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'''تبه''' (ته په طبي اصطلاح '''pyrexia'''، يا '''febrile ځواب''' وايي، دا ويي د لاطيني لغت [[febris]] نه چې په مانه د تبې ده راوتلی، په لرغوني پېر کې د '''ague''' يا آګو په نامه پېژندل کېده) يوه عامه طبي نښه ده چې د بدن داخلي تودوخه څرګندوي |
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{{SignSymptom infobox | |
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Name = Fever | |
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ICD10 = {{ICD10|R|50||r|50}} | |
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ICD9 = {{ICD9|780.6}} | |
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ICDO = | |
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Image = | |
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Caption = | |
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OMIM = | |
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MedlinePlus = | |
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eMedicineSubj = med | |
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eMedicineTopic = 785 | |
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DiseasesDB = 18924 |}} |
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'''تبه''' (ته په طبي اصطلاح '''pyrexia'''، يا '''febrile ځواب''' وايي، دا ويي د لاطيني لغت [[febris]] نه چې په مانه د تبې ده راوتلی، په لرغوني پېر کې د '''ague''' يا آګو په نامه پېژندل کېده) يوه عامه طبي نښه ده چې د بدن داخلي تودوخه څرګندوي a frequent [[medicine|medical]] [[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). In hospitals fever is daily recorded with fever charts. |
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The elevation in thermoregulatory set-point means that the previous "normal body temperature" is considered [[hypothermia|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. |
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== مېچنه == |
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When a patient has or is suspected of having a fever, that person's body temperature is measured using a [[medical thermometer|thermometer]]. At a first glance, fever is present if: |
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* [[rectum|rectal]] temperature (in the anus) is at, or higher than 38 degrees [[Celsius]] (100.4 degrees [[Fahrenheit]]) |
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* oral temperature (in the mouth) is at, or higher than 37.5 degrees Celsius (99.5 degrees Fahrenheit) |
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* axillar temperature (in the [[armpit]]) is at, or higher than 37.2 degrees Celsius (99 degrees Fahrenheit) |
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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. |
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There are different locations where you can measure temperature, and these differ in temperature variability. [[Tympanic membrane]] [[thermometer]]s measure radiant heat energy from the tympanic membrane (=infrared). These may be very convenient, but may also show more variability. |
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Children develop higher temperatures with activities like playing, but this is not fever because their set-point is normal. Elderly patients may have a decreased ability to generate body heat during a fever, so even a low-grade fever can have serious underlying causes in [[geriatrics]]. |
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In conclusion, temperature is ideally always measured the same moment of the day, in the same way, after the same amount of activity. |
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== مېکانيزم == |
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Temperature is regulated in the hypothalamus. Substances <!--"which" incorrect: NOT ALL substances induce fever; a distinction is to be made-->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]]. |
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[[دوتنه:fever-conceptual.svg|thumb|right|400px|'''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.<br />'''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.<br />'''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.]] |
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One model for the mechanism of fever is the detection of [[lipopolysaccharide]] (LPS), which is a cell wall component of [[Gram-negative|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 [[organ (anatomy)|organs]] of the [[brain]], where the [[blood-brain barrier]] is reduced. The cytokine factors bind with [[endothelium|endothelial receptors]] on vessel walls, or interact with local [[microglial cell]]s. When these cytokine factors bind, they activate the [[arachidonic acid]] pathway. This pathway (as it relates to fever), is mediated by the [[enzyme]]s [[phospholipase|phospholipase A2]] (PLA2), [[cyclooxygenase|cyclooxygenase-2]] (COX-2), and [[Prostaglandin|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. |
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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]]. |
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The brain ultimately orchestrates '''heat effector mechanisms'''. These may be |
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* increased heat production by increased [[muscle tone]], [[shivering]] and hormones like epinephrine and [[thyroid hormone]]s, or, |
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* prevention of heat loss, such as [[vasoconstriction]]. |
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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. |
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== د تبې ډولونه == |
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Pyrexia can be classed as |
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* low-grade: 38 - 39 °C (100.4 - 102.2 °F) |
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* moderate: 39 - 40 °C (102.2 - 104 °F) |
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* high-grade: > 40 °C (> 104 °F) |
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* [[Hyperpyrexia]]: > 42 °C (> 107.6 °F) |
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The last is clearly a medical emergency because it approaches the upper limit compatible with human life. |
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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]]: |
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* Pel-Ebstein fever is a specific kind of fever associated with [[Hodgkin's lymphoma|Hodgkin disease]], being high for one week and low for the next week and so on. However, there is some debate ([http://content.nejm.org/cgi/content/short/333/1/66]) whether this pattern truly exists. |
