Unit I. Classification of medicine text a. Antipyretics
Antipyretics comes from the Greek anti (against), and pyreticus (pertaining to fever). Antipyretics are drugs or herbs that reduce fever. Antipyretics cause the hypothalamus to override an interleukin-induced increase in temperature. The body then works to lower the temperature, resulting in a reduction in fever.
Most antipyretic medications have other purposes. The most common antipyretics are ibuprofen and aspirin, which are used primarily as pain relievers. Non-steroidal anti-inflammatory drugs (NSAIDs) are antipyretic, anti-inflammatory, and pain relievers. There is some debate over the appropriate use of such medications, as fever is part of the body’s immune response to infection.
Non-pharmacological treatment
Bathing or sponging with lukewarm or cool water can effectively reduce body temperature in those with heat illness but not usually in those with fever. The use of alcohol baths is not an appropriate cooling method, because there have been reported adverse events associated with systemic absorption of alcohol.
Medications
Many medications have antipyretic effects and thus are useful for fever but not heat illness, including: 1) NSAIDs such as ibuprofen, naproxen, ketoprofen, and nimesulide; 2) aspirin, and related salicylates like choline salicylate, magnesium salicylate, and sodium salicylate; 3) paracetamol; 4) metamizole, banned in over 30 countries for causing agranulocytosis; 5) nabumetone; 6) phenazone, also known as antipyrine, available in combination with benzocaine; and 7) quinine.
Plants
Traditional use of higher plants with antipyretic properties is a common worldwide feature of many ethnobotanical cultural systems. In ethnobotany, plants with naturally occurring antipyretic properties are commonly referred to as febrifuges.
Text b. Analgesics
An analgesic is any member of the group of drugs used to achieve analgesia, relief from pain. The word analgesic derives from Greek αν - (without) and άλγος - (pain).
Commonly known as painkillers, analgesic drugs act in various ways on the peripheral and central nervous systems. They are distinct from anesthetics, which reversibly eliminate sensation, and include paracetamol, the non-steroidal anti-inflammatory drugs such as the salicylates, and opioid drugs such as morphine and opium.
Analgesic choice is also determined by the type of pain: for neuropathic pain, traditional analgesics are less effective, and there is often benefit from classes of drugs that are not normally considered analgesics, such as tricyclic antidepressants and anticonvulsants.
Major classes of analgesics
Paracetamol and NSAIDs. The exact mechanism of action of paracetamol or acetaminophen is uncertain but appears to act centrally in the brain rather than peripherally in nerve endings. Aspirin and the other non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenases, leading to a decrease in prostaglandin production. In contrast to paracetamol and the opioids, this not only reduces pain but inflammation as well. Paracetamol has few side effects and is regarded as generally safe, although excess or sustained use can lead to potentially life-threatening liver damage and occasionally kidney damage. While paracetamol is usually taken orally or rectally, an intravenous preparation introduced in 2002 has been shown to improve pain relief and reduce opioid consumption in the perioperative setting. NSAIDs predispose to peptic ulcers, renal failure, allergic reactions, and occasionally hearing loss, and they can increase the risk of hemorrhage by affecting platelet function. The use of aspirin in children under 16 suffering from viral illness has been linked to Reye's syndrome, a rare but severe liver disorder.
COX-2 inhibitors. These drugs have been derived from NSAIDs. The cyclooxygenase enzyme inhibited by NSAIDs was discovered to have at least 2 different versions: COX1 and COX2. Research suggested that most of the adverse effects of NSAIDs were mediated by blocking the COX1 (constitutive) enzyme, with the analgesic effects being mediated by the COX2 (inducible) enzyme. These drugs (such as rofecoxib, celecoxib and etoricoxib) are equally effective analgesics when compared with NSAIDs, but cause less gastrointestinal hemorrhage in particular. After widespread adoption of the COX-2 inhibitors, it was discovered that most of the drugs in this class increased the risk of cardiovascular events by 40% on average. This led to the withdrawal of rofecoxib and valdecoxib, and warnings on others. Etoricoxib seems relatively safe, with the risk of thrombotic events similar to that of non-coxib NSAID diclofenac.