PAIN

Answer

Pathophysiology of Acute, Chronic, and Referred Pain

Pain can be defined as an unpleasant sensation that occurs in response to processes that have the potential of damaging body tissues such as injuries or diseases. Pain can be classified into acute, chronic, and referred pain.  The purpose of this paper is to identify the pathophysiology of the three common types of pain; acute, chronic, and referred pain. Further, the paper addresses on the impacts of genetics and ethnicity on pathophysiology, diagnosis and prescription of treatment for acute, chronic and referred pain. As the paper suggests, both genetic and ethnicity factors influence pain sensitivity, pain susceptibility, prescription and pain management.

Acute pain, commonly linked to anxiety and sympathetic hyperactivity such as tachycardia and diaphoresis, occurs as a response to tissue damage. (Schug, 2015). Acute pain can be described as a normal response to injury resulting from a normal physiological process in the nociceptive system. Normally, acute pain results from activation of nociceptors in response to an injury or tissue damage.  The nociceptors (delta and C sensory) are free nerve fibers that function as receptors to damaging stimuli known as noxious stimuli (Pozek, 2016). The common causes of acute pain include dental work, surgery, labor, or burns.

Chronic pain occurs as a result of persistent activation of the nociceptors in the verge of ongoing tissue injury or damage. Chronic pain may also result from a dysfunction of the central nervous system, a condition commonly known as neuropathic pain (Flor, 2015). Chronic pain is frequently linked to illness such as cancer, arthritis, or fibromyalgia pain. Chronic pain can impact physical and emotional effects on an individual, which may manifest themselves in the form of muscle pains, appetite changes, depression, anxiety, or re-injury.

Referred pain is pain that is perceived at a site other than where it originated from or the source of the painful stimulus. Referred pain mechanisms are associated with interconnecting of sensory nerves, whereby, the nerve fibers of higher region sensory response like the skin interconnect with lower sensory response nerve fibers like the pancreases. In other words, referred pain is as a result of many principal sensory neurons unite on a single ascending tract (Arendt-Nielsen, 2015). For instance, pain ascending in the visceral receptors may be interpreted to arise from the somatic receptors since they have more common signals and higher sensory response, unlike the visceral (Luz et al., 2015). Referred pain is frequently caused by pain arising from viscera, tumors, spine, sacroiliac joint, or infections. Arendt-Nielsen (2015) affirms that the size of referred pain is associated with the intensity and duration of induced pain. Therefore, while acute pain may range from being mild (within a moment) or severe (weeks or months), chronic pain is more persistent and ordinarily takes longer than six months (Pozek, 2016). Meanwhile, referred pain differs from acute and chronic pain due to its predisposition of occurring in locations other than the source of the painful stimulus.

Recent studies on pain response across ethnicities suggest that regardless of efforts made to advance pain care, the minority ethnic groups are still at risk for inadequate pain control. Multiple research studies have confirmed that pain prevalence is higher among minority groups when compared to the Whites or Caucasians. For instance, when compared to the Caucasian patients, the African American, Asian, and minority ethnic (BAME) groups are reported to receiving fewer analgesics after a surgical procedure (Kvachadze, 2015). Further, studies suggest that sub-optimal diagnosis and treatment is common among the minority groups, which causes under-treatment of pain. The potential barriers associated with under-treatment among minority groups include communication barriers and inadequate pain assessment. Under-treatment of acute pain inclines to chronic pain. Further, ethnic impacts on prescriptions as different races may differ in terms of hepatic metabolism, bioavailability and genetic makeup. For instance, African Americans and Asians do not benefit from codeine prescription due to their lack of an enzyme responsible for metabolizing codeine to morphine (Kvachadze, 2015).

Recent studies suggest that elusive changes in the DNA could partially explain the variants in individual’s sensitivity and reception to pain. Also, multiple studies have suggested that the several genes play a key role in shaping pain sensitivity, pain diagnosis, pain susceptibility and treatment. Additionally, research has also revealed that a mutual connection between certain pain conditions and genetic factors. For instance, chronic fatigue syndrome (CFS) has been linked to two genes, the neuronal tryptophan hydroxylase (TH2) gene and the 5-hydroxytryptamine-transporter (HTT) gene (Schlauch, 2016). While TH2 is involved in the production of serotonin, the HTT functions as a serotonin transporter gene. Hence, studies claim that the tempered concentration of extracellular serotonin due to longer allelic variants is linked to amplified susceptibility for CFS. Further, individuals differ in their genetic ability to metabolize medication which is a vital consideration when prescribing. Schlauch (2016) suggest that individual’s ability to metabolize drugs is categorized into poor metabolizer, normal metabolizer and rapid metabolizer. A poor metabolizer has two abnormal alleles; a normal metabolizer has at least one active allele while a rapid metabolizer portrays at least one highly active allele.

succeeding [] ]