උණ

විකිපීඩියා, නිදහස් විශ්වකෝෂය වෙතින්
වෙත පනින්න: සංචලනය, සොයන්න
For other uses, please see Fever (disambiguation).

සැකිල්ල:SignSymptom infobox

An analogue medical thermometer showing the temperature of 38.7 °C - වෛද්‍ය උෂ්ණත්ව මානය (උණ කටුව) සෙල්සියස් අංශක 38.7 පෙන්වයි.

උණ is a frequent වෛද්‍ය විද්‍යාත්මක symptom that describes an increase in internal body temperature to levels that are above normal (37 °C, 98.6 °F). Fever is most accurately characterized as a temporary elevation in the body’s thermoregulatory set-point, which is usually by about 1-2 °C. Fever differs from hyperthermia, which is an increase in body temperature over the body’s thermoregulatory set-point (due to excessive heat production or insufficient thermoregulation, or both).

The elevation in thermoregulatory set-point means that the previous "normal body temperature" is considered hypothermic, and effector mechanisms kick in. The person who is developing the fever has a cold sensation, and an increase in heart rate, muscle tone and shivering attempt to counteract the perceived hypothermia, thereby reaching the new thermoregulatory set-point.

මැනීම[සංස්කරණය]

රෝගියෙකුට උණ වැළඳී ඇතැයි සැක කල විට එම උෂ්ණත්ව වැඩිවීම වෛද්‍ය උෂ්ණත්ව මානය (උණ කටුව) මගින් පහත පරිදි මැන ගත හැක.

  • ගුද මාර්ගය තුල උෂ්ණත්වය මැණීම - මෙහිදී උෂ්ණත්වය සෙල්සියස් අංශක 38 (ෆැරන්හයිට් අංශක 100.4) ට වඩා වැඩිනම් උණ ඇතැයි සැළෙකේ.
  • මුඛය තුල උෂ්ණත්වය මැණීම - මෙහිදී උෂ්ණත්වය සෙල්සියස් අංශක 37.5 (ෆැරන්හයිට් අංශක 99.5) ට වඩා වැඩිනම් උණ ඇතැයි සැළෙකේ.
  • කිහිල්ලේ උෂ්ණත්වය මැණීම - මෙහිදී උෂ්ණත්වය සෙල්සියස් අංශක 37.2 (ෆැරන්හයිට් අංශක 99) ට වඩා වැඩිනම් උණ ඇතැයි සැළෙකේ.


However, there are many variations in normal body temperature, and this needs to be considered when measuring fever. Body temperature normally fluctuates over the day, with the lowest levels at 4 A.M. and the highest at 6 P.M.. Therefore, an oral temperature of 37.5 °C would strictly be a fever in the morning, but not in the afternoon. Normal body temperature may differ as much as 0.4 °C (0.7 °F) between individuals. In women, temperature differs at various points in the menstrual cycle, and this can be used for family planning (although it is only one of the variables of temperature). Temperature is increased after meals, and psychological factors (like the first day in the hospital) also influence body temperature.

There are different locations where you can measure temperature, and these differ in temperature variability. Tympanic membrane thermometers measure radiant heat energy from the tympanic membrane (=infrared). These may be very convenient, but may also show more variability.

Children develop higher temperatures with activities like playing, but this is not fever because their set-point is normal. Elderly patients may have decreased ability to generate body heat during fever, so even a low-grade fever can have serious underlying causes in geriatrics.

In conclusion, temperature is ideally always measured the same moment of the day, in the same way, after the same amount of activity.

ඇතිවන අයුරු[සංස්කරණය]

Temperature is regulated in the hypothalamus. Substances that induce fever are called pyrogens. These are both external or exogenous, such as the bacterial substance LPS, and internal or endogenous. The endogenous pyrogens (such as interleukin 1) are a part of the innate immune system, produced by phagocytic cells, and cause the increase in the thermoregulatory set-point in the hypothalamus. The endogenous pyrogens may also come directly from tissue necrosis.

ගොනුව:Fever-conceptual.jpg
Hyperthermia: Characterized on the left. Normal body temperature (thermoregulatory set-point) is shown in green, while the hyperthermic temperature is shown in red. As can be seen, hyperthermia can be conceptualized as an increase above the thermoregulatory set-point.
Hypothermia: Characterized in the center: Normal body temperature (thermoregulatory set-point) is shown in green, while the hypothermic temperature is shown in blue. As can be seen, hypothermia can be conceptualized as a decrease below the thermoregulatory set-point.
Fever: Characterized on the right: Normal body temperature (thermoregulatory set-point) is shown in green. It reads “New Normal” because the thermoregulatory set-point has risen. This has caused what was the normal body temperature (in blue) to be considered hypothermic.

One model for the mechanism of fever is the detection of lipopolysaccharide (LPS), which is a cell wall component of gram-negative bacteria. An immunological protein called Lipopolysaccharide-Binding Protein (LBP) binds to LPS. The LBP-LPS complex then binds to the CD14 receptor of a nearby macrophage. This binding results in the synthesis and release of various cytokine factors, such as interleukin 1 (IL-1), interleukin 6 (IL-6), and the tumor necrosis factor-alpha. These cytokine factors are released into general circulation where they migrate to the circumventricular organs of the brain, where the blood-brain barrier is reduced. The cytokine factors bind with endothelial receptors on vessel walls, or interact with local microglial cells. When these cytokine factors bind, they activate the arachidonic acid pathway. This pathway (as it relates to fever), is mediated by the enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), and prostaglandin E2 synthase (membrane-associated protein involved in eicosanoid and glutathione metabolism, also known as mPEGS-1). These enzymes ultimately mediate the synthesis and release of PGE2.