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* [[Typhoid fever]] may show a specific fever pattern, with a slow stepwise increase and a high plateau. |
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* 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. |
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Febricula<ref name=biologyonline>Febricula, definition from [http://www.biology-online.org/ Biology-Online.org], consulted June 7, 2006 [http://www.biology-online.org/dictionary/Febricula http://www.biology-online.org/dictionary/Febricula]</ref> is a mild fever of short duration, of indefinite origin, and without any distinctive pathology. |
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== د تبې لاملونه == |
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Fever is a common [[symptom]] of many medical conditions: |
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* [[infectious disease]], e.g. [[common cold]], [[HIV]], [[malaria]], [[infectious mononucleosis]], [[gastroenteritis]], ''etc.''. |
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* [[Immunology|Immunological]] diseases like [[lupus erythematosus]], [[sarcoidosis]], [[inflammatory bowel disease]]s, ''etc.''. |
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* Tissue destruction, which can occur in [[hemolysis]], [[surgery]], [[infarction]], [[crush syndrome]], [[rhabdomyolysis]], [[cerebral hemorrhage]], ''etc.''. |
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* [[Drug fever]] |
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** directly caused by the drug (e.g. [[progesterone]], [[chemotherapeutics]] causing [[tumor]] [[necrosis]]) |
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** as an adverse reaction to drugs (e.g. [[antibiotic]]s, [[Sulfonamide (medicine)|sulfa drugs]], ''etc.'') |
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** after drug discontinuation, like with [[heroin]] withdrawal |
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* [[Cancer]]s such as [[Hodgkin disease]] (with [[Pel-Ebstein fever]]) |
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* [[Metabolic disorder]]s like [[gout]], [[porphyria]], ''etc.''. |
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* Thrombo-embolic processes (i.e. [[pulmonary embolism]], [[deep venous thrombosis]]) |
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Persistent fever which cannot be explained after repeated routine clinical inquiries, is called [[fever of unknown origin]]. |
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== آيا تبه ګټوره ده؟ == |
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There are arguments for and against, and the issue is controversial<ref name=Schaffner>Schaffner A. Fever--useful or noxious symptom that should be treated? ''Ther Umsch'' 2006; '''63''': 185-8. PMID 16613288</ref><ref name=value>Soszynski D. The pathogenesis and the adaptive value of fever. ''Postepy Hig Med Dosw'' 2003; '''57''': 531-54. PMID 14737969</ref>. There are studies using [[warm blooded]] [[vertebrates]]<ref name=VUB>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</ref> and [[human]]s <ref name=humans>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</ref> ''[[in vivo]]'', with some suggesting that they recover more rapidly from infections or critical illness due to fever. |
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Theoretically, fever has been conserved during evolution because of its advantage for host defense<ref name=Schaffner>Schaffner A. Fever--useful or noxious symptom that should be treated? ''Ther Umsch'' 2006; '''63''': 185-8. PMID 16613288</ref>. There are certainly some important immunological reactions that are sped up by temperature, and some [[pathogen]]s with strict temperature preferences could be hindered<ref name=Fischler>Fischler MP, Reinhart WH. Fever: friend or enemy? ''Schweiz Med Wochenschr'' 1997; '''127''': 864-70. PMID 9289813</ref>. The overall conclusion seems to be that both aggressive treatment of fever<ref name=humans>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</ref> and too little fever control<ref name=Schaffner>Schaffner A. Fever--useful or noxious symptom that should be treated? ''Ther Umsch'' 2006; '''63''': 185-8. PMID 16613288</ref> can be detrimental. This depends on the clinical situation, so careful assessment is needed. |
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== درملنه == |
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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. |
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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]]. |
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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. |
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Treatment of fever should primarily be based on lowering the setpoint, but facilitating heat loss may contribute. The former is accomplished with [[antipyretic]]s. 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. |
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== سرچينې == |
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=== ليکنې === |
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<references/> |
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=== کتابونه === |
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* Rhoades, R and Pflanzer, R. Human physiology, third edition, chapter 27 ''Regulation of body temperature'', p. 820 ''Clinical focus: pathogenesis of fever''. ISBN 0-03-005159-2 |
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* Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL. ''[[Harrison's Principles of Internal Medicine]]''. New York: McGraw-Hill, 2005. ISBN 0-07-139140-1. |
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== باندنۍ تړنې == |
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* [http://www.seattlechildrens.org/child_health_safety/health_advice/fever.asp What to do if your child has a fever] from Seattle Children's Hospital |
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* [http://kidshealth.org/parent/general/body/fever.html Fever and Taking Your Child's Temperature] |
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* [http://www.nlm.nih.gov/medlineplus/ency/article/003090.htm US National Institute of Health factsheet] |
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* [http://hcd2.bupa.co.uk/fact_sheets/html/fever.html BUPA factsheet] |
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[[وېشنيزه:Symptoms]] |
[[وېشنيزه:Symptoms]] |
د ۲۳:۳۳, ۷ نومبر ۲۰۱۰ بڼه
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تبه (ته په طبي اصطلاح pyrexia، يا febrile ځواب وايي، دا ويي د لاطيني لغت febris نه چې په مانه د تبې ده راوتلی، په لرغوني پېر کې د ague يا آګو په نامه پېژندل کېده) يوه عامه طبي نښه ده چې د بدن داخلي تودوخه څرګندوي