An antipyretic is a type of medication that will prevent or reduce fever by

lowering body temperature from a raised state. They will not affect normal
body temperature if the patient does not have a fever. Generally, most nonsteroidal anti-inflammatory drugs (NSAIDs) work by inhibiting prostaglandin
synthetase within the hypothalamus. Fever, or pyrexia, occurs when the body
reaches a temperature above what is considered "average"
it is generally accepted fever exists at a temperature above 37 degrees
Celsius (98.6 degrees Fahrenheit) when the thermometer is placed under the
armpit, or over 37.5 degrees Celsius (99.5 degrees Fahrenheit) when measured
orally or rectally.Fever usually results from microbes such as bacteria or viruses
triggering the body's defence mechanisms. This activates certain types of cells,
some of which release the substance interleukin. Prostaglandin is another
chemical released by the body that plays a part in this process. Prostaglandin is
induced by bacterial pyrogens and is produced in the Central Nervous System
(CNS). Interleukin affects the hypothalamus, which is the part of the brain that
regulates body temperature, signalling it to raise the temperature by a few
degrees. The hypothalamus works like a thermostat while the interleukin that is
released serves to raise its preset temperature.The body has a number of
techniques that it uses to achieve this change in temperature. Shivering
involves physical movement that produces heat. Vasoconstriction, which entails
the constriction of blood flow beneath the skin, reduces the amount of heat lost
from the body. It also causes one to feel cold in their extremities, such as the
hands and feet, prompting them to be covered up.How is this increase in
temperature part of the body's defence mechanism? The body raises the
temperature in an effort to create an inhospitable environment for the microbes
that cause the infection. Fever is a symptom of illness is part of the body's
attempts to rid itself of the infection and inhibit its spread. Once the infection
has been dealt with, the fever is said to have "broken" and the patient feels
overheated, breaking out in a sweat as the body tries to cool down to its normal
temperature. Vasodilatation of peripheral blood vessels also occurs at this
stage, increasing the blood flow once again.Antipyretics work by getting the
"thermostat" in the hypothalamus to override the interleukin-induced increase
in temperature. The body will then work to lower the temperature to the new,
lower temperature and the result is a reduction in the fever. Antipyretics will
also reduce prostaglandin synthesis in the hypothalamus by inhibiting the
effect of endogenous or microbial pyrogens on the heat regulating sensors of
the hypothalamus. By blocking prostaglandin synthetase, antipyretics prevent a
rise in prostaglandin levels in the brain.
Fever is a complex physiologic response triggered by infectious or aseptic stimuli. Elevations in body
temperature occur when concentrations of prostaglandin E(2) (PGE(2)) increase within certain areas of the
brain. These elevations alter the firing rate of neurons that control thermoregulation in the hypothalamus.
Although fever benefits the nonspecific immune response to invading microorganisms, it is also viewed as

a source of discomfort and is commonly suppressed with antipyretic medication. Antipyretics such as
aspirin have been widely used since the late 19th century, but the mechanisms by which they relieve fever
have only been characterized in the last few decades. It is now clear that most antipyretics work by
inhibiting the enzyme cyclooxygenase and reducing the levels of PGE(2) within the hypothalamus.
Recently, other mechanisms of action for antipyretic drugs have been suggested, including their ability to
reduce proinflammatory mediators, enhance anti-inflammatory signals at sites of injury, or boost antipyretic
messages within the brain. Although the complex biologic actions of antipyretic agents are better
understood, the indications for their clinical use are less clear. They may not be indicated for all febrile
conditions because some paradoxically contribute to patient discomfort, interfere with accurately assessing
patients receiving antimicrobials, or predispose patients to adverse effects from other medications. The
development of more selective fever-relieving agents and their prudent use with attention to possible
untoward consequences are important to the future quality of clinical medicine.

Aspirin is a white crystalline powder with a melting point of 135C.

