Part – 1
Pain associated with peripheral nephropathy directly influences the peripheral nervous system. Peripheral neuralgia might arise because of trauma, toxicity, inflammation, infection, metabolic complications or hereditary causes (Marchettini, et al., 2006). The peripheral neuropathic pain appears with elevated intensity and requires immediate medical intervention. Peripheral neuralgia exacerbates by intraneural microstimulation that considerably disrupts the sensation of small and large fibres, thereby leading to the feeling of tingling, numbness, cramping and burning (Marchettini, et al., 2006). Neuropathic pain usually varies with the type of stimulus and might also exhibit episodic paroxysm. Peripheral neuralgia might result from the triggering by nerve lesions that molecular alterations in the nociceptive neurons (Baron, 2009). The hypersensitivity of these neurons leads to the spontaneous activity of sodium channels and TRPM8/TRPV1 receptors (Baron, 2009). This resultantly, leads to the development of shooting pain that appears in the form of cold and heat hyperalgesia. The pathology in the nociceptive A-fibers leads to the development of paresthesia and associated clinical manifestations (Baron, 2009). The defects in nociceptors lead to the pattern of hyperexcitability of the neurons of brain and spinal cord. Peripheral neuralgia might also result from the sustained defects in the mitochondrial function and structure. The pattern of peripheral neuropathy is manifested by the elevation in vacuolated mitochondria in the myelinated axons and C-fibers in the peripheral nerves (Park, 2014). Resultantly, intracellular calcium is dysregulated because of mitochondrial abnormality that leads to the development of peripheral neuropathic pain. The pattern of peripheral neuropathic pain might also originate under the influence of hyperglycemia in the diabetic patients (Juster-Switlyk & Smith, 2016). The hyperglycemia episode causes microvascular and axonal trauma, polyol activation, oxidative stress, toxic adiposity, induction of inflammatory markers and accumulation of the products of advanced glycation (Juster-Switlyk & Smith, 2016). This eventually leads to the gradual damage of nerve fibers, hypertrophy of endothelial cells and thickening of the endoneurial basement membrane. Patients experience the pattern of severe allodynia, hyperalgesia and burning sensation in the peripheral region. The disassociation of the sensory nerves results in the development of burning and stabbing pain. However, motor nerves damage leads to the development of myalgia and abnormal gait (Medical_Marijuana_INC, 2015).
Neuralgia remains localized in the lower back region and impacts the individuals for a duration of three months (Allegri, et al., 2016). The psychological attributes including anxiety, depression and stress considerably influence the onset and establishment of peripheral neuralgia and low back pain. Low back pain originates from the intervertebral discs, joints, bones, fascial structures, muscles and nerve roots (Allegri, et al., 2016). Diseases like lumbar disc degeneration or herniation leads to the central sensitization that eventually excites the neurons of the central nervous system. The patients experience the pattern of tactile allodynia and pain does not remain confined to the region of tissue damage (Allegri, et al., 2016). The chronification of low back pain primarily results from the process of central sensitization that produces long term inflammation in the muscles, ligaments and joints of individuals. The delta fibres associated with the muscles, discs, bones, ligaments and joints prove to the source of chronic pain following their consistent stimulation by the external factors (Allegri, et al., 2016). The existence of diseases like fibromyalgia, cancer and arthritis also exacerbates the pattern of neuralgia and associated low back pain (Kasper, et al., 2015). Secondary perpetuating factors after the resolution of a disease continue to cause chronic pain. These factors include the painful reflex muscle contraction, sympathetic efferent activity and traumatized sensory nerves. The sleep pattern, appetite, mood and daily activity of the patients considerably influence the pattern of their chronic pain (Kasper, et al., 2015,). The assessment of organic as well as emotional factors is of paramount importance while assessing the pattern of chronic neuralgia. The sustained disruption of the inhibitory pain pathways as well as neurotransmitters result in defective neuro-chemical execution of sensory signals in the central nervous system (Jahan, et al., 2012). This eventually reduces the pain threshold, thereby leading to the enlargement of sensory signals that continuously transmit pain sensations in the treated patients. Any associated gastrointestinal disturbance might also aggravate the pattern of patient’s chronic neuralgia at the lower back. In the majority of cases of chronic lower back neuralgia, the causative factors attribute to the non-pathological functional abnormalities and associated clinical manifestations (Casser, et al., 2016). For example, the conditions like hypermobility, incoordination, localized swelling, muscle dysfunction, hyperlordosis, SI joint syndrome and segmental dysfunction lead to the establishment of chronic lower back neuralgia (Casser, et al., 2016).
