STUDY - Technical - New Dacian's Medicine
Fever
and hyperthermia (1)
Translation Draft
Here comes the time for a new sign of disease, fever and all the associated manifestations.
Fever is an increase in body temperature exceeding the normal circadian range as a result of a change in the center of thermoregulation, located in the anterior hypothalamus. A normal body temperature is usually maintained, despite environmental variations, by the ability of the thermoregulation center to balance the heat production of tissues (especially the muscle and liver) with heat loss.
In the case of fever, the balance is shifted in the direction of the central temperature increase. Hyperthermia is an increase in body temperature above the hypothalamic threshold due to insufficient heat dissipation (e.g. in combination with exercise, sweat-inhibiting drugs or a very hot environment).
While the "normal" temperature in humans is considered to be 37 degrees Celsius (98.6 degrees Fahrenheit) based on Wunderlich's original observations, long ago, the overall average oral temperature of healthy individuals aged 18 to 40 years (which is actually 36.8 +/- 0.4 degrees Celsius or 98.2 +/- 0.7 degrees Fahrenheit, with a lower limit at 6 o'clock and an upper limit between 16 and 18).
The maximum normal oral temperature at 6 o'clock is 37.2 degrees Celsius (98.9 degrees Fahrenheit) and the maximum normal oral temperature at 6 o'clock is 37.7 degrees Celsius (99.9 degrees Fahrenheit), both of which define 99% of normal individuals. Given these criteria, a temperature measured in the morning, greater than 37.2 degrees Celsius (98.9 degrees Fahrenheit) or a temperature measured in the afternoon, greater than 37.7 degrees Celsius (99.9 degrees Fahrenheit) will define a fever.
Rectal temperatures are generally higher by 0.6 degrees Celsius (1 degree Fahrenheit). Temperatures in the lower esophagus closely reflect the central temperature. The temperature of a recently collected urine sample is close to rectal values. The normal 24-hour circadian temperature rate is associated with temperatures typically ranging from 0.5 degrees Celsius (0.9 degrees Fahrenheit) and sometimes even one degree Celsius, between the minimum morning and the maximum in the afternoon.
This aspect of morning minimum and maximum towards evening is usually preserved in febrile diseases, but not in hyperthermia. In women with menstruation, the morning temperature is generally lower in the 2 weeks preceding ovulation, increasing by about 0.6 degrees Celsius (a degree Fahrenheit) in ovulation and remaining at this level until menstruation occurs.
In addition, there may be a seasonal variation in body temperature. Finally, physiological factors such as postprandial status, pregnancy, endocrine changes and age can influence basal temperatures.
Pyrogens are substances that cause fever and can be either exogenous or endogenous. Exogenous pyrogens come from outside the host, while endogenous pyrogens are produced by the host, generally in response to provocative stimuli, which are usually triggered by infection or inflammation.
Most exogenous pirogens are microorganisms, their products or toxins. The best known type of external pyrogen consists of a heterogeneous group of molecules that is common to all gram-negative bacteria and which is called endotoxin (lipopolysaccharide, LPZ - in vivo, a minimum amount of 1 nanogram/ kilogram body is capable of producing fever in humans).
Gram-positive microorganisms are also sources of powerful pyrogens. These include lipoprotein acid, derived from the cell wall, and peptidoglicans. Several exo and endotoxins produced by pathological strains of streptococci and staphylococci behave as bacterial superantigens, attracting through lymphocytic T processes, release of mediators and tissue damage. These toxins are thought to contribute to both staphylococcal and streptococcal shock.
In general, exogenous pyrogens act mainly by inducing the formation of endogenous pyrogens on the way to stimulating host cells, usually monocytes and macrophages. However, the distinction between exogenous and endogenous pyrogens is sometimes unclear.
For example, LPZ can act directly on endothelial cells in the brain to generate fever, while many exogenous products lead to the release of endogenous pyrogens, thus producing fever. Such endogenous substances include antigen-antibody complexes with complement, complement splitting products, steroid hormone metabolites, bile acids and some cytokines.