PGE2 is the ultimate mediator of the febrile response. The set-point temperature of the body will remain elevated until PGE2 is no longer present. PGE2 acts near the ventromedial preoptic area (VMPO) of the anterior hypothalamus and the parvocellular portion of the periventricular nucleus (PVH), where the thermal properties of fever emerge. It is presumed that the elevation in thermoregulatory set-point is mediated by the VMPO, whereas the neuroendocrine effects of fever are mediated by the PVH, pituitary gland, and various endocrine organs.

The brain ultimately orchestrates heat effector mechanisms. These may be

The autonomic nervous system may also activate brown adipose tissue to produce heat (=non-exercise associated thermogenesis, also known as non-shivering thermogenesis), but this seems mostly important for babies. Increased heart rate and vasoconstriction contribute to increased blood pressure in fever.

වරගීකරණය[සංස්කරණය]

Pyrexia can be classed as

  • low-grade: 38 - 39 °C (99.5 - 102.2 °F)
  • moderate: 39 - 40 °C (102.2 - 104 °F)
  • high-grade: > 40 °C (> 104 °F)
  • Hyperpyrexia: > 42 °C (> 107.6 °F)

The last is clearly a medical emergency because it approaches the upper limit compatible with human life.

Most of the times, fever types can't be used to find the underlying cause. However, there are specific fever patterns that may occasionally hint the diagnosis:

  • Pel-Ebstein fever is a specific kind of fever associated with Hodgkin disease, being high for one week and low for the next week and so on. However, there is some debate ([1]) whether this pattern truly exists.
  • Typhoid fever may show a specific fever pattern, with a slow stepwise increase and a high plateau.
  • In malaria, there may be a fever with a periodicity of 48 hours (tertian fever) or 72 hours (quartan fever, indicating Plasmodium vivax). These patterns may be less clear in travelers.

Febricula[1] is a mild fever of short duration, of indefinite origin, and without any distinctive pathology.

‍ඇතිවන හේතු[සංස්කරණය]

Fever is a common symptom of many medical conditions:

Persistent fever which cannot be explained after repeated routine clinical inquiries, is called fever of unknown origin.

Is fever useful?[සංස්කරණය]

There are arguments for and against, and the issue is controversial[2][3]. There are studies using warm blooded vertebrates[4] and humans [5] in vivo, with some suggesting that they recover more rapidly from infections or critical illness due to fever.

Theoretically, fever has been conserved during evolution because of its advantage for host defense[2]. There are certainly some important immunological reactions that are sped up by temperature, and some pathogens with strict temperature preferences could be hindered[6]. The overall conclusion seems to be that both aggressive treatment of fever[5] and too little fever control[2] can be detrimental. This depends on the clinical situation, so careful assessment is needed.

ප්‍රතිකාර[සංස්කරණය]

Fever should not necessarily be treated. Fever is an important signal that there's something wrong in the body, and it can be used for follow-up. Fever might help the immune system or hinder specific pathogens, but this is generally considered of little importance. Moreover, not all fevers are of infectious origin.

Even when treatment is not indicated, however, febrile patients are generally advised to keep themselves adequately hydrated, as the dehydration produced by a mild fever can be more dangerous than the fever itself. Water is generally used for this purpose, but there is always a small risk of hyponatremia if the patient drinks too much water. For this reason, some patients drink sports drinks or products designed specifically for this purpose, such as Pedialyte.

Most people take medication against fever because the symptoms cause discomfort. Fever increases heart rate and metabolism, thus potentially putting an additional strain on elderly patients, patients with heart disease, etc. This may even cause delirium. Therefore, potential benefits (if any) must be weighed against risks in these patients. In any case, fever must be brought under control in instances when fever escalates to hyperpyrexia, and tissue damage is imminent.

Treatment of fever should primarily be based on lowering the setpoint, but facilitating heat loss may contribute. The former is accomplished with antipyretics. Heat loss may be an effect of heat conduction, convection, radiation or evaporation (sweating, perspiration). This may be particularly important in babies, where drugs should be avoided. However, when someone would use water that is too cold, this induces vasoconstriction and prevents adequate heat loss.

References[සංස්කරණය]

Articles[සංස්කරණය]

  1. Febricula, definition from Biology-Online.org, consulted June 7, 2006 http://www.biology-online.org/dictionary/Febricula
  2. 2.0 2.1 2.2 Schaffner A. Fever--useful or noxious symptom that should be treated? Ther Umsch 2006; 63: 185-8. PMID 16613288
  3. Soszynski D. The pathogenesis and the adaptive value of fever. Postepy Hig Med Dosw 2003; 57: 531-54. PMID 14737969
  4. Su F, Nguyen ND, Wang Z, Cai Y, Rogiers P, Vincent JL. Fever control in septic shock: beneficial or harmful? Shock 2005; 23: 516-20. PMID 15897803
  5. 5.0 5.1 Schulman CI, Namias N, Doherty J, et al. The effect of antipyretic therapy upon outcomes in critically ill patients: a randomized, prospective study. Surg Infect (Larchmt) 2005; 6:369-75. PMID 16433601
  6. Fischler MP, Reinhart WH. Fever: friend or enemy? Schweiz Med Wochenschr 1997; 127: 864-70. PMID 9289813

Books[සංස්කරණය]

බාහිර යොමු (External links)[සංස්කරණය]

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