms in these areas. The leading mechanism involves sequential activation of hypothalamic neurons, the sympathetic nervous system, neurosecretory cells (synthesizing thyrotropin-releasing hormone), and adenohypophysis cells producing thyroid-stimulating hormone (TSH).
Reflexogenic. They occur in response to strong, typically painful stimulation of various organs and tissues. The main cause is exposure to reflexogenic zones. This happens during irritation of the hepatic bile ducts, renal pelvicalyceal system, and urinary tract (e.g., during stone passage). Endoscopic manipulations also serve as triggers: gastroscopy, colonoscopy, laparoscopy, and cystoscopy. Pathogenesis is driven by the activation of the sympathoadrenal and thyroid systems, leading to metabolism intensification and increased heat generation.
Exogenous Hyperthermic Reactions
Exogenous reactions are provoked by environmental factors and are subdivided into drug-induced and non-drug-induced.
Drug-induced. They occur upon administration of medications with adverse thermogenic effects. The main groups of such drugs include catecholamine-based agents, caffeine, ephedrine, L-DOPA, and thyroid hormones. In addition, the reaction is caused by oxidation and phosphorylation uncouplers containing calcium ions, non-esterified fatty acids (NEFA), and oligomycin.
Non-drug-induced. Caused by chemical substances with pronounced thermogenic action. Etiology includes research purposes (animal experiments), accidental toxin ingestion, or occupational safety violations. Examples of such substances include 2,4-dinitrophenol, cyanides, and amobarbital. The mechanism of their action consists in activating the sympathoadrenal and thyroid systems with subsequent uncoupling of tissue respiration processes.
Mnemonic
To quickly recall the types of endogenous reactions, use the abbreviation PEN: Psychogenic, Endocrine, Neurogenic.
Frequently asked questions
What stages are distinguished in the pathogenesis of a hyperthermic reaction (hyperthermia)?
Two main stages are distinguished in the pathogenesis of hyperthermia:
Compensation stage — adaptation stage.
Decompensation stage — maladaptation of thermoregulation mechanisms.
Hyperthermic coma — the final stage, sometimes highlighted.
For a hyperthermic reaction, sources indicate: temporary elevation of body temperature above the norm due to transient predominance of heat production over heat loss; thermoregulation mechanisms remain preserved.
How does a hyperthermic reaction fundamentally differ from fever regarding the set-point mechanism?
The fundamental difference according to sources lies in the mechanism of temperature elevation.
Criterion
Fever
Hyperthermic Reaction
Mechanism
Temporary dynamic restructuring of the thermoregulation system with a shift of the 'set point' to a higher level
Temporary elevation of body temperature above the norm due to transient predominance of heat production over heat loss; thermoregulation mechanisms remain preserved
Formulations about 'breakdown of the thermoregulation mechanism itself' for hyperthermic reaction are not supported by sources.
Do thermoregulatory mechanisms remain intact during a hyperthermic reaction?
Yes, during a hyperthermic reaction (just as in fever), the physiological mechanisms of thermoregulation remain fully intact; only a temporary imbalance between heat production and heat loss occurs.
Why can body temperature rise during renal colic or passing kidney stones?
Severe painful irritation of the renal pelvis triggers a reflexogenic hyperthermic reaction. Pain stimulates the sympathoadrenal and thyroid systems, sharply accelerating metabolism and heat production.
Which drugs most commonly produce an adverse thermogenic effect?
Catecholamine preparations, thyroid hormones, ephedrine, caffeine, and L-DOPA can lead to temperature elevation because they accelerate metabolism and stimulate exothermic processes.
Go deeper
Topography of the thermoregulation center in the hypothalamus and associated zones of the cerebral cortex and brainstem.
Biochemical mechanism of uncoupling of oxidation and phosphorylation processes.
Role of thyrotropin-releasing hormone and TSH in the pathogenesis of centrogenic heat balance disorders.
Pathogenesis of sympathoadrenal system activation during psychoemotional stress and pain syndrome.
Effect of non-esterified fatty acids, oligomycin, and cyanides on cellular respiration.