Endogenous pyrogens are polypeptides produced by a variety of host cells, especially monocytes/ macrophages. Endogenous pyrogens, produced either systemically or locally, enter circulation and produce fever by action at the center of thermoregulation in the hypothalamus.
Body temperature is controlled by the hypothalamus. Neurons, both from the anterior preoptic hypothalamus and the posterior hypothalamus, receive two types of signals, one from the peripheral nerves, which represent the receptors for hot or cold and the other from the blood temperature that irrigates the area.
These two signals are integrated by the center of thermoregulation in the hypothalamus in order to maintain normal temperature. In a neutral environment, people's metabolic rate produces considerably more heat than is needed to keep the central body temperature at 37 degrees Celsius.
Therefore, the hypothalamus controls the temperature through the mechanisms of heat loss. Groups of neurons in the preoptic/anterior hypothalamus are irrigated by a rich and permeable vascular network with a limited function of the blood-brain barrier. The specialized vascular network is called "organum vasculosum laminae terminalis".
Endothelial cells of this network are likely to release metabolites of arachidonic acid when exposed to endogenous pyrogen cytokines in circulation (I would continue the description of the process but the term "probably" is often used). The fact is that when a higher "new thermostat value" appears, the signals go to various eferential nerves, especially those sympathetic fibers that irritate the peripheral blood vessels, which in turn initiate vasoconstriction and contribute to the preservation of heat.
The center of thermoregulation also sends signals to the cerebral cortex initiating behavioral changes such as looking for a warm environment, dressing more thick clothes or special postures. With the shearing of blood circulation from the periphery and these behavioral changes, the body temperature usually increases by 2 to 3 degrees Celsius, and if the hypothalamus requires more heat, the tremor (involuntary muscle contractions) is triggered to increase heat production.
The combination of heat conservation with increased heat production continues until the blood temperature that irrigates neurons in the anterior hypothalamus coincides with the "new adjustment threshold". At that point, the hypothalamus maintains the new temperature feverish. The hypothalamic adjustment threshold decreases with the disappearance of stimulating pyrogen cytokines or with inhibition of local prostaglandin synthesis by cycloxigenase inhibitors such as aspirin and ibuprofen.
Reduction of fever with acetaminophen involves the metabolism of the drug by cytochromes in the brain and subsequent inhibition of cyclooxygenase in the brain by metabolites. vasodilation and sweat dissipate heat from the skin through radiation and conduction. Behavioural changes can be triggered, such as removing thick clothing or mobilizing from the bed.
There are also antipyretic endogenous substances such as arginin-vasopressin, adenocorticotropin, etc., each of them seeming to alter the amount of endogenous pyrogens to stimulate the production of prostagrandins. Specific cytokine antagonists and inhibitorcy cytokines may play a role in fever modulation. And the description of all kinds of agents could continue...
From an evolutionary perspective, the phenomenon of fever exists from the first vertebrates, being present in fish, amphibians, reptiles and mammals. In many situations, increasing body temperature improves survival through some kind of fever therapy.
The growth and virulence of several bacterial species is affected at high temperatures, so fever therapy was, for example, used to treat neurosyphilis before the period of antibiotic introduction. similarly, type III pneumococcus have a particular sensitivity to high temperatures and at 41 degrees Celsius they grow slowly and can autolyse.
On the other hand, the temperature values of the febrile beach seem to increase the phagocytic and bactericidal activity of neutrophils and the cytotoxic effects of lymphocytes, thus probably the fever increases the ability to survive an infection.
However, fever involves numerous costs of the host, in addition to discomfort. For each one degree Celsius increase in body temperature, there is an increase in oxygen consumption by 13% and increased caloric and liquid needs. increased metabolic needs may affect the fetuses during pregnancy (a single episode of fever in the first trimester of pregnancy doubling the risk of neural tube defects in the fetus), as well as patients with borderline damage to cardiac or cerebral circulation.
