1. Discuss the pathophysiology of fever. Fever is caused by infection. Noninfectious causes are cancer,collagen vascular diseases,granulomatous Diseases etc.

Infectious causes releses pyrogens which produce pyrogenic cytokines, and non infectious causes directly stimulates release of pyrogenic cytokines, which go to vessels supplying hypothalamus(lamina ventricularis), where they produce PGE2 from endothelium of blood vessels,which makes thermostat of hypothalamus in a higher level, which causes fever The body temperature is controlled by the hypothalamus, a section of the brain that acts just like your household thermostat. That is, if the body gets too cold, the thermostat sends out instructions to warm things up, and if it gets too hot, the thermostat tries to cool things down. When the body is faced with an infection, it responds in a number of ways. In addition to making antibodies that kill the offending germs, it sends various white blood cells to the location of the infection, where they act very much like soldiers at a battle. Temperature is ultimately regulated in the hypothalamus. A trigger of the fever, called a pyrogen, causes a release of prostaglandin E2(PGE2). PGE2 then in turn acts on the hypothalamus, which generates a systemic response back to the rest of the body, causing heat-creating effects to match a new temperature level. In many respects, the hypothalamus works like a thermostat. When the set point is raised, the body increases its temperature through both active generation of heat and retaining heat. Vasoconstriction both reduces heat loss through the skin and causes the person to feel cold. If these measures are insufficient to make the blood temperature in the brain match the new setting in the hypothalamus, then shivering begins in order to use muscle movements to produce more heat. When the fever stops, and the hypothalamic setting is set lower; the reverse of these processes (vasodilation, end of shivering and nonshivering heat production) and sweating are used to cool the body to the new, lower setting. This contrasts with hyperthermia, in which the normal setting remains, and the body overheats through undesirable retention of excess heat or over-production of heat. Hyperthermia is usually the result of an excessively hot environment (heat stroke) or an adverse reaction to drugs. Fever can be differentiated from hyperthermia by the circumstances surrounding it and its response to anti-pyretic medications. Pyrogens A pyrogen is a substance that induces fever. These can be either internal (endogenous) or external (exogenous) to the body. The bacterial substance lipopolysaccharide (LPS), present in the cell wall of some bacteria, is an example of an exogenous pyrogen. Pyrogenicity can vary: In extreme examples, some bacterial pyrogens known as superantigens can cause rapid and dangerous fevers. Depyrogenation may be achieved through filtration, distillation, chromatography, or inactivation. Endogenous In essence, all endogenous pyrogens are cytokines, molecules that are a part of the innate immune system. They are produced by phagocytic cells and cause the increase in the thermoregulatory set-point in the hypothalamus. Major endogenous pyrogens are interleukin 1 ( and ), Interleukin 6 (IL-6) and tumor necrosis factor-alpha. Minor endogenous pyrogens include interleukin-8, tumor necrosis factor-, tumor necrosis factor, macrophage inflammatory protein- and macrophage inflammatory protein- as well as interferon, interferon-, and interferon-. These cytokine factors are released into general circulation, where they migrate to the circumventricular organs of the brain due to easier absorption caused by the blood-brain barrier's reduced filtration action there. The cytokine factors then bind with endothelial receptors on vessel walls, or interact with local microglial cells. When these cytokine factors bind, the arachidonic acid pathway is then activated. Exogenous One model for the mechanism of fever caused by exogenous pyrogens includes LPS, which is a cell wall component of gram-negative bacteria. An immunological protein calledlipopolysaccharide-binding protein (LBP) binds to LPS. The LBPLPS complex then binds to the CD14 receptor of a nearby macrophage. This binding results in the synthesis and release of various endogenous cytokine factors, such as interleukin 1 (IL-1), interleukin 6 (IL-6), and the tumor necrosis factor-alpha. In other words, exogenous factors cause release of endogenous factors, which, in turn, activate the arachidonic acid pathway. PGE2 release

PGE2 release comes from the arachidonic acid pathway. This pathway (as it relates to fever), is mediated by the enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), andprostaglandin E2 synthase. 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 on neurons in the preoptic area (POA) through the prostaglandin E receptor 3 (EP3). EP3-expressing neurons in the POA innervate the dorsomedial hypothalamus (DMH), the rostral raphe pallidus nucleus in themedulla oblongata (rRPa), and the paraventricular nucleus (PVN) of the hypothalamus . Fever signals sent to the DMH and rRPa lead to stimulation of the sympathetic output system, which evokes non-shivering thermogenesis to produce body heat and skin vasoconstriction to decrease heat loss from the body surface. It is presumed that the innervation from the POA to the PVN mediates the neuroendocrine effects of fever through the pathway involving pituitary gland and various endocrine organs. Hypothalamus The brain ultimately orchestrates heat effector mechanisms via the autonomic nervous system. These may be:

Increased heat production by increased muscle tone, shivering, and hormones like epinephrine Prevention of heat loss, such as vasoconstriction.

In infants, the autonomic nervous system may also activate brown adipose tissue to produce heat (nonexercise-associated thermogenesis, also known as non-shivering thermogenesis). Increased heart rate and vasoconstriction contribute to increased blood pressure in fever. 2. Give the nursing management for the patient with fever. Fever should not necessarily be treated. Most people recover without specific medical attention. Although it is unpleasant, fever rarely rises to a dangerous level even if untreated. Damage to the brain generally does not occur until temperatures reach 42 C (107.6 F), and it is rare for an untreated fever to exceed 105 F (41 C). Some limited evidence supports sponging or bathing feverish children with tepid water. The use of a fan or air conditioning may somewhat reduce the temperature and increase comfort. If the temperature reaches the extremely high level of hyperpyrexia, aggressive cooling is required. In general, people are advised to keep adequately hydrated. Whether increased fluid intake improves symptoms or shortens respiratory illnesses such as the common cold is not known. 3. Why do patient with fever chill? When you have a fever your internal thermostat is set too high therefore a room temperature, which would feel comfortable if your temperature was normal, gives you a chill if your temperature is raised. The above answer is an oversimplification. When you shiver, it is your body's way of warming itself up. The repetitive oscillations of your muscles give off heat that raises the body's core temperature. When you have a fever, it is because your body is using the heat to kill off the invading organisms. When it needs a little more help getting the core temperature up, it signals the body to begin shivering to raise the temperature even more. 4. Why and how does high fever result to seizures?
Febrile seizures are most common in small children. This is because a child's brain is still in the developmental stages and is much more susceptible to the effects of a high fever than the brain of an adult. When the body's temperature rises beyond a certain point in a short period of time, it can cause a seizure to occur. The pathophysiology that causes these seizures to occur are unknown to the medical community. However, there is some measure of consensus that the condition may be genetically related. Therefore, parents who experienced the condition as children may be more likely to have children who also experience a febrile seizure. There is also strong evidence to suggest that children who have had a sibling experience a fever seizure are 50 percent more likely to experience one themselves. References

http://www.ehow.com/how-does_4916926_why-does-fever-cause-seizures.html#ixzz1iPd6ZgYs http://en.wikipedia.org/wiki/Fever#Management http://wiki.answers.com/Q/Why_do_you_get_chills_when_you_have_a_fever http://nursingcrib.com/nursing-care-plan/nursing-care-plan-fever/ http://en.wikipedia.org/wiki/Febrile_seizure