Pain and Painkillers

The perception of pain and the emotions that control intensity differ in individuals. Since feeling pain is somewhat adaptive, when one experiences it, he or she becomes aware of an injury and tries to remove oneself from the source that caused the injury. For this reason, pain is considered neuropathic or inflammatory in nature. Thus, when pain is the outcome from the damage caused to the neurons of the peripheral and central nervous system, then that pain is neuropathic. However, if the pain signals any kind of tissue damage, then the pain is inflammatory in nature. Due to various types of pain, the interpretation of pain by neurons and the source of that pain

Pain not only involves the physical reaction to damaged tissue, but also involves an emotional and cognitive response by the person experiencing the pain (Backer, 1994). A person's prior experience will influence how pain is managed. Pain is a signal that something is not

The reason that this drug can be so intense and dangerous is because it falls into the category II narcotics. Many commonly known narcotics include opium, morphine, and heroin. The addiction rate of any of these drugs is phenomenal. Narcotics are central nervous system depressants that relieve pain without causing the loss of consciousness. They can also produce feelings drowsiness, mental confusion and euphoria. The analgesic effects of narcotics result from the drugs’ effects on the emotional aspects of pain. Many patients that experience intense pain say that after the administration of the narcotic, their pain is as intense as ever but no longer as bothersome. Because narcotics block the emotional side effects of pain they make it much more bearable.

The opioid epidemic in America continues to grow at an alarming rate with no end in sight. All narcotics are derived from the opium poppy plant and then manufactured into different forms of drugs such as morphine, heroin, and other pharmaceutical and synthetic opioid drugs sold on the market for pain. Opium derived drugs block and suppress pain by binding to and stimulating the natural receptor sites for endorphins found in the central nervous system of a user’s brain. Patients who are prescribed narcotic drugs can quickly become addicted to the drugs because their body’s will stop producing endorphins and instead

The binding could only occur in the receptors active site if the size, shape and charge of the morphine’s meet the requirement of the receptor. Once the match is identified, the following binding process would take place. The flat benzene ring in morphine would fit securely in the flat surface of the receptor’s active site to allow the rest of the molecule to fall in place easily. The adjacent carbon atoms would fit into a nearby groove, while the nitrogen atom would attach to the negatively charged group receptor, hence joining the two together. After the binding occurred, the morphine would be able to block the sending of the painful information from the pre-synaptic neuron on the nociceptor. This is because, it caused a reactionary changed in the cell which blocks its ability to produces the substance that causes the feeling of pain during and/or after an operation and injury.

The media portrays opioid abuse as a new dilemma, but it actually extends as far back as 1898 when Bayer Co. produced heroin, a drug made from opium, and commercialized it to be a “wonder drug” for those in need of pain relief (Moghe 2016). Today, heroin is known to be a dangerous, illegal, and addictive drug. Before doctors

“Amid Opioid Crisis, Insurers Restrict Pricey, Less Addictive Painkillers” by Katie Thomas & Charles Ornstein

noniceptors to reduce inflammation. They also have some effect on the nervous system to act on

“The total toll from prescription opioid overdoses exceeds 175,000, three times the U.S. body count in the Vietnam war” (“Pain Medications are Killing…” 1). In 2013, half as many people died in a traffic accident than overdosed, and 2,000 less had been murdered (“Pain Medications are Killing…” 1). Opioid prescription has contributed to a rise in heroin abuse and deaths, because opioid patients turn to find new and stronger drugs and seek a street equivalent chemical that is easy to find and cheap to use (“Pain Medications are Killing…” 2). It has also lead to a rise in other drugs, and today there is the highest prescription and drug abuse rates ever. Not only is it causing deaths, but it is causing debt in America. To address the scale of

