searchspell:blisterscorrected for fever blisters
Fever (also known as pyrexia, or a febrile response, and archaically known as ague) is a medical symptom that describes an increase in internal body temperature to levels that are above normal (37°C, 98.6°F). Fever should not be confused with hyperthermia, which is an increase in body temperature over the body’s thermoregulatory set-point (normally approximately 37°C, but increased during a fever). A fever is most accurately characterized as a temporary elevation in the body’s thermoregulatory set-point, which is usually by about 1-2°C. This elevation in thermoregulatory set-point means that the previous "normal body temperature" would be considered hypothermic. Effector mechanisms, such as increased blood pressure, increased heart rate, activation of brown adipose tissue, and muscular shivering attempt to counteract the perceived hypothermia, thereby reaching the new thermoregulatory set-point. It is the most common symptom of many diseases. An adaptive mechanism, fever is the body's reaction to pathogens; it attempts to raise core body temperature to levels that will speed up the actions of the immune system, and may also directly denature, debilitate, or kill the pathogen. Most fevers are caused by infections, and almost all infectious diseases can cause fever. When a patient has or is suspected of having a fever, that person's body temperature is measured using a thermometer. If successful in ridding the body of an invasive pathogen, fever is an important protective immune mechanism and should generally not be suppressed. However, there are instances when fever escalates to temperatures where the body is at risk of destroying its own cells and must be brought under control with suppressive medication. 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. By using a reliable thermometer, you can tell if a fever is present if temperature is at or higher than one of the following levels:
MechanismFever is a positive feedback mechanism that acts toward the direction of change (as opposed to negative feedback, which acts opposite to change to maintain homeostasis). Therefore, fever is the opposite of thermoregulation. Substances that induce fever are called pyrogens. Although external pathogens may be the ultimate reason for a fever, it is the internal or endogenous pyrogens that directly cause the increase in the thermoregulatory set-point. 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, interleukin-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 PGE2 synthase (membrane-associated protein involved in eicosanoid and glutathione metabolism, also known as mPEGS-1). These enzymes ultimately mediate the synthesis and release of prostaglandin E2 (PGE2). PGE2 is the ultimate mediator of the febrile response. It 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. Other heat effector mechanisms are mediated by the brain stem/medullary premotor sympathetic activation to the autonomic nervous system, which ultimately leads to the activation of brown adipose tissue. The body can also induce shivering, or raise blood pressure through a mechanism of vasoconstriction. The set-point temperature of the body will remain elevated until PGE2 is no longer present (something that is likely to follow the disappearance of the foreign pathogen). TypesPyrexia can be classed as low-grade (38 to 39 °C, 99.5 to 102.2 °F), moderate (39 to 40 °C, 102.2 to 104 °F), or high-grade (more than 40 °C or 104 °F) depending on how much the body temperature has deviated from normal. Fever may be of benefit and is part of the body's response to a disease; however, if the fever goes above 42 °C (107.6 °F), then it may cause significant tissue damage. This is termed hyperpyrexia. 43.3oC (110oF) is considered the upper limit compatible with life. Temperature normally fluctuates over the day, and the same applies to fever. If this characteristic pattern is lost, the raised body temperature may be due to hyperthermia, a more dangerous disorder. Hyperthermia is commonly caused by overheating or sunstroke, which elevates the body's temperature above the thermoregulatory set-point. TreatmentSome research suggests that artificially suppressing fever may increase the duration of illness, however it can also increase comfort level. Drugs that reduce fever are known as antipyretics. Common antipyretics are acetaminophen, also called paracetamol, and NSAIDs such as ibuprofen. These drugs act on the cyclooxygenase enzyme used to create prostaglandin E2 synthesis. Therefore, they work as prostaglandin synthesis inhibitors, stopping the creation of PGE2. Vasopressin is also a potential antipyretic, which is released from the hypothalamus to the posterior pituitary gland, where it then acts on the body through the bloodstream. A popular household remedy is soaking a cloth in cold water and placing it on the patient's forehead. Sometimes, for various reasons, mild fevers are intentionally induced. Naturopath Paavo Airola claimed that, because cancer cells are known to die at lower temperatures than normal body cells, they can sometimes be fought with fevers. [3] However, Quackwatch has questioned Airola's scientific credentials.[4] ReferencesPrimary Sources
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