Accelerating muscle catabolism leads to a decrease in body weight and a negative nitrogen balance. Essentially, skeletal muscle is used as an energy source, with the release of amino acids for gluconeogenesis and for the synthesis of acute phase proteins and the formation of immune cell clones. Fever reduces mental acuity and can cause delirium or stupor. Children are at increased risk of having seizures during fever, especially if there is a history of such seizures.
As expected, many of the symptoms associated with fever, including dorsolumbar pain, generalized myalgia, arthralgia, anorexia and drowsiness, can be reduced by infusions of purified cytokines. These symptoms can be improved by cyclooxygenase inhibitors.
Chills, a feeling of cold that occurs during most febrile states, are part of the central nervous system (CNS) response to the thermoregulation "threshold", which requires more heat. Rigor, a deep, pieloerection ("chicken skin"), associated with tooth clattering and severe tremor, is common in bacterial infections, rickettsii and protozoa infections and influenza (but not in other viral infections).
Septic states, systemic infections such as leptospirosis, brucellosis, rat bite fever, endocarditis, malaria and intermittent septic state observed in abscesses can produce rigor, as well as lymphomas, renal cell carcinoma and hepatoma. Rigor is also common in drug-induced fevers.
Sweating occurs by activating heat loss mechanisms, antipyretic treatment, touching the new "thermal ceiling" or eliminating the feverish stimulus. Intermittent administration of antipyretics may exaggerate temperature swings, causing coldness, discomfort and exhaustion. Hypothalamic reflexes trigger perspiration, allowing rapid dissipation of heat by evaporation.
Changes in mental status and seizures are common in very young and very old patients and patients with dementia, liver failure and chronic kidney failure. Progression from irritability to delirium and frank obnubilation usually disappears with fever failure.
Seizures typically occur in infants and febrile children under 5 years of age, especially at the onset of a febrile disease and at temperatures higher than 40 degrees Celsius. Febrile seizures in children are not necessarily a sign of significant brain disease, but an CNS disease should be excluded in these cases. Fever can also precipitate seizures in adult epileptic patients.
Here comes the time for a new sign of disease, fever and all the associated manifestations.
Fever is an increase in body temperature exceeding the normal circadian range as a result of a change in the center of thermoregulation, located in the anterior hypothalamus. A normal body temperature is usually maintained, despite environmental variations, by the ability of the thermoregulation center to balance the heat production of tissues (especially the muscle and liver) with heat loss.
In the case of fever, the balance is shifted in the direction of the central temperature increase. Hyperthermia is an increase in body temperature above the hypothalamic threshold due to insufficient heat dissipation (e.g. in combination with exercise, sweat-inhibiting drugs or a very hot environment).
While the "normal" temperature in humans is considered to be 37 degrees Celsius (98.6 degrees Fahrenheit) based on Wunderlich's original observations, long ago, the overall average oral temperature of healthy individuals aged 18 to 40 years (which is actually 36.8 +/- 0.4 degrees Celsius or 98.2 +/- 0.7 degrees Fahrenheit, with a lower limit at 6 o'clock and an upper limit between 16 and 18).
The maximum normal oral temperature at 6 o'clock is 37.2 degrees Celsius (98.9 degrees Fahrenheit) and the maximum normal oral temperature at 6 o'clock is 37.7 degrees Celsius (99.9 degrees Fahrenheit), both of which define 99% of normal individuals. Given these criteria, a temperature measured in the morning, greater than 37.2 degrees Celsius (98.9 degrees Fahrenheit) or a temperature measured in the afternoon, greater than 37.7 degrees Celsius (99.9 degrees Fahrenheit) will define a fever.
Rectal temperatures are generally higher by 0.6 degrees Celsius (1 degree Fahrenheit). Temperatures in the lower esophagus closely reflect the central temperature. The temperature of a recently collected urine sample is close to rectal values. The normal 24-hour circadian temperature rate is associated with temperatures typically ranging from 0.5 degrees Celsius (0.9 degrees Fahrenheit) and sometimes even one degree Celsius, between the minimum morning and the maximum in the afternoon.