Opioids, which includes drugs such as morphine and codeine, bind to opioid receptors and help to relieve pain through the activation of K+ ATP channels. While these analgesic effects of opioids have been studied for decades, the rise of opioid tolerance and addiction creates a very interesting question: How did opioid tolerance and addiction evolve, and what are the ancestral reasons for these traits? To first understand this question, the evolutionary history of opioid receptors needs to be examined. Looking at the evolutionary history of the four opioid receptors seen today in Homo sapiens will help to understand how the functions of each receptor evolved. Secondly, following the evolution of the pathways involved with opioid receptor signaling and comparing that to other pathways would be helpful to understand if there are opioid-like receptor pathways in species besides vertebrates. Finally, looking at the evolution of the pathways involved with physical and social pain will be crucial to understanding why humans are vulnerable to addiction. Examining the effects of social interactions

A nerve cell has a negative charge at a resting state due to negatively charged proteins within the cell.[3] Although the inside of the cell contains positively charged potassium ions as well, overall the charge is still negative. Along with potassium on the inside of the cell, positively charged sodium ions are located around the exterior of the cell.[3] When an action potential occurs, the cell becomes even more negatively charged. In turn, this causes sodium transport molecules in the membrane of the cell to open.[3] Sodium will then enter the cell during active transport. The positively charged sodium will cancel out the negatively charged active potential which will depolarize the cell. This allows neurotransmitters to transfer from cell to cell.[3] These neurotransmitters are what allows the body to feel pain. Local anesthetics work by diffusing through nerve fibers. Once they’ve reached the cells, they block the sodium transport molecules in the cell.[2] Therefore neurotransmitters cannot transfer information from cell to cell and the feeling of

Nociception is the sensation of pain which is normally a warning signal to brain in respond to a potential hazard. Generally noxious stimulations are detected by specialised high-threshold sensory neurons, which are refer to nociceptors. The signals are then transferred to an electrical potential and conducted to the brain via spinal cord. However sometimes abnormal nociception can lead to a moderate to severe pain although a noxious stimulus is missing. This kind of pain are usually trigger by nerve injury, while the pain sensation remains after the tissue had been healed. Although the prevalence of neuropathic pain is not significant, about 7% to 8% of the European population is affected, and about 5% are suffering severe pain (Torrance et al., 2006; Bouhassira et al., 2008). Normally the neuropathic pain is induced by injury of somatosensory nerves, and the pain remains after the tissue being healed. It can bring abnormal nociception while noxious stimuli are missing, which called dysesthesia. Beside, pain can be triggered by non-painful stimuli, which is called allodynia). Many research has linked the neuropathic pain to neuronal damages where endogenous ATP being released. Therefore purinergic receptors that can respond to ATP are involved. In this essay, after a brief introduction of P2X receptors, the role of microglial P2X4 and P2X7 in neuropathic pain will be discussed.

The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (1979). Pain is actually the culprit behind warranting a visit to a physician office for many people (Besson, 1999). Notoriously unpleasant, pain could also pose a threat as both a psychological and economic burden (Phillips, 2006). Sometimes pain does happen without any damage of tissue or any likely diseased state. The reasons for such pain are poorly understood and the term used to describe such type of pain is “psychogenic pain”. Also, the loss of productivity and daily activity due to pain is also significant. Pain engulfs a trillion dollars of GDP for lost work time and disability payments (Melnikova, 2010). Untreated pain not only impacts a person suffering from pain but also impacts their whole family. A person’s quality of life is negatively impacted by pain and it diminishes their ability to concentrate, work, exercise, socialize, perform daily routines, and sleep. All of these negative impacts ultimately lead to much more severe behavioral effects such as depression, aggression, mood alterations, isolation, and loss of self-esteem, which pose a great threat to human society.

4.) Acetaminophen-Oxycodone (Trade Name: Percocet 5/325) 1-2 tablets by mouth, every four hours; used for decreasing pain as well as decreasing a temperature (Deglin & Vallerand, 2007).

In this discussion, I will be looking at the different forms of pain and how this pain is caused within the body. The number of different types of drugs used to treat pain is forever expanding but I will examine the main types of painkiller, how they were discovered and how they work to relieve the symptoms of pain.