The common chemical name for aspirin is acetylsalicylic acid. Its systematic
name is 2-(acetyloxy)benzoic acid.The chemical formula of aspirin is C 9H8O4 and
the atoms are arranged according to the following diagram.
Structural formula of aspirin

Structural diagram of aspirin

An expanded structural diagram of aspirin

Aspirin is commonly used as a medicinal drug to relieve headaches, minor

pains and fevers. It also helps prevents blooding clotting but it higher doses
may cause ulcers in stomach and the gastrointestinal tract.
Paracetamolis4acetamidophenolandmayberepresentedbythefollowingformula:

Insomepublications,itisdescribedas4hydroxyacetanilideorNacetylpaminophenolandinthe
USPharmacopoeiaitisknownasacetaminophen.
Paracetamolisawhite,odourlesscrystallinepowderwithabittertaste,solublein70partsofwater
(1in20boilingwater),7partsofalcohol(95%),13partsofacetone,40partsofglycerol,9partsof
propyleneglycol,50partsofchloroform,or10partsofmethylalcohol.Itisalsosolublein
solutionsofalkalihydroxides.Itisinsolubleinbenzeneandether.Asaturatedaqueoussolutionhas
apHofabout6andisstable(halflifeover20years)butstabilitydecreasesinacidoralkaline
conditions,theparacetamolbeingslowlybrokendownintoaceticacidandpaminophenol.
Mixturesofparacetamolandaspirinarestableindryconditions,buttabletscontainingthesetwo
ingredients,particularlyinthepresenceofmoisture,magnesiumstearate,orcodeine,producesome
diacetylpaminophenolwhenstoredatroomtemperature,andthislattercompoundishydrolyzed
inthepresenceofmoisturetoparacetamolandpaminophenol.Paracetamolis4acetamidophenol
andmayberepresentedbythefollowingformula:

Insomepublications,itisdescribedas4hydroxyacetanilideorNacetylpaminophenolandinthe
USPharmacopoeiaitisknownasacetaminophen.
Paracetamolisawhite,odourlesscrystallinepowderwithabittertaste,solublein70partsofwater
(1in20boilingwater),7partsofalcohol(95%),13partsofacetone,40partsofglycerol,9partsof
propyleneglycol,50partsofchloroform,or10partsofmethylalcohol.Itisalsosolublein
solutionsofalkalihydroxides.Itisinsolubleinbenzeneandether.Asaturatedaqueoussolutionhas
apHofabout6andisstable(halflifeover20years)butstabilitydecreasesinacidoralkaline

conditions,theparacetamolbeingslowlybrokendownintoaceticacidandpaminophenol.
Mixturesofparacetamolandaspirinarestableindryconditions,buttabletscontainingthesetwo
ingredients,particularlyinthepresenceofmoisture,magnesiumstearate,orcodeine,producesome
diacetylpaminophenolwhenstoredatroomtemperature,andthislattercompoundishydrolyzed
inthepresenceofmoisturetoparacetamolandpaminophenol.

Phenacetin was introduced in 1887, and was used principally as an analgesic; it was one of the first synthetic fever
reducers to go on the market. It is also known historically to be one of the first non-opioid analgesics without antiinflammatory properties.
[edit]

Known mechanism of action

Its analgesic effects are due to its actions on the sensory tracts of the spinal cord. In addition, phenacetin has a
depressant action on the heart, where it acts as a negative inotrope. It is an antipyretic, acting on the brain to decrease
the temperature set point. It is also used to treat rheumatoid arthritis (subacute type) and intercostal neuralgia.
It is metabolised in the body to paracetamol.
[edit]

Preparation
The first synthesis was reported in 1878 by Harmon Northrop Morse.[1]
Phenacetin may be synthesized as an example of the Williamson ether synthesis: ethyl iodide, paracetamol, and
anhydrous potassium carbonate are refluxed in 2-butanone to give the crude product, which is recrystallized from
water.[2]