د "تبه" د بڼو تر مېنځ توپير

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۱۶ کرښه:
[[انځور:Clinical thermometer 38.7.JPG|thumb|کيڼ|An analogue medical thermometer showing the temperature of 38.7 °C]]
 
'''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.
 
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.
 
== مېچنه ==
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:
* [[rectum|rectal]] temperature (in the anus) is at, or higher than 38 degrees [[Celsius]] (100.4 degrees [[Fahrenheit]])
۲۶ کرښه:
* axillar temperature (in the [[armpit]]) is at, or higher than 37.2 degrees Celsius (99 degrees Fahrenheit)
 
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]] [[thermometer]]s measure radiant heat energy from the tympanic membrane (=infrared). These may be very convenient, but may also show more variability.
۳۴ کرښه:
In conclusion, temperature is ideally always measured the same moment of the day, in the same way, after the same amount of activity.
 
== مېکانيزم ==
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]].
 
[[Imageدوتنه: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.]]
 
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)|organorgans]]s of the [[brain]], where the [[blood-brain barrier]] is reduced. The cytokine factors bind with [[endothelium|endothelial receptorreceptors]]s 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.
 
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
۴۸ کرښه:
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.
 
== د تبې ډولونه ==
Pyrexia can be classed as
* low-grade: 38 - 39 &nbsp;°C (100.4 - 102.2 &nbsp;°F)
* moderate: 39 - 40 &nbsp;°C (102.2 - 104 &nbsp;°F)
* high-grade: > 40 &nbsp;°C (> 104 &nbsp;°F)
* [[Hyperpyrexia]]: > 42 &nbsp;°C (> 107.6 &nbsp;°F)
The last is clearly a medical emergency because it approaches the upper limit compatible with human life.
 
۶۳ کرښه:
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.
 
== د تبې لاملونه ==
Fever is a common [[symptom]] of many medical conditions:
* [[infectious disease]], e.g. [[common cold]], [[HIV]], [[malaria]], [[infectious mononucleosis]], [[gastroenteritis]], ''etc.''.
۶۹ کرښه:
* Tissue destruction, which can occur in [[hemolysis]], [[surgery]], [[infarction]], [[crush syndrome]], [[rhabdomyolysis]], [[cerebral hemorrhage]], ''etc.''.
* [[Drug fever]]
** directly caused by the drug (e.g. [[progesterone]], [[chemotherapeutics]] causing [[tumor]] [[necrosis]])
** as an adverse reaction to drugs (e.g. [[antibiotic]]s, [[Sulfonamide (medicine)|sulfa drugdrugs]]s, ''etc.'')
** after drug discontinuation, like with [[heroin]] withdrawal
* [[Cancer]]s such as [[Hodgkin disease]] (with [[Pel-Ebstein fever]])
۷۸ کرښه:
Persistent fever which cannot be explained after repeated routine clinical inquiries, is called [[fever of unknown origin]].
 
== آيا تبه ګټوره ده؟ ==
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.
 
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.
 
== درملنه ==
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.
 
۹۲ کرښه:
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.
 
== سرچينې ==
=== ليکنې ===
<references/>
=== کتابونه ===
* 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
* 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.
 
== باندنۍ تړنې ==
* [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
* [http://kidshealth.org/parent/general/body/fever.html Fever and Taking Your Child's Temperature]
۱۰۶ کرښه:
 
[[وېشنيزه:Symptoms]]
[[Categoryوېشنيزه:روغتيا]]
 
[[ar:حمى]]
۱۲۵ کرښه:
[[fi:Kuume]]
[[fr:Fièvre]]
[[gl:Febre]]
[[he:חום (תסמין)]]
[[hi:ज्वर]]
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