This aspect of morning minimum and maximum towards evening is usually preserved in febrile diseases, but not in hyperthermia. In women with menstruation, the morning temperature is generally lower in the 2 weeks preceding ovulation, increasing by about 0.6 degrees Celsius (a degree Fahrenheit) in ovulation and remaining at this level until menstruation occurs.
In addition, there may be a seasonal variation in body temperature. Finally, physiological factors such as postprandial status, pregnancy, endocrine changes and age can influence basal temperatures.
Pyrogens are substances that cause fever and can be either exogenous or endogenous. Exogenous pyrogens come from outside the host, while endogenous pyrogens are produced by the host, generally in response to provocative stimuli, which are usually triggered by infection or inflammation.
Most exogenous pirogens are microorganisms, their products or toxins. The best known type of external pyrogen consists of a heterogeneous group of molecules that is common to all gram-negative bacteria and which is called endotoxin (lipopolysaccharide, LPZ - in vivo, a minimum amount of 1 nanogram/ kilogram body is capable of producing fever in humans).
Gram-positive microorganisms are also sources of powerful pyrogens. These include lipoprotein acid, derived from the cell wall, and peptidoglicans. Several exo and endotoxins produced by pathological strains of streptococci and staphylococci behave as bacterial superantigens, attracting through lymphocytic T processes, release of mediators and tissue damage. These toxins are thought to contribute to both staphylococcal and streptococcal shock.
In general, exogenous pyrogens act mainly by inducing the formation of endogenous pyrogens on the way to stimulating host cells, usually monocytes and macrophages. However, the distinction between exogenous and endogenous pyrogens is sometimes unclear.
For example, LPZ can act directly on endothelial cells in the brain to generate fever, while many exogenous products lead to the release of endogenous pyrogens, thus producing fever. Such endogenous substances include antigen-antibody complexes with complement, complement splitting products, steroid hormone metabolites, bile acids and some cytokines.
Endogenous pyrogens are polypeptides produced by a variety of host cells, especially monocytes/ macrophages. Endogenous pyrogens, produced either systemically or locally, enter circulation and produce fever by action at the center of thermoregulation in the hypothalamus.
Body temperature is controlled by the hypothalamus. Neurons, both from the anterior preoptic hypothalamus and the posterior hypothalamus, receive two types of signals, one from the peripheral nerves, which represent the receptors for hot or cold and the other from the blood temperature that irrigates the area.
These two signals are integrated by the center of thermoregulation in the hypothalamus in order to maintain normal temperature. In a neutral environment, people's metabolic rate produces considerably more heat than is needed to keep the central body temperature at 37 degrees Celsius.
Therefore, the hypothalamus controls the temperature through the mechanisms of heat loss. Groups of neurons in the preoptic/anterior hypothalamus are irrigated by a rich and permeable vascular network with a limited function of the blood-brain barrier. The specialized vascular network is called "organum vasculosum laminae terminalis".
Endothelial cells of this network are likely to release metabolites of arachidonic acid when exposed to endogenous pyrogen cytokines in circulation (I would continue the description of the process but the term "probably" is often used). The fact is that when a higher "new thermostat value" appears, the signals go to various eferential nerves, especially those sympathetic fibers that irritate the peripheral blood vessels, which in turn initiate vasoconstriction and contribute to the preservation of heat.
The center of thermoregulation also sends signals to the cerebral cortex initiating behavioral changes such as looking for a warm environment, dressing more thick clothes or special postures. With the shearing of blood circulation from the periphery and these behavioral changes, the body temperature usually increases by 2 to 3 degrees Celsius, and if the hypothalamus requires more heat, the tremor (involuntary muscle contractions) is triggered to increase heat production.
The combination of heat conservation with increased heat production continues until the blood temperature that irrigates neurons in the anterior hypothalamus coincides with the "new adjustment threshold". At that point, the hypothalamus maintains the new temperature feverish. The hypothalamic adjustment threshold decreases with the disappearance of stimulating pyrogen cytokines or with inhibition of local prostaglandin synthesis by cycloxigenase inhibitors such as aspirin and ibuprofen.
Reduction of fever with acetaminophen involves the metabolism of the drug by cytochromes in the brain and subsequent inhibition of cyclooxygenase in the brain by metabolites. vasodilation and sweat dissipate heat from the skin through radiation and conduction. Behavioural changes can be triggered, such as removing thick clothing or mobilizing from the bed.
There are also antipyretic endogenous substances such as arginin-vasopressin, adenocorticotropin, etc., each of them seeming to alter the amount of endogenous pyrogens to stimulate the production of prostagrandins. Specific cytokine antagonists and inhibitorcy cytokines may play a role in fever modulation. And the description of all kinds of agents could continue...
From an evolutionary perspective, the phenomenon of fever exists from the first vertebrates, being present in fish, amphibians, reptiles and mammals. In many situations, increasing body temperature improves survival through some kind of fever therapy.
The growth and virulence of several bacterial species is affected at high temperatures, so fever therapy was, for example, used to treat neurosyphilis before the period of antibiotic introduction. similarly, type III pneumococcus have a particular sensitivity to high temperatures and at 41 degrees Celsius they grow slowly and can autolyse.
On the other hand, the temperature values of the febrile beach seem to increase the phagocytic and bactericidal activity of neutrophils and the cytotoxic effects of lymphocytes, thus probably the fever increases the ability to survive an infection.
However, fever involves numerous costs of the host, in addition to discomfort. For each one degree Celsius increase in body temperature, there is an increase in oxygen consumption by 13% and increased caloric and liquid needs. increased metabolic needs may affect the fetuses during pregnancy (a single episode of fever in the first trimester of pregnancy doubling the risk of neural tube defects in the fetus), as well as patients with borderline damage to cardiac or cerebral circulation.
Accelerating muscle catabolism leads to a decrease in body weight and a negative nitrogen balance. Essentially, skeletal muscle is used as an energy source, with the release of amino acids for gluconeogenesis and for the synthesis of acute phase proteins and the formation of immune cell clones. Fever reduces mental acuity and can cause delirium or stupor. Children are at increased risk of having seizures during fever, especially if there is a history of such seizures.
As expected, many of the symptoms associated with fever, including dorsolumbar pain, generalized myalgia, arthralgia, anorexia and drowsiness, can be reduced by infusions of purified cytokines. These symptoms can be improved by cyclooxygenase inhibitors.
Chills, a feeling of cold that occurs during most febrile states, are part of the central nervous system (CNS) response to the thermoregulation "threshold", which requires more heat. Rigor, a deep, pieloerection ("chicken skin"), associated with tooth clattering and severe tremor, is common in bacterial infections, rickettsii and protozoa infections and influenza (but not in other viral infections).
Septic states, systemic infections such as leptospirosis, brucellosis, rat bite fever, endocarditis, malaria and intermittent septic state observed in abscesses can produce rigor, as well as lymphomas, renal cell carcinoma and hepatoma. Rigor is also common in drug-induced fevers.
Sweating occurs by activating heat loss mechanisms, antipyretic treatment, touching the new "thermal ceiling" or eliminating the feverish stimulus. Intermittent administration of antipyretics may exaggerate temperature swings, causing coldness, discomfort and exhaustion. Hypothalamic reflexes trigger perspiration, allowing rapid dissipation of heat by evaporation.
Changes in mental status and seizures are common in very young and very old patients and patients with dementia, liver failure and chronic kidney failure. Progression from irritability to delirium and frank obnubilation usually disappears with fever failure.
Seizures typically occur in infants and febrile children under 5 years of age, especially at the onset of a febrile disease and at temperatures higher than 40 degrees Celsius. Febrile seizures in children are not necessarily a sign of significant brain disease, but an CNS disease should be excluded in these cases. Fever can also precipitate seizures in adult epileptic patients.
Week
full of achievements, peace, understanding, love and
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Dorin, Merticaru