Part – 2
The most rational approach for treating the pain arising from the pattern of diabetic peripheral neuropathy attributes to the effective controlling of hyperglycemia episode (Javed, et al., 2015). The control of glucose with the administration of insulin or other antidiabetic medications assists in the secondary prevention of peripheral diabetic neuropathy and associated neuralgia. Evidence-based research literature advocates the requirement of administering tricyclic antidepressants for effectively treating the pattern of neuropathic pain (Dworkin, et al., 2010). Indeed, the administration of anti-depressant therapy is a two-way tool for controlling the intensity and establishment of neuropathic pain. The pain mechanism influenced by the co-morbid state of depression is controlled by the administration of antidepressants (Dworkin, et al., 2010). Furthermore, the analgesic effect of these drugs helps in reducing the frequency and severity of neuropathic pain. The administration of Pregabalin and Gabapentin is recommended for controlling the establishment of peripheral neuropathic pain because of their sedation property (Dworkin, et al., 2010). These drugs require administration in a dose dependent manner for effectively inducing dizziness in the treated patients. The patients exhibit elevated tolerability for these drugs following their initial administration. The administration of tramadol in cases of peripheral neuropathy results in the sustained inhibition of reuptake of norepinephrine and serotonin (Dworkin, et al., 2010). The pattern of neuropathic pain arising from small fiber neuropathy requires the systematic administration of topical interventions, opioids and anticonvulsants in accordance with their safety profile and tolerability in the treated patients (Hovaguimian & Gibbons, 2011). The drugs with anticonvulsant properties influence the voltage-gated α2δ calcium channels for reducing the accumulation of calcitonin gene–related peptide, substance P and glutamate. The tolerability of these drugs in the treated patients makes them as the treatment of choice for controlling the pattern of peripheral neuropathic pain. Nursing approaches warranted for controlling the state of peripheral neuropathic pain advocate the requirement of systematic assessment of patient’s psychological state, sociocultural background and harmful effects of neuropathic pain (Karahan, et al., 2014). Accordingly, nurse professionals might utilize psychosocial counselling for remediating the intensity of neuropathic pain experienced by the patients of various age groups. The exercise interventions produce promising results in terms of treating the pattern of peripheral neuropathic pain episodes (Dobson, et al., 2014). They enhance the endothelial function and systematically improve the peripheral vascular supply that reciprocally increases the muscle health and controls the level of blood glucose in the treated patients. Resultantly, patients experience gradual improvement in the pattern of their peripheral pain.
Exercise interventions warranted for treating the for treating the pattern of chronic low back pain advocate the requirement of normalizing the duration, intensity and frequency of body movements for restoring physiological functions of the painful body parts (Dreisinger, 2014). The spinal strengthening interventions assist in restoration of resistance in the lumbar extensor muscles that eventually reduces the intensity of chronic low back pain (Dreisinger, 2014). The elevation in muscle resistance reciprocally improves the vascular supply of the diseased muscles that sequentially reduce the propagation of painful signals in the treated patients. The administration of topical herbal drug like Capsaicin desensitises the region of pain through localized analgesia (Hebert, et al., 2014). Similarly, the administration of coxibs and NSAIDs assists in reducing the pattern of inflammation and associated chronic pain in the lower back region. However, the concomitant administration of proton pump inhibitors is required for reducing the establishment of gastrointestinal toxicity following the systematic administration of NSAIDs to the individuals experiencing chronic low back pain (Kuritzky & Samraj, 2012). Topical NSAIDs require transdermal administration in the form of patch and gel for producing localized anti-inflammatory effect on the target location (Kuritzky & Samraj, 2012). However, the administration of NSAID intervention is a short-term approach warranting administration for acquiring temporary relief from the pattern of intense chronic pain. Eventually, blend of psychosocial and pharmacotherapeutic interventions is recommended for effectively controlling the pattern of chronic low back pain. The treatment of chronic pain conditions requires the thorough evaluation of history and physical of the patient (Kasper, et al., 2015, p. 93). The physician might opt to administer the antidepressant drugs like desipramine and nortriptyline for the effective reduction in pain manifestation. Chronic opioid therapy requires administration in the context of reducing the chronic pain of the patients receiving treatment for their malignant states. Elevated peak plasma levels of these drugs lead to the development of analgesia in the treated